24 Shock
Cardiac Nursing
DEBRA LAURENT-BOPP
JULIE A. SHINN
DATABASE FOR NURSING MANAGEMENT
Shock is a complex clinical syndrome characterized by impaired cellular metabolism due to decreased tissue perfusion. This inadequacy of tissue perfusion results in cellular hypoxia, the accumulation of cellular metabolic wastes, cellular destruction, and, ultimately, organ and system failure. The syndrome begins as an adaptive response to some insult or injury and progresses to multiple organ system failure.6,8,38,44,59 The pathophysiologic mechanisms of shock include decreased circulating blood volume, decreased cardiac contractility, and increased venous capacitance. One of these mechanisms predominates in each type of shock; however, the mechanisms are interactive, with more than one occurring in each of the shock syndromes.
Classification
This chapter discusses three basic types of shock: hypovolemic, cardiogenic, and vasogenic. Hypovolemic shock exists when there is a decrease in the circulating blood volume. Losses of blood volume may be external (e.g., hemorrhage) or internal (e.g., sequestration of fluid in the abdomen secondary to intestinal obstruction). Cardiogenic shock is characterized by a decreased strength of contraction of myocardial fibers, leading to a decreased cardiac output. The decrease in myocardial contractile strength may be due to ischemia, infarction, trauma, myocarditis, or cardiomyopathy. Distributive or vasogenic shock is characterized by vasodilation in response to neurologic or hormonal stimuli. Profound vasodilation results in an inequality between the circulating blood volume and the capacity of the vascular bed. Septic shock is the most often encountered form of distributive shock and is the representative form discussed in this chapter. Two other forms of distributive shock are anaphylactic and neurogenic.38,51,59
A variety of labels can be found in the literature to describe the various types of shock. Display 24-1 classifies the types of shock according to the primary physiologic deficit.
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Pathophysiology
Although the clinical syndrome of shock has various etiologies and basic pathophysiologic defects, all three types are characterized by tissue hypoperfusion, which, if untreated or inadequately treated, results in generalized cellular and systemic dysfunction. In response to tissue hypoperfusion, compensatory mechanisms are activated and are directed at the restoration and maintenance of adequate blood volume and pressure and at the adequate perfusion of the heart and brain. If the basic physiologic defect is not corrected, compensatory mechanisms become counterproductive, resulting in the vicious cycle of irreversible shock.18,38,51
Clinical shock is a dynamic continuum. The prominence of its features and compensatory mechanisms varies with time and with treatment. Although other features (e.g., low blood pressure or decreased cardiac output) are present, the basic problem is acute, generalized tissue hypoperfusion.
HYPOVOLEMIC SHOCK
Hypovolemic shock exists when the volume of blood is inadequate to fill the intravascular space. A significant reduction in the venous return to the right heart results in a decreased cardiac output, a reduced mean arterial blood pressure (MAP), and renal hypoperfusion. A 10% reduction in blood volume initiates compensatory mechanisms, and a rapid reduction of 20% of blood volume produces the clinical signs and symptoms of hypovolemic shock.18,51,64
CARDIOGENIC SHOCK
Cardiogenic shock results from the impaired ability of the heart to pump blood.38,51 As the endpoint on the clinical continuum of left ventricular (LV) failure, cardiogenic shock includes shock due to ineffective cardiac contractility and myocardial failure. This can happen with a myocardial infarction (MI) when there is inadequate contractility of the heart muscle (pump failure), or when the heart rate and rhythm are disrupted and the efficiency of myocardial contractions is impaired (power failure). MI usually involves the left ventricle, but a small percentage of patients have damage to the right ventricle. Right ventricular infarctions can lead to cardiogenic shock because the damaged right ventricle does not propel sufficient blood to the left ventricle, resulting in a decreased cardiac output and inadequate systemic circulation.51 Cardiogenic shock may also occur after cardiac surgery, in association with episodes of cardiac tamponade, or as a result of severe heart failure (HF) due to coronary heart disease, myocardial disease (e.g., the cardiomyopathies), or valvular dysfunction. Acute HF can be grouped clinically into acute cardiogenic pulmonary edema, cardiogenic shock, and acute decompensation of chronic HF.21
DISTRIBUTIVE SHOCK
Massive peripheral vasodilation causes shock because the blood volume, although within normal limits, is insufficient to fill the enlarged vascular capacity. This leads to a decreased venous return and a diminished cardiac output.38 Several types of distributive shock exist, including septic, anaphylactic, and neurogenic shock.
Septic Shock. In septic shock, cellular derangements precede and contribute to cardiovascular abnormalities.5 Any type of microorganism can produce septic shock, including gram-negative bacteria, gram-positive bacteria, viruses, fungi, and rickettsiae; however, gram-negative bacteria are the most common cause, producing more than two-thirds of the reported cases.51 The gram-negative bacteria include Escherichia coli, Klebsiella, Enterobacter, and Serratia species, Pseudomonas aeruginosa, and Bacteroides and Proteus species. A complex hormonal and chemical release of substances is produced through the body's immune system in response to the adverse effects of endotoxins. The invading microorganisms elaborate vasoactive toxins (histamine and kinins), which results in selective but profound vasodilation. In addition, the pathogens create a focus of inflammation, which creates a high-flow, low-resistance state.51,58 There is a persistent decreased ability to extract oxygen from inspired air and from the blood, which results in tissue hypoxia. These abnormalities in oxygen diffusion result from destruction of pulmonary alveolar type I and II cells, a reduction in 2,3-diphosphoglycerate, and a shift of the oxyhemoglobin dissociation curve to the left.18,38 In late stages (see section on Irreversible Stage), septic shock is remarkably similar to cardiogenic and hypovolemic shock, with hypotension, vasoconstriction, decreased cardiac output, hypoxia, and acidosis.15,58,59
Anaphylactic Shock. Anaphylactic shock is the result of a severe allergic, antigen–antibody reaction. Examples of substances that can act as antigens include drugs, contrast media, transfused blood and blood products, and insect venoms.51,59 This reaction results in the release of histamine, serotonin, and bradykinin, causing direct vasodilation and increased capillary permeability. Slow-reacting substances of anaphylaxis are also released, causing bronchoconstriction.38,44,51
Neurogenic Shock. In neurogenic shock, there is a reduction of vasomotor tone, which occurs at the level of the vasomotor centers in the brainstem and causes decreased vasoconstriction, resulting in generalized systemic vasodilation. This form of shock can develop with spinal anesthesia, spinal cord injury, or altered function of the vasomotor center in response to low blood sugar or drugs, including sedatives, barbiturates, and narcotics.38,51
Compensatory Mechanisms
The following equations illustrate the physiologic relation of the hemodynamic variables. Here, CO = cardiac output, SV = stroke volume, HR = heart rate, MAP = mean arterial pressure, and SVR = systemic vascular resistance:
In the pathophysiologic state of shock, the decrease in MAP is brought about by an alteration in one of the variables. In hypovolemic and cardiogenic shock, the reduction in MAP results from a decrease in stroke volume, whereas in distributive shock, the reduction in MAP results from a decrease in systemic vascular resistance:
Compensatory mechanisms consist of reflex reactions to an initial fall in blood pressure. They are activated immediately and increase in intensity in an attempt to restore adequate tissue perfusion. The compensatory mechanisms are directed at the restoration and maintenance of adequate blood volume, cardiac output, and vascular tone. The initial compensatory mechanisms vary with the primary pathophysiologic derangement, but the intermediate and final stages are similar. The initial compensatory mechanisms in hypovolemic and cardiogenic shock are increased heart rate and increased systemic vascular resistance. In vasogenic shock, the initial compensatory mechanism is increased heart rate and cardiac output.38,51,59
INITIAL STAGE
The initial stage of hypovolemic shock is characterized by selective venoconstriction of the renal, cutaneous, muscular, and splanchnic beds, with preservation of circulation to the heart and brain.38,53
In cardiogenic shock, the decreased coronary blood flow results in profound local compensatory events. There is an increase in myocardial oxygen extraction and dilation of the coronary arteries. The myocardial cells shift to anaerobic metabolism and use glycolysis in the production of adenosine triphosphate (ATP).38,53 These events occur immediately in response to myocardial ischemia. If inadequate, myocardial contractility decreases, leading to a fall in cardiac output and systemic hypoperfusion.
The initial stage of septic shock is characterized by a hyperdynamic cardiovascular and metabolic state. This hyperdynamism results from the interrelation between the inflammatory responses and those caused by the endotoxins. Various vasoactive substances (e.g., vasodilators, histamine, and kinins) are released early in septic shock.38,53,59 It is in the late stages of sepsis that a hypodynamic state characterized by reduced cardiac output, vasoconstriction, and additional blood shunting occurs and initiates compensatory mechanisms similar to those in cardiogenic and hypovolemic shock (Fig. 24-1).
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FIGURE 24-1 In the initial stage of shock, all three types of shock lead to a decrease in mean arterial pressure. Compensatory mechanisms attempt to reduce the effects of this decreased mean arterial pressure and, if successful, lead to an increase in cardiac output and mean arterial pressure.
A reduction in arterial blood pressure secondary to decreased blood volume, decreased cardiac output, or increased venous capacitance initiates the body's compensatory mechanisms to maintain adequate tissue perfusion. These mechanisms serve to increase cardiac output and arterial blood pressure through increasing heart rate, enhancing myocardial contractility, providing selective vasoconstriction, conserving sodium and water, and shifting fluid from the interstitial to the intravascular space.53,59,60
Specialized nerve endings (mechanoreceptors) in the carotid sinus, aortic arch, heart, and lungs sense the decrease in blood pressure and transmit their impulses to the vasomotor center. The vasomotor center stimulates the sympathetic nervous system, inhibits the parasympathetic, and initiates the secretion of catecholamines from the adrenal gland. Sympathetic nervous system stimulation unopposed by parasympathetic effects results in increased heart rate, increased myocardial contractility, and selective vasoconstriction. Reflexes of the sympathetic nervous system are active within 30 seconds of an acute decrease in circulating blood volume and are able to compensate for a 20% loss in blood volume by increasing cardiac output by 20% to 25%.18,58
In response to ischemia and sympathetic stimulation, hormones are released from the adrenal medulla, adrenal cortex, anterior and posterior pituitary gland, and kidney, which further compensate for decreased circulating blood volume. The adrenal medulla releases epinephrine and norepinephrine, which enhance vasoconstriction, myocardial contractility, and heart rate. Epinephrine and norepinephrine also stimulate glycogenolysis, thus increasing serum glucose. The adrenal cortex releases glucocorticoids, which also increase serum glucose. Decreased renal blood flow results in the release of renin, which initiates a series of reactions in the liver and elsewhere, resulting in the production of angiotensin. Angiotensin promotes the release of aldosterone by the adrenal cortex and, in situations of hypovolemia, promotes profound vasoconstriction. Aldosterone enhances renal sodium reabsorption accompanied by increased water reabsorption. Antidiuretic hormone is released from the posterior pituitary and further enhances renal water reabsorption. Thirst is stimulated and also causes increased fluid intake.18,53,60 As a result of decreased capillary pressure, Starling capillary balance is shifted, and fluid is transferred from the interstitial space to the capillary.
INTERMEDIATE STAGE
If shock is not recognized and reversed in the initial compensatory stage, it progresses. Compensatory mechanisms are no longer able to maintain homeostasis and may become counterproductive. For example, continued profound vasoconstriction in the presence of decreased MAP promotes inadequate tissue perfusion and cellular hypoxia.6,8,53 (Fig. 24-2).
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FIGURE 24-2 In the intermediate stage of shock, compensatory mechanisms fail, resulting in decreased tissue perfusion and organ function. Decreased myocardial contractility leading to a decrease in cardiac output sets up a positive feedback mechanism (+) to decrease further cardiac output and mean arterial pressure. SGOT, serum glutamic oxaloacetic transaminase; SGPT, serum glutamic pyruvic transaminase; LDH, lactate dehydrogenase.
Decreased delivery of oxygen and nutrients causes cells to shift to anaerobic metabolic pathways.5,18 Increasing amounts of lactic acid are produced and accumulate in the cells owing to decreased perfusion.36 Because anaerobic metabolism is less efficient in meeting the energy requirements of the cells, ATP is depleted. Reduction in the available ATP results in failure of the membrane transport mechanisms, intracellular edema, and rupture of the cell membrane. Progressive tissue ischemia results in increased anaerobic metabolism and the further production of metabolic acidosis.
Impairment of cellular function disrupts all body organs and organ systems. Splanchnic ischemia results in the release of endotoxin from the intestine. The reticuloendothelial (tissue macrophage) system (RES) is suppressed by splenic and hepatic ischemia. The continued renal response to ischemia leads to further vasoconstriction, stimulating the release of aldosterone from the adrenal gland and promoting the reabsorption of sodium in the kidney. This response is no longer useful because the increased volume cannot be pumped by the failing heart and results in ventilatory failure. The increased volume begins to pool in tissues secondary to profound venoconstriction and increased capillary permeability.53,59
Myocardial ischemia results in the deterioration of cardiac function. In addition to the direct detrimental effects of myocardial ischemia, there is some evidence that a peptide secreted by the pancreas, the myocardial depressant factor (MDF), may further depress myocardial function.58 MDF has been identified in the serum of patients in the early stages of septic shock.42 Its presence in other forms of shock remains controversial.
IRREVERSIBLE STAGE
In this stage, the compensatory mechanisms are nonfunctioning or no longer effective, and hypotension has reached the critical level of adversely affecting the heart and brain (Fig. 24-3). Myocardial hypoperfusion, resulting from hypotension and tachycardia, produces acidosis, which leads to further depression of myocardial function. Decreased cerebral blood flow leads to depressed neuronal function and activity and loss of the central neuronal compensatory mechanisms.6,8,53
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FIGURE 24-3 In the irreversible stage of shock, a prolonged decrease in cardiac output and mean arterial pressure leads to cellular necrosis and multiple organ failure.
The progressive general hypoxia and reduction in cardiac output further deprive body cells of oxygen and nutrients needed for cell growth and result in microcirculatory insufficiency. The microcirculation responds by vasodilation to secure the necessary nutrients and oxygen for the deprived cells. Microcirculatory vasodilation in association with systemic vasoconstriction results in the sequestration of blood in the capillary beds, further limiting the volume of blood returning to the systemic circulation. This loss of circulating blood volume and impaired capillary flow result in reduced venous return, further reducing cardiac output and arterial pressure. This situation creates a positive feedback mechanism in which the low-flow state produces a further reduction in flow.18
CLINICAL MANIFESTATIONS
Patients in the initial stages of shock exhibit a variety of behavioral and physiologic symptoms, depending on the cause of shock. Changes noted on physical examination during the initial stages are primarily due to sympathetic stimulation. Regardless of the classification of shock, the principal physiologic defect remains the same: reduced cellular perfusion. Continued tissue hypoxia and acidosis affect specific vital organs in specific ways.
Brain. Decreased cerebral blood flow and coagulopathy can lead to a cerebral infarction or cerebral thrombus formation. Alterations in cellular metabolism throughout the body, metabolic acidosis, and the accumulation of toxins further depress cerebral function. Lethargy, stupor, and coma develop as shock progresses. Finally, in the irreversible stage of shock, the vasomotor center in the brain is disrupted, causing failure of the circulatory mechanisms.53,59
Myocardium. Because it cannot greatly increase oxygen extraction as other organs and tissues can, the myocardium is more vulnerable to the effects of decreased blood flow. A drop in aortic pressure decreases coronary perfusion pressure. Myocardial cells convert to anaerobic metabolism due to the underperfused hypoxic myocardium, and lactate production increases. The normal functioning of the sodium–potassium pump is disrupted. Because of ischemia and necrosis of the pancreas, MDF is released and has a direct negative inotropic effect on the myocardium, contributing to further ischemia. MDF is thought to interfere with calcium in coupling electrical excitation with contraction of the heart.42,58
Kidney. Adequate renal perfusion produces a minimum of 400 mL urine/24 hours, or 20 mL/h. Impaired renal perfusion in shock results in hourly urine outputs of less than 20 mL/h.53,59,64 The excretion of high volumes of low-solute urine may also represent renal hypoperfusion. Prolonged hypoperfusion may lead to acute tubular necrosis and acute renal failure.
Gastrointestinal Tract. Compensatory vasoconstriction in shock may result in mucosal ischemia, an ileus, and full-thickness gangrene of the bowel. If the bowel wall becomes disrupted, the normal bacterial flora of the intestines enter the abdomen and can then enter the circulation. Gastrointestinal bleeding may also occur.8,53
Liver. Factors that cause damage to the liver include decreased blood flow, splanchnic vasoconstriction, pooling of blood in the microcirculation, right HF, and bacterial invasion. The subsequent changes include a loss of RES function, increasing the risk of infection; a decreased lactic acid conversion, contributing to metabolic acidosis; altered protein, fat, and carbohydrate metabolism; and altered bilirubin function.
Jaundice, increased serum bilirubin levels, and increased serum enzymes are early indicators of liver damage associated with shock. Serum globulin is increased, and serum albumin is decreased.53
Lungs. The lung is fairly resistant to short-term ischemia. Thus, it is unlikely that low blood flow is the sole cause of pulmonary insufficiency associated with shock. Other contributory factors have been implicated, including thromboemboli or fat emboli in the pulmonary tree, the toxic effect of fibrin degradation products resulting from intravascular coagulation, serum complement depletion with sequestration of granulocytes in the lung, and sepsis.6,8,53 These factors lead to increased pulmonary capillary permeability. As the ensuing alveolar edema impairs surfactant production, massive atelectasis develops. Clinically, this is called shock lung, adult respiratory distress syndrome (ARDS), or primary pulmonary edema and is characterized by severe hypoxemia, dyspnea, a marked reduction in lung compliance, and the presence of extensive lung infiltrates.
In cardiogenic shock, failure of the left ventricle leads to acute cardiogenic pulmonary edema. Because of the increase in LV end-diastolic pressure, there is an increase in left atrial pressure and dilation. Pressure is increased within the pulmonary capillary bed, forcing plasma or whole blood into the pulmonary interstitial compartment and, finally, into the pulmonary alveoli.
Coagulation. Disseminated intravascular coagulation is a disorder characterized by simultaneous thrombosis and hemorrhage, which occurs in the stage of irreversible shock. Procoagulants initiate uncontrolled microcirculatory clotting. The rapid thrombin formation causes three major problems: fibrin deposits in the microcirculation, consumption of clotting factors, and provocation of the fibrinolytic system. The prothrombin time and the partial thromboplastin time are prolonged, the platelet count and fibrinogen levels are decreased, and the fibrin degradation products are increased. Diffuse bleeding, which may ultimately lead to massive bleeding, may occur from the mucosal surfaces in the trachea, gastrointestinal tract, or urinary tract.
Immune System. Patients sustaining shock or trauma are at heightened risk of serious infection. The RES function is depressed in shock. The ability of the RES to clear damaged red cells, fibrin degradation products, and bacteria is impaired and contributes to the increased susceptibility to infection.6,8,44,53
Physical Assessment
Ongoing assessment of the patient at risk for or in shock, with early detection of subtle changes in the patient's condition, is essential. Subjective and objective data must be correlated with adjunctive clinical measurements such as the measurement of cardiac output and oxygen consumption. The clinical assessment of the patient provides the basis for medical and nursing intervention.4
INTEGUMENTARY
Skin appearance and temperature provide a clinical measure of peripheral circulation. Progressive peripheral vasoconstriction results in a change from the initial normal skin appearance to cool, moist, pale skin with mottling. In cardiogenic shock, cool, moist skin with barely perceptible peripheral pulses is commonly observed. Patients with vasogenic shock initially appear flushed, followed by pallor and mottling as shock progresses. Capillary refill and peripheral pulses are other indicators of the relative adequacy of cardiac output. Normal capillary refill is almost instantaneous; in cardiogenic and hypovolemic shock, capillary refill is often prolonged. Dry mucous membranes and thirst may be seen in association with an elevated serum sodium.8,50,59
CIRCULATORY
Blood pressure is one of the defining characteristics of shock. A MAP of 65 to 75 mm Hg is required to maintain myocardial and renal perfusion.18,58 Shock is defined clinically as the pathophysiologic state that results from a MAP of less than 65 mm Hg over time. Narrowing of the pulse pressure indicates arteriolar vasoconstriction and a decreasing cardiac output.
Pulse rate usually increases in response to sympathetic stimulation to compensate for decreased stroke volume and to maintain cardiac output. In vasogenic shock, the pulse may be full and bounding; in hypovolemic and cardiogenic shock, the pulse is weak and thready.
Jugular veins are flat in hypovolemic and vasogenic shock. Distended neck veins may be seen with cardiogenic shock associated with right ventricular failure.
NEUROREGULATORY
Level of consciousness is an indicator of the adequacy of cerebral blood flow. With cerebral ischemia, the patient initially exhibits hypervigilance, restlessness, agitation, and mild confusion. Persistent cerebral hypoxia results in progressive unresponsiveness to verbal stimuli with eventual coma.50,59
RENAL
Urine output is an indicator of the adequacy of renal perfusion and may decrease early in hypovolemic and cardiogenic shock. Distributive shock may initially cause polyuria. Oliguria is defined by a urine output of less than 20 mL/h. Urine osmolarity and specific gravity increase, and urine sodium decreases with decreased urine output. Nonoliguric renal insufficiency is characterized by the output of large volumes of urine with low specific gravity. An elevated serum creatinine is an early, nonspecific indicator of impaired renal perfusion.8,50
PULMONARY
Respiratory rate and depth are initially increased in all forms of shock, and patients may experience dyspnea or air hunger. This increased ventilation represents the body's attempt to eliminate lactic acid resulting from decreased tissue perfusion. Increased respiratory depth also enhances blood return to the right heart. Arterial blood gases initially reveal respiratory alkalosis. As shock progresses, this is followed by a combined metabolic and respiratory acidosis.
Medical Management Plan
DIAGNOSIS
The diagnosis of shock is made by the history, physical examination, and collection of data from adjunctive diagnostic tests. The primary measurements that document the relative adequacy of blood flow include continuous monitoring of arterial blood pressure and central venous pressure (CVP), monitoring of the electrocardiogram (ECG), and repeated measurements of pulmonary artery wedge pressure (PAWP) and of cardiac output by thermal dilution technique.6,8,50,59
Continuous measurement of urine output and urine studies is the best indicator of adequate organ perfusion because the kidney is sensitive to decreased blood flow. Serial measurements of arterial blood gases reflect the overall metabolic state of the patient, the adequacy of ventilation, and the adequacy of the circulation in providing for oxygen and metabolic needs. Measurement of mixed venous oxygen content (S
O2) by direct blood sampling or by continuous invasive monitoring reflects peripheral oxygen extraction and use. Serial arterial lactate levels can also be measured because the presence of lactic acidosis helps identify critical hypoperfusion as marked by anaerobic metabolism.3,36,49 Elevation of other substances in the blood that reflect the function of specific organs, such as blood urea nitrogen, creatinine, bilirubin, aspartate aminotransferase, and lactate dehydrogenase, may be useful in the diagnosis of shock.8,50
Hypovolemic Shock. Hypovolemic shock is a diagnosis based on the history and clinical assessment. Patients admitted after injury or surgery and those experiencing dehydration, gastrointestinal hemorrhage or obstruction, burns, liver disease, or peritonitis are all at risk for development of hypovolemic shock. In the initial stages of hypovolemia, interstitial fluids tend to move into the capillaries. The hematocrit value reflects the relation between red cells and intravascular fluid and drops 6 to 8 hours after hemorrhage. Hematocrit initially is stable in hemorrhage because both red cells and plasma are lost. It is elevated in situations in which intravascular fluid is sequestered in the abdomen or selectively lost from the body, as in burns. If the fluid volume is monitored invasively, a worsening fluid volume deficit is indicated by a sustained decrease in CVP or PAWP.
Cardiogenic Shock. Cardiogenic shock is diagnosed by the presence of systemic and pulmonary hemodynamic alterations and neurohormonal mechanisms that reflect ventricular failure and result in an inadequate cardiac output and the retention of sodium and water. Primary indicators of cardiogenic shock include a systolic blood pressure less than 85 mm Hg or a MAP less than 65 mm Hg; cardiac index less than 2.2 L/min/m2; and an elevated PAWP greater than 18 mm Hg.16,60 (Forrester subset IV; Fig. 24-4). Noninvasive assessments of a rapid, thready pulse, arrhythmias, oliguria, and decreased mentation are important clinical indices of an inadequate cardiac output.
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FIGURE 24-4 Forrester subsets: Clinical states and therapy. IABP, intra-aortic balloon pumping.
Radiographically, the heart may be enlarged, and there may be evidence of pulmonary congestion. The arterial blood gases frequently show a decreased PaO2, which provides an important indicator of intrapulmonary shunting.
Septic Shock. Septic shock has no universal pattern of signs and symptoms. Its many variations make it difficult to diagnose. The diagnosis is confirmed by microbiologic data, usually from two sets of blood cultures and cultures of sputum and urine.15,44,50
PROGNOSIS
The stages of shock depict a series of pathophysiologic changes that occur if medical and nursing interventions are delayed or inappropriate. The stages do not progress at the same speed in all patients. The length of time tissues are hypoxic is a major factor in determining the occurrence of complications. The early and intermediate stages of shock are reversible with aggressive management. The irreversible stage, due to cellular necrosis and multiple organ failure, is not. The chance of recovery in the irreversible stage without permanent injury is low.
In cardiogenic shock, patients with a cardiac index less than 1.81 L/min/m2 have a 70% mortality rate.16 Patients with an SO2 less than 55% also have a high mortality rate.36 Patients in septic shock are at greater risk for development of disseminated intravascular coagulation and ARDS than are patients with cardiogenic or hypovolemic shock. The survival rate with ARDS varies from 50% to 70% and depends on early recognition and management.
TREATMENT
The main goal of treatment of the metabolic defects produced by shock is the restoration of adequate tissue perfusion. Treatment should be aimed at (1) restoring the blood volume, (2) strengthening the heart, and (3) restoring the normal luminal size of blood vessels. Depending on the cause of shock, treatment must revolve around the manipulation of one or more of these three mechanisms.6,8,15,26,38,52,64
Hypovolemic Shock. Hypovolemic shock requires restoration of fluids and the circulating plasma volume. The amount of fluids and the speed at which they are infused is dictated by the severity of the loss and clinical status of each patient. Parental fluids used in shock include blood and blood products, colloids (e.g., dextran, hespan, albumin, or plasma protein fraction [Plasmanate]), and crystalloids (e.g., normal saline or lactated Ringer's solution).19,29,52
After severe hypotension from massive hemorrhage, volume replacement should be given rapidly enough to maintain the systolic pressure greater than 100 mm Hg and the MAP greater than 80 mm Hg. To maximally augment stroke volume, the CVP should be raised to 15 cm H2O or the PAWP to 16 to 20 mm Hg.
The type of fluid to be given is determined by the type lost, although opinions vary as to the amount and type.20,22,29,52
Crystalloid solutions such as lactated Ringer's are the most appropriate replacement solutions in hypovolemia due to vomiting, intestinal obstruction, or other sequestration of fluids. Much work has focused on the efficacy of hypertonic saline solutions (3%, 5%, and 7.5%) for fluid resuscitation in various forms of circulatory shock.20,26,68 Volume replacement with hypertonic solutions was reduced, but careful monitoring was essential to avoid complications. Until more studies are conclusive regarding the safety and efficacy of hypertonic saline solutions, they should not be considered for widespread clinical use.26
Crystalloid solutions can be given initially while blood is being crossmatched for the patient who has hemorrhaged, and resuscitation with Ringer's alone may be adequate if blood loss is 20% or less.29 When acute hemorrhage reaches 20% to 50% blood loss, nonprotein plasma expanders (e.g., dextran) are indicated. Major losses of whole blood (>50%) should be replaced with whole blood and fresh or frozen plasma to maintain a hematocrit of at least 24% and a hemoglobin of 8 g/dL.29,41,52 Packed cells should be used if the CVP is high or if myocardial failure limits the amount and speed of fluid resuscitation. If the blood loss exceeds 80%, for every 5 units of blood, 1 to 2 units of fresh frozen plasma and 1 to 2 units of platelets should be given to prevent hemodilution of clotting factors and bleeding.26,29,37,41,52
Cardiogenic Shock. Cardiogenic shock requires the institution of therapeutic measures to protect the ischemic myocardium. The three major goals of treatment are (1) to increase the oxygen supply to the myocardium, (2) to maximize the cardiac output, and (3) to decrease the workload of the left ventricle.10,16
- Increase the oxygen supply to the myocardium. Increased inspired oxygen concentrations, including the institution of mechanical ventilation with positive end-expiratory pressure, may be required to maintain arterial blood gases within normal limits. Narcotic analgesics are used to control the patient's pain and aid in reducing myocardial oxygen demands. Reperfusion of the coronary arteries can be undertaken by invasive and noninvasive approaches, including percutaneous transluminal coronary angioplasty, atherectomy or stent placement, coronary artery bypass grafting, and thrombolytic therapy.
- Maximize the cardiac output. Because the cardiac output is already compromised, arrhythmias, which occur as a result of ischemia, acid–base alterations, or MI, can cause a further decline in cardiac output. Antiarrhythmic agents, pacing, or cardioversion may be used to maintain a stable heart rhythm. Volume loading is undertaken with caution and in the presence of adequate hemodynamic monitoring. Optimal preload (LV end-diastolic pressure) ranges between 14 and 18 mm Hg.16 However, fluid loading must be abandoned when the increase in filling pressure occurs without increase in cardiac output. A diuretic such as furosemide is given when symptoms of pulmonary edema occur. Pharmacologic agents are also used in an attempt to increase the cardiac output. Sympathomimetic amines such as dopamine, epinephrine, and norepinephrine may improve contractility and cardiac output; however, the peripheral vasoconstriction and increase in myocardial oxygen requirements associated with these agents may outweigh the benefit and prove deleterious. Other agents used for positive inotropic effect include dobutamine and the phosphodiesterase inhibitors, such as amrinone or milrinone.52
- Decrease the LV workload. The efficacy of vasodilators has been shown in the treatment of cardiogenic shock. The major physiologic effect of vasodilators is a reduction in LV end-diastolic pressure and systemic vascular resistance, with a subsequent increase in stroke volume and improved LV function.10,38 Intravenous nitroprusside remains the drug of choice in cardiogenic shock because it acts rapidly and has a balanced effect, dilating both veins and arterioles, thereby reducing both preload and afterload.14 Other vasodilators that provide a reduction in preload, afterload, or a combined effect include nitroglycerin, hydralazine, captopril, and enalapril. Mechanical support of circulation may be used in the reduction of LV workload in cardiogenic shock. The intra-aortic balloon pump (IABP) is used to reduce afterload at the time of systolic contraction and to increase myocardial perfusion during diastole. Other mechanical assist devices may be used. An in-depth discussion of circulatory assist devices follows this treatment section.
ACUTE PULMONARY EDEMA. The Forrester subsets (see Fig. 24-4) can be used as guidelines for the patient in cardiogenic pulmonary edema.16,17 In subset II, the goal of therapy is to reduce the PAWP below a level that causes pulmonary congestion but above a level that causes a deleterious reduction in cardiac output by the Starling mechanism. There are several options, because diuretics, peripheral vasodilators, and inotropic agents all reduce PAWP. The management strategy for the patient in acute cardiogenic pulmonary edema is outlined in Display 24-2.
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CARDIOGENIC SHOCK AND DECOMPENSATED HEART FAILURE. In the high-risk Forrester subset IV (see Fig. 24-4), simultaneous improvement of both cardiac index and PAWP is the goal of therapy. Afterload reduction by peripheral vasodilators appears particularly well suited to this goal. Inotropic agents are also used to increase systemic and coronary artery perfusion pressure. IABP counterpulsation may also be indicated.16,17 Figure 24-5 provides a general approach to the selection of specific intravenous pharmacologic agents based on hemodynamic profile.23
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FIGURE 24-5 Algorithm for hemodynamically directed pharmacologic support of cardiogenic shock and decompensated heart failure. AP, arterial pressure; CO, cardiac output; PCWP, pulmonary capillary wedge pressure; SVR, systemic vascular resistance; IABP, intra-aortic balloon pump. (From Haas GJ, Young JB: Acute heart failure management. In Topol EJ [ed]: Textbook of Cardiovascular Medicine, p 2262. Philadelphia, Lippincott–Raven, 1998.)
The initial therapeutic decision is influenced by the systemic arterial pressure. Display 24-3 reviews the hemodynamically directed protocol for decompensated HF.21,23
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Septic Shock. Treatment of septic shock has two primary therapeutic goals: (1) to eradicate the causative organism and (2) to support vital life functions compromised by circulatory failure.15,38,52 Interventions directed at identifying, localizing, and controlling the microorganisms include surgery, removal of the source of the contaminating organisms, and antimicrobial drugs.
Fluid replacement is the most common therapy used to support vital functions in septic shock. As with hypovolemic shock, there is disagreement about which fluid to use. Advantages of one fluid type over another have not been conclusively demonstrated.25 Two types of fluids are used: crystalloids (e.g., lactated Ringer's, normal saline) and colloids (e.g., Plasmanate, hespan, or dextran).20,24,26 Weil and Shubin66 advocate a “7/3 rule” for fluid replacement. They give fluid challenges of 5 to 20 mL/min for 10 min. If the PAWP reading is elevated more than 7 mm Hg above the beginning level, the infusion is stopped. If the PAWP or pulmonary artery diastolic pressure rises only 3 mm Hg above the starting point, or decreases, another fluid challenge is given.66 Inotropic agents are sometimes indicated to maximize cardiac output. The most commonly recommended inotropic agent in septic shock is dopamine. Dobutamine is not an optimal drug for this clinical setting owing to its peripheral vasodilator effects. Epinephrine has been shown to be effective in dopamine-resistant septic shock.38
Clinical research studies report conflicting results from the use of steroids in septic shock. Steroids at high doses appear to block inhibition of gluconeogenesis by endotoxin and thus prevent intracellular hypoglycemia.15,38,60 Other actions of steroids include reduction of lactic acid concentration and stabilization of the endothelial wall of the pulmonary microcirculation. Future therapies will focus on the immune system, with interferon and the prostaglandins as agents involved in the immune response.38,52,59
One of the greatest challenges in septic shock is maintaining adequate tissue oxygenation. A recent study addressed the optimization of oxygen delivery (
O2) to “supranormal” levels, with the O2 indexed goal of 600 mL/min/m2.69 This study suggested that the standard of care of treating these critically ill patients to a normal indexed O2 of 450 to 550 mL/min/m2 should be reconsidered.
CIRCULATORY ASSIST DEVICES
Circulatory assist devices have been clinically used, in various forms, since the mid-1960s. IABP counterpulsation is now commonly used in a variety of hospital centers for both medical and surgical patients. Temporary extracorporeal circulatory support devices, once restricted to a few large centers, are now used with increasing frequency in most larger hospitals as an adjunct to cardiovascular surgery programs. Such devices are used to support circulation temporarily when the injured myocardium cannot generate adequate cardiac output. In centers with heart transplantation programs, these devices are being used temporarily to support patients with end-stage HF until a donor heart becomes available. One such device has been used successfully to support patients for over 2 years. We are on the horizon of the clinical application of chronic, long-term support of circulation with totally implantable devices for situations in which myocardial recovery is not expected to occur. It is estimated that 17,000 to 35,000 patients younger than 70 years of age could benefit from the increased life span with an acceptable quality of life provided by implantable, long-term circulatory support devices.65
With early recognition, the rapid deterioration of patients with acute LV failure can be arrested with circulatory assist devices. The type of device used depends on the degree of myocardial injury and the degree to which LV function is compromised. The purpose of therapy is to stabilize the patient until (1) the left ventricle recovers from acute injury, (2) mechanical problems causing acute failure (e.g., ruptured ventricular septum) can be surgically corrected, or (3) possible heart transplantation can be performed. As implied, the goal of any circulatory assist device is to arrest deterioration and to stabilize or improve hemodynamics and secondary organ function. The major principles governing all devices are that they (1) decrease LV workload, (2) partially or totally support the systemic circulation, and (3) enhance oxygen supply to the injured myocardium. The extent to which each principle is achieved depends on the type of device used. The IABP offers only partial support, whereas an implantable LV assist device (LVAD) can assume the total workload of the left ventricle.
Most cardiovascular critical care nurses encounter patients requiring IABP support, which is the emphasis of this chapter. For completeness, examples of various other types of circulatory assist devices and a nursing care plan are included. Because LV support is used most commonly, examples are limited to this scenario.
Intra-aortic Balloon Pump Counterpulsation. The IABP was introduced clinically in the late 1960s as a therapy for cardiogenic shock after MI.28 Since then, its application has expanded to include patients with acute LV failure after cardiac surgery and potential heart transplant recipients whose end-stage condition begins to deteriorate. Another large group of patients who benefit from IABP therapy are those with unstable angina that is refractory to pharmacologic therapy.67 In most of these patients, IABP therapy eliminates rest pain accompanied by ischemic ECG changes and allows for surgical revascularization under less emergent conditions. IABP therapy also may be used to stabilize patients with papillary muscle rupture or ventricular septal rupture after MI, allowing for safer anesthesia induction before the surgical repair of these injuries. Major indications are summarized in Display 24-4.
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DESCRIPTION. The intra-aortic balloon is constructed of biocompatible polyurethane and mounted on a catheter constructed of the same material. Perforation at the catheter–balloon connection allows pressurized gas to move in and out of the balloon, causing inflation and deflation to occur. Helium is preferred as the inflating gas. Properly positioned, the balloon catheter rests just distal to the left subclavian artery and proximal to the renal arteries. Figure 24-6 illustrates proper anatomic position of the IABP catheter. The catheter is inserted by way of a direct femoral or iliac arteriotomy or by percutaneous insertion using a Seldinger technique. It can also be inserted through a femoral artery sheath or introducer. A direct arteriotomy approach is used infrequently today; it was once the only method available owing to previous catheter designs. It may still be the choice for a patient with serious peripheral vascular disease when direct visualization is desired, or in pediatric patients. The approach requires an incision in the groin for access to the femoral or iliac artery. A major disadvantage of this technique is its increased invasiveness, the required surgical procedure for removal, and the time required for insertion. The percutaneous technique allows for more rapid insertion and is less invasive. Catheters used for this technique are designed especially for this approach and can be passed through a large-bore sheath that has been placed in the artery. The balloon is wrapped tightly around its own guide wire so that it slides easily through the sheath. Once in proper position, the balloon is unwrapped in the aorta, allowing inflation and deflation to commence. This catheter is secured in place by suturing it to the skin. Figure 24-7 illustrates the percutaneous insertion technique.
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FIGURE 24-6 Proper placement of the balloon catheter is just distal to the left subclavian artery and proximal to the renal arteries. (From Shinn JA: Intra-aortic balloon pump counterpulsation. In Hudak CM, Gallo BM, Lohr TS [eds]: Critical Care Nursing: A Holistic Approach, 4th ed, p 190. Philadelphia, JB Lippincott, 1986.)
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FIGURE 24-7 Percutaneous insertion of the balloon catheter through an introducer or sheath. Note the right wrap of the balloon. (From Bull SO: Principles and techniques of intra-aortic balloon counterpulsation. In Woods SL [ed]: Cardiovascular Critical Care Nursing, p 171. New York, Churchill Livingstone, 1983.)
PHYSIOLOGIC PRINCIPLES. Goals of IABP therapy are to increase coronary artery perfusion pressure and thus coronary artery blood flow and to decrease LV workload. These goals are achieved by displacement of volume in the aorta during systole and diastole with alternating inflation and deflation of the balloon. A typical adult-sized balloon contains 40 mL of gas or volume. For smaller patients, a 34-mL balloon is available. The size of the catheter ranges from 7 to 9 French.
When the balloon is rapidly inflated at the onset of diastole, 40 mL of volume is suddenly added to the aorta. This acute increase in volume creates a pressure rise in the aorta and generates retrograde flow toward the aortic valve. The increase in aortic pressure early in diastole effectively increases pressure at the aortic root, where the coronary ostia are located. As a result, the perfusion pressure of the coronary arteries is increased. Figure 24-8 illustrates this effect. The objective is to increase coronary artery perfusion and subsequently oxygen delivery to the ischemic ventricle. The desired outcome is decreased ischemia. The period of time early in diastole in which diastolic pressure is enhanced is referred to as diastolic augmentation. Diastolic augmentation also contributes to enhanced flow to other organs. Diastolic pressure gradually tapers off, as it normally does when diastolic run-off occurs.
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FIGURE 24-8 Balloon inflation during diastole displaces volume retrograde toward the aortic root. The result is increased coronary artery perfusion pressure. Enhanced distal flow may also occur. (From Quaal SJ: Comprehensive Intra-Aortic Balloon Pumping, p 82. St. Louis, CV Mosby, 1984.)
Rapid evacuation of the 40 mL of gas out of the balloon during deflation displaces 40 mL of volume out of the aorta. This sudden drop in aortic volume rapidly decreases pressure. Deflation is timed to occur at the end of diastole, just before the patient's next systole. Effective deflation, which decreases end-diastolic pressure, decreases the impedance or resistance to systolic ejection. Impedance to ejection is what determines the amount of wall tension (afterload) that the ventricle must generate to force the aortic valve open and to sustain ejection during systole. The greater the impedance, the greater the LV workload. In shock states, high systemic vascular resistance contributes to greater impedance, resulting in a greater workload for the failing left ventricle. With properly timed deflation, which lowers end-diastolic pressure and impedance to ejection, the LV workload requirement is reduced. In this situation, it is not necessary for the ventricle to generate higher degrees of wall tension or to maintain high pressures to sustain ejection. Figure 24-9 illustrates this effect. Systolic pressure is actually decreased when deflation of the balloon is timed properly. As a result of decreased afterload, contractility improves and there is more effective forward flow during systole. Improved forward flow contributes to decreased end-systolic volume in the ventricle. Improved emptying leads to decreased subsequent preload. A decrease in excessive preload also contributes to decreasing LV workload. Improved forward flow results in increased cardiac output with a resultant increase in blood pressure. Tachycardia that resulted from decreased stroke volume in the shock state is not necessary for compensation as forward flow (stroke volume) improves. As a result, rapid heart rate should diminish, decreasing oxygen demand. Better systemic perfusion helps to reverse the acidosis often seen in shock states and improves secondary organ dysfunction related to the previous hypoperfused state. Display 24-5 and Display 24-6 summarize the physiologic effects of IABP therapy.
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FIGURE 24-9 Impedence or resistance to left ventricular (LV) ejection is decreased by abrupt balloon deflation before systole. Properly timed deflation decreases aortic end-diastolic pressure (A0EDP), which decreases the workload of the left ventricle. (From Quaal SJ: Comprehensive Intra-Aortic Balloon Pumping, p 83. St. Louis, CV Mosby, 1984.)
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CONTRAINDICATIONS. Inflation of the balloon during diastole dictates that the aortic valve be competent. If aortic regurgitation is present, inflation serves to generate more aortic regurgitation because of the increased pressure and retrograde flow against the aortic valve. This effect actually increases the workload of the ventricle. Thus, IABP therapy is of no benefit to this patient and actually may contribute to further deterioration of the patient's condition.
The presence of an aortic aneurysm also contraindicates IABP therapy. First, the tip of the catheter may advance into the aneurysm during insertion, resulting in perforation of the weakened wall or dislodgement of thrombus. A second concern is the effect of inflation and deflation adjacent to the thrombotic debris that accumulates in the aneurysm. There is a great potential for thrombus material to break free, resulting in emboli and possibly precipitating a catastrophic event.
Severe peripheral vascular occlusive disease is considered a contraindication to IABP therapy. More accurately, a femoral or iliac artery insertion site is the actual contraindication. Catheter insertion may be difficult or impossible in this situation. There is a potential for dislodgement of plaque from the vessel wall, which can embolize and totally disrupt distal flow. Dissection of the vessel is also possible in this situation. Another possibility is disruption of flow caused by the presence of the catheter in an already compromised vessel. Such a situation jeopardizes the distal extremity by depriving it of oxygen. This potential problem can be avoided by selecting an alternate method of insertion. In the cardiac surgery patient, the catheter may be inserted directly into the thoracic aorta. The obvious disadvantage of this approach is the requirement for reopening the sternotomy incision to remove the catheter. Another, less conventional approach is antegrade aortic insertion of the balloon catheter by way of the right subclavian artery.33 This approach requires a subperiosteal clavicular resection to access the artery, but is less invasive than a sternotomy incision. Newer catheters of smaller diameter minimize the risk of occluding distal blood flow. When distal flow to the extremity is threatened by iliac or femoral insertion and other options are not ideal, femorofemoral crossover Dacron grafts have been used to shunt arterial flow from one femoral artery to the femoral artery compromised by the presence of the catheter.2 In this way, blood flow to the affected extremity can be maintained.
A final contraindication is balloon catheter insertion in any patient who has a terminal condition in which no medical or surgical therapy exists that might alter the outcome. It would serve no purpose to introduce more aggressive therapy to support such a patient. The only time this may be considered is when the patient meets the criteria for heart transplantation.
PROPER TIMING TO ACHIEVE EXPECTED CLINICAL OUTCOMES. Proper timing of IABP therapy is crucial to achieving the beneficial hemodynamics previously outlined. Proper timing requires coordination of inflation and deflation of the balloon with the patient's cardiac cycle. The R wave from the ECG, pacemaker spikes on the ECG, or the arterial systolic pressure are used to identify individual cardiac cycles. All these act as signals to the IABP console to discriminate systole from diastole. The R wave signals the onset of electrical depolarization, which precedes mechanical systole. A ventricular pacemaker spike essentially represents the same event. Arterial systolic pressure signals the onset of mechanical systole. Any of these can be used as a reference point to determine when deflation of the balloon should optimally occur. An arterial waveform is necessary to determine the onset of mechanical diastole and systole and to verify timing. Diastole has begun when the dicrotic notch appears on the arterial waveform. Balloon inflation is timed to occur at this point in the cardiac cycle. The deflation point can be optimally adjusted by observing the end-diastolic drop in pressure created by balloon deflation. The goal is to create the greatest pressure drop possible. Ideally, the difference between end-diastolic pressure without the balloon effect and end-diastolic pressure created by balloon deflation is at least 10 mm Hg. Evidence that afterload reduction has occurred is seen in the following systolic pressure. With afterload reduction, the next systolic pressure after balloon deflation is lower than the systolic pressure with no balloon effect. This is evidence that LV workload has been decreased.
To evaluate balloon timing properly, the assist ratio is set at 1:2, meaning the balloon is assisting every other cardiac cycle. In this way, the observer can compare the effect of balloon inflation and deflation with unassisted beats. Most patients tolerate this well for a brief period. Five criteria can be used to determine the effectiveness of IABP timing, as illustrated on the arterial pressure tracing (Fig. 24-10).
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FIGURE 24-10 Criteria for effective intra-aortic balloon pump (IABP) timing: (1) inflation occurs at the dicrotic notch; (2) the slope of rise of balloon inflation is straight and runs parallel with the preceding systolic upstroke; (3) augmented diastolic pressure is at least equal to the preceding systolic pressure; (4) end-diastolic pressure at balloon deflation is lower than the preceding unassisted end-diastolic pressure; (5) the next systolic pressure is assisted systole and is lower than the preceding systole, which was not affected by balloon deflation. (From Shinn JA: Intra-aortic balloon pump counterpulsation. In Hudak CM, Gallo BM, Lohr TS [eds]: Critical Care Nursing: A Holistic Approach, 5th ed, p 213. Philadelphia, JB Lippincott, 1990.)
The first step is to ensure that inflation occurs at the dicrotic notch, the beginning of diastole. Inflation should actually be timed to obliterate the notch. The interval between the onset of systolic upstroke and the point of balloon inflation should not be shorter than the interval between the systolic upstroke and dicrotic notch on the unassisted beat. Inflation that occurs too early is detrimental to the patient because the abrupt increase in diastolic pressure may force the aortic valve closed prematurely. Complete ejection may be impaired. Late inflation, past the dicrotic notch, does not harm the patient, but the duration of assistance is unnecessarily shortened so that maximal benefit from augmented pressure is not achieved.
Next, the upstroke of balloon inflation should be sharp and parallel with the preceding systolic upstroke. This creates a V-shaped appearance on the ECG, with the nadir of the V being the point of inflation. The sharp upslope ensures that maximal early augmentation is occurring. A slope that is not straight may indicate that the balloon is inflating late, perhaps off of some other artifact during early diastole. In this case, the loss of the V configuration also is evident.
The third criterion is that the augmented diastolic pressure peak be at least equal to the preceding systolic pressure peak. A decrease in this pressure peak may indicate gas loss from the balloon. This loss can occur by natural diffusion. A balloon normally requires refilling every 2 to 4 hours because of natural diffusion of gas through the membrane. Most consoles automatically purge and refill the balloon and catheter every 2 hours. An abrupt loss of the pressure peak may indicate the development of a leak in the balloon or the catheter. Occasionally, augmentation greater than the systolic pressure is not achievable owing to the size of the balloon relative to the size of the aorta. To fit properly, the balloon should occlude 80% of the aorta when inflated. If a smaller balloon was used because of insertion difficulties, or if the aorta is dilated, diastolic augmentation may be less than the patient's systole. In this instance, balloon inflation does not generate as much volume displacement or rise in aortic pressure during diastole.
The fourth point to evaluate is balloon deflation at the end of diastole. Proper deflation results in a drop in pressure at the end of diastole. This drop in pressure creates an end-diastolic pressure much lower than diastolic pressure without the balloon effect. Timing is adjusted so that the lowest pressure possible is achieved. It is important to make sure that the systolic upstroke that follows is straight and that a sharp, V-shaped configuration is present. The V shape indicates that systole began immediately after deflation. Any plateau indicates that deflation occurred too early. In this case, early deflation does not relieve the ventricle of impedance, and afterload reduction does not occur. Late deflation results in higher impedance because the balloon remains inflated at the onset of systolic ejection. An end-diastolic pressure that is the same or greater than the end-diastolic pressure without balloon assistance is evidence of late deflation. The following systolic pressure is the same as the unassisted systole because no afterload reduction has occurred. It can also be lower than the unassisted systole because of the inability of the failing ventricle to work against the higher impedance to ejection.
Finally, the observer should note what effect balloon deflation has on the next systolic pressure, for reasons just described. The goal is to ensure that the lower systolic pressure that follows balloon deflation is caused by afterload reduction and not by improper timing, which resulted in late deflation. Proper balloon fit has an impact on the ability to achieve afterload reduction. If the balloon size is small, volume displacement may have less of an effect on lowering end-diastolic pressure. Figure 24-11 illustrates the four possible errors that can occur with timing.
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FIGURE 24-11 Possible errors in balloon timing. (From Shinn JA: Intra-aortic balloon pump counterpulsation. In Hudak CM, Gallo BM, Lohr TS [eds]: Critical Care Nursing: A Holistic Approach, 4th ed, p 198. Philadelphia, JB Lippincott, 1986.)
COMPLICATIONS. Intra-aortic balloon pump therapy carries a relatively low risk of morbidity given the clinical condition of the patient. Most complications are vascular. The incidence has been reported to be 10% to 45%.1,19,27,57 Vascular injuries that may occur during insertion include plaque dislodgement, dissection, laceration, and compromised circulation to the distal extremity. If a cutdown was used during insertion, peripheral nerve injury is another complication that may be incurred during the insertion procedure. Compromised circulation can occur any time during IABP therapy as a result of the presence of the indwelling catheter, compartment syndrome, or embolus from thrombus formation along the catheter or on the balloon.11,47,61 These complications occur with greater frequency in patients with peripheral vascular occlusive disease, in women with small vessels, and in patients with insulin-dependent diabetes.19 Nursing functions involved in monitoring or preventing compromised circulation include careful assessment of peripheral perfusion; preventing the patient from flexing the hip of the affected extremity, which may compromise blood flow; and maintaining coagulation times within prescribed parameters by careful titration of anticoagulants. The nurse should be aware that multiple or prolonged attempts at insertion increase the risk of vascular injury and thrombus formation.
Infection is reported to occur in approximately 0.2% of patients.57 Insertion site infections may dictate the removal of the IABP catheter. Careful efforts must be made to maintain the sterility of insertion site dressings. Other problems that may be encountered include thrombocytopenia; compromised circulation to the left subclavian, renal, or mesenteric arteries owing to balloon malposition; and bleeding from the insertion site or other line insertion sites. Mechanical problems related to the balloon include improper timing or a leak or perforation in the balloon, necessitating its removal. A leak in the balloon becomes evident as augmentation becomes less effective. Eventually, blood backs up in the catheter and can be detected. When a leak has occurred, the balloon must be removed immediately to avoid the possibility of gas embolus.
NURSING MANAGEMENT PLAN. Good cardiovascular assessment of the patient provides indicators that IABP therapy is effectively assisting LV function. Assessment includes vital signs, cardiac output, heart rhythm, heart regularity, heart ischemia, urine output, color, peripheral perfusion, and mentation. All these parameters should reflect an improvement in the patient's condition. The patient on IABP therapy is relatively immobile owing to the need to avoid hip flexion and to multiple invasive monitoring and infusion lines. Often, the patient requires endotracheal intubation and ventilator support. Care must be taken to prevent or minimize extensive atelectasis. These patients also are at greater risk for respiratory tract infection. Careful suctioning technique and prevention of aspiration reduce this risk. Prolonged hypotension from the shock state may jeopardize renal function. Monitoring urine output and quality closely may contribute to early recognition and treatment of renal dysfunction, thus avoiding acute renal failure. Psychosocial support of both the patient and family is important. The patient requires interventions that minimize stress, disorientation, and sleep deprivation. Families benefit from honest communication and help with the interpretation of the patient's condition. Nursing Care Plan 24-1 outlines a plan of care for the patient on IABP therapy. Because this patient is experiencing acute LV failure or cardiogenic shock, many nursing diagnoses used for those conditions apply. The plan of care that is outlined focuses on issues unique to IABP therapy.
Left Ventricular Assist Devices. In patients who have catastrophic myocardial injury or deteriorating end-stage HF, IABP therapy may provide inadequate support. IABP therapy depends on ventricular function to maintain systemic blood pressure. The IABP is not capable of contributing to cardiac output directly. With profound ventricular failure, mean blood pressure is less than 60 mm Hg, systolic blood pressure is less than 90 mm Hg, and the cardiac index typically is less than 1.8 L/min/m2.7,30,45 IABP therapy increases cardiac output only marginally (500 to 800 mL/min), and the expectation of long-term support in this scenario is unrealistic.13 Therefore, more aggressive therapy with an LVAD, which can provide a physiologic cardiac output, is warranted.
PATIENT INDICATIONS. The most frequent indications for use of an LVAD are to support a patient awaiting a donor for heart transplantation or for patients who cannot be weaned from cardiopulmonary bypass after conventional treatment, including IABP therapy. Approximately 1% to 4% of cardiac surgery patients cannot be weaned from cardiopulmonary bypass after major myocardial injury.31,34,43 Between 30% and 50% of those patients may survive with LVAD support.45,55, Some centers use LVADs to support the patient in cardiogenic shock after MI. The LVAD is used to decrease LV work and to maintain systemic blood pressure while the left ventricle recovers from injury. If allowed to rest for 48 to 96 hours, there is potential for myocardial function to return.7 Indications of initial ventricular recovery should appear within 24 hours.31 The decision to insert an LVAD must be made quickly but carefully. The longer the patient remains on cardiopulmonary bypass, the more likely the patient is to have profound coagulopathy, which may become difficult or impossible to amend. Situations that may contraindicate LVAD placement include preexisting disease states, severe debilitation making recovery unlikely, massive myocardial injury in which recovery is not possible, multisystem organ failure, and prolonged cardiac arrest associated with neurologic damage.31 Unless cardiac transplantation is an option, a major factor in the decision-making process is to select patients in whom recovery is possible, thus avoiding a situation in which the patient becomes totally LVAD dependent without potential for weaning.
MECHANISM OF SUPPORT. Left ventricular assist devices are designed temporarily to replace the pumping function of the left ventricle by being placed in the circuit of normal blood flow. Blood is diverted from the left atrium or left ventricle and shunted to the LVAD by the pressure gradient between those chambers and the LVAD. Blood is returned to the aorta with continuous flow from the LVAD or in a pulsatile fashion with pump ejection occurring during the patient's diastole or asynchronous to the patient's cardiac cycle. Available pumps are divided into two categories: continuous-flow pumps and pulsatile pumps.
Continuous-flow pumps are continuously filled by left atrial blood flow, and blood is returned to the aorta at a continuous rate. There is no ability to mimic systole or diastole, but constant flow rates and mean blood pressure are maintained. Left atrial blood flow is captured by a cannula placed in the chamber. As a result, LV preload is markedly diminished, and LV workload is reduced. Continuous-flow pumps are capable of flow rates of up to 6 L/min.34,45
Pulsatile pumps are filled during atrial contraction or ventricular systole, depending on whether the LVAD inflow cannula is placed in the left atrium or left ventricle. In the latter case, the LV acts as an “atrium” to fill the LVAD, and filling of the LVAD occurs during the patient's native systole. Because the LVAD is empty before LV contraction, impedance to LV ejection is reduced dramatically, and minimal work is required to fill the pump. LV pressures as low as 10 mm Hg may be all that is required to fill the LVAD. The aortic valve remains closed, and no blood is ejected from the ventricle into the aorta during systole. Once the LVAD is filled, ejection from the LVAD pump into the aorta occurs. This coincides with the patient's native diastole. The LVAD is in counterpulsation with the patient's heart. It is in its filling phase during LV contraction and is ejecting during LV relaxation. Blood pressure during true diastole in these patients actually is higher than blood pressure during true systole. Pumps can also run in a fill-to-empty mode, with ejection occuring any time the pump is fully filled. The LVAD is capable of assuming total responsibility for maintaining physiologic cardiac output.
| Nursing Care Plan 24–1 u The Patient with an Intra-aortic Balloon Pump |
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TYPES OF CONTINUOUS-FLOW DEVICES. One type of device provides continuous flow by means of a roller pump. This pump is filled from a left atrial cannula, and flow is returned to the ascending aorta after passing through the roller pump (Fig. 24-12). Long cannulas are required that create high resistance to blood flow. This high resistance necessitates the use of high pressure to maintain flow. Tubing occlusion that causes a pressure back-up is one of the disadvantages of this system. Heparinization is required to prevent thrombus formation along the long cannulas.32,34 Roller pumps also traumatize blood cells, causing hemolysis. This device is best applied for short-term situations. After long periods, hemolysis and coagulopathies become problematic. An example of this support would be the maintenance of partial cardiopulmonary bypass after a cardiac surgical procedure.
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FIGURE 24-12 Continuous flow to the aorta is provided by a roller pump. Cannulas are tunneled through the abdominal wall to the external roller pump. (From Litwak RS, Koffsky RM, Lukban SB et al: Implanted heart assist devices after intracardiac surgery. N Engl J Med 291: 1342, 1974. Copyright © 1974 Massachusetts Medical Society. All rights reserved.)
The centrifugal-kinetic energy pump is an example of a frequently used continuous-flow LVAD (Fig. 24-13). The Bio-Medicus pump is an example of this type of device. With this system, blood is taken from the left atrium and returned to the aorta. The major advantage of such a device is the ability to function at low pressure while delivering high volume or flow. As blood enters the pump, it is whirled by centrifugal force, creating a vortex or tornado effect.32 The higher the speed of the pump (revolutions per minute), the greater the centrifugal force and the greater the output of the pump. Thus, flow rates are controlled by the number of revolutions per minute that the pump spins. An advantage of this design is that any air accumulates at the top of the vortex while blood accumulates at the bottom, thus avoiding the possibility of air microembolus. Chipping from the inner surfaces of the tubing or other wear and tear on the tubing does not occur with this pump design. Trauma to blood cells is markedly decreased, compared to cardiopulmonary bypass. Heparinization is not required for up to 48 hours, as long as flow rates are kept at greater than 1 L/min.31 This pump also minimizes the buildup of excessive outflow pressure that can result in tubing disconnections. These devices can support patients for longer times than roller pump designs, primarily owing to the decreased trauma to blood cells.
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FIGURE 24-13 Continuous-flow centrifugal-kinetic energy pump. PA, pulmonary artery; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. (From Marchetta S, Stennis E: Ventricular assist devices: Applications for critical care. J Cardiovasc Nurs 2[2]: 45, 1988.)
A new device undergoing clinical trials also works in series with the native heart, like IABP therapy. This device, called the Hemopump (Johnson & Johnson), is capable of generating up to 3.5 L/min of continual, nonpulsatile blood flow, which more effectively rests the left ventricle.56 This device is classified as an axial flow pump. The pump is mounted in a cannula that is inserted through the femoral artery and passed up the aorta. The tip of the cannula crosses the aortic valve and is positioned in the LV chamber (Fig. 24-14). Axial flow is achieved by rotating blades contained within the pump housing, which rotate at speeds of up to 25,000 rpm.56 This action draws blood from the left ventricle and propels it into the systemic circulation. Nonrotating blades placed more distally in the cannula maintain unidirectional flow. An external motor magnet is connected to a drive shaft, which is housed in the inner lumen of the cannula. This drive shaft connects to the pump and provides it with a means to turn the pump's rotating blades. A newer version of the Hemopump is being developed by Thermo Cardiosystems Inc., (Woburn, MA) that is totally implantable.
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FIGURE 24-14 Placement of the Hemopump cannula in the left ventricle, with exit out the femoral artery. The driving motor is located externally. (From Rutan PM, Roundtree WD, Myers KK et al: Initial experience with the hemopump. Critical Care Nursing Clinics of North America 1: 527–534, 1989.)
Advantages of this system are that it does not have to be synchronized with a cardiac cycle, so its function does not depend on secure ECG electrode placement or nursing time for timing adjustments. Its insertion and removal are also relatively minor procedures (except the implanted design), which make it more available to medical patients. Its major disadvantage, which may exclude smaller patients, is the size of the cannula. The patient's femoral anatomy must be able to accommodate a large cannula. Because of the size, there is also risk of compromised distal blood flow. All placements require arteriotomy under direct vision using a cutdown technique.
TYPES OF PULSATILE PUMPS. Pulsatile LVAD pumps are either pneumatic (air driven) or electric. Either can be used as temporary support, but the electrically driven pump has the potential to be totally implantable.
The Thoratec pump (Thoratec Laboratories, Inc., Pleasanton, CA) is an example of a pneumatic system. Pulsatile flow is created by air compression of a polyurethane sac that contains up to 65 mL of blood. Positive air pressure compresses the sac, causing ejection from the LVAD to the aorta. Negative pressure is applied after ejection, causing the blood sac to fill. Backward flow is prevented by placement of inflow and outflow disk valves in the pump. The blood sac is filled by means of a cannula placed in either the left atrium or left ventricle. It can be controlled by three modes: (1) a fixed rate that is asynchronous with the patient's heart and delivers variable stroke volumes, (2) triggering of the pump by the R wave of the ECG (not practical for long-term support), or (3) triggering of pump ejection by reaching full fill (also called fill-to-empty mode).30,39 A major advantage is pulsatile flow, which allows for longer term support. Pulsatile flow provides better kidney perfusion, decreases peripheral vascular resistance, and increases systemic circulation.32 A major disadvantage is the risk of infection associated with a pump that is placed externally. Conduits from the atrium and to the aorta are tunneled through the chest and connected to the external pump (Fig. 24-15). Epithelial cells ingrow into the Dacron-covered conduits. Tissue ingrowth acts as a seal from the surface of the body.
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FIGURE 24-15 Cannula placement of two Thoratec pumps during support of both right and left ventricles. Arrows indicate direction of blood flow. (From Ruzevich SA, Swartz MI, Pennington DG: Nursing care of the patient with a pneumatic ventricular assist device. Heart Lung 17: 399–405, 1988.)
Another pulsatile pump is the Novacor pump (Baxter Healthcare Corporation, Oakland, CA). This electrically driven pump is designed to be totally implanted in a preperitoneal pocket just anterior to the posterior rectus sheath. Chronic support is possible because electrical energy can be stored in battery cells that are small enough to implant, although the electric power unit currently used is an exchangeable five hour battery. Filling of the pump occurs from a cannula that is placed in the LV apex. The cannula is tunneled through to the abdomen, where the pump is implanted. Blood is returned to the ascending aorta through another cannula. The device also uses inflow and outflow valves. Ejection is triggered by either a fixed rate, changes in the velocity of filling, or in a fill-to-empty mode. When the blood sac is filled, or the trigger is recognized, two electrically powered pusher plates compress the blood sac, which is located between the two plates. Ejection occurs when the sac is compressed.61 The major advantage of this system is the ability to implant the device, eliminating much of the risk of infection. Another major advantage is the potential for storing and implanting the energy source. Figure 24-16 illustrates the appearance of the device in its totally implantable form. In the device's current configuration, patients must wear the controller on a belt and carry a power source with them. The controller and battery packs can also be carried in a shoulder bag or in specially designed vests that have pockets for the controller and two battery packs. One battery serves as a reserve supply when the patient switches from AC power to battery operation, and vice versa. The other primary battery pack can supply power for up to 5 hours, allowing the patient freedom from a tethered set-up. Figure 24-17 shows the first patient in the United States who is ambulatory with the wearable system.
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FIGURE 24-16 Illustration of the Novacor left ventricular assist device shows the design of the totally implanted system. Power is transmitted from the belt, through the skin, to the implanted controller (ECP) and storage batteries. (From Ream AK, Portner PM: Cardiac assist devices and the artificial heart. In Ream AK, Fogdall RP [eds]: Acute Cardiovascular Management, Anesthesia, and Intensive Care, p 864. Philadelphia, JB Lippincott, 1982.)
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FIGURE 24-17 A patient with the wearable Novacor left ventricular assist system. The patient carries a 5-hour battery pack on a specially designed belt, allowing him to be totally untethered to a heavy operating console, as with many other types of devices. This patient is shown at approximately 3 weeks after implantation and is waiting for a donor heart.
Another pump that can also be totally implanted is the Heartmate implantable pneumatic system (Thermo Cardiosystems, Inc., Woburn, MA). With this design, an external source of pressurized air is used to pressurize the chamber housing the blood sac. With pressure, the blood sac is compressed by a single pusher plate, causing ejection to occur. A second Heartmate pump is electrically driven, with a controller and battery pack system similar to those of the Novacor pump. Ejection occurs as a result of compression of the blood sac by a single, motor-driven pusher plate.25
Both the Novacor and Heartmate systems can support patients for extended periods with a relatively low risk of thromboembolism or mechanical problems. All are used to support patients awaiting heart transplantation. The portability of the systems allows patients to be ambulatory and care for themselves. As a result, these patients are now routinely discharged from the hospital while they wait for suitable donor hearts.40,46
NURSING MANAGEMENT PLAN FOR THE PATIENT IN SHOCK
When caring for the acutely ill patient in shock, the goals of nursing and medicine merge to preserve life through the maintenance of oxygenation and circulation. In addition, the nurse considers the human responses to shock and the extent to which normal daily activities must be supplemented by nursing care.9 This is done through a careful functional assessment of the individual patient. Cues are collected within functional categories, and patterns are recognized, which provide the basis for nursing diagnosis and intervention. Altered tissue perfusion, self-care deficit, and altered family processes are among the nursing diagnoses encountered in association with shock.9,35
Decreased Cardiac Output
Decreased cardiac output is a clinical problem requiring the specialized intervention of nursing and medicine for resolution. Both disciplines possess the knowledge necessary to recognize the signs and symptoms and to diagnose the problem. The accepted therapy (e.g., fluid replacement, inotropes, vasopressors, IABP) legally falls within the definition of medical practice. The physician must define the parameters of therapy. The nurse uses knowledge and judgment in administering the prescribed therapy.12 In addition, the nurse considers the impact that a reduction in cardiac output has on other functional categories, such as perceptual awareness or activity tolerance. After confirming the specific response of the patient, the nurse intervenes directly to foster a salutary response.9,35
Decreased Tissue Perfusion
Decreased tissue perfusion requires further specification to provide direction for nursing care. Because a nursing diagnosis must describe a problem for which nurses are educated and licensed to treat, use of the customary “related to” clause is inappropriate. Instead, the nurse must specify the impact of decreased tissue perfusion on the health of the patient—for example, altered tissue perfusion: decreased, cerebral, resulting in restlessness, agitation. The independent nursing interventions are then directed toward patient protection, the maintenance of the current level of function, and early recognition and prevention of further deterioration.
Self-Care Deficit
Carpenito9 defines self-care deficit as “The state in which the individual experiences an impaired motor function or cognitive function, causing a decreased ability to feed, bathe, dress, or toilet oneself.” Critical illness implies the inability to meet one's care needs. Self-care requires energy and endurance, which may surpass the strengths of the critically ill patient. Detailed assessment is required to determine the scope and extent of the deficit and to provide appropriate supportive or supplemental intervention. Nursing activities designed to meet these needs include turning, positioning,63 bathing, massaging, and communicating. Knowing when to help and when to refrain from helping are equally important. There is an interrelatedness among the self-care deficits—feeding, bathing, toileting—and interventions instituted in one category may affect other categories.
Altered Family Processes Related to an Ill Family Member
This nursing diagnosis refers to the state in which a normally supportive family experiences a stressor that challenges its previously effective functioning ability.9 It is frequently seen in caring for people who are critically ill, with the stressors being the critical illness and the intensive care environment.54 Defining characteristics include a family system that cannot, or does not (1) meet the physical, emotional, or spiritual needs of its members; (2) accept or express a full range of feelings; (3) seek or accept help appropriately; (4) communicate openly with its members; or (5) adapt constructively to crisis. Nursing interventions must be individualized but may include actions such as conducting family orientation to the hospital, providing a private place for family to wait, providing information regarding changes in the patient's condition or treatment, acknowledging family strengths, and facilitating the expression of feelings.
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Books@Ovid
Copyright © 2000 Lippincott Williams & Wilkins
Susan L. Woods, Erika S. Sivarajan Froelicher, and Sandra Underhill Motzer
Cardiac Nursing
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