Finals THEORY

Complications from H eart Disease Right-sided heart failure (right ventricular failure) - inability of
the right ventricle to fill or eject sufficient blood into the
Acute decompensated heart failure - acute exacerbation of heart
pulmonary circulation
failure, w/ s/sx of severe respiratory distress & poor systemic
Systolic heart failure - inability of the heart to pump sufficiently
perfusion
because of an alteration in the ability of the heart to contract; term
Anuria - urine output of less than 50 mL/24 h
used to describe a type of heart failure
Ascites - an accumulation of serous fluid in the peritoneal cavity
Cardiac resynchronization therapy (CRT) - a treatment for heart
failure in w/c a device paces both ventricles to synchronize
contractions
Congestive heart failure - a fluid overload condition (congestion)
associated w/ heart failure
Diastolic heart failure - the inability of the heart to pump
sufficiently because of an alteration in the ability of the heart to
fill; term used to describe a type of heart failure
Ejection fraction (EF) - percentage of blood volume in the
ventricles at the end of diastole that is ejected during systole; a
measurement of contractility HEART FAILURE (HF) - is a clinical syndrome resulting from
Heart failure (HF) - a clinical syndrome resulting from structural structural or functional cardiac disorders that impair the ability of
or functional cardiac disorders that impair the ability of a ventricle the ventricles to fill or eject blood
to fill or eject blood - The term heart failure indicates myocardial disease in
Left-sided heart failure (left ventricular failure) - inability of the which impaired contraction of the heart (systolic
left ventricle to fill or eject sufficient blood into the systemic dysfunction) or filling of the heart (diastolic dysfunction)
circulation may cause pulmonary or systemic congestion. Some cases
Oliguria - diminished urine output; less than 0.5 mL/kg/h of HF are reversible, depending on the cause
Orthopnea - shortness of breath when lying flat CHRONIC HEART FAILURE - as w/ coronary heart disease, the
Paroxysmal nocturnal dyspnea (PND) - shortness of breath that incidence of HF increases w/ age. Approx. 6 million people in the
occurs suddenly during sleep US have HF & 550,000 new cases are diagnosed each y.o Although
Pericardiocentesis - procedure that involves aspiration of fluid HF can affect people of all ages, it is most common in people older
from the pericardial sac than 75 y.o
Pericardiotomy - surgically created opening of the pericardium 2 Major types of HF:
Pulmonary edema - abnormal accumulation of fluid in the 1. Systolic Heart Failure - the most common type is an
interstitial spaces and alveoli of the lungs alteration in ventricular contraction, w/c is characterized
Pulseless electrical activity (PEA) - condition in which electrical by a weakened heart muscle
activity is present on an electrocardiogram, but there is not an 2. Diastolic Heart Failure - is a less common type, w/c is
adequate pulse or blood pressure characterized by a stiff & non compliant heart muscle,
Pulsus paradoxus - systolic blood pressure that is more than 10 making it difficult for the ventricle to fill
mm Hg lower during inhalation than during exhalation; difference CLASSIFICATION OF HEART FAILURE
is normally less than 10 mm Hg STAGE A - pt at high risk for developing left ventricular
dysfunction but w/o structural heart disease or s/sx of HF
Pt characteristic:
➔ Hypertension
➔ Atherosclerotic disease
➔ Diabetes
➔ obesity
Treatment recommendation for appropriate pt:
Risk factor control
➔ ACE inhibitor or ARBS
STAGE B - pt w/ left ventricular dysfunction or structural heart
disease who have not developed s/sx of HF
Pt characteristic:
➔ History of MI
➔ Left ventricular hypertrophy
➔ Low ejection fraction
Treatment recommendation for appropriate pt:
Implement stage A recommendation, plus:
➔ Beta blocker
STAGE C - pt w/ left ventricular dysfunction or structural heart
disease w/ current or prior s/sx of heart disease
Pt characteristics:
➔ Shortness of breath
➔ Fatigue Be alert for the ff s/sx:
➔ Decreased exercise tolerance Congestion:
Treatment recommendations for appropriate pt: ★ Dyspnea
Implement stage A & B recommendations, plus: ★ Orthopnea
➔ Diuretics ★ Paroxysmal nocturnal dyspnea
➔ Sodium restriction ★ Cough (recumbent or exertional)
➔ Implantable defibrillator ★ Pulmonary crackles that do not clear w/ cough
➔ Cardiac resynchronization therapy ★ Dependent edema
STAGE D - pt w/ refractory end-stage HF requiring specialized ★ Abdominal bloating or discomfort
interventions ★ Weight gain
Pt characteristics: ★ Ascites
➔ s/sx despite maximal medical therapy ★ Jugular venous distention
➔ Recurrent hospitalizations ★ Sleep disturbance (anxiety or air hunger)
Treatment recommendations for appropriate pt: ★ Fatigue
Implement stage A,B, & C recommendations, plus: Poor Perfusion/Low Cardiac Output:
➔ End life care ★ Decrease exercise tolerance
Extraordinary measures: ★ Muscle wasting or weakness
➔ Cardiac transplantation ★ Anorexia or nausea
➔ Mechanical support ★ Unexplained weight loss
★ Lightheadedness or diziness
★ Unexplained confusion or altered mental status
 ★ Resting tachycardia ❖ Echocardiogram
★ Daytime oliguria w. Recumbent nocturia ❖ Chest x ray
★ Cool or vasoconstricted extremities ❖ 12-lead ECG
★ Pallor or cyanosis ❖ Lab studies : serum electrolytes, BUN, creatinine, liver
LEFT-SIDED HEART FAILURE function tests, thyroid-stimulating hormone, CBC, BNP &
- Pulmonary congestion occurs when the left ventricle routine urinalysis
cannot effectively pump blood out of the ventricle into the Management:
aorta & the systemic circulation. 1. Oral & IV medication
- The increased left ventricular end-diastolic blood volume Several medications are routinely prescribed for HF,
increases the left ventricular end-diastolic pressure, which including ACE inhibitors, beta blockers & diuretics. Many
decreases blood flow from the left atrium into the left of these medications, particularly ACE inhibitors & beta
ventricle during diastole. blockers, improve symptoms & extends survival. Others,
- The blood volume & pressure build up in the left atrium, such as diuretics, improve symptoms but may not affect
decreasing flow through the pulmonary veins into the left survival.
atrium. Pharmacologic Therapy
- Pulmonary venous blood volume and pressure increase in Intravenous Infusions
the lungs, forcing fluid from the pulmonary capillaries into IV inotropes
the pulmonary tissues & alveoli, causing pulmonary - Milrinone (Primacor)
interstitial edema & impaired gas exchange - Dobutamine (Dobutrex)
Clinical manifestations of pulmonary congestion: IV vasodilators
★ Dyspnea - Nitroprusside (Nipride)
★ Cough - Nitroglycerin
★ Pulmonary crackles & low 02 saturation levels - Nesiritide (Natrecor)
★ Extra heart sound, the S3 or “ventricular gallop” may be 2. Major lifestyle changes (restriction of dietary sodium -
detected on auscultation. It is caused by abnormal no more than 2g/day; avoidance of smoking, including
ventricular filling. passive smoke; avoidance of excessive fluid and alcohol
RIGHT-SIDED HEART FAILURE intake; weight reduction when indicated; and regular
- When the right ventricle fails, congestion in the peripheral exercise
tissues and the viscera predominates. This occurs because An Exercise Program for Patients With Heart Failure
the right side of the heart cannot eject blood effectively Before undertaking physical activity, the pt should be given the ff
and cannot accommodate all of the blood that normally guidelines:
returns to it from the venous circulation. ● Talk with your primary provider for specific exercise
- Increased venous pressure leads to jugular venous program recommendations.
distention (JVD) and increased capillary hydrostatic ● Begin with low-impact activities such as walking.
pressure throughout the venous system. Start with warm-up activity followed by sessions that
Clinical manifestations include: gradually build up to about 30 minutes.
★ Edema of the lower extremities (dependent edema) ● Follow your exercise period with cool-down activities.
★ Hepatomegaly (enlargement of the liver) Avoid performing physical activities outside in extreme
★ Ascites (accumulation of fluid in the peritoneal cavity) hot, cold, or humid weather.
★ Weight gain due to retention of fluid ● Wait 2 hours after eating a meal before performing the
Assessment & Diagnostic findings: physical activity.
❖ Physical signs
 ● Ensure that you are able to talk during the physical ★ Incessant coughing may occur, producing increasing
activity; if you cannot do so, decrease the intensity of quantities of foamy sputum
activity. ★ Drowning in secretions
● Stop the activity if severe shortness of breath, pain, or Assessment & Diagnostic Findings
dizziness develops. ❖ The patient’s airway and breathing are assessed to
3. Supplemental oxygen, implantation of cardiac devices determine the severity of respiratory distress, along with
4. Surgical approaches including cardiac transplantation vital signs
➔ PCI ❖ Laboratory tests are obtained, including arterial blood
➔ CABG gases, electrolytes, BUN, and creatinine & CBC
➔ CRT ❖ chest x-ray is obtained to confirm the extent of pulmonary
➔ Ultrafiltration edema in the lung fields.
Nursing Diagnoses: ❖ Abrupt onset of signs of left-sided HF and pulmonary
➢ Activity intolerance related to decreased CO edema may occur without evidence of right-sided HF (e.g.,
➢ Excess fluid volume related to the HF syndrome no JVD, no dependent edema)
➢ Anxiety-related symptoms related to complexity of the Medical Management:
therapeutic regimen 1. Oxygen therapy
➢ Powerlessness related to chronic illness & hospitalizations 2. Diuretics
➢ Ineffective family therapeutic regimen management 3. Vasodilators
PULMONARY EDEMA CARDIOGENIC SHOCK
- is the abnormal accumulation of fluid in the interstitial - occurs when decreased CO leads to inadequate tissue
spaces and alveoli of the lungs. It is a diagnosis associated perfusion and initiation of the shock syndrome
with acute decompensated HF that can lead to acute - Cardiogenic shock most commonly occurs following acute
respiratory failure and death. MI when a large area of myocardium becomes ischemic
Pathophysiology: and hypokinetic
Left sided heart failure - It also can occur as a result of end stage HF, cardiac
↓ tamponade, pulmonary embolism (PE), cardiomyopathy,
Decreased pumping ability to the systemic circulation and dysrhythmias. Cardiogenic shock is a life-threatening
↓ condition with a high mortality rate.
Congestion & accumulation of blood in pulmonary area
↓
Fluid leaks out of intravascular space to the interstitium
↓
Accumulation of fluid
↓
Pulmonary edema
Clinical Manifestations:
★ Onset of breathlessness & a sense of suffocation
Medical management:
★ Tachypneic w/ noisy breathing & low oxygen sat rates
1. Mechanical Circulatory Assistive - such as the Intra-aortic
★ Skin & mucous membranes ,ay be pale to cyanotic & the
balloon pump (IABP). The IABP is a catheter with an
hands may be cool & moist
inflatable balloon at the end. The catheter is usually
★ Tachycardia & JVD are common signs
inserted through the femoral artery & threaded toward the
 heart, & the balloon is positioned in the descending caused by blood clots in the lungs.
thoracic aorta. - Blood clots that form in the deep veins of the legs and
2. Ventricular Assistive Device (VAD) - is an implantable embolize to the lungs can cause a pulmonary infarction
mechanical pump that helps pump blood from the lower where emboli mechanically obstruct the pulmonary
chambers of your heart (ventricles) to rest of your body. A vessels, cutting off the blood supply to sections of the lung
VAD is used in people who have weakened hearts or heart Clinical Manifestations
failure ★ Dyspnea
Nursing Management: ★ Pleuritic chest pain, tachypnea
➢ The pt in cardiogenic shock requires constant monitoring. ★ Cough, hemoptysis, tachycardia & hemodynamic
➢ The critical care nurse must carefully assess the patient, instability
observe the cardiac rhythm, monitor hemodynamic Diagnostic tests
parameters, monitor fluid status, and adjust medications ❖ Chest x ray
and therapies based on the assessment data ❖ Ventilation-perfusion lung scan, high resolution helical
➢ The patient is continuously evaluated for responses to the computed tomography, or computed tomographic
medical interventions and for the development of pulmonary angiogram
complications so that problems can be addressed ❖ Blood D-dimer assay - is a helpful screening test that
immediately. identifies whether clotting & fibrinolysis are taking place
THROMBOEMBOLISM somewhere in the body
- Pt w/ cardiovascular disorders are at risk for the Management:
development of arterial and venous thromboemboli 1. Anticoagulant therapy w/ unfractionated heparin, low
- Intracardiac thrombi can form in pts w/ atrial fibrillation molecular weight heparin, or fondaparinux (Arixtra)
because the atria do not contract forcefully, 2. Thrombolytic therapy
resulting in slow & turbulent flow, & increasing the 3. Warfarin for at least 6 months
likelihood of thrombus formation 4. Mechanical devices (pneumatic compression devices)
- Mural thrombi can also form on ventricular walls when PERICARDIAL EFFUSION & CARDIAC TAMPONADE
contractility is poor. - (accumulation of fluid in the pericardial sac) may
- Intracardiac thrombi can break off & travel through the accompany advanced HF, pericarditis, metastatic
circulation to other structures, including the brain, where carcinoma, cardiac surgery, or trauma. Normally, the
they cause a stroke (cerebrovascular accident). pericardial sac contains about 20 mL of fluid, which is
- Decreased mobility & other factors in pts w/ cardiac needed to decrease friction for the beating heart. An
disease also can lead to clot formation in the deep veins of increase in pericardial fluid raises the pressure within the
the legs pericardial sac & compresses the heart. This has the
- Although s/sx of deep vein thrombosis (DVT) can vary, pts following effects:
may report leg pain & swelling & the leg may appear ➔ Elevated pressure in all cardiac chambers
erythematous & feel warm. Diagnosis of DVT can be ➔ Decreased venous return due to atrial compression
confirmed by duplex ultrasound of the lower extremities ➔ Inability of the ventricles to distend and fill adequately
These clots can break off & travel through the inferior - Pericardial fluid may build up slowly without causing
vena cava & through the right noticeable symptoms until a large amount (1-2L)
- side of the heart into the pulmonary artery, where they accumulates
can cause a pulmonary embolus. - As pericardial fluid increases, pericardial pressure
PULMONARY EMBOLISM increases, reducing venous return to the heart and
- is a potentially life-threatening disorder typically
 decreasing CO. This can result in cardiac tamponade, ★ Pallor & cyanosis are seen in the skin & mucous
which causes low CO and obstructive shock. membranes
★ Irreversible brain damage
Cardiopulmonary Resuscitation
- Cardiopulmonary resuscitation (CPR) provides blood flow
to vital organs until effective circulation can be
reestablished
- The resuscitation process begins with the immediate
assessment of the patient and action to call for assistance,
as CPR can be performed most effectively with the
addition of more health care providers and equipment
(e.g., defibrillator).
The 4 basic steps in CPR are as follows:
1. Recognition of sudden cardiac arrest.
Clinical Manifestations: 2. Activation of the emergency Response Systems (ERS).
★ Dyspnea/ Tachypnea 3. Performance of high-quality CPR.
★ Hypertension paradoxical pulse 4. Rapid cardiac rhythm analysis & defibrillation as soon as it
★ Prominent neck vein due to elevated venous pressure is available
★ Chest pain/ tachycardia/ distant heart sounds Emergency Assessment & Management:
Assessment & Diagnostic findings: ❖ CArdiopulmonary Resuscitation
❖ An echocardiogram is performed to confirm the diagnosis ❖ Maintaining Airway & Breathing
and quantify the amount of pericardial fluid ❖ Defibrillation
❖ A chest x-ray may show an enlarged cardiac silhouette due ❖ Advanced Cardiac Life Support
to pericardial effusion. ❖ Follow-up Monitoring & Care
❖ The ECG shows tachycardia & may also show low voltage Medications used in Cardiopulmonary Resuscitation
Medical Management: 1. Epinephrine - vasopressor used to optimate BP & cardiac
1. Pericardiocentesis output; improves perfusion & myocardial contractility
2. Pericardiotomy 2. Vasopressin - increases systemic vascular resistance & BP
CARDIAC ARREST 3. Norepinephrine - vasopressor given to increases BP
- the heart is unable to pump and circulate blood to the 4. Dopamine - vasopressor given to increases BP &
body’s organs and tissues. It is often caused by a contractility
dysrhythmia such as ventricular fibrillation, progressive 5. Atropine - blocks parasympathetic action; increases SA
bradycardia, or asystole (absence of cardiac electrical node automaticity & AV conduction
activity and heart muscle contraction). 6. Amiodarone - acts on sodium-potassium & calcium
- Cardiac arrest can also occur when electrical activity is channels to prolong action potential & refractory period
present on the ECG but cardiac contractions are 7. Sodium bicarbonate (NaHCO2) - corrects metabolic
ineffective, a condition called pulseless electrical activity acidosis
(PEA). 8. Magnesium sulfate - promotes adequate functioning of
Clinical Manifestations: cellular sodium-potassium pump
★ Consciousness, pulse & BP are lost immediately
★ Breathing usually ceases, but ineffective respiratory
gasping may occur. Dilating pupils in less than a minute
★ Seizures may occur
Shock and Multiple Organ effective cardiac pump, adequate vascular or circulatory system,
and sufficient blood volume. If one of these components is

Dysfunction Syndrome impaired, perfusion to the tissues is threatened or compromised.

Without treatment, inadequate blood flow to the cells results in
anaphylactic shock - distributive shock state resulting from a poor delivery of oxygen and nutrients, cellular hypoxia, and cell
severe allergic reaction producing an acute systemic vasodilation death that progresses to organ dysfunction and eventually death.
and relative hypovolemia Normal Cellular Function & Effects of Shock
biochemical mediators - messenger substances that may be
released by a cell to create an action at that site or may be carried
by the bloodstream to a distant site before being activated; also
called cytokines or inflammatory mediators
cardiogenic shock - shock state resulting from impairment or
failure of the myocardium
Colloids - intravenous solutions that contain molecules that are
too large to pass through capillary membranes
Crystalloids - intravenous electrolyte solutions that move freely
between the intravascular compartment and interstitial spaces
distributive shock - shock state resulting from displacement of
intravascular volume creating a relative hypovolemia and
inadequate delivery of oxygen to the cells
hypovolemic shock - shock state resulting from decreased
intravascular volume due to fluid loss Physiology/Pathophysiology
multiple organ dysfunction syndrome - presence of altered
function of two or more organs in an acutely ill patient such that
interventions are necessary to support continued organ function
neurogenic shock - shock state resulting from loss of sympathetic
tone causing relative hypovolemia
Sepsis - life-threatening organ dysfunction caused by a
dysregulated host response to infection
septic shock - a subset of sepsis in which underlying circulatory
and cellular metabolism abnormalities are profound enough to
substantially increase mortality
Shock - physiologic condition in which there is inadequate blood
flow to tissues and cells of the body
systemic inflammatory response syndrome - a syndrome resulting
from a clinical insult that initiates an inflammatory response that
is systemic, rather than localized to the site of the insult
Overview of Shock
Shock can best be defined as a clinical syndrome that results from
inadequate tissue perfusion, creating an imbalance between the
delivery of oxygen and nutrients needed to support cellular
function. Adequate blood flow to the tissues and cells requires an
 STAGES OF SHOCK obtaining necessary lab tests to rule out & treat metabolic
1 . Compensatory Stage imbalances or infection
- BP remains within normal limits. A. Monitoring Tissue Perfusion
- Vasoconstriction, increased heart rate, and increased ➢ changes in level of consciousness,
contractility of the heart contribute to maintaining ➢ VS (including pulse rate), urinary output, skin, respiratory
adequate cardiac output. This results from stimulation of rate, & laboratory values (base deficit, lactic acid levels)
the sympathetic nervous system and subsequent release of ➢ In the compensatory stage of shock, serum sodium &
catecholamines (epinephrine, norepinephrine). blood glucose levels are elevated in response to the release
- Pts display the often-described fight-or-flight response. of aldosterone & catecholamines.
- The body shunts blood from organs such as the skin, ➢ The nurse should report a systolic BP lower than 90 mm
kidneys, & gastrointestinal (GI) tract to the brain, heart, & Hg or a drop in systolic BP of 40 mm Hg from baseline or a
lungs to ensure adequate blood supply to these vital MAP less than 65 mm Hg
organs ➢ Interventions focus on decreasing tissue oxygen
- As a result, the skin may be cool and pale, bowel sounds requirements & increasing perfusion to deliver more
are hypoactive, & urine output decreases in response to oxygen to the tissues
the release of ➢ Administration of IV fluids & medications supports BP &
- aldosterone and ADH. cardiac output, & the transfusion of packed RBC enhances
Clinical Manifestations: oxygen transport
★ BP - Normal B. Reducing Anxiety
★ HR - >100 bpm ➢ Provide brief explanations about the diagnostic &
★ RR - >20 breaths/min PaCO2 <32mmHg treatment procedures,
★ Skin - Cold clammy ➢ supporting the pt during these procedures, & providing
★ Urinary output - Decreased information about their outcomes are usually effective in
★ Mentation - Confusion and/or agitation reducing stress & anxiety
★ Acid-base balance - Respiratory alkalosis ➢ Speaking in a calm, reassuring voice & using gentle touch
Medical Management: also help ease the pt’s concerns
- Medical treatment is directed toward identifying the cause ➢ The nurse should advocate that family members be
of the shock, correcting the underlying disorder so that present during procedures & while pt care is provided
shock does not progress, & supporting those physiologic C. Promoting Safety
processes that thus far have responded successfully to the ➢ The nurse must be vigilant for potential threats to the pt’s
threat. Because compensation cannot be maintained safety, because a high anxiety level & altered mental
indefinitely, measures such as fluid replacement & status impair judgment. In this stage of shock, pts who
medication therapy must be initiated to maintain an were previously cooperative and followed instructions may
adequate BP & reestablish and maintain adequate tissue now disrupt IV lines & catheters & complicate their
perfusion condition. Close monitoring, frequent reorientation,
Nursing Management: hourly rounding, & implementing interventions to
- The nurse must systematically assess the pt at risk for prevent falls (bed alarms) are essential.
shock, recognizing subtle clinical signs of the 2. Progressive Stage
compensatory stage before the pt’s BP drops. Early - In the second stage of shock, the mechanisms that
interventions include identifying the cause of shock, regulate BP can no longer compensate, & the MAP falls
administering intravenous (IV) fluids & oxygen, & below normal limits. Pts are clinically hypotensive; this is
defined as a systolic BP of less than 90 mm Hg or a
 decrease in systolic BP of 40 mm Hg from baseline. The pt This condition is called acute lung injury (ALI); as ALI
shows signs of declining mental status continues, interstitial inflammation and fibrosis
Pathophysiology: Cardiovascular Effects:
➔ The overworked heart becomes dysfunctional, the body’s - A lack of adequate blood supply leads to dysrhythmias and
inability to meet increased oxygen requirements produces ischemia. The heart rate is rapid, sometimes exceeding 150
ischemia, & biochemical mediators cause myocardial bpm. The pt may complain of chest pain & even suffer a
depression. This leads to failure of the heart myocardial infarction (MI). Levels of cardiac biomarkers
➔ the autoregulatory function of the microcirculation fails in (cardiac troponin I [cTn-I]) increase. In addition,
response to the numerous biochemical mediators released myocardial depression and ventricular dilation may
by the cells, resulting in increased capillary permeability, further impair the heart’s ability to pump enough blood to
w/ areas of arteriolar & venous constriction further the tissues to meet increasing oxygen requirements
compromising cellular perfusion Neurologic Effects:
➔ The relaxation of precapillary sphincters causes fluid to - As blood flow to the brain becomes impaired, mental
leak from the capillaries, creating interstitial edema & status deteriorates. Changes in mental status occur w/
decreased return to the heart decreased cerebral perfusion & hypoxia. Initially, the pt
➔ The body mobilizes energy stores and increases oxygen may exhibit subtle changes in behavior, become agitated,
consumption to meet the increased metabolic needs of the confused, or demonstrate signs of delirium
underperfused tissues & cells. Anaerobic metabolism Renal Effects:
ensues, resulting in a buildup of lactic acid & disruption of - When the MAP falls below 65 mm Hg, the glomerular
normal cell function filtration rate of the kidneys cannot be maintained, &
Clinical Manifestations: drastic changes in renal function occur. Acute kidney
★ BP - systolic <90 mm Hg. MAP <65 mm Hg. Requires fluids injury (AKI) is characterized by an increase in blood urea
resuscitation to support blood pressure nitrogen (BUN) & serum creatinine levels, fluid &
★ HR - >150 bpm electrolyte shifts, acid–base imbalances, & a loss of the
★ RR - rapid, shallow respirations; crackles. PaO2 <80 mm renal–hormonal regulation of BP. Urinary output usually
Hg, PaCO2 >45 mm Hg decreases to less than 0.5 mL/kg per hr (or less than 30 mL
★ Skin - Mottled, petechiae per hour) but may vary depending on the phase of AKI.
★ Urinary output - 0.5 mL/kg/h Hepatic Effects:
★ Mentation - Lethargy - Hepatic Effects Decreased blood flow to the liver impairs
★ Acid-base balance - Metabolic acidosis the ability of liver cells to perform metabolic & phagocytic
Respiratory Effects: functions. Consequently, the pt is less able to metabolize
- Respirations are rapid & shallow. Crackles are heard over medications & metabolic waste products, such as
the lung fields. Decreased pulmonary blood flow causes ammonia & lactic acid. Metabolic activities of the liver,
arterial oxygen levels to decrease & CO2 levels to increase. including gluconeogenesis & glycogenolysis, are impaired.
Hypoxemia and biochemical mediators cause an intense The pt becomes more susceptible to infection as the liver
inflammatory response & pulmonary vasoconstriction, fails to filter bacteria from the blood. Liver enzymes
perpetuating pulmonary capillary hypoperfusion and (aspartate aminotransferase, alanine aminotransferase,
hypoxemia. The hypoperfused alveoli stop producing lactate dehydrogenase,) & bilirubin levels are elevated,
surfactant & subsequently collapse. Pulmonary capillaries and the pt develops jaundice
begin to leak, causing pulmonary edema, diffusion Gastrointestinal Effects:
abnormalities (shunting), & additional alveolar collapse. - GI ischemia can cause stress ulcers in the stomach, putting
the patient at risk for GI bleeding. In the small intestine,
 the mucosa can become necrotic & slough off, causing ● histamine-2 (H2) blockers, or antipeptic medications to
bloody diarrhea. Beyond the local effects of impaired reduce the risk of GI ulceration and bleeding.
perfusion, GI ischemia leads to bacterial translocation & Nursing Management:
organ dysfunction, in w/C bacterial toxins enter the Early interventions are essential to the survival of pts; therefore,
bloodstream through the lymphatic system. In addition to suspecting that a pt may be in shock and reporting subtle changes
causing infection, bacterial toxins can cause cardiac in assessment are imperative. PTS in the progressive stage of
depression, vasodilation, increased capillary permeability, shock are cared for in the intensive care setting to facilitate close
& an intense inflammatory response w/ activation of monitoring (hemodynamic monitoring, ECG monitoring, ABG
additional biochemical mediators. The net result is serum electrolyte levels, physical & mental status changes); rapid
interference w/ healthy cellular functioning & the ability & frequent administration of various prescribed medications and
to metabolize nutrients fluids; and possibly interventions w/ supportive technologies, such
Hematologic Effects: as mechanical ventilation, dialysis (continuous renal replacement
- The combination of hypotension, sluggish blood flow, therapy), intra-aortic balloon pump.
metabolic acidosis, coagulation system imbalance, & Preventing complications
generalized hypoxemia can interfere w/ normal hemostatic ➢ Monitoring includes evaluating blood levels of
mechanisms. In shock states, the inflammatory cytokines medications, observing invasive vascular lines for signs of
activate the clotting cascade, causing deposition of infection, & checking neurovascular status if arterial lines
microthrombi in multiple areas of the body & are inserted, especially in the lower extremities
consumption of clotting factors. The alterations of the ➢ the nurse promotes the pt’s safety & comfort by ensuring
hematologic system, including imbalance of the clotting that all procedures, including invasive procedures &
cascade, are linked to the overactivation of the arterial & venous punctures, are carried out using correct
inflammatory response of injury. Disseminated aseptic techniques
intravascular coagulation (DIC) may occur either as a ➢ Nursing interventions that reduce the incidence of
cause or as a complication of shock. In this condition, ventilator-associated pneumonia (VAP) must also be
widespread clotting & bleeding occur simultaneously. implemented. These include frequent oral care, aseptic
Bruises (ecchymoses) & bleeding (petechiae) may appear suction technique, turning, elevating the head of the bed
in the skin. Coagulation times (prothrombin time, at least 30 degrees to prevent aspiration, & implementing
activated partial thromboplastin time) are prolonged. daily interruption of sedation as prescribed to evaluate
Clotting factors & platelets are consumed & require patient readiness for extubation
replacement therapy to achieve hemostasis ➢ Positioning & repositioning of the pt to promote comfort
Medical Management: & maintain skin integrity are essential.
Specific medical management in the progressive stage of shock ➢ The nurse must also be vigilant in assessing for acute
depends on the type of shock, its underlying cause, & the degree delirium,
of decompensation in the organ systems ➢ characterized by an acute change in mental status,
● Supporting the respiratory system inattention, disorganized thinking, & altered level of
● Optimizing intravascular volume consciousness. Nursing interventions that can prevent
● Supporting the pumping action of the heart delirium include engaging the pt in frequent reorientation
● Improving the competence of the vascular system activities (to date, time, place), assessing & treating pain,
Other aspects of management may include promoting sleep, providing early mobilization activities, &
● early enteral nutritional support, limiting sedation, especially sedation w/ benzodiazepines
● targeted hyperglycemic control with IV insulin and use of (lorazepam [Ativan])
antacids,
Promoting Rest and Comfort ➔ Fluid replacement to restore intravascular volume
➢ Efforts are made to minimize the cardiac workload by ➔ Vasoactive medications to restore vasomotor tone and
reducing the pt’s physical activity & treating pain & improve cardiac function
anxiety. Because promoting pt rest & comfort is a priority, ➔ Nutritional support to address the metabolic
the nurse performs essential nursing activities in blocks of requirements that are often dramatically increased in
time, allowing the pt to have periods of uninterrupted rest, shock
w/c may prevent acute delirium, as noted previously. To Fluid Replacement
conserve the pt’s energy, the nurse should protect the pt - Fluid replacement, also referred to as fluid resuscitation, is
from temperature extremes (excessive warmth or cold, given in all types of shock. The fluids given may include
shivering), w/c can increase the metabolic rate & oxygen crystalloids(electrolyte solutions that move freely between
consumption & thus the cardiac workload. intravascular compartment & interstitial spaces)
3 . Irreversible Stage colloids(large-molecule IV solutions) & blood components
- The irreversible (or refractory) stage of shock represents (packed red blood cells, fresh frozen plasma, & platelets).
the point along the shock continuum at which organ Complications of Fluid Administration
damage is so severe that the pt does not respond to - Cardiovascular overload
treatment & cannot survive. Despite treatment, BP - Pulmonary edema
remains low. Renal & liver dysfunction, compounded by - Abdominal compartment syndrome
the release of biochemical mediators, creates an acute The pt receiving fluid replacement must be monitored
metabolic acidosis. Anaerobic metabolism contributes to a frequently for;
worsening lactic acidosis. Reserves of ATP are almost - adequate urinary output,
totally depleted, & mechanisms for storing new supplies - changes in mental status,
of energy have been destroyed. Respiratory system - skin perfusion, & changes in vital signs.
dysfunction prevents adequate oxygenation & ventilation - Lung sounds are auscultated frequently to detect
despite mechanical ventilatory support, & the signs of fluid accumulation
cardiovascular system is ineffective in maintaining an The CVP is used to assess preload in the right side of the heart.
adequate MAP for tissue perfusion. The CVP value assists in monitoring the pt’s response to fluid
Medical Management: replacement, especially when it is used in conjunction w/
- Medical management during the irreversible stage of additional assessment parameters (urine output, heart rate, BP
shock is similar to interventions & treatments used in the response to fluid challenge) A normal CVP ranges from 4 to 12 mm
progressive stage. Although the pt may have progressed to Hg or cm H2O
the irreversible stage, the judgment that the shock is Vasoactive Medication Therapy
irreversible can be made only retrospectively on the basis Inotropic Agents
of the pt’s failure to respond to treatment. Strategies that Dobutamine (Dobutrex)
may be experimental (investigational medications, such as Dopamine (Intropin)
immunomodulation therapy) may be tried to reduce or Epinephrine (Adrenalin)
reverse the severity of shock. Milrinone (Primacor)
General Management Strategies in Shock Desired action in shock:
management in all types and all phases of shock includes the Improve contractility, increases stroke
following: volume, increases cardiac output
➔ Support of the respiratory system w/ supplemental Disadvantages:
oxygen & /or mechanical ventilation to provide optimal Increase oxygen demand of the hearT
oxygenation
Vasodilators Pathophysiology
Nitroglycerin (Tridil)
Nitroprusside (Nipride)
Desired action in shock:
Reduces preload & afterload, reduce
oxygen demand of the heart
Disadvantages:
Cause hypertension
Vasopressor Agents
Norepinephrine (Levophed)
Dopamine (Intropin)
Phenylephrine (Neo-Synephrine)
Vasopressin (Pitressin)
Epinephrine (Adrenalin)
Desired action in shock:
Increase BP by vasoconstriction Risk Factors: HYPOVOLEMIC SHOCK
Disadvantages: External Fluid Losses
Increases afterload, thereby increasing ➔ Trauma
cardiac workload; compromise perfusion ➔ Surgery
to skin, kidneys, lungs, GI ➔ Vomiting
Nutritional Support ➔ Diarrhea
- Increased metabolic rates during shock increase energy ➔ Diuresis
requirements & therefore caloric requirements. Pts in ➔ Diabetes insipidus
shock may require more than 3000 calories daily. Enteral Internal Fluid Losses
nutrition is preferred, promoting GI function through ➔ Hemorrhage
direct exposure to nutrients & limiting infectious ➔ Burns
complications associated w/ parenteral feeding Stress ➔ Ascites
ulcers occur frequently in acutely ill pts because of the ➔ Peritonitis
compromised blood supply to the GI tract. Therefore, ➔ Dehydration
antacids, H2 blockers (famotidine [Pepcid]), & proton ➔ Necrotizing pancreatitis
pump inhibitors (lansoprazole [Prevacid], esomeprazole Medical Management:
magnesium [Nexium]) are prescribed to prevent ulcer 1. Treatment of the underlying cause
formation by inhibiting gastric acid secretion or increasing If the pt is hemorrhaging, efforts are made to stop the
gastric pH bleeding. This may involve applying pressure to the
Hypovolemic Shock bleeding site or surgical interventions to stop internal
- Hypovolemic shock, the most common type of shock, is bleeding. If the cause of the hypovolemia is diarrhea or
characterized by decreased intravascular volume. Body vomiting, medications to treat diarrhea & vomiting are
fluid is contained in the intracellular & extracellular given while efforts are made to identify & treat the cause.
compartments. Hypovolemic shock occurs when there is a In older adult pts, dehydration may be the cause of
reduction in intravascular volume by 15% to 30%, which hypovolemic shock
represents an approximate loss of 750 to 1,500 mL of Fluid and Blood Replacement:
blood in a 70-kg (154-lb) person ● Crystalloids - 0.9% sodium chloride (Normal saline
solution)
 Lactated Ringer’s given for diabetes insipidus, antidiarrheal agents for
Advantages: diarrhea, & antiemetic medications for vomiting
Widely available, inexpensive. Lactate ion that Nursing Management:
helps buffer metabolic acidosis Primary prevention of shock is an essential focus of nursing care.
Disadvantages: Hypovolemic shock can be prevented in some instances by closely
Requires large volume of infusion, can cause monitoring pts who are at risk for fluid deficits & assisting w/ fluid
hypernatremia, pulmonary edema, abdominal replacement before intravascular volume is depleted.
compartment syndrome General nursing measures include
● Colloids - albumin (5%, 25%) - ensuring safe administration of prescribed fluids &
Advantages: - medications & documenting their administration &
Rapidly expands plasma volume effects.
Disadvantages: Administering Blood and Fluids
Expensive, requires human donors, limited supply, ➢ The nurse monitors the pt closely for cardiovascular
can cause heart failure overload & signs of difficulty breathing, a condition known
● Blood Products - plasma, packed RBCs and platelets as transfusion-associated circulatory overload.
Advantages: Transfusion-related acute lung injury may occur and is
Rapidly replaces volumes lost due to hemorrhage characterized by pulmonary edema, hypoxemia,
Disadvantages: respiratory distress, & pulmonary infiltrates, usually w/in
Cross-match type specific blood is desired for hrs after massive transfusion. ACS is also a possible
optimal massive transfusion protocols to reduces complication of excessive fluid resuscitation & may
transfusion related complications (acute lung initially present
injury, hemolytic reactions) ➢ Hemodynamic pressure, VS, ABG, serum lactate levels,
2. Redistribution of Fluid hemoglobin & hematocrit levels, bladder pressure
In addition to administering fluids to restore intravascular monitoring, & fluid intake & output are among the
volume, positioning the patient properly assists fluid parameters monitored. Temperature should also be
redistribution. A modified Trendelenburg position, also monitored closely to ensure that rapid fluid resuscitation
known as passive leg raising, is recommended in does not cause hypothermia. IV fluids may need to be
hypovolemic shock. Elevation of the legs promotes the warmed when large volumes are given
return of venous blood & can be used as a dynamic ➢ Physical assessment focuses on observing the jugular
assessment of a pt’s fluid responsiveness. The nurse veins for distention & monitoring jugular venous pressure.
assesses for an improvement in the pts VS, specifically a Jugular venous pressure is low in hypovolemic shock; it
rise in the BP & return of the pulse pressure to normal or increases w/ effective treatment & is significantly
near normal. A full Trendelenburg position makes increased w/ fluid overload & heart failure. The nurse
breathing difficult & does not increase BP or cardiac must monitor cardiac & respiratory status closely & report
output changes in BP, pulse pressure, CVP, heart rate & rhythm,
3. Pharmacologic therapy & lung sounds to the primary provider
If fluid administration fails to reverse hypovolemic shock, Implementing other measures:
then vasoactive medications that prevent cardiac failure ➢ Oxygen is given to increase the amount of oxygen carried
are given. Medications are also given to reverse the cause by available hemoglobin in the blood. A pt who is confused
of the dehydration. For ex. insulin is given if dehydration may feel apprehensive w/ an oxygen mask or cannula in
is secondary to hyperglycemia, desmopressin (DDAVP) is place, & frequent explanations about the need for the
mask may reduce some of the pt’s fear & anxiety.
 Simultaneously, the nurse must direct efforts to the safety Clinical manifestations:
& comfort of the pt ★ Pain of angina
Cardiogenic Shock ★ Developed dysrhythmias
- occurs when the heart’s ability to contract & to pump ★ Complain of fatigue
blood is impaired & the supply of oxygen is inadequate for ★ Express feeling of doom
the heart & the tissues. The causes of cardiogenic shock ★ Signs of hemodynamic instability
are known as either coronary or noncoronary. Coronary Medical Management:
cardiogenic shock is more common than non coronary The goals of medical management in cardiogenic shock are to limit
cardiogenic shock and is seen most often in pts w/ acute further myocardial damage & preserve the healthy myocardium &
MI resulting in damage to a significant portion of the left to improve cardiac function by increasing cardiac contractility,
ventricular myocardium decreasing ventricular afterload, or both. In general, these goals
- Noncoronary cause of cardiogenic shock are related to are achieved by increasing oxygen supply to the heart muscle while
conditions that stress the myocardium (severe hypoxemia, reducing oxygen demands.
acidosis,hypoglycemia,hypocalcemia,tension 1. Correction of underlying cause
pneumothorax) as well as conditions that result in As with all forms of shock, the underlying cause of
ineffective myocardial function (cardiomyopathies, cardiogenic shock must be corrected. It is necessary first to
valvular damage, cardiac tamponade, dysrhythmias). treat the oxygenation needs of the heart muscle to ensure
Pathophysiology its continued ability to pump blood to other organs. In the
In cardiogenic shock, cardiac output, which is a function of both case of coronary cardiogenic shock (acute coronary
stroke volume & heart rate, is compromised. When stroke volume syndromes, acute MI), the pt may require thrombolytics
& heart rate decrease or become erratic, BP falls & tissue (fibrinolytics) therapy, a percutaneous coronary
perfusion is reduced. Blood supply for tissues & organs & for the intervention, coronary artery bypass graft surgery,
heart muscle itself is inadequate, resulting in impaired tissue intra-aortic balloon pump therapy, ventricular assist
perfusion. Because impaired tissue perfusion weakens the heart & device, or some combination of these treatments. In the
impairs its ability to pump, the ventricle does not fully eject its case of non coronary cardiogenic shock, interventions
volume of blood during systole. As a result, fluid accumulates in focus on correcting the underlying cause, such as
the lungs. This sequence of events can occur rapidly or over a replacement of a faulty cardiac valve, correction of a
period of days dysrhythmia, correction of acidosis & electrolyte
disturbances, or treatment of a tension pneumothorax. If
the cause of the cardiogenic shock was related to a cardiac
arrest, once the pt is successfully resuscitated, targeted
temperature management, also called therapeutic
hypothermia, may be initiated to actively lower the body
temperature to a targeted core temperature (32°C [89.6°F]
to 36°C [96.8°F]) to preserve neurologic function
2. Oxygenation
In the early stages of shock, supplemental oxygen is given
by nasal cannula at a rate of 2 to 6 L/min to achieve an
oxygen saturation exceeding 95%. Monitoring of ABG
values, pulse oximetry values, & ventilatory effort (work of
breathing) helps determine whether the pt requires a more
 aggressive method of oxygen delivery (including myocardial activity & improving cardiac output.
noninvasive & invasive mechanical ventilation). Myocardial alpha-adrenergic receptors are also stimulated,
3. Pain Control resulting in decreased pulmonary & systemic vascular
If a pt experiences chest pain, IV morphine is given for resistance
pain relief. In addition to relieving pain, morphine dilates Nitroglycerin
the blood vessels. This reduces the workload of the heart IV nitroglycerin in low doses acts as a venous vasodilator
by both decreasing the cardiac filling pressure (preload) & & therefore reduces preload. At higher doses, nitroglycerin
reducing the pressure against w/c the heart muscle has to causes arterial vasodilation & therefore reduces afterload
eject blood (afterload). Morphine may also decrease the as well. These actions, in combination w/ dobutamine,
pt’s anxiety. increase cardiac output while minimizing cardiac
4. Hemodynamic Monitoring workload. In addition, vasodilation enhances blood flow to
Hemodynamic monitoring is initiated to assess the pt’s the myocardium, improving oxygen delivery to the
response to treatment. In many institutions, this is weakened heart muscle
performed in the intensive care unit (ICU), where an Dopamine
arterial line can be inserted. The arterial line enables Dopamine is a sympathomimetic agent that has varying
accurate & continuous monitoring of BP & provides a port vasoactive effects depending on the dosage. It may be used
from which to obtain frequent arterial blood samples w/o w/ dobutamine & nitroglycerin to improve tissue
having to perform repeated arterial punctures. A perfusion. Doses of 2 to 8 μg/kg/min improve contractility
multilumen central venous & pulmonary artery catheter (inotropic action), slightly increase the heart rate
may be inserted to allow measurement of myocardial (chronotropic action), & may increase cardiac output.
filling pressures, pulmonary artery pressures, cardiac Doses that are higher than 8 μg/kg/min predominantly
output, & pulmonary & systemic resistance cause vasoconstriction, which increases afterload & thus
5. Laboratory Marker Monitoring increases cardiac workload. Because this effect is
Laboratory biomarkers for ventricular dysfunction (B-type undesirable in pts w/ cardiogenic shock, dopamine doses
natriuretic peptide), cardiac enzyme levels and biomarkers must be carefully titrated. In severe metabolic acidosis,
(cTn-I), and serum lactate are measured, a transthoracic w/c occurs in the later stages of shock, metabolic acidosis
echocardiography may be performed at the bedside, & must first be corrected to ensure maximum effectiveness
serial 12-lead ECG are obtained to assess the degree of of vasoactive medications
myocardial damage. Continuous ECG & ST segment Other Vasoactive Medications:
monitoring is also done to closely monitor the pt for - Norepinephrine
ischemic changes - Epinephrine
6. Fluid Therapy - Milrinone
Appropriate fluid administration is also necessary in the - Vasopressin &
treatment of cardiogenic shock. Administration of fluids - Phenylephrine
must be monitored closely to detect signs of fluid Antiarrhythmic Medications
overload. Incremental IV fluid boluses are cautiously given Multiple factors, such as hypoxemia, electrolyte imbalances, &
to determine optimal filling pressures for improving acid– base imbalances, contribute to serious cardiac dysrhythmias
cardiac output in all pts w/ shock. In addition, as a compensatory response to
Pharmacologic Therapy decreased cardiac output & BP, the heart rate increases beyond
Dobutamine normal limits. This impedes cardiac output further by shortening
Dobutamine produces inotropic effects by stimulating diastole & thereby decreasing the time for ventricular filling.
myocardial beta receptors, increasing the strength of
Consequently, antiarrhythmic medications are required to stabilize venous puncture sites must be observed for bleeding, &
the heart rate. pressure must be applied at the sites if bleeding occurs. IV
Mechanical Assistive Devices infusions must be observed closely because tissue necrosis
If cardiac output does not improve despite supplemental oxygen. & sloughing may occur if vasopressor medications
vasoactive medications, & fluid boluses, mechanical assistive infiltrate the tissues. When possible, vasoactive
devices are used temporarily to improve the heart’s ability to medications should be given using central IV lines.
pump. Intra-aortic balloon counterpulsation is one means of Furthermore, the need for the central IV access devices
providing temporary circulatory assistance. Other means of should be reviewed daily to reduce the risk of CLABSIs.
mechanical assistance include left & right ventricular assist The nurse must also monitor urine output, serum
devices & total temporary artificial hearts. Another short-term electrolytes, BUN, & serum creatinine levels to detect
means of providing cardiac or pulmonary support to the pt in decreased renal function secondary to the effects of
cardiogenic shock is through an extracorporeal device similar to cardiogenic shock or its treatment.
the cardiopulmonary bypass (CPB) system used in open-heart Maintaining Intra-Aortic Balloon Counterpulsation
surgery. CPB is used only in emergency situations until definitive ➢ The nurse plays a critical role in caring for the pt receiving
treatment, such as heart transplantation, can be initiated. intraaortic balloon counterpulsation. The nurse makes
Nursing Management: ongoing timing adjustments of the balloon pump to
Preventing Cardiogenic shock maximize its effectiveness by synchronizing it w/ the
➢ Identifying at-risk pts early, promoting adequate cardiac cycle. The pt is at risk of circulatory compromise to
oxygenation of the heart muscle, & decreasing cardiac the leg on the side where the catheter for the balloon has
workload can prevent cardiogenic shock. This can be been inserted; therefore, the nurse must check the
accomplished by conserving the pt’s energy, promptly neurovascular status of the lower extremities frequently.
relieving angina, & administering supplemental oxygen Enhancing Safety and Comfort
Monitoring Hemodynamic status ➢ The nurse must take an active role in safeguarding the pt,
➢ A major role of the nurse is monitoring the pt’s enhancing comfort, & reducing anxiety. This includes
hemodynamic & cardiac status. Arterial lines & ECG administering medication to relieve chest pain, preventing
monitoring equipment must be well maintained & infection at the multiple arterial & venous line insertion
functioning properly. The nurse anticipates the sites, protecting the skin, & monitoring respiratory &
medications, IV fluids, & equipment that might be used & renal function. Proper positioning of the pt promotes
is ready to assist in implementing these measures. effective breathing w/o decreasing BP & may also increase
Changes in hemodynamic, cardiac, & pulmonary status & pt comfort while reducing anxiety. Brief explanations
lab values are documented and reported promptly about procedures that are being performed & the use of
Administering Medications and Intravenous Fluids comforting touch often provide reassurance to the pt &
➢ The nurse plays a critical role in the safe & accurate the family. The family is usually anxious & benefits from
administration of IV fluids & medications. Fluid overload opportunities to see and talk to the pt. Explanations of
& pulmonary edema are risks because of ineffective treatments & the pt’s responses are often comforting to
cardiac function & accumulation of blood & fluid in the family members.
pulmonary tissues. The nurse documents medications & Distributive Shock
treatments that are given as well as the pt’s response to - Distributive shock occurs when intravascular volume pools
treatment. The nurse must be knowledgeable about the in peripheral blood vessels. This abnormal displacement of
desired effects as well as the side effects of medications. intravascular volume causes a relative hypovolemia
For ex. the nurse monitors the pt for decreased BP after because not enough blood returns to the heart, which
administering morphine or nitroglycerin. Arterial & leads to inadequate tissue perfusion. The ability of the
 blood vessels to constrict helps return the blood to the Activation of inflammatory response
heart. The vascular tone is determined both by central ↓
regulatory mechanisms, as in BP regulation, & by local Maldistribution of intravascular volume
regulatory mechanisms, such as tissue demands for ↓
oxygen & nutrients. Therefore, distributive shock can be Decreased venous return
caused by either a loss of sympathetic tone or a release of ↓
biochemical mediators from cells that causes vasodilation. Decreased cardiac output
The varied mechanisms leading to the initial vasodilation ↓
in distributive shock provide the basis for the further Decreased tissue perfusion
subclassification of shock into three types: septic shock, Risk Factors: Septic Shock
neurogenic shock, and anaphylactic shock. These subtypes ● Immunosuppression
of distributive shock cause variations in the ● Extremes of age (<1 yr & >65 yrs)
pathophysiologic chain of events & are explained here ● Malnourishment
separately. In all types of distributive shock, massive ● Chronic Illness
arterial & venous dilation promotes peripheral pooling of ● Invasive procedures
blood. Arterial dilation reduces systemic vascular ● Emergent and/or multiple surgeries
resistance. Initially, cardiac output can be high, both from Medical Management:
the reduction in (systemic vascular resistance) & from the 1. Correction of Underlying Causes
heart muscle’s increased effort to maintain perfusion Current treatment of sepsis & septic shock involves rapid
despite the incompetent vasculature. Pooling of blood in identification & elimination of the cause of infection.
the periphery results in decreased venous return. Current goals are to identify & treat pts in early sepsis
Decreased venous return results in decreased stroke w/in 3 hrs to optimize pt outcome
volume & decreased cardiac output. Decreased cardiac 2. Fluid Replacement Therapy
output, in turn, causes decreased BP & ultimately must be instituted to correct tissue hypoperfusion that
decreased tissue perfusion. results from the incompetent vasculature & the
Sepsis and Septic Shock inflammatory response. Reestablishing tissue perfusion
- Septic shock, the most common type of distributive shock, through aggressive fluid resuscitation is key to the
is caused by widespread infection or sepsis. management of sepsis and septic shock.
- sepsis is “life-threatening organ dysfunction caused by a An initial fluid challenge, w/c includes an IV infusion of at
dysregulated host response to infection least 30 mL/kg of crystalloids over 30 minutes, may be
- septic shock is “a subset of sepsis in which underlying required to aggressively treat sepsis-induced tissue
circulatory & cellular metabolism abnormalities are hypoperfusion
profound enough to substantially increase mortality” Monitor:
- Despite the increased sophistication of antibiotic therapy, - BP, CVP, fluid responsiveness
the incidence of both sepsis & septic shock has continued - Passive leg raise
to rise. They are the leading cause of death in noncoronary - Urine output & serum lactate levels
ICU pts Pharmacologic Therapy
Pathophysiology: ● Inotropic agents may also be given to provide
Precipitating event pharmacologic support to the myocardium.
↓ ● Packed RBC may be ordered to support oxygen delivery &
Vasodilation transport to the tissues.
↓
 ● Neuromuscular blockade agents & sedation agents may be Medical Management:
required to reduce metabolic demands & provide comfort 1. restoring sympathetic tone, either through the
to the pt. stabilization of a spinal cord injury or, in the instance of
● Deep vein thrombosis (DVT) prophylaxis w/ low-dose spinal anesthesia, by positioning the pt properly.
● unfractionated heparin or low–molecular-weight heparin, 2. Specific treatment depends on the cause of the shock.
in combination w/ mechanical prophylaxis (sequential Nursing Management:
compression devices) should be initiated, as well as ➢ elevate & maintain the head of the bed at least 30 degrees
medications for stress ulcer prophylaxis to prevent neurogenic shock when a pt receives spinal or
Nutritional Therapy epidural anesthesia.
- Aggressive nutritional supplementation should be ➢ The nurse must check the pt daily for any lower extremity
initiated w/in 24 to 48 hours of ICU admission to address pain, redness, tenderness, & warmth.
the hypermetabolic state present w/ septic shock ➢ If the pt complains of pain & objective assessment of the
- Enteral feedings are preferred to the parenteral route calf is suspicious, the pt should be evaluated for DVT.
because of the increased risk of iatrogenic infection ➢ Passive range of motion of the immobile extremities helps
associated w/ IV catheters promote circulation.
Nursing Management: ➢ Early interventions to prevent VTE include the application
➢ All invasive procedures must be carried out w/ aseptic of pneumatic compression devices often combined w/
technique after careful hand hygiene. antithrombotic agents (low–molecular-weight heparin).
➢ IV lines, arterial & venous puncture sites, surgical ➢ nurse must monitor the pt closely for signs of internal
incisions, traumatic wounds, & urinary catheters must be bleeding that could lead to hypovolemic shock.
monitored for signs of infection. Anaphylactic Shock
➢ Nursing interventions to prevent infection need to be - caused by a severe allergic reaction when pts who have
implemented in the care of all pts. already produced antibodies to a foreign substance
Neurogenic Shock (antigen) develop a systemic antigen–antibody reaction;
- vasodilation occurs as a result of a loss of balance between specifically,an immunoglobulin E (IgE)-mediated response
parasympathetic & sympathetic stimulation. - This antigen–antibody reaction provokes mast cells to
- Sympathetic stimulation causes vascular smooth muscle release potent vasoactive substances, such as histamine or
to constrict, and parasympathetic stimulation causes bradykinin, & activates inflammatory cytokines, causing
vascular smooth muscle to relax or dilate. widespread vasodilation and capillary permeability.
- The pt experiences a predominant parasympathetic - The most common triggers are
stimulation that causes vasodilation lasting for an foods (especially peanuts),
extended period, leading to a relative hypovolemic state. medications, and
- The overriding parasympathetic stimulation that occurs insect
with neurogenic shock causes a drastic decrease in the pt’s Anaphylaxis has 3 defining characteristics:
systemic vascular resistance and bradycardia. ➔ Acute onset of symptoms
- Inadequate BP results in the insufficient perfusion of ➔ Presence of two or more symptoms that include
tissues & cells that is common to all shock states. respiratory compromise,
Risk Factors: Neurogenic Shock reduced BP,
● Spinal cord injury GI distress, and
● Spinal anesthesia skin or mucosal tissue irritation
● Depressant action and/or multiple surgeries ➔ Cardiovascular compromise from minutes to hours after
exposure to the antigen
Risk Factors: Anaphylactic Shock Nursing Management:
● History of medication sensitivity ➢ The nurse must assess all pts for allergies or previous
● Transfusion reaction reactions to antigens (medications, blood products, foods,
● History of reaction to insect bites/stings contrast agents, latex) & communicate the existence of
● Food Allergies these allergies or reactions to others
● Latex sensitivity ➢ The nurse assesses the pt’s understanding of previous
Clinical Manifestations: reactions & steps taken by the pt & the family to prevent
May present within 2-30 mins after exposure to the antigen; further exposure to antigens.
★ headache, ➢ When new allergies are identified, the nurse advises the pt
★ lightheadedness, to wear or carry identification that names the specific
★ nausea, allergen or antigen.
★ vomiting, ➢ When administering any new medication, the nurse
★ acute abdominal observes all pts for allergic reactions
★ pain or discomfort, ➢ The nurse must be knowledgeable about the clinical signs
★ pruritus, and of anaphylaxis, must take immediate action if signs &
★ feeling of impending doom symptoms occur, & must be prepared to begin CPR if
Assessment may reveal diffuse cardiorespiratory arrest occurs.
❖ erythema and generalized flushing, Multiple Organ Dysfunction Syndrome
❖ difficulty breathing (laryngeal edema), - Multiple organ dysfunction syndrome (MODS) is altered
❖ bronchospasm, organ function in acutely ill pts that requires medical
❖ cardiac dysrhythmias, and intervention to support continued organ function.
❖ hypotension - It is another phase in the progression of shock states
Anaphylactoid reactions present similarly to anaphylaxis but are - The actual incidence of MODS is difficult to determine,
not mediated by IgE responses. Anaphylaxis & anaphylactoid because it develops w/ acute illnesses that compromise
reactions are often clinically indistinguishable tissue perfusion. Dysfunction of one organ system is
Medical Management: associated w/ 20% mortality, & if more than 4 organs fail,
1. Intramuscular epinephrine is given for its vasoconstrictive the mortality is at least 60%
action Pathophysiology
2. Diphenhydramine (Benadryl) is given intravenously to - MODS may be a complication of any form of shock, but it
reverse the effects of histamine, thereby reducing capillary is most commonly seen in pts w/ sepsis & is a result of
permeability inadequate tissue perfusion.
3. albuterol (Proventil), may be given to reverse - The precise mechanism by w/c MODS occurs remains
histamine-induced bronchospasm unknown.
4. If cardiac arrest and respiratory arrest are imminent or - MODS frequently occurs toward the end of the continuum
have occurred, cardiopulmonary resuscitation (CPR) is of septic shock when tissue perfusion cannot be effectively
performed. restored.
5. Endotracheal intubation may be necessary to establish an - tissues become hypoperfused at both a microcellular and
airway. macrocellular level, eventually causing organ dysfunction
6. IV lines are inserted to provide access for administering that requires mechanical & pharmacologic intervention to
fluids and medications support organ function
 - Organ failure usually begins in the lungs, & cardiovascular goals, because massive loss of skeletal muscle mass makes
instability, as well as failure of the hepatic, GI, renal, rehabilitation a long, slow process
immunologic, & central nervous systems Educating Patients About Self-Care
Clinical Manifestations: ➢ Ps who experience & survive shock may have been unable
Lungs are the first organs to show signs of dysfunction to get out of bed for an extended period of time & are
★ Progressive dyspnea likely to have a slow, prolonged recovery.
★ respiratory failure that are manifested as ALI or ARDS ➢ The pt & the family are educated about strategies to
Hypermetabolic states prevent further episodes of shock by identifying the
★ Hyperglycemia factors implicated in the initial episode
★ Hyperlactic acidemia Continuing and Transitional Care
★ Increase BUN ➢ Because of the physical toll associated w/ recovery from
Severe loss of skeletal muscle mass shock, pts may be cared for in a long-term care facility or
Renal dysfunction rehabilitation setting after hospital discharge
★ elevated creatinine and anuria ➢ The adequacy of treatments continued at home & the
Cardiovascular system becomes unstable and unresponsive to ability of the pt & the family to cope w/ these treatments
vasoactive agents are also assessed
Neurologic state ➢ The pt is likely to require close medical supervision until
★ Unresponsiveness complete recovery occurs
★ coma
Medical Management:
Vascular disorders and Problems
1. Early detection & documentation of initial signs of
infection are essential in managing MODS in older adult
of Peripheral Circulation
pts. Anastomosis - junction of two vessels
2. Subtle changes in mentation & a gradual rise in Aneurysm - a localized sac or dilation of an artery formed at a
temperature are early warning signs. weak point in the vessel wall
3. Other pts at greater risk for MODS are those w/ chronic Angioplasty - an invasive procedure that uses a balloon-tipped
illness, malnutrition, immunosuppression, or surgical or catheter to dilate a stenotic area of a blood vessel
traumatic wounds ankle-brachial index (ABI) - ratio of the ankle systolic pressure to
If preventive measures fail, treatment measures to reverse MODS the brachial systolic pressure; an objective measurement of
are aimed at arterial disease that provides quantification of the degree of
(1) controlling the initiating event, stenosis
(2) promoting adequate organ perfusion, Arteriosclerosis - diffuse process whereby the muscle fibers & the
(3) providing nutritional support, and endothelial lining of the walls of small arteries & arterioles
(4) maximizing patient comfort thicken
Nursing Management: Atherectomy - an invasive procedure that uses a cutting device or
Promoting Communication laser to remove or reduce plaque in an artery
➢ Nurses should encourage frequent & open communication Atherosclerosis -inflammatory process involving the accumulation
about treatment modalities & options to ensure that the of lipids, calcium, blood components, carbohydrates, & fibrous
pt’s wishes regarding medical management are met. tissue on the intimal layer of a large or medium-sized artery
➢ Pts who survive MODS must be informed about the goals Bruit - sound produced by turbulent blood flow through an
of rehabilitation & expectations for progress toward these irregular, tortuous, stenotic, or dilated vessel
Dissection - separation of the weakened elastic and fibromuscular
elements in the medial layer of an artery of the atrioventricular valves makes the first heart sounds,
duplex ultrasonography - combines B-mode grayscale imaging of the “lub”; closure of the semilunar valves makes the
tissue, organs, & blood vessels w/ capabilities of estimating second heart sound, the “dub”
velocity changes by the use of a pulsed Doppler Conduction System
intermittent claudication - a muscular, cramp-like pain or fatigue - Contraction of the heart, occurring as a result of its
in the extremities consistently reproduced w/ the same degree of conduction system, causes blood to move throughout the
exercise or activity & relieved by rest body
Ischemia - deficient blood supply Cardiac Cycle
rest pain - persistent pain in the foot or digits when the pt is - The period from the beginning of one heartbeat to the
resting, indicating a severe degree of arterial insufficiency beginning of the next. During this cycle, electrical &
Rubor - reddish-blue discoloration of the extremities; indicative of mechanical events must occur in the proper sequence & to
severe peripheral arterial damage in vessels that remain dilated & the proper degree to provide adequate cardiac output to
unable to constrict the body
Stenosis - narrowing or constriction of a vessel - Has two phases: “systole” and “diastole”
The Heart has actually 2 separate pumps: Cardiac Output
1. Right side - pumps the blood to the lungs to receive - Refers to the amount of blood the heart pumps in 1
oxygen minute. It’s equal to the heart rate multiplied by the stroke
2. Left side - pumps the oxygenated blood to the rest of the volume, the amount of blood ejected with each heartbeat
body Blood Flow
Where the Heart lies? - As blood makes its way through the vascular system, it
➔ About the size of a closed fist, the heart lies beneath the travels through five types of blood vessels, involving
sternum in the mediastinum (the cavity bet the lungs), methods of circulation.
between the second & sixth ribs Arteries - have a thick walls to accommodate the flow of blood at
high speed & pressures
Arterioles - have thinner walls than arteries, they constrict or
dilate to control blood flow to the capillaries
Capillaries - which (being microscopic) have walls composed of
only a single layer of endothelial cells
Venules - gather blood from the capillaries, their walls are
thinner than those of the arterioles
Veins - have thinner walls than arteries but have larger diameters,
because of the low blood pressures of venous return to the heart.
Heart Structures:
About 60,000 miles of arteries, arterioles, capillaries, venules &
➔ Surrounded by a sac called the pericardium
veins keep blood to & from every functioning cell in the body
➔ Has a wall made up of 3 layers : myocardium, endocardium
Circulation
& epicardium
- There are 3 methods of circulation that carry blood
➔ Within the heart lie:
throughout the body
◆ 4 chambers (2 atria & 2 ventricles)
1. Pulmonary circulation - blood travels to the lungs to
◆ 4 valves (2 atrioventricular [AV] & 2 semilunar
pick up oxygen & release carbon dioxide
valves
2. Systemic circulation - blood pumped from the left
Memory Jogger:
ventricle carries oxygen & other nutrients to body cells &
➔ If you can remember that there are 2 distinct heart sounds,
transports waste products for excretion
you can recall that there are 2 sets of heart valves. Closure
 3. Coronary circulation - the heart relies on the coronary e. Angiography
arteries & their branches for its supply of oxygenated Used to confirm the diagnosis of occlusive arterial disease
blood & depends on the cardiac veins to remove oxygen when surgery or other interventions are considered.
depleted blood Involves injecting a radiopaque contrast agent directly
Assessment parameters appropriate for determining the into the arterial system to visualize the vessels.
status of peripheral circulation. f. Magnetic Resonance Angiography
1. Health history - obtains an in depth description from the pt w/ Performed w/ a standard magnetic resonance imaging
peripheral vascular disease of any pain & its precipitating factors (MRI) scanner & special software programmed to isolate
2. Physical assessment - inspection of the skin the blood vessels
Rubor g. Contrast Phlebography (Venography) -Involves injecting a
- Reddish-blue discoloration of the extremities radiopaque contrast agent into the venous system.
- Indicative of severe peripheral arterial damage in vessels If a thrombus exists, the x-ray image reveals an unfilled
that remain dilated & unable to constrict segment of vein in an otherwise completely filled vein.
Palpation of pulses h. Lymphoscintigraphy
- Stenosis (narrowing or constriction), absence of pulse Involves injection of a radioactively labeled colloid
Palpation of arterial pulses subcutaneously in the second interdigital space.
❖ Radial Causes, pathophysiologic changes, clinical manifestations,
❖ Brachial management and prevention of:
❖ Femoral ARTERIAL DISORDERS
❖ Popliteal A. Arteriosclerosis and atherosclerosis
❖ Dorsalis pedis Arteriosclerosis - hardening of the arteries
❖ Posterior tibial ➔ Most common disease of the arteries
3. Diagnostic evaluation ➔ A diffuse process whereby the muscle fibers & the
a. Doppler Ultrasound Flow Studies endothelial lining of the walls of small arteries &
To hear (insonate) the blood flow in vessels arterioles become thickened
- Ankle-Brachial index (ABI) Atherosclerosis
- Ratio of the ankle systolic pressure to the brachial ➔ Involves a different process, affecting the intima of large
systolic pressure & medium-sized arteries
An objective measure of arterial disease that provide ➔ These changes consist of accumulation of lipids, calcium,
quantification of the degree of stenosis blood components, carbohydrates & fibrous tissue on the
b. Exercise Testing intimal layer of the artery.
To determine how long a pt can walk and to measure the ➔ Accumulation are referred as atheromas or plaques
ankle systolic blood pressure in response to walking ➔ A generalized disease of the extremities, it is usually
c. Duplex Ultrasonography present elsewhere in the body
Involves B-mode grayscale imaging of the tissue, organs & ➔ Inflammatory process involving the accumulation of
blood vessels (arterial & venous) & permits estimation of lipids, calcium, blood components, carbohydrates &
velocity changes by use of a pulsed doppler fibrous tissue on the intimal layer of a large or
d. Computed Tomography Scanning medium-sized artery
Provides cross-sectional images of soft tissue & visualizes Most common affected:
the area of volume changes to an extremity & the - Abdominal aorta - carotid
compartment where changes take place - Coronary
- Popliteal
Pathophysiology ★ Sedentary lifestyle
Risk factors: pathologic changes to the arterial vasculature > ★ Elevated C-reactive protein
diffuse process (muscle & the endothelial lining of the walls of ★ hyperhomocysteinemia
small arteries/arterioles become thickened Non-modifiable Risk Factors
↓ ★ Increasing age
Arteriosclerosis) ★ Female gender
narrowing of the lumen (stenosis, due to obstruction by thrombus, ★ Familial predisposition/genetics
aneurysm, ulceration & rupture) Prevention
↓ ◆ Reducing the amount of fat ingested in a healthy
indirect results are malnutrition (subsequent fibrosis of the organs diet
that are sclerotic arteries supply with blood) ◆ Substituting unsaturated fats for saturated fats
↓ ◆ Decreasing cholesterol intake (to reduce the risk of
cells undergo ischemic necrosis or ischemia) cardiovascular disease)
↓ ◆ Elimination of all controllable risk factors,
replaced by fibrous tissue (requires much less blood flow particularly the use of nicotine products, is
Atherosclerosis) strongly recommended
↓ Signs and symptoms:
Stenosis narrowing or constriction of a vessel ★ Depends on the organ or tissue affected
Atherosclerosis occurs through the following events Medical Management:
● Endothelial injury - Modification of risk factors
- Causes increased vascular permeability, leukocyte - Controlled exercise program (to improve circulation & its
adhesion & thrombosis functioning capacity)
● Accumulation of lipoproteins - in the vessel wall - Medication therapy
- Mainly LDL & its oxidized forms - Interventional or surgical graft procedures
● Monocyte adhesion to the endothelium Surgical Management: (vascular surgical procedures)
- Followed by migration into the intima & ★ Inflow procedures (improve blood supply from the aorta
transformation into macrophages and form cells into the femoral artery)
● Platelet adhesion ○ Are described w/ diseases of the aorta & outflow
● Factor release - from activated platelets, macrophages & procedures w/ peripheral arterial occlusive disease
vascular wall cells inducing smooth muscle cell ★ Outflow procedure (provide blood supply to vessels below
recruitment the femoral artery)
● Smooth muscle cell proliferation and ECM production Radiologic Intervention:
● Lipid accumulation - both extracellularly & w/in cells ➔ Angioplasty (Percutaneous transluminal angioplasty or
(macrophages & smooth muscle cells) PTA), if an isolated lesion or lesions are identified during
Risk factors of atherosclerosis and peripheral arterial disease the arteriography
Modifiable Risk Factors ◆ An invasive procedure that uses a balloon-tipped
★ Nicotine use (tobacco smoking or chewing) catheter to dilate a stenotic area of a blood vessel
★ Diet (contributing to hyperlipidemia Dissection
★ Hypertension ➔ Separation of the weakened elastic &
★ Diabetes fibromuscular elements in the medial layer of an
★ Hyperlipidemia artery
★ Stress
 ◆ Complication of PTA (hematoma formation, The age of onset and the severity are influenced by the
ambolus, dissection) type & number of atherosclerotic risk factors
➔ Atherectomy Pathophysiology:
◆ Removing plaque makes the artery wider, so blood Risk Factors: >obstruction or narrowing of the lumen of the aorta
can flow more freely to the heart, muscle & its major branches (carotid, vertebral, innominate, subclavian,
◆ The plaques is shaved or vaporized away with tiny mesenteric and celiac arteries)
rotating blades or a laser on the end of a catheter ↓
(a thin flexible tube) interruption of blood, usually to the legs & feet (arterial
Nursing Management: insufficiency( intermittent claudication or severe rest pain
Improving peripheral arterial circulation Arterial Insufficiency vs. Venous Insufficiency
➢ Positioning the part below the level of the heart, elevating Arterial insufficiency (PAD)
the head of the bed or use a reclining chair or sit w/ the - Narrowing of the anterior, commonly the pelvic & legs
feet resting on the floor Clinical symptoms:
➢ Assist the pt w/ walking or other moderate or grade Cramping pain, tired legs & hip muscles that
isometric exercises(to promote blood flow & encourage worsen during walking/activity & subsides w/ rest
the development of collateral circulation) Venous Insufficiency (PVD)
➢ Instruct the pt to walk w/ the point of pain, rest until the - Inadequate return of venous blood from the legs to the
pain subsides, then resume walking (so that endurance can heart
be decreased) as circulation develops Clinical symptoms:
➢ Regular exercise program (can result in increased walking tired/heavy itchy straining in the legs, pain
distance before the onset of claudication), but not for all pt worsen when standing & improves w/ leg
Promoting vasodilation and preventing vascular compression elevation and activity
➢ Application of warmth (to promote arterial flow) Signs & Symptoms:
➢ Avoid exposure to cold temp(causes vasoconstriction) ★ Intermittent claudication (hallmark symptom), pain may
➢ Adequate clothing & warm temp(protect from chilling) be described as aching, cramping or inducing fatigue or
➢ Stress management program(to minimize emotional stress weakness that occurs w/ the same degree of exercise or
due to stressful situations) activity as id relieved w/ rest
➢ Counseling services or relaxation training (for people who ★ Decreased ability to walk w/ same distance as before or
cannot cope effectively w/ situational stressors may notice increased pain w/ ambulation
➢ Avoid constrictive clothing & accessories (may impede ★ Rest pain (severe insufficiency), usually worse at night &
circulation to the extremities & promote venous stasis) often wakes the pt
➢ Discouraged crossing the legs for more than 15mins at a ★ Persistent pain in the foot or digits when the pt is resting,
time (it compresses vessels in the legs indicating severe degree of arterial insufficiency
Relieving Pain Diagnostic test
➢ Analgesic agents (hydrocodone plus acetaminophen) ● Examination of peripheral pulses
B . Peripheral arterial occlusive disease ● Careful history of the s/sx & by physical examination
Arterial insufficiency of the extremity ● CW Doppler and ABIs
- Occurs most in men and common cause of ● Treadmill testing for claudication
disability ● Duplex ultrasonography or other imaging studies
The legs are most frequently affected, however the upper Medical Management:
extremities may be involved. - Exercise program
 - Walking program combined w/ weight reduction & Promoting home and community-based care (discharge planning)
cessation of tobacco use (to improve activity tolerance) ➢ Assess the pt's ability to manage activities of daily living
- Arm-ergometer exercise training (improve physical fitness, independently & determines whether the pt has a network
central cardio-respiratory function & walking capacity of family & friends to assist w/ ADLs
Pharmacologic therapy ➢ Encouraged to make the lifestyle changes necessitated by
➔ Pentoxifylline (trental) & cilostazol (Pletal) Treatment of the onset of the chronic disease (pain management &
symptomatic claudication modification in diet, activity & hygiene -skin care)
➔ Antiplatelet agents, aspirin or clopidogrel (Plavix) Prevent ➢ Ensures that the pt has the knowledge & ability to assess
the formation of thromboemboli can lead to myocardial for any postoperative complications (infection, occlusion
infarction & stroke of the artery or graft, decreased blood flow)
➔ Statins -Beneficial effects on vascular inflammation, ➢ Assists in developing & implementing a plan to stop using
plaque stabilization, endothelial dysfunction &thrombosis tobacco
Surgical Management: Upper extremity arterial occlusive disease
Surgery is reserved for treatment of severe & disabling C. Arterial occlusions
claudication or when the limb is at risk of amputation because of - occur less frequently in the upper extremity (arms) than in
tissue necrosis the legs & cause less severe symptoms(because the
★ Endarterectomy to removed atheromatous obstruction collateral circulation is significantly better in the arms
★ Bypass grafts to reroute the blood flow around the stenosis - The arms also have less muscle mass & are not subjected
or occlusion to the workload of the legs
○ Before bypass grafting, the surgeon determines Signs and Symptoms
where the distal anastomosis (site where the ★ Typically complains of arm fatigue & pain w/ exercise
vessels are surgically joined) will be placed (forearm claudication)
★ Vein-graft ★ Inability to hold or grasp objects
Nursing Management (post op care) ★ Occasionally difficulty driving
Maintaining circulation through arterial repair ★ Develop a "subclavian steal" syndrome * characterized by
➢ Doppler assessment, color & temp, capillary refill, & reverse flow in the vertebral & basilar artery to provide
sensory & motor function of the affected extremity are blood flow to the arm.
checked & compared w/ those of the other extremity & ★ This syndrome may cause vertebrobasilar (cerebral)
recorded initially every 15 mins until stable symptoms: vertigo, ataxia, syncope or bilateral visual
➢ ABI monitored at least once every 8 hrs for the first 24 changes
hours & then once each day until discharge Diagnostic test:
Monitoring and managing potential complications - Assessment findings
➢ Continuous monitoring of urine output, central venous - Upper and forearm BP determination (to evaluate upper
pressure, mental status & pulse rate & volume (permits extremity arterial occlusions
early recognition & treatment of fluid imbalances) - Duplex ultrasonography (to identify the anatomic location
➢ Leg crossing & prolonged extremity are avoided (to of the lesion & to evaluate the hemodynamics of the blood
prevent thrombosis) flow
➢ Elevating the extremities & encouraging to exercise the - Transcranial Doppler evaluation (to evaluate the
extremities while in bed (to reduces edema) intracranial circulation & to detect any siphoning of blood
➢ Graduated compression or anti-embolism stocking may be flow to the affected arm
prescribed, but care must be taken (to avoid compressing - Arteriogram
distal vessel bypass grafts Medi cal Management:
 - PTA w/ possible stent or stent graft placement (if a short ▸ Risk factors: (Atherosclerosis) >
lesion is identified) Damaged or degenerating tunica media (vascular layer of the aorta
- Surgical bypass (if the lesion involves the subclavian ↓
artery w/ documented siphoning of blood flow from media loses its elasticity
- the intracranial circulation & an interventional radiologic ↓
procedure is not possible aortic walls weakens (from mechanical stress and hemodynamic
Nursing Management (post op care) forces)
➢ Arm kept at heart level or elevated, w/ the fingers at the ↓
highest level causes the lumen to dilate & protrude (aneurysm) eventually
➢ Pulse are monitored w/ Doppler assessment of the arterial rupture or dissection (as the vessels enlarges or weakens)
flow every hr for 4 hrs & then every shift I Are serious because they can rupture, leading to hemorrhage &
➢ BP obtained by stethoscope & Doppler) every 4 hrs & then death
every shift 1 .Thoracic aortic aneurysms
➢ Monitor motor & sensory function, warmth, color & - 85% cause by atherosclerosis
capillary refill w each arterial flow - Occurs most frequently in men between 50 to 70 years
D. Aortoiliac disease - The thoracic area is the most common site for a dissecting
- If collateral circulation has develop, pt w/ a stenosis or aneurysm
occlusion of the aortoiliac segment may be asymptomatic, - ⅓ of pts die of rupture of the aneurysm
or they may complain of buttocks or low back discomfort Sign and Symptoms:
associated w/ walking ★ Some pain are asymptomatic
- Men may experience impotence.(these pts may have ★ Pain (the most preeminent symptom), usually constant &
decreased or absent femoral pulses) boring but may occur only when the person is supine
E . Aneurysm Other conspicuous symptoms:
- A localized sac or dilation of an artery formed at a weak ★ Dyspnea (the result of pressure of the aneurysm sac
point in the vessel wall against the trachea, a man bronchus or the lung itself)
- A localized sac or dilation formed at a weak point in the ★ Cough, frequently paroxysmal & w/ a brassy quality
wall of the artery ★ Hoarseness, stridor or weakness or complete loss of the
- May be classified by its shape and form: voice (aphonia) resulting from pressure against the
1. Saccular (most common), projects from only laryngeal nerve
one side of the vessel ★ Dysphagia due to impingement on the esophagus by the
2. Fusiform (most common), if an entire arterial aneurysm
segment becomes dilated Diagnostic test:
3. Mycotic, very small due to localized infection - Chest x-ray
Etiologic classification of Arterial Aneurysms - Computed tomography angiography (CTA)
1. Congenital - Transesophageal echocardiography
2. Mechanical Medical Management:
3. Traumatic - Controlling blood pressure (antihypertensive agents)
4. Inflammatory - Correcting risk factors
5. Infectious - Surgery(to repair the aneurysm & restore vascular
6. Pregnancy-related degenerative continuity with a vascular graft
7. Anatosmatic 2 . Abdominal aortic aneurysm
Pathophysiology: - Most common cause is atherosclerosis
 - Affects men two to six time more often than women Surgical repair is performed w/ replacement grafts or endovascular
- Two to three times more common in caucasian versus repair using a stent graft, w/c is a Dacron or PTFE graft w/ external
black men structures made from a variety of materials(for additional support
- Most prevalent in older adult pts Nursing Management (post op care)
- Most of these aneurysms occur below the renal arteries ➢ Lie supine for 6 hrs
(infrarenal aneurysms) ➢ Head may be elevated up to 45 degrees after 2 hrs
Signs and Symptoms (only 40%) ➢ Bed rest without TP
★ Can feel their heart beating in the abdomen when lying ➢ Vital signs & Doppler assessment of peripheral pulses
down, or they may say that they feel an abdominal mass or ➢ Monitor complications
abdominal throbbing 1 . Dissecting aorta
★ Cyanosis & mottling of the toes(due to small cholesterol, - An aorta diseased by arteriosclerosis, a tear develops in
platelet or fibrin emboli may lodge in the interosseous or the intima or the media degenerates, resulting in a
digital arteries dissection
★ The most important indication is a pulsatile mass in the - Arterial dissections 3x more common in men
middle and upper abdomen (80% are palpated) - Occurs most commonly in the 50 to 70 year age group
★ A systolic bruit may be heard over the mass Pathophysiology:
Diagnostic test: › Causes: Unknown, degenerative changes etc.
- Duplex ultrasonography or CTA ( to determine the size, sudden tear in the intimal layer of the aorta. permits blood to
length & location of the aneurysm) enter the media
- Ultrasonography at 6minutes interval (when the ↓
aneurysm is small) creates a dissection within the wall of the aorta
Medical Management: ↓
Pharmacologic Therapy pressure from the contraction of the heart forces blood through
- Antihypertensive agents including diuretics, beta blockers, the tear
ACE inhibitors, angiotensin II receptor antagonists & ↓
calcium channel blockers (to maintain the pt's blood creates hemorrhage in the medial layer
pressure w/in acceptable limits ↓
Surgical Management: forming a false lumen between the intima and adventitia
- Surgery is the treatment of choice, for more than 5.5cm (2 Signs and Symptoms (onset is usually sudden)
inches) wide or those that are enlarging ★ Severe & persistent pain (described as tearing or ripping)
- Open surgical repair of the aneurysm by resecting the in the anterior chest or back & extends to the shoulders,
vessel & sewing a bypass graft in place epigastric area or abdomen
- Endovascular grafting (alternative treatment) ★ May appear pale, seating & tachycardia may be detected
Nursing Management: ★ Blood pressure may be elevated or marked different from
➢ Postoperative care requires frequent monitoring of one arm to the other if dissection involves the orifice of
pulmonary, cardiovascular, renal & neurologic status the subclavian artery on one side
➢ Monitor for complications
3 . Other Aneurysm Diagnostic Test:
- Aneurysms may be arise in the peripheral vessels (vessels - Arteriography
as the subclavian artery, renal artery, femoral artery or - Multidetector computed tomography
popliteal artery (most frequently) - angiography(MDCTA) Duplex ultrasonography
Medical Management: - MRA
Medical Management: - Minimally invasive interventional management:
- depends on the type of dissection (same w/ thoracic aortic - Emergen embolectomy (the procedure of choice if
aneurysms) the involved extremity is viable, involves incising
Nursing Management: the vessel & removing the clot)
➢ Same w/ aortic aneurysms Endovascular Management:
2. Arterial embolism and arterial thrombosis - Percutaneous mechanical thrombectomy devices
- Acute vascular occlusion may be caused by an embolus or (treatment of an acute thrombosis)
acute thrombosis Pharmacologic Therapy
- Acute arterial occlusions may result from iatrogenic injury, - IV anticoagulation w/ heparin (prevent the thrombus from
w/c can occur during insertion of invasive catheters spreading & reduce muscle necrosis)
(arteriography, PTA or stent placement, intra-aortic - Intra-arterial thrombolytic medications(dissolve the
balloon pump or may occur as a result of IV drug abuse embolus)
- Other causes: trauma from a fracture, crush injury, - Fibrin-specific thrombolytic medications(prevents the
penetrating wounds(that disrupt the arterial intima) development of systemic fibrinolysis
Pathophysiology: Nursing Management:
Causes: Atrial fibrillation, MI, etc. ➢ Bed rest w/ affected extremity level or slightly dependent
Thrombi develops in the chamber of the heart (15degress)
↓ ➢ The affected part is kept at room temperature & protected
Thrombi become detached from trauma
↓ ➢ VS every 15 mins if admitted to a critical care unit
Carried from the left side of the heart (arterial system) & lodge in ➢ closely monitor for bleeding
↓ ➢ Minimizes the number punches & avoids intramuscular
Obstruct an artery (smaller) than embolus injections.
Signs and symptoms: 3 . Raynaud phenomenon and other across syndromes
Acute arterial embolism /thrombosis in extremity with poor - A form of intermittent arteriolar vasoconstriction that
collateral flow results in coldness, pain & pallor of the finger or toes
★ Acute, severe pain - Symptoms may result from a defect in basal heat
★ Gradual loss of sensory and motor function production that eventually decreases the ability of
★ 5Ps (pain, pallor, pulselessness, paresthesia, cutaneous vessels to dilate
poikilothermia (coldness) & paralysis) - Episodes may be triggered by emotional factors or by
★ Collapse superficial veins, due to decreased blood flow to unusual sensitivity to cold
the extremity - Most common in between 16 - 40 years of age
★ Marked colder and paler part Pathophysiology:
Diagnostic test: Causes: unknown, connective tissue disorder
- Two-dimensional transthoracic echocardiography or TEE, Intrinsic vascular wall hyperactivity to cold or antigen-antibody
chest x-ray & ECG (may reveal the cardiac disease) immune response
- Noninvasive duplex & Doppler ultrasonography determine ↓
the presence & extent of underlying atherosclerosis Episodic constriction of the arterioles/arteries of the extremities
- Arteriography ↓
Medical Management: Reduced digital blood flow
- Heparin therapy(to prevent further development of emboli ↓
& to prevent the extension of existing thrombi) Results in pallor, cyanosis of the fingers
TWO FORMS - Sympathectomy, interrupting the sympathetic nerves by
1. Primary or idiopathic Raynaud’s disease removing the sympathetic ganglia or dividing their
- Occurs in the absence of an underlying disease branches
2. Secondary Raynaud’s (Raynaud’s syndrome) - Avoidance of exposure to cold & trauma & implementing
- Occurs in association w/ underlying disease, measures to improve local circulation as the primary focus
usually a connective tissue-disorder (SLE, RA, of treatment
scleroderma, trauma & obstructive arterial Nursing Management:
lesions) ➢ Avoid stressful & unsafe situations(stress management
- Characterized by vasospasms & fixed blood vessel classes)
obstructions that may lead to ischemia, ulceration ➢ Exposure ro cool must be minimized(wear layers of
& gangrene clothing, hats, mittens or gloves)
Signs and symptoms: ➢ Avoid all forms of nicotine to prevent complication
★ Pallor brought on by sudden vasoconstriction (classic (gangrene and amputation)
clinical picture) ➢ Cautioned to handle sharp objects to avoid injuring their
★ Cyanotic or bluish skin, due to pooling of deoxygenated fingers
blood during vasospasm, as a result of exaggerated reflow Venous disorders
(hyperemia) due to vasodilation, a red color (rubor) is - cause reduction in venous blood flow, causing blood stasis
produced when oxygenated blood returns to the digits A . Venous Thromboembolism
after the vasospasms stops. The characteristic sequence of - Deep vein thrombosis (DVT) occurs when a blood clot
color change is white, blue & red (rhombus) forms in one or more of the deep veins in body,
★ Numbness, tingling and burning pain occur as the color usually in the legs. Deep vein thrombosis can cause leg
changes, & the manifestations tend to be bilateral & pain or swelling but also can occur w/ no symptoms.
symmetric & may involve toes & fingers You can get DVT if you have certain medical conditions
Acrocyanosis that affect how your blood clots
- A variant of Raynaud’s phenomenon because both are - Pulmonary embolism is a blockage in one of the
aggravated by cold & emotional stress & both present w/ pulmonary arteries in the lungs. In most cases, pulmonary
the blue discoloration of the fingers & hyperhidrosis embolism is caused by blood clots that travel to the lungs
(excessive sweating) from deep veins in the legs or, rarely from veins in other
Signs and Symptoms: parts of the body (deep vein thrombosis)
★ Relative presence of skin color changes RISK FACTORS: Deep Vein Thrombosis and Pulmonary
★ Symmetry & an absences of the paroxysmal pallor Embolism
★ Marked clamminess & hyperhidrosis of the hands & feet, 1. Endothelial Damage
which tend to worsen in warmer temp. while the color ➔ Trauma
changes improve ➔ Surgery
★ Finger color normalizes when the hands are transferred ➔ Pacing wires
from the dependent to horizontal position ➔ Central venous catheters
Medical Management: ➔ Dialysis access catheters
- Avoiding the particular stimuli(cold, tobacco) that provoke ➔ Local vein damage
vasoconstriction is a primary factor in controlling RP ➔ Repetitive motion injury
- Calcium channel blockers(Nifedipine,Amlodipine) 2. Venous Stasis
effective in relieving symptoms ➔ Bed rest or immobilization
➔ Obesity
 ➔ History of varicosities ★ Edema & swelling of the extremity the outflow of venous
➔ Spinal cord injury blood is inhibited
➔ Age (>65 years) ★ Warmer affected extremity
3. Altered Coagulation ★ Prominent superficial veins
➔ Cancer ★ Tenderness produce by inflammation of the vein wall
➔ Pregnancy ★ In Some cases, s/sx of pulmonary embolism (PE) are the
➔ Oral contraceptive use first indication of DVT
➔ Protein C deficiency ★ Thrombosis of superficial veins pain or tenderness,
➔ Protein S deficiency redness & warmth in the involved area
➔ Antiphospholipid antibody syndrome Diagnostic test:
➔ Factor V Leiden defect - Nursing assessment includes measuring the circumference
➔ Prothrombin G20210A defect of the affected extremity at various level for comparison
➔ Hyperhomocysteinemia Prevention:
➔ Elevated factors II, VIII, IX, XI ❖ Application of graduated compression stockings
➔ Antithrombin III deficiency ❖ Use of intermittent pneumatic compression devices
➔ Polycythemia ❖ Encouragement of early ambulation & leg exercises
➔ Septicemia ❖ Administration of subcutaneous unfractionated or low
Pathophysiology: molecular weight heparin (LMWH) to prevent thrombosis
Causes: endothelial damage, venous stasis, for surgical pts
Altered coagulation ❖ Lifestyle changes(weight loss, smoking cessation & regular
↓ exercise)
Damage to the intimal lining of the blood vessels Medical Management: The goal are:
↓ - To prevent the thrombus from growing & fragments,
Creates s site for clot formation recurrent thromboemboli & post thrombotic syndrome
↓ - Anticoagulant therapy administration of a medication to
Thrombus develops delay the clotting time of blood, prevent formation of a
Complications of Venous Thrombosis thrombus in postoperative pts & forestall the extension of
● Chronic venous occlusion a thrombus after it has formed
● Pulmonary emboli from dislodged thrombi - Combining anticoagulant therapy with mechanical &
● Valvular destruction ultrasonic-assisted thrombolytic therapy may eliminate
● Chronic venous insufficiency post thrombotic syndrome by early removal of the
● Increased venous pressure thrombus
● Varicosities Pharmacologic Therapy:
● Venous ulcers ➔ Unfractionated Heparin
● Venous destruction ➔ Low molecular weight heparin
● Increased distal pressure ➔ Oral anticoagulant
● Fluid status ➔ Factor Xa inhibitors
● Edema ➔ Thrombolytic (Fibrinolytic) therapy
● Venous gangrene Endovascular Management:
Signs and Symptoms: ❖ Thrombectomy - a mechanical method of clot removal
★ Obstruction of the deep veins involve using intraluminal catheter w/ a balloon or other
devices
 ❖ Ultrasound assisted thrombolysis - uses bursts or 6. Promoting Home and Community-Based Care
continuous high frequency ultrasound waves emanating - Educate about the prescribed anticoagulant,its purpose &
from the catheters to cause cavitation of the thrombus, the need to take the correct amount at the specific times
making it more permeable to the thrombolytic agent prescribed
❖ Vena Cava Filter - may be placed at the same time of the - Aware that periodic blood tests are necessary to determine
thrombectomy or thrombolysis to traps large emboli & if a change in medication or dosage is required
prevents PE Signs and Symptoms:
❖ Balloon Angioplasty w/ stent placement - to treat chronic ★ Postthrombotic syndrome characterized by chronic venous
leg symptoms in pts w/ chronic iliac vein compression stasis resulting in edema, altered pigmentation, pain &
Nursing Management: stasis dermatitis
1. Assessing and monitoring anticoagulant therapy ★ Obstruction or poor calf muscle pumping in addition to
- (frequently monitor the aPTT, prothrombin time (PT), valvular reflux (severe)
INR, ACT, hemoglobin & hematocrit values, platelet ★ Dilated superficial veins
count, & fibrinogen level) ★ Stasis ulcer (results of the rupture of small skin veins &
2. Monitoring and managing potential complications ulcerations
- Bleeding(spontaneous)the principal complication of ★ Hemosiderm staining(when the vessels rupture RBC
anticoagulant therapy) escape into surrounding tissues & then degenerate,
- Thrombocytopenia, HIT may be a complication of heparin leaving a brownish discoloration of the tissues
therapy ★ Pigmentation & ulcerations in the lower part of the
- Drug Interactions with other medications extremity, in the area of the medial malleolus of the ankle
3. Proving comfort (are adjunct to therapy) ★ Dry crack & itches skin fibrose subcutaneous tissues
- Elevation of the affected extremity ★ Atrophy & firbrose subcutaneous tissues
- Graduated compression stockings Diagnostic test:
- Analgesic agents for pain relief - Duplex ultrasonography confirms the obstruction &
- Warm, moist packs applied to the affected extremity identifies the level of valvular incompetence
reduce the discomfort associated with DVT Complications
- Encouraged to walk once anticoagulation therapy has been ● Venous ulceration (most serious)
initiated ● Cellulitis dermatitis
- Bed exercises such as repetitive dorsiflexion of the foot Management:
4. Compression therapy - Goal-directed at reducing venous stasis & preventing
- Stockings ulcerations
- External Compression Devices & Wraps Intermittent - Elevating the legs (decreases edema, promotes venous
Pneumatic Compression Devices return & provides symptomatic relief Compression of
5. Positioning the body and encouraging exercise superficial veins w/ graduated
- Periodic elevation of the feet & lower legs above the level - compression stockings (reduces the pooling of venous
of the heart (allows the superficial & tibial veins to empty blood, entre ces venous return to the heart)
rapidly and to remain collapsed
- Active & passive leg exercises (calf muscles), to increase Leg ulcers
venous flow - An excavation of the skin that occurs when inflamed
- Early ambulation to prevent venous stasis Deep breathing necrotic tissue sloughs off
exercises, they produce increased negative pressure in the Pathophysiology:
thorax, which assists in emptying the large veins Cellular metabolism cannot maintain energy balance
 ↓ - Minimal unless extremity kept in dependent position
alterations in blood vessels at the arterial, capillary & venous level constantly to relieve pain
↓ Venous
inadequate exchange of oxygen and other nutrients in the tissue Location:
↓ - Medial malleolus or anterior tibial area
cell death (necrosis) Pain:
↓ - Minimal pain or very painful
formation of leg ulcers Depth of ulcer:
Characteristics of ARTERIAL & VENOUS insufficiency & - superficial
resulting ulcer Shape:
Arterial - irregular
Pain: Ulcer base:
- Intermittent claudication to sharp, unrelenting, constant. - Granulation tissue-beefy red to yellow fibrinous in chronic
Pulses: long term, ulcer
- Diminished or absent Leg edema:
Skin characteristics: - Moderate to severe
- Dependent rubor-elevation pallor of the foot, dry skin, Diagnostic test:
cool to cold temperature, loss of hair over toes & dorsum - Doppler & duplex ultrasound studies
of foot; nails thickened and ridged - Arteriography
Venous - Venography
Pain: - Cultures of the ulcer
- Aching, cramping Medical Management:
Pulses: 1. Pharmacologic therapy
- Present but may be difficult to palpate through edema - Anticoagulant agent *oral antibiotics
Skin characteristics: 2. Compression therapy to facilitate venous return to the
- Pigmentation in gaiter area (area of medial and lateral heart
malleolus) skin thickened & tough, may be reddish blue, 3. Debridement for removal of nonviable tissue from wounds
frequently associated dermatitis 4. Topical therapy to promote wound healing
ULCER characteristics 5. Wound dressing to favor healing
Arterial 6. Stimulated healing
Location: 7. Hyperbaric Oxygenation enhances the ability of leukocytes
- Tip of toes, toe web or other pressure areas if confined to to phagocytize and kill bacteria
bed. 8. Negative pressure wound therapy decreases time to
Pain: healing in complex wounds that have not healed in a 3
- Very painful week period
Depth of ulcer: Varicose Veins
- Deep, often involving joint space - Abnormally dilated, tortuous, superficial veins caused by
Shape: incompetent venous valves
- circular - Occurs ots commonly in the lower extremities, saphenous
Ulcer base: veins, lower trunk, esophagus
- Pale to black and dry gangrene. Pathophysiology:
Leg edema:
Causes: hereditary weakness of the vein, occupations requiring ➢ Worn graduated compression stocking
prolonged standing, pregnancy etc. Reflux of venous blood (lower ➢ Leg exercises
extremities, saphenous veins, lower trunk, esophagus) >Venous ➢ Analgesic agents
stasis (incompetent venous valves >Dilated tortuous superficial Lymphatic disorders
Changes in vein wall A . Lymphangitis and Lymphadenitis
↓ Lymphangitis
Over stretching of veins ➔ Is an acute inflammation of the lymphatic channels
↓ ➔ Arises most commonly from a focus of infection in an
Increase in size of veins but valve leaflets don’t expand extremity w/ usually the infectious organisms is a
↓ hemolytic streptococcus
Secondary valvular Incompetence ➔ The characteristics red streaks that extend up to arm or
↓ the leg from an infected wound outline the course of the
Backflow (reflux) lymphatic vessels as they drain
↓ Lymphadenitis
Pooling and further dilation of veins ➔ When the lymph nodes located along the course of the
↓ lymphatic channels become enlarged, red and tender
Varicosity-Dilated Tortuous Veins Suppurative lymphadenitis
Signs and Symptoms: ➔ When become a necrotic and form an abscess
★ Dull aches Pathophysiology:
★ Nocturnal Cramps (common) Causes: Infectious organism (haemolytic streptococcus)
★ Increased muscle fatigue in the lower legs ↓
★ Ankle edema lymph nodes become enlarged, red (streaks) and tender
★ Feeling of heaviness of the legs ↓
★ Chronic Insufficiency Symptoms (edema, pain, tissue swelling occur (a quantity of lymph)
pigmentation and ulceration) ↓
★ Increases susceptibility to infection obstruction of the lymphatic vessel (Lymphedema)
Diagnostic test: ↓
- Duplex ultrasound - documents the anatomic site of reflux caused by parasite (filarial)
& provides a quantitative measure of the severity of ↓
valvular reflux leads to chronic fibrosis, thickening of the subcutaneous tissues,
- Venography - to evaluate valvular reflux hypertrophy of the skin
Prevention: ↓
- Avoid wearing socks that are too tight at the top or that chronic swelling of the extremity (elephantiasis)
have marks on the skin Elephantiasis
- Avoid crossing the legs - Chronic obstruction of the extremity due to lymphatic
- Avoid sitting and standing for long periods obstruction caused by a parasite (filarial)
Medical Management: Signs and symptoms:
- Ligation & stripping to remove the vein ★ frequent bouts of acute infection (high fever, chills) and
- Thermal ablation to seal the vein ★ increased residual edema after the inflammation has
- Sclerotherapy by obliterating the lumen of the vein resolved
Nursing Management: B. Lymphedema and Elephantiasis
➢ Encourage ambulation (Walking) Lymphedema
 - Tissue swelling occurs in the extremities because of an Bacteria release their toxins in the subcutaneous tissue
increased quantity of lymph that results from obstruction ↓
of lymph vessels. Localized swelling and redness
Types: Signs and symptoms:
1. Primary (congenital malformations/Lymphedema ★ Acute onset of swelling,
praecox)) - most common, caused by hypoplasia of the ★ localized redness (may not be uniform and often skips
lymphatic system of the lower extremity area),
2. Secondary (acquired obstructions) ★ pain,
Signs and symptoms: ★ systemic infection (fever, chills, sweating),
★ Soft & pitting edema (initial) ★ tender and enlarged regional lymph nodes
★ Firm & nonpitting edema ( as conditions progresses) Medical Management:
Management 1. Oral antibiotic therapy (mild cases)
Medical: Goal to reduce and control edema and prevent 2. IV antibiotics (severe)
1. Active & passive exercises to assist in moving lymphatic Nursing Management:
fluid into the bloodstream 1. Elevate the affected area 3 to 6 inches above heart level
2. External compression devices milk the fluid proximally 2. Apply warm, moist packs to the site every 2 to 4 hours
from the foot to the hip or from the hand to the axilla 3. Education about skin and foot care
3. Custom-fitted graduated compression stockings or sleeves
to prevent long term edema
4. Bedrest
5. Leg elevated to aid in mobilizing the fluid
6. Manual lymphatic drainage to direct or shift the congested
lymph through functioning lymphatics that have
preserved drainage
Pharmacologic:
1. Diuretic furosemide (Lasix) initial therapy to prevent
overload due to mobilization of extracellular fluid
2. Antibiotherapy for infection
Surgical:
- Excision of the affected subcutaneous tissue & fascia w/
skin grafting to cover the defect
- Surgical relocation by buried dermal flap to provide a
conduit of lymphatic drainage
Nursing:
➢ Constant elevation of the affected extremity
➢ Observation for complications
C. Cellulitis
- Most common infectious cause of limb swelling
- Occur as single isolated event or recurrent events
Pathophysiology:
Entry of bacteria to the normal skin barriers >
↓