RN Expert Guides: Cardiovascular Care, 1st Edition (2008)

Chapter 10. Cardiovascular Complications

CARDIAC TAMPONADE

Cardiac tamponade involves a rapid increase in intrapericardial pressure, which impairs diastolic filling of the heart and reduces cardiac output. The increase in pressure usually results from blood or fluid accumulation in the pericardial sac. If fluid accumulates rapidly, as little as 250 ml can create an emergency situation.

Prognosis depends on the rate of fluid accumulation. If it accumulates rapidly, cardiac tamponade requires emergency life-saving measures to prevent death. Slow accumulation and an increase in pressure, as in pericardial effusion associated with cancer, may not produce immediate signs and symptoms because the fibrous wall of the pericardial sac can gradually stretch to accommodate as much as 1 to 2 L of fluid.

Pathophysiology

In cardiac tamponade, the progressive accumulation of fluid in the pericardial sac causes compression of the heart chambers. This compression obstructs blood flow into the ventricles and reduces the amount of blood that can be pumped out of the heart with each contraction. (See Understanding cardiac tamponade, page 476.)

Each time the ventricles contract, more fluid accumulates in the pericardial sac. This further limits the amount of blood that can fill the ventricular chambers—especially the left ventricle—during the next cardiac cycle.

ff2-b01382759RED FLAG

Cardiac tamponade may cause a cardiac condition called pulseless electrical activity (PEA). In PEA, isolated electrical activity occurs sporadically without evidence of myocardial contraction. Unless the underlying cardiac tamponade is identified and treated quickly, PEA results in death.

UP CLOSE

ff4-b01382759UNDERSTANDING CARDIAC TAMPONADE

The pericardial sac, which surrounds and protects the heart, is composed of several layers. The fibrous pericardium is the tough outermost membrane; the inner membrane, called the serous membrane, consists of the visceral and parietal layers. The visceral layer clings to the heart and is also known as the epicardial layer of the heart. The parietal layer lies between the visceral layer and the fibrous pericardium. The pericardial space—between the visceral and parietal layers-contains 10 to 30 ml of pericardial fluid. This fluid lubricates the layers and minimizes friction when the heart contracts.

NORMAL HEART AND PERICARDIUM

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In cardiac tamponade, blood or fluid fills the pericardial space, compressing the heart chambers, increasing intracardiac pressure, and obstructing venous return. As blood flow into the ventricles falls, so does cardiac output. Without prompt treatment, low cardiac output can be fatal.

CARDIAC TAMPONADE

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The amount of fluid necessary to cause cardiac tamponade varies greatly; it may be as little as 50 ml when the fluid accumulates rapidly or more than 2 L when the fluid accumulates slowly and the pericardium stretches to adapt.

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effusion (in patients with cancer, bacterial infection, tuberculosis or, rarely, acute rheumatic fever)

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hemorrhage from trauma (such as a gunshot or stab wound to the chest and perforation by catheter during cardiac or central venous catheterization, or after cardiac surgery)

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hemorrhage from nontraumatic causes (such as rupture of the heart or great vessels, or anticoagulant therapy in a patient with pericarditis)

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viral, postirradiation, or idiopathic pericarditis

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acute myocardial infarction

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pneumothorax causing pressure against the heart

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drug reaction (such as with procainamide, hydralazine, minoxidil, isoniazid, penicillin, methysergide, and daunorubicin)

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a connective tissue disorder (such as rheumatoid arthritis, systemic lupus erythematosus, rheumatic fever, vasculitis, or scleroderma).

Complications

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Reduced cardiac output (fatal without prompt treatment)

Assessment findings

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The patient's history may show a disorder that can cause cardiac tamponade.

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He may report acute pain and dyspnea, sitting upright and leaning forward to facilitate breathing and lessen the pain. He may be orthopneic, diaphoretic, anxious, and restless, and appear pale or cyanotic.

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You may note jugular vein distention produced by increased venous pressure, although this may not be present if the patient is hypovolemic.

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Palpation of the peripheral pulses may disclose rapid, weak pulses. Palpation of the upper quadrant may reveal hepatomegaly.

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Percussion may disclose a widening area of flatness across the anterior chest wall, indicating a large effusion. Hepatomegaly may also be noted.

 

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Auscultation of the blood pressure may demonstrate a decreased arterial blood pressure, paradoxical pulse (an abnormal inspiratory drop in systemic blood pressure greater than 15 mm Hg), and narrow pulse pressure.

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Heart sounds may be muffled. A quiet heart with faint sounds usually accompanies only severe tamponade and occurs within minutes of the tamponade, as happens with cardiac rupture or trauma. The lungs are clear.

Diagnostic test results

The following test results are characteristic of cardiac tamponade:

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Chest X-rays show slightly widened mediastinum and enlargement of the cardiac silhouette.

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Electrocardiography (ECG) is useful to rule out other cardiac disorders. The QRS complex may be reduced, and electrical alternans of the P wave, QRS complex, and T wave may be present. Generalized ST-segment elevation is noted in all leads.

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Pulmonary artery pressure monitoring detects increased right atrial pressure, right ventricular diastolic pressure, and central venous pressure (CVP).

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Echocardiography records pericardial effusion with signs of right ventricular and atrial compression.

Treatment

The goal of treatment is to relieve intrapericardial pressure and cardiac compression by removing accumulated blood or fluid. Pericardiocentesis (needle aspiration of the pericardial cavity) or surgical creation of an opening dramatically improves systemic arterial pressure and cardiac output with aspiration of as little as 25 ml of fluid. A drain may be inserted into the pericardial sac to drain the effusion. (See Aspirating pericardial fluid.) This may be left in until the effusion process stops or the corrective action (pericardial window) is performed.

If tamponade or effusions or adhesions from chronic pericarditis recur, a portion or all of the pericardium may need to be removed to allow adequate ventricular filling and contraction. A pericardial window may be performed, which involves removing a portion of the pericardium to permit excess pericardial fluid to drain into the pleural space. In more severe cases, removal of the toughened encasing pericardium (pericardectomy) may be necessary.

In the hypotensive patient, trial volume loading with I.V. normal saline solution with albumin and, perhaps, an inotropic drug such as dopamine is necessary to maintain cardiac output.

ASPIRATING PERICARDIAL FLUID

In pericardiocentesis, a needle and syringe assembly is inserted through the chest wall into the pericardial sac, as illustrated here. Electrocardiographic monitoring with a leadwire attached to the needle and electrodes placed on the limbs (right arm [RA], right leg [RL], left arm [LA], and left leg [LL]) helps to ensure proper needle placement and to avoid damage to the heart.

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Depending on the cause of tamponade, additional treatment may include:

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for traumatic injury, blood transfusion or a thoracotomy to drain reaccumulating fluid or to repair bleeding sites

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for heparin-induced tamponade, the heparin antagonist protamine

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for warfarin-induced tamponade, vitamin K.

Nursing interventions

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Monitor the patient with cardiac tamponade in the intensive care unit. Check for signs of increasing tamponade, increasing dyspnea, and arrhythmias.

FOR A PATIENT WHO HAS UNDERGONE PERICARDIOCENTESIS

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Reassure the patient to reduce his anxiety.

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Gather a pericardiocentesis tray, an ECG machine, and an emergency cart with a defibrillator at the bedside. Make sure the equipment is turned on and ready to be used. Position the patient at a

45- to 60-degree angle. Connect the precordial ECG lead to the hub of the aspiration needle with an alligator clamp and connecting wire, and assist with fluid aspiration. When the needle touches the myocardium, you see ST-segment elevation or premature ventricular contractions.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH CARDIAC TAMPONADE

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Teach the patient signs and symptoms of recurrent effusion, infection, and cardiac arrhythmias to report to the practitioner.

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Review medications and adverse effects.

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Review incisional care if appropriate.

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Monitor blood pressure and CVP during and after pericardiocentesis. Infuse I.V. solutions, as ordered, to maintain blood pressure. Watch for a decrease in CVP and a concomitant increase in blood pressure, which indicate relief of cardiac compression.

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Administer oxygen therapy as needed.

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Watch for complications of pericardiocentesis, such as ventricular fibrillation, vasovagal arrest, and coronary artery or cardiac chamber puncture. Closely monitor cardiac rhythm strip changes, blood pressure, pulse rate, level of consciousness, and urine output.

FOR A PATIENT WHO HAS UNDERGONE THORACOTOMY

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Give an antibiotic, protamine, or vitamin K.

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Postoperatively monitor critical parameters, such as vital signs and arterial blood gas levels, and assess heart and breath sounds. Give an analgesic as ordered. Maintain the chest drainage system, and be alert for complications, such as hemorrhage and arrhythmias. (See Teaching the patient with cardiac tamponade.)

CARDIOGENIC SHOCK

Cardiogenic shock is a condition of diminished cardiac output that severely impairs tissue perfusion. It's sometimes called pump failure. Cardiogenic shock can occur as a serious complication in nearly 15% of all patients who are hospitalized with acute myocardial infarction (MI). It typically affects patients whose area of infarction involves 40% or more of left ventricular muscle mass; in such patients, mortality may exceed 85%.

Pathophysiology

In cardiogenic shock, the left ventricle can't maintain adequate cardiac output. Compensatory mechanisms increase heart rate, strengthen myocardial contractions, promote sodium and water retention, and cause selective vasoconstriction. However, these mechanisms increase myocardial workload and oxygen consumption, which reduces the heart's ability to pump blood, especially if the patient has myocardial ischemia. Consequently, blood backs up, resulting in pulmonary edema. Eventually, cardiac output falls and multisystem organ failure develops as the compensatory mechanisms fail to maintain perfusion.

Cardiogenic shock can result from any condition that causes significant left ventricular dysfunction with reduced cardiac output, such as an MI (most common), myocardial ischemia, papillary muscle dysfunction, and end-stage cardiomyopathy.

Other causes include myocarditis and depression of myocardial contractility after cardiac arrest and prolonged cardiac surgery. Mechanical abnormalities of the ventricle, such as acute mitral or aortic insufficiency or an acutely acquired ventricular septal defect or ventricular aneurysm, may also result in cardiogenic shock.

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Acute respiratory distress syndrome

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Acute tubular necrosis

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Disseminated intravascular coagulation

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Death

Assessment findings

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Typically, the patient's history includes a disorder that severely decreases left ventricular function, such as an MI or cardiomyopathy.

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Patients with underlying cardiac disease may complain of angina because of decreased myocardial perfusion and oxygenation.

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Urine output is usually less than 20 ml/hour.

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Palpation of peripheral pulses may reveal a rapid, thready pulse. The skin feels cold and clammy.

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Auscultation of blood pressure usually discloses a mean arterial pressure of less than 60 mm Hg in adults and a narrowing pulse pressure.

CLASSIFYING SHOCK

 

TYPE

DESCRIPTION

 

Cardiogenic

Results from a direct or indirect pump failure with decreasing cardiac output. Total body fluid isn't decreased. Causes include valvular stenosis or insufficiency, myocardial infarction, cardiomyopathy, arrhythmias, cardiac arrest, cardiac tamponade, pericarditis, pulmonary hypertension, and pulmonary emboli.

 

Distributive

Results from inadequate vascular tone that leads to massive vasodilation. Vascular volume remains normal and heart pumps adequately, but size of vascular space increases. Result is maldistribution of blood within the circulatory system. It includes the following subtypes:

• Anaphylactic shock: characterized by massive vasodilation and increased capillary permeability secondary to a hypersensitivity reaction to an antigen.

• Neurogenic shock: characterized by massive vasodilation from loss or suppression of sympathetic tone. Causes include head trauma, spinal cord injuries, anesthesia, and stress.

• Septic shock: a form of severe sepsis characterized by hypotension and altered tissue perfusion. Vascular tone is lost and cardiac output may be decreased.

 

Hypovolemic

Results from a decrease in central vascular volume. Total body fluids may or may not be decreased. Causes include hemorrhage, dehydration, and fluid shifts (caused by trauma, burns, or anaphylaxis).

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In a patient with chronic hypotension, the mean pressure may fall below 50 mm Hg before he exhibits signs of shock.

     

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The heart is auscultated to detect gallop rhythm, faint heart sounds and, possibly (if shock results from rupture of the ventricular septum or papillary muscles), a holosystolic murmur.

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Although many of these clinical features also occur in heart failure and other shock syndromes, they are usually more profound in cardiogenic shock. (See Classifying shock.)

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Patients with pericardial tamponade may have distant heart sounds.

Diagnostic test results

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Pulmonary artery pressure (PAP) monitoring reveals increased PAP and pulmonary artery wedge pressure (PAWP), reflecting an increase in left ventricular end-diastolic pressure (preload) and

heightened resistance to left ventricular emptying (afterload) caused by ineffective pumping and increased peripheral vascular resistance. Thermodilution catheterization reveals a reduced cardiac index (less than 1.8 L/minute/ml).

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Invasive arterial pressure monitoring shows hypotension caused by impaired ventricular ejection.

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Arterial blood gas analysis may show metabolic and respiratory acidosis and hypoxia.

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Electrocardiography demonstrates possible evidence of an acute MI, ischemia, or a ventricular aneurysm.

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Cardiac catheterization and echocardiography reveal other conditions that can lead to pump dysfunction and failure, such as cardiac tamponade, papillary muscle infarct or rupture, ventricular septal rupture, pulmonary emboli, venous pooling (associated with venodilators and continuous intermittent positive pressure breathing), and hypovolemia.

Treatment

Treatment aims to enhance cardiovascular status by increasing cardiac output, improving myocardial perfusion, and decreasing cardiac workload with combinations of cardiovascular drugs and mechanical-assist techniques.

I.V. drug therapy may include dopamine (Inocor), a vasopressor to increase cardiac output, blood pressure, and renal blood flow; milrinone (Primacor) or dobutamine (Dobutrex), an inotropic agent to increase myocardial contractility; and norepinephrine (Levophed), when a more potent vasoconstrictor is necessary. Nitroprusside, a vasodilator, may be used with a vasopressor to further improve cardiac output by decreasing peripheral vascular resistance (afterload) and reducing left ventricular end-diastolic pressure (preload). The patient's blood pressure must be adequate to support nitroprusside therapy and must be monitored closely. Furosemide (Lasix) is used to decrease pulmonary congestion.

Treatment may also include the intra-aortic balloon pump (IABP), a mechanical-assist device that attempts to improve coronary artery perfusion and decrease cardiac workload. The inflatable balloon pump is inserted through the femoral artery into the descending thoracic aorta. The balloon inflates during diastole to increase coronary artery perfusion pressure and deflates before systole (before the aortic valve opens) to reduce resistance to ejection (afterload) and, therefore, lessen cardiac workload. Improved ventricular ejection, which significantly improves cardiac output, and a subsequent vasodilation in the peripheral vessels lead to lower preload volume.

When drug therapy and IABP insertion fail, a ventricular assist device may be used.

Nursing interventions

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In the intensive care unit, start I.V. infusions with normal saline solution or lactated Ringer's solution, using a large-bore (14G to 18G) catheter, which allows easier administration of later blood transfusions.

ff2-b01382759RED FLAG

Don't start I.V. infusions in the legs of a shock patient who has suffered abdominal trauma because infused fluid may escape through the ruptured vessel into the abdomen.

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Monitor and record blood pressure, pulse and respiratory rates, and peripheral pulses every 1 to 5 minutes until the patient's condition is stabilized. Record hemodynamic pressure readings every 15 minutes. Monitor cardiac rhythm continuously. Systolic blood pressure less than 80 mm Hg usually results in inadequate coronary artery blood flow, cardiac ischemia, arrhythmias, and further complications of low cardiac output. When blood pressure drops below 80 mm Hg, increase the oxygen flow rate, and notify the practitioner immediately.

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A progressive drop in blood pressure accompanied by a thready pulse generally signals inadequate cardiac output from reduced intravascular volume. Notify the practitioner, and increase the infusion rate.

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Using a pulmonary artery catheter, closely monitor PAP, PAWP, and cardiac output. A high PAWP indicates heart failure, increased systemic vascular resistance, decreased cardiac output, and decreased cardiac index and should be reported immediately.

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Insert an indwelling urinary catheter if necessary to measure hourly urine output. If the output is less than 30 ml/hour in an adult, increase the fluid infusion rate, but watch for signs of fluid overload such as an increase in PAWP. Notify the practitioner if the patient's urine output doesn't improve.

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Give an osmotic diuretic, such as mannitol, to increase renal blood flow and urine output. Determine how much fluid to give by checking blood pressure, urine output, central venous pressure (CVP), or PAWP. To increase accuracy, measure CVP at the level of the right atrium, using the same reference point on the chest each time.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH CARDIOGENIC SHOCK

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Teach the patient the early warning signs of myocardial infarction and how to access emergency care.

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Educate the patient about signs and symptoms of heart failure and cardiac arrhythmias.

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Review home care instructions, medications, and special equipment needs such as oxygen.

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Draw an arterial blood sample to measure blood gas levels. Administer oxygen by face mask or airway to ensure adequate oxygenation of tissues. Adjust the oxygen flow rate to a higher or lower level as blood gas measurements indicate. Many patients need 100% oxygen, and some require 5 to 15 cm H2O of positive endexpiratory or continuous positive airway pressure ventilation.

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Monitor complete blood count and electrolyte levels.

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During therapy, assess skin color and temperature, and note any changes. Cold, clammy skin may be a sign of continuing peripheral vascular constriction, indicating progressive shock.

ff2-b01382759RED FLAG

When a patient is on the IABP, move him as little as possible. Never flex the patient's leg at the hip because this may displace or fracture the catheter. Never place the patient in a sitting position (including for chest X-rays) while the balloon is inflated; the balloon may tear through the aorta and cause immediate death. Assess pedal pulses and skin temperature and color to make sure circulation to the leg is adequate. Check the dressing on the insertion site frequently for bleeding, and change it according to facility protocol. Also check the site for hematoma or signs of infection, and culture any drainage.

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If the patient becomes hemodynamically stable, gradually reduce the frequency of balloon inflation to wean him from the IABP. During weaning, carefully watch for monitor changes, chest pain, and other signs and symptoms of recurring cardiac ischemia and shock.

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To ease emotional stress, plan your care to allow frequent rest periods, and provide for as much privacy as possible. Allow family members to visit and comfort the patient as much as possible.

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Allow the family to express their anger, anxiety, and fear. (See Teaching the patient with cardiogenic shock.)

HYPOVOLEMIC SHOCK

Hypovolemic shock is a potentially life-threatening situation in which reduced intravascular blood volume causes circulatory dysfunction and inadequate tissue perfusion. Tissue anoxia prompts a shift in cellular metabolism from aerobic to anaerobic pathways. This produces an accumulation of lactic acid, resulting in metabolic acidosis.

Without sufficient blood or fluid replacement, hypovolemic shock may lead to irreversible cerebral and renal damage, cardiac arrest and, ultimately, death. (See .) Hypovolemic shock necessitates early recognition of signs and symptoms and prompt, aggressive treatment to improve the prognosis.

Pathophysiology

In hypovolemic shock, venous return to the heart is reduced when fluid is lost from the intravascular space through external losses or the shift of fluid from the vessels to the intersitial or intracellular spaces. This reduction in preload decreases ventricular filling, leading to a drop in stroke volume. Then, cardiac output falls, causing reduced perfusion of the tissues and organs.

Hypovolemic shock usually results from acute blood loss—about one-fifth of total volume. Massive blood loss may result from GI bleeding, internal hemorrhage (such as hemothorax or hemoperitoneum), external hemorrhage (caused by accidental or surgical trauma), or any condition (such as severe burns) that reduces circulating intravascular plasma volume or other body fluids.

Other causes of hypovolemic shock include intestinal obstruction, peritonitis, acute pancreatitis, ascites and dehydration from excessive perspiration, severe diarrhea or protracted vomiting, diabetes insipidus, diuresis, and inadequate fluid intake.

Complications

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Acute respiratory distress syndrome

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Disseminated intravascular coagulation (DIC)

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Multiple-organ-dysfunction syndrome

Assessment findings

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The patient's history includes disorders or conditions that reduce blood volume, such as GI hemorrhage, trauma, and severe diarrhea and vomiting.

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A patient with cardiac disease may complain of angina because of decreased myocardial perfusion and oxygenation.

HOW HYPOVOLEMIC SHOCK PROGRESSES

Vascular fluid volume loss causes the extreme tissue hypoperfusion that characterizes hypovolemic shock. Internal fluid loss results from internal hemorrhage (such as GI bleeding) and third-space fluid shifting (such as in diabetic ketoacidosis). External fluid loss results from severe bleeding or from severe diarrhea, diuresis, or vomiting.

Inadequate vascular volume leads to decreased venous return and cardiac output. The resulting drop in arterial blood pressure activates the body's compensatory mechanisms in an attempt to increase vascular volume. If compensation is unsuccessful, decompensation and death may rapidly ensue.

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Inspection may reveal pale skin, decreased sensorium, and rapid, shallow respirations.

     

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Palpation of peripheral pulses may disclose a rapid, thready pulse; the skin feels cold and clammy.

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Auscultation of blood pressure usually detects a mean arterial pressure of less than 60 mm Hg in adults and a narrowing pulse pressure.

CHECKING FOR EARLY HYPOVOLEMIC SHOCK

Orthostatic vital signs

Measure the patient's blood pressure and pulse rate while lying in a supine position, sitting, and standing. Wait at least 1 minute between each position change. A systolic blood pressure decrease of 10 mm Hg or more between positions or a pulse rate increase of 10 beats/minute or more is a sign of volume depletion and impending hypovolemic shock.

Tilt test

With the patient lying in a supine position, raise his legs above heart level. If his blood pressure increases significantly, the test is positive, indicating volume depletion and impending hypovolemic shock.

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In patients with chronic hypotension, the mean pressure may fall below 50 mm Hg before signs of shock appear.

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Orthostatic vital signs and the tilt test may help determine the presence of hypovolemic shock. (See Checking for early hypovolemic shock.)

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Central venous pressure (CVP), right atrial pressure, pulmonary artery pressure, pulmonary artery wedge pressure (PAWP), and cardiac output are reduced.

Diagnostic test results

Characteristic laboratory findings include:

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low hematocrit and decreased hemoglobin level and red blood cell and platelet counts

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elevated serum potassium, sodium, lactate dehydrogenase, creatinine, and blood urea nitrogen levels

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increased urine specific gravity (greater than 1.020) and urine osmolality

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decreased urine creatinine levels

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decreased pH and partial pressure of arterial oxygen and increased partial pressure of carbon dioxide.

Tests to identify internal bleeding sites include:

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X-rays

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aspiration of gastric contents through a nasogastric tube

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tests for occult blood

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coagulation studies may detect coagulopathy from DIC.

Treatment

Emergency treatment measures include prompt and adequate blood and fluid replacement to restore intravascular volume and to raise blood pressure and maintain it above 60 mm Hg. Infusion of normal saline solution or lactated Ringer's solution and then possibly plasma proteins (albumin) or other plasma expanders may produce adequate volume expansion until packed cells can be matched. A rapid solution infusion system can provide these crystalloids or colloids at high flow rates.

For severe cases, an intra-aortic balloon pump, ventricular assist device, or pneumatic antishock garment may be helpful.

Treatment may also include oxygen administration, bleeding control by direct application of pressure and related measures, dopamine or another inotropic agent, and possibly surgery to correct the underlying problem. To be effective, dopamine or other inotropics must be used with vigorous fluid resuscitation.

Nursing interventions

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Check for a patent airway and adequate circulation. If blood pressure and heart rate are absent, start cardiopulmonary resuscitation.

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Record the patient's blood pressure, pulse and respiratory rates, and peripheral pulses every 15 minutes until the patient's condition is stabilized. Monitor cardiac rhythm continuously.

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When systolic blood pressure drops below 80 mm Hg, increase the oxygen flow rate, and notify the practitioner immediately because systolic blood pressure less than 80 mm Hg usually results in inadequate coronary artery blood flow, cardiac ischemia, arrhythmias, and further complications of low cardiac output.

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Start an I.V. infusion with normal saline solution or lactated Ringer's solution, using a large-bore (14G to 18G) catheter, which allows easier administration of later blood transfusions.

ff2-b01382759RED FLAG

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Notify the practitioner and increase the infusion rate if the patient has a progressive drop in blood pressure accompanied by a thready pulse. This generally signals inadequate cardiac output from reduced intravascular volume.

·

Insert an indwelling urinary catheter if necessary to measure hourly urine output. If output is less than 30 ml/hour in adults, increase the fluid infusion rate, but watch for signs of fluid overload such as

an increase in PAWP. Notify the practitioner if urine output doesn't improve.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH HYPOVOLEMIC SHOCK

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Instruct the patient and his family about early signs and symptoms of reduced blood volume.

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Review all discharge medications and instruct the patient to carry a list of drugs.

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Make sure the patient knows when to schedule follow-up care with the practitioner.

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An osmotic diuretic, such as mannitol, may be ordered to increase renal blood flow and urine output. Determine how much fluid to give by checking blood pressure, urine output, CVP, or PAWP. (To increase accuracy, CVP should be measured at the level of the right atrium, using the same reference point on the chest each time.)

·

Draw an arterial blood sample to measure blood gas levels. Administer oxygen by face mask or endotracheal tube to ensure adequate tissue oxygenation. Adjust the oxygen flow rate to a higher or lower level, as blood gas measurements indicate.

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Draw venous blood for a complete blood count, electrolyte measurements, typing and crossmatching, and coagulation studies.

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During therapy, assess skin color and temperature, and note any changes. Cold, clammy skin may be a sign of continuing peripheral vascular constriction, indicating progressive shock.

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Watch for signs of impending coagulopathy (petechiae, bruising, bleeding or oozing from gums or venipuncture sites).

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Provide emotional support to the patient and his family. (See Teaching the patient with hypovolemic shock.)

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Members of some groups (such as Jehovah's Witnesses) are opposed to blood transfusion and may refuse this type of treatment because of religious reasons. In an emergency, a court order may be obtained to allow such treatment if it's in the patient's best interest.

VENTRICULAR ANEURYSM

Ventricular aneurysm is a potentially life-threatening condition that involves an outpouching—almost always of the left ventricle—that produces ventricular wall dysfunction in 10% to 20% of patients after a myocardial infarction (MI). It may develop within days to weeks after an MI or may be delayed for years. Resection improves the prognosis in patients with ventricular failure or ventricular arrhythmias.

Pathophysiology

Understanding ventricular aneurysm, page 492.)

During systolic ejection, the abnormal muscle-wall movements associated with the aneurysm cause the remaining normally functioning myocardial fibers to increase the force of contraction to maintain stroke volume and cardiac output. At the same time, a portion of the stroke volume is lost to passive distention of the noncontractile sac.

Complications

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Ventricular arrhythmias

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Cerebral embolization

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Death

Assessment findings

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The patient may have a history of a previous MI. However, sometimes an MI is silent, so the patient may be unaware of having had one. He may complain of palpitations and angina.

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If the patient has developed heart failure as a result of the aneurysm, he may report dyspnea, fatigue, and edema.

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Inspection of the chest may reveal a visible or palpable systolic precordial bulge.

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Jugular vein distention may be apparent if heart failure is present.

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Palpation of peripheral pulses may reveal an irregular rhythm caused by arrhythmias (such as premature ventricular contractions). An alternating pulse may be felt.

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Palpation of the chest usually detects a double, diffuse, or displaced apical impulse.

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Auscultation of the heart may detect an irregular rhythm and a gallop rhythm.

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Crackles and rhonchi may be present in the lung if heart failure is present.

UP CLOSE

ff4-b01382759UNDERSTANDING VENTRICULAR ANEURYSM

When myocardial infarction destroys a large, muscular section of the left ventricle, necrosis reduces the ventricular wall to a thin layer of fibrous tissue. The thin wall stretches under intracardiac pressure and forms a ventricular aneurysm. Ventricular aneurysms usually occur on the anterior or apical surface of the heart.

Ventricular aneurysms balloon outward with each systole (dyskinesia). Blood is diverted to the distended muscle wall of the aneurysm, which doesn't contract (akinesia). Mural thrombus is present about half of the time—thromboembolism rarely is. Calcification of the thrombus is common.

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To maintain stroke volume and cardiac output, the remaining normally functioning myocardial fibers increase contractile force. If they can't, overall ventricular function is impaired and complications, such as heart failure and ventricular arrhythmias, may develop.

Diagnostic test results

The following tests may determine the presence of a ventricular aneurysm:

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Echocardiography demonstrates abnormal motion in the left ventricular wall.

 

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Left ventriculography reveals left ventricular enlargement, with an area of akinesia or dyskinesia (during cineangiocardiography) and diminished cardiac function.

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Electrocardiography may show persistent ST-segment and T-wave elevations at rest. ST-segment elevation over the aneurysm creates an elevated rounded appearance.

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Chest X-rays may disclose an abnormal bulge distorting the heart's contour if the aneurysm is large; X-rays may be normal if the aneurysm is small.

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Noninvasive nuclear cardiology scan may indicate the site of infarction and suggest the area of aneurysm.

Depending on the size of the aneurysm and the presence of complications, treatment may require only routine medical examination to follow the patient's condition, or aggressive measures for intractable ventricular arrhythmias, heart failure, and emboli.

Emergency treatment of ventricular arrhythmia includes an I.V. antiarrhythmic, cardioversion, and defibrillation. Preventive treatment continues with an oral antiarrhythmic, such as procainamide (Procan), quinidine, or disopyramide (Norpace).

Emergency treatment for heart failure with pulmonary edema includes oxygen, I.V. digoxin, I.V. furosemide, potassium replacement, I.V. morphine sulfate and, when necessary, I.V. nitroprusside and endotracheal (ET) intubation. Maintenance therapy may include an oral nitrate and an angiotensin-converting enzyme inhibitor, such as captopril (Capoten) or enalapril (Vasotec).

Systemic embolization requires anticoagulation therapy or embolectomy. Refractory ventricular tachycardia, heart failure, recurrent arterial embolization, and persistent angina with coronary artery occlusion may require surgery. The most effective surgery is aneurysmectomy with myocardial revascularization.

Nursing interventions

·

In a patient with heart failure, closely monitor vital signs, heart sounds, intake and output, fluid and electrolyte balance, and blood urea nitrogen and serum creatinine levels.

·

Be alert for sudden sensory changes that indicate cerebral embolization and for signs that suggest renal failure or MI.

·

Arrhythmias require elective cardioversion. If the patient is conscious, give diazepam I.V. as ordered before cardioversion.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH VENTRICULAR ANEURYSM

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Teach the patient how to check for pulse irregularity and rate changes. Encourage him to follow his prescribed drug regimen—even during the night—and to watch for adverse reactions.

·

Because arrhythmias can cause sudden death, refer the family to a community-based cardiopulmonary resuscitation training program.

·

If the patient is receiving an antiarrhythmic, check appropriate laboratory results. For instance, if the patient takes procainamide, check for antinuclear antibodies because the drug may induce signs and symptoms that mimic lupus erythematosus.

·

Provide psychological support for the patient and his family to reduce anxiety. (See Teaching the patient with ventricular aneurysm.)

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If the patient is scheduled to undergo resection, explain expected postoperative care in the intensive care unit (such as an ET tube, a ventilator, hemodynamic monitoring, and chest tubes).

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After surgery, monitor vital signs, intake and output, heart sounds, and pulmonary artery catheter. Watch for signs of infection, such as fever and drainage.