This section addresses the diverse acute and chronic etiologies of left ventricular dysfunction and concludes with principles of management for each.
Decreased Left Ventricular Systolic Function
Dilated cardiomyopathies are the best-known chronic causes of decreased left ventricular contractility.21 Dilated cardiomyopathy is often idiopathic with evidence that genetic, viral, and immune factors contribute. Dilated cardiomyopathy may also be associated with coronary artery disease, presumably due to previous ischemic events and subsequent adverse remodeling and apoptosis of cardiomyocytes leading to a dilated, poorly functional left ventricle.22 Alcoholic cardiomyopathy is an important cause of chronic dilated ventricular dysfunction to be considered in critically ill patients.21 Particularly in younger patients, inflammatory cardiomyopathy (myocarditis), usually viral, is an important cause of acute dilated cardiomyopathy that may lead to a chronic dilated cardiomyopathy in 10% of cases. Evidence of familial occurrence of similar disease is common, suggesting a genetic contribution in up to 25% of cases.21,23 Rare causes such as the glycogen storage diseases also may be found in young patients. Multiple, less common causes may be encountered (Table 22-1).
Table 22–1. Chronic Causes of Decreased Contractility (Dilated Cardiomyopathies) ||Download (.pdf)
Table 22–1. Chronic Causes of Decreased Contractility (Dilated Cardiomyopathies)
- Coronary artery disease
- Inflammatory (viral, toxoplasmosis, Chagas disease)
- Infection with the human immunodeficiency virus
- Nutritional deficiency (selenium deficiency)
- Metabolic disorder (Fabry disease, Gaucher disease)
- Toxic (Adriamycin, cobalt)
These multiple, different etiologies of dilated cardiomyopathy lead to decreased ventricular contractility in a number of ways. Loss of myocardium with degradation of the normal collagen architecture by matrix metalloproteinases and replacement with fibrous connective tissue leads to remodeling and decreased contractility.24 Increased levels of circulating renin, angiotensin II, endothelin, and norepinephrine promote cardiomyocyte hypertrophy, apoptosis, myocardial fibrosis, and vascular cell hypertrophy. Myocardial norepinephrine stores are depleted and β-receptor density is reduced in chronic dilated cardiomyopathy.24,25 Biochemical changes that may contribute to decreased contractility include decreased efficiency of the sarcoplasmic reticulum calcium pump, decreased actin-myosin adenosine triphosphatase activity, and change in myosin isoenzyme composition.
In the ICU, acute causes of decreased left ventricular contractility are important because the acute causes are potentially reversible (Table 22-2). Acute causes of depressed left ventricular contractility include ischemia, hypoxemia, respiratory acidosis, metabolic acidosis, ionized hypocalcemia, hypo- and hyperthermia, exogenous toxins such as alcohol and drugs, endogenous toxins such as circulating depressant factors of sepsis, inflammatory cytokines, and increased nitric oxide (NO) production.
Table 22–2. Acute Reversible Contributors to Decreased Contractility ||Download (.pdf)
Table 22–2. Acute Reversible Contributors to Decreased Contractility
- Respiratory acidosis
- Metabolic acidosis
- Possibly other electrolyte abnormalities (Mg2+, K+)
- Exogenous substances (alcohol, β blockers, calcium channel blockers, antiarrhythmics)
- Endogenous substances (endotoxin, histamine, tumor necrosis factor, interleukin 1, platelet-activating factor)
- Hypo- and hyperthermia
Transient ischemic episodes occur frequently in critically ill patients. The onset of ischemia is due to myocardial oxygen demand exceeding the ability of the myocardium to extract oxygen from the oxygen supply (coronary blood flow multiplied by arterial oxygen content). Myocardial oxygen demand is increased by increasing heart rate, contractility, afterload, preload, and the basal metabolic rate of the myocardium (which increases with increased sympathetic tone and catecholamines).26 Many of the underlying illnesses encountered in the critically ill and many of the therapies, including fluid and inotropic or vasoactive drug infusion, contribute to markedly increased oxygen demand. Because of the prevalence of coronary artery disease in older patient populations, ischemia in the ICU is frequently regional with associated wall motion abnormalities. Accordingly, a high index of suspicion and an early aggressive diagnostic approach are indicated and facilitate the early treatment of ischemic coronary artery disease, as discussed in more detail in Chap. 25.
In the absence of coronary artery disease, critically ill patients with sepsis also may manifest global heterogeneous left ventricular hypoxia with increased creatine kinase MB and troponin levels. The heart consumes less lactic acid and may produce lactic acid.27 If inadequate oxygen delivery in relation to demand is not corrected quickly, then the heart may enter a detrimental positive-feedback loop of decreasing contractility, decreasing cardiac output and coronary perfusion, and, hence, decreasing contractility leading to precipitous cardiac arrest.28 In the canine model, this vicious cycle occurred when arterial O2 saturation decreased below 75% (arterial partial pressure of O2 = 40 mm Hg) when hemoglobin concentration was 14 g/dL. Accordingly, aggressive measures to prevent this level of hypoxemia by keeping arterial O2 saturation above 85% to 90% are indicated; maintaining a reasonable hematocrit in hypoxic critically ill patients with risks for myocardial ischemia is part of this therapy.
Respiratory acidosis results in myocardial intracellular acidosis, and intracellular acidosis decreases the effect of intracellular calcium on the contractile proteins so that contractility is decreased.29 In critically ill patients, respiratory acidosis may significantly contribute to depressed contractility and reduced cardiac output at partial pressure of CO2 (PCO2) levels of 60 mm Hg and certainly by PCO2 levels of 90 mm Hg.30 Whether long-term elevations in PCO2 have the same myocardial depressant effect is uncertain because intracellular pH will normalize, despite high PCO2, over time. These considerations may be particularly important in patients in whom the clinician actually seeks a high PCO2 during mechanical ventilation (permissive hypercapnia) to minimize ventilator-associated lung injury (see Chaps. 37, 38, and 40).
Metabolic acidosis also may decrease left ventricular contractility, but its effects are less marked. Arterial blood gas measurement identifies metabolic acidosis in the extracellular compartment. The intracellular compartment is affected to the extent that the metabolic acid anion permeates the cell. Common organic acids such as lactic acid and ketoacids have anions that do not easily cross into the intracellular compartment, so a severe metabolic acidosis may not be associated with significant intracellular acidosis and therefore may not depress ventricular contractility much. For example, lactic acidosis at a normal PCO2 begins to depress contractility at pH 7.1 to 7.2, but even at a pH of 7.0 the depression in contractility remains quite small.31
During septic shock and in patients critically ill from diverse causes, serum ionized calcium levels are often low.32 Further acute reductions may result in a substantial decrease in left ventricular contractility. Decreased extracellular ionized calcium concentration results in decreased calcium flux during systole and decreased contractility.33 After transfusion of red blood cells stored in standard citrated media, serum ionized calcium levels can decrease dramatically because calcium is bound by citric acid. During shock and other conditions, lactic acid, like citric acid, also appears to bind ionized calcium.34 Bicarbonate infusion also can rapidly decrease ionized calcium levels and, as a result, may depress ventricular contractility.35 In addition to ionized hypocalcemia, other electrolyte abnormalities, including hypophosphatemia, hypomagnesemia, and hypokalemia or hyperkalemia, may contribute to decreased contractility or, more importantly, to arrhythmias.
Side Effects of Common Drugs
Exogenous toxins may result in acutely depressed myocardial contractility. Ethanol is a commonly encountered substance that acutely depresses contractility. Drugs commonly used in the ICU that significantly depress contractility include β blockers, calcium channel blockers, and antiarrhythmics such as disopyramide and procainamide.
Septic Shock and Systemic Inflammatory Responses
Many inflammatory pathways triggered by bacterial endotoxins and sepsis have been suggested to contribute to myocardial dysfunction of sepsis. A number of proinflammatory cytokines, including tumor necrosis factor α (TNF), interleukin (IL)–1, IL-2, and IL-6, decrease myocardial contractility in humans and in animal models of sepsis.36,37 Proinflammatory cytokines trigger increased NO production. NO is normally an important regulator of beat-to-beat contractility and, in the setting of enhanced NO production, becomes an important myocardial depressant factor.37 Reactive oxygen intermediates released by leukocytes and cardiomyocytes contribute directly, and by formation of peroxy nitrite radicals, to myocardial damage and dysfunction. Coronary capillary endothelial activation, damage, and dysfunction also contribute, in part due to impaired regulation of coronary microvascular blood flow, which impairs myocardial oxygen extraction.38 Thus, multiple pathways of the intramyocardial inflammatory response may contribute to myocardial dysfunction of systemic inflammation and sepsis.
During hyperdynamic sepsis, the etiology of the hypoperfusion state likely resides in the septic paralysis of arteriolar (and in part venular) smooth muscle, with a minor contribution from decreased contractility, because cardiac output is maintained or elevated. However, the late decrease in cardiac output leading to death involves significant decreases in systolic contractility and increases in diastolic stiffness.
During anaphylactic shock, histamine depresses left ventricular contractility in human beings,39 although the primary cause of hypoperfusion is hypovolemia (see Chap. 106). Hyperthermia and hypothermia may decrease myocardial contractility and contribute to depressed left ventricular function observed during sepsis and other critical illnesses associated with marked abnormalities of body temperature (see Chaps. 110 and 111).
Management of Decreased Left Ventricular Contractility in Critical Illness
Identify and Correct Acute Reversible Causes
It is important to identify the multiple, different potentially reversible causes for depressed contractility in critically ill patients because, although alone they may be insufficient to account for the left ventricular dysfunction, together they may significantly depress function. For example, if ischemia or hypoxemia is present, aggressive attempts to correct it should be instituted. In the presence of coronary artery disease, standard care including heparin, antiplatelet therapy (when indicated), β blockade, and coronary vasodilation using nitrates may be helpful. Thrombolytic therapy within 4 to 6 hours of acute coronary thrombosis or emergency angioplasty decreases the incidence of congestive heart failure and improves outcome (see Chap. 25). Correction of hypoxemia and anemia may result in substantial improvement in ventricular function. Attention should be paid to decreasing factors that increase myocardial oxygen demand. Therefore, when β blockade is not feasible, choosing the lowest level of inotropic and vasoactive drugs that produces the desired therapeutic effect will minimize their contribution to myocardial oxygen demand. Likewise, alleviating pain is important to diminish the associated tachycardia and increased sympathetic tone.
In ventilated patients with left ventricular dysfunction, the detrimental effects of acute respiratory acidosis should be considered; mixed venous and, hence, tissue PCO2 is much higher than the arterial partial pressure of CO2 when the cardiac output is low. In general, metabolic acidosis should be treated by reversing its etiology. Alkali therapy for increased anion gap metabolic acidosis is of no benefit and may be dangerous even at pH values as low as 7.0 for a number of reasons.35 Bicarbonate infusion results in an increase in PCO2 due to chemical equilibrium of HCO3− with H2O and CO2 unless compensatory hyperventilation is also instituted. Particularly during rapid bolus injection, local PCO2 may climb to extremely high values so that myocardial intracellular acidosis transiently may be severe, leading to decreased ventricular contractility.30 Bicarbonate therapy is associated with an increase in lactic acid production because bicarbonate increases the rate-limiting step of glycolysis. Bicarbonate therapy also decreases blood levels of ionized calcium.34,35
Decreased contractility due to ionized hypocalcemia can be corrected with an intravenous infusion of calcium. After approximately 6 U of transfusion, ionized hypocalcemia should be measured and corrected, if necessary. Hypophosphatemia, hypomagnesemia, hypokalemia, hyperkalemia, and other metabolic disturbances also should be corrected because they may lead directly or indirectly to altered cardiovascular function.
Treatment of myocardial depression due to circulating myocardial depressant factors has been attempted with antibodies to endotoxin and TNF, naloxone, and dialysis, but these investigational treatments have not led to improved clinical outcomes. Inhibitors of circulating inflammatory mediators appear to be beneficial in severe sepsis but are limited in less severe sepsis,40 possibly because circulating factors (endotoxin, TNF, and IL-1) are present for only limited periods early in the course of sepsis. Naloxone administered over short periods is not consistently effective, but longer-duration infusions of 1 or more days may result in improvement of hemodynamic measurements. Dialysis, hemofiltration, and plasmapheresis have not been tested adequately in human septic shock, but preclinical evidence suggests that depressed left ventricular contractility due to a myocardial depressant factor of sepsis can be reversed with these treatments.41
Managing the Depressed Heart
Having reversed the acute contributors to depressed left ventricular contractility, standard therapy of decreased left ventricular contractility includes optimizing ventricular filling pressure, decreasing afterload using angiotensin-converting enzyme inhibitors or alternatives when arterial pressure is adequate, increasing contractility using inotropic agents, resynchronization therapy using biventricular pacing,42,43 and, when appropriate, using intraaortic balloon counterpulsation followed by surgical correction of coronary artery stenosis or other surgically correctable lesions24,44 (see Chap. 23).
The ventricular pump function curve illustrates the Frank-Starling mechanism, which shows that increased ventricular filling results in increased ejection even when contractility is depressed. The limit to increased ventricular filling is generally set by the onset of pulmonary edema. Pulmonary edema fluid enters the lung interstitium according to the Starling equation. At normal protein osmotic pressures (largely due to albumin) and normal permeability of the pulmonary endothelium, pulmonary edema starts to develop at Ppw values of at least 20 to 25 mm Hg.45 In the presence of decreased oncotic pressure due to decreased albumin or in the presence of a leaky pulmonary endothelium, pulmonary edema may form at considerably lower Ppw values; in acute respiratory distress syndrome (ARDS) or pneumonia, pulmonary edema may form at very low Ppw values. With this in mind, it is appropriate to search for the Ppw that produces the highest cardiac output without resulting in substantial pulmonary edema. Most often, this search necessitates preload reduction using diuretics and vasodilating agents (Table 22-3). However, when pulmonary edema does not limit oxygenation, it is appropriate to consider increasing cardiac output by intravascular fluid expansion.
Table 22–3. Effect of Direct-Acting Vasodilators ||Download (.pdf)
Table 22–3. Effect of Direct-Acting Vasodilators
|Drug||Route of Administration||Dosage||Onset of Effect||Duration of Effect||Large Arteries||Arterioles||Veins|
|Sodium nitroprusside (Nipride)||Intravenous||25–400 μg/min||Immediate||—||+||+++||+++|
|Nitroglycerin (Tridil)||Intravenous||10–200 μg/min||Immediate||—||++||+||+++|
|Isosorbide dinitrate (Isordil; Sorbitrate, Isobid; Isotrate; Sorate, Sorbide; Dilatrate)
||Oral||20–60 mg||30 min||4–6 h||++||+||+++|
|Hydralazine (Apresoline)||Oral||50–100 mg||30 min||6–12 h||0||+++||±|
|Hydralazine (Apresoline)||IV or IM||5–40 mg||15 min||4–8 h||0||+++||±|
|Minoxidil (Loniten)||Oral||10–30 mg||30 min||8–12 h||0||+++||0|
|Diazoxide (Hyperstat)||IV bolus||100–300 mg||Immediate||4–12 h||0||+++||±|
|Nifedipine (Procardia)||Oral||10–20 mg||20–30 min||2–4 h||++||+++||±|
|Sublingual||10–20 mg||15 min||2–4 h||++||+++||±|
Further management of decreased ventricular contractility then proceeds with afterload reduction14 and inotropic agents.46,47 These therapies are considered in detail below (Acute on Chronic Heart Failure). When vasodilator and inotropic therapy is insufficient, temporary support using intraaortic balloon counterpulsation is appropriate when damaged myocardium is expected to recover or as supportive therapy leading to surgical correction of an anatomic abnormality.24,44 Balloon inflation during diastole improves diastolic perfusion of the coronary and systemic arterial beds. During systole, deflation of the balloon reduces afterload, allowing for increased ejection by a ventricle with markedly decreased contractility (see Chap. 25). Stem cell transplantation is a promising new approach under investigation to repair damaged myocardium.48
Increased Diastolic Stiffness
In normal hearts and in hearts with depressed ventricular function, increasing preload is an important mechanism of increasing cardiac output. For hearts with normal systolic function, left ventricular end-diastolic filling pressures are often in the range of 0 to 10 mm Hg and result in an adequate cardiac output. For hearts with depressed contractility, higher filling pressures are usually required for an adequate cardiac output. Therefore, there is no uniformly optimal filling pressure. Left ventricular function may be substantially impaired by increased diastolic stiffness of the left ventricle—a shift up and to the left of the diastolic pressure-volume relation.16,49 This is a problem whose importance is equal at least to depressed contractility in the critically ill patient.8 Depressed systolic function reduces stroke volume because ESV increases; in contrast, increased diastolic stiffness reduces stroke volume because EDV decreases. Increased diastolic stiffness is a relatively frequent problem encountered in critically ill patients. It differs from depressed ventricular contractility because it is much more difficult to treat and does not respond to conventional therapy of decreased left ventricular pump function.50 In fact, in the absence of an imaging study that demonstrates increased diastolic stiffness (small EDV in relation to the end-diastolic pressure [EDP]), the diagnosis of increased diastolic stiffness is suggested by finding depressed ventricular pump function unresponsive to fluid loading, afterload reduction, and inotropic agents. Occasionally, the diagnosis of increased diastolic stiffness is suggested by the observation that cardiac output is unusually sensitive to changes in heart rate.
Chronic diseases that increase diastolic stiffness include concentric left ventricular hypertrophy due to hypertensive cardiovascular disease, hypertrophic cardiomyopathy, and restrictive myocardial diseases. In addition, diseases of the pericardium, including constriction and effusion, and other processes that increase intrathoracic pressure result in increased diastolic stiffness, as discussed in Chap. 28. Concentric hypertrophy due to chronic hypertension is very common; although it seldom primarily accounts for severe depression in ventricular pump function, it may be an important contributor in combination with acute diseases depressing systolic function. Hypertrophic cardiomyopathy results in increased diastolic stiffness and, in the setting of hypovolemia, may also result in greatly increased afterload due to dynamic aortic outflow obstruction. Over a period of days and months, β blockers and calcium channel blockers, in particular verapamil, may reduce evidence of increased diastolic stiffness. More rapidly, these agents alleviate dynamic outflow obstruction in patients with hypertrophic cardiomyopathy due to their negative inotropic effect.51 Restrictive cardiomyopathies include amyloidosis, hemochromatosis, sarcoidosis, endomyocardial fibrosis, some glycogen storage diseases, and restriction because of surgical correction of acquired and congenital abnormalities. Amyloidosis is uncommon at age 40 but by age 90 has a prevalence of 50%.
Clinical examination may show a Kussmaul sign, rapid x and y descents in the jugular venous pressure waveform so that a and v waves are prominent, and a fourth heart sound. Hepatojugular reflux may be prominent because the increased venous return produced by this maneuver cannot be accommodated by the stiff heart. Diastolic ventricular pressure measurements may show a square root sign, which is a rapid early rise in diastolic pressure to a relatively constant plateau. Echocardiographic evaluation may demonstrate rapid early diastolic filling to a relatively fixed diastolic diameter similar to the square root sign, and increased myocardial echogenicity may be observed in amyloidosis.52,53
As with diseases resulting in depressed left ventricular systolic function, it is important to consider the acute, potentially reversible causes of increased diastolic stiffness.8 Regional or global ischemia results in delayed systolic relaxation, contributing to increased diastolic stiffness. This change in diastolic stiffness usually precedes depressed contractility because the sarcoplasmic reticulum calcium pump has a lower affinity for adenosine triphosphate than do the contractile proteins. In addition, ischemia may result in increased diastolic stiffness by increasing pericardial pressure as a result of increased CVP.54 Therefore, in the setting of increased diastolic stiffness, any ischemia should be treated aggressively.55 Nitrates increase coronary blood flow and decrease tone in the venous capacitance bed, thereby reducing pericardial pressure; nitroprusside also decreases diastolic stiffness.
Increased intrathoracic or intrapericardial pressure is a common reversible cause of apparent increased diastolic stiffness in critical illness. Intrathoracic pressure is increased by positive-pressure mechanical ventilation and more so by the addition of positive end-expiratory pressure (PEEP). Positive airway pressures and PEEP are variably transmitted to the heart, depending on the distensibility of the lungs and chest wall. If the lungs are very distensible and the chest wall is relatively rigid (as with a tense abdomen), then most of an increase in airway pressure will be transmitted to the heart; to maintain the same chamber volumes, the atrial and ventricular pressures have to increase as much. This accounts for part of the reduction in venous return and cardiac output if and when Pms does not increase by a similar amount. A common misconception is that, if the lungs are very stiff, as in the early exudative phase of ARDS, then less of an increase in airway pressures will be transmitted to the heart. However, because PEEP reduces shunt by re-aerating flooded lung regions, the chest wall volume and pleural pressure increase as much or more in ARDS, so the increase in Pra with PEEP may be just as much as in patients with normal lungs. Increased intrathoracic pressure due to pneumothorax or massive pleural effusion may tamponade the heart and thereby result in apparent increased diastolic stiffness. Greatly increased intraabdominal pressure may elevate the diaphragm and similarly increase diastolic stiffness. Pericardial pressure may be increased by pericardial effusion and rarely by massive pneumopericardium. Because all these causes of increased intrathoracic or intrapericardial pressure leading to apparent increased diastolic stiffness are treatable, they must be identified or excluded early in critically ill patients.
Hypovolemic shock and septic shock may result in increased diastolic stiffness.56 The increased diastolic stiffness associated with these kinds of shock is associated with irreversibility of the shock state and increased mortality rate. In septic shock, when depressed left ventricular systolic contractility occurs, the response of surviving patients is that of decreased diastolic stiffness or increased diastolic ventricular compliance.57 This is the usual response to decreased left ventricular systolic contractility seen with other dilated cardiomyopathies.58 However, in patients with septic shock who do not survive, the diastolic left ventricles do not dilate to increase EDV and, hence, do not compensate normally for decreased systolic contractility. The diastolic ventricles of those who do not survive are therefore much stiffer than the ventricles of those who do survive.59 Infusion of catecholamines and calcium may further contribute to increased diastolic stiffness by contraction band formation.
Hypothermia with body temperature falling below 35.8°C (95.8°F) also results in increased left ventricular diastolic stiffness. This is a reversible phenomenon as temperature is increased. This is an important consideration during massive fluid resuscitation and mandates resuscitation with warmed infusions.
Management of Diastolic Dysfunction
Whereas acute diastolic stiffness due to ischemia, tamponade, and tension pneumothorax are readily treated, acute therapy to reverse diastolic stiffness in the critical care setting is limited. Therefore, searching for an optimal filling pressure that maximizes ventricular diastolic filling without resulting in substantial pulmonary edema is a critically important component of care in these patients. In addition, hypovolemia and sepsis should be treated aggressively and promptly, inotropic agents should be avoided or used at the smallest dose that results in the desired systolic or vascular effect, hypothermia should be prevented and treated, and tachycardia or atrioventricular arrhythmias should be treated early (see below). Intrathoracic pressure is minimized by appropriate ventilator management and by decompressing surrounding compartments (pericardial, pleural, and abdominal) when these cause cardiac tamponade.
Special Effects of Altered Afterload on Ventricular Function in Critical Illness
An increase in afterload decreases left ventricular pump function because stroke volume is reduced as a result of increased ESV (see Fig. 22-2). In malignant hypertension, elevated aortic pressure results in decreased cardiac output and elevated left ventricular filling pressures leading to pulmonary edema even if contractility is normal. Antihypertensive therapy results in rapid improvement. When contractility is depressed, increased afterload may worsen cardiac function even more. This is particularly important in dilated cardiomyopathies, in which increased afterload may be observed due to increased sympathetic tone, activation of the renin-angiotensin-aldosterone axis, and abnormally increased vascular smooth muscle tone.
Aortic valvular stenosis or dynamic obstruction of the aortic outflow tract also may increase afterload and contribute to decreased left ventricular pump function14 (see Chap. 29). Dynamic outflow tract obstruction is most commonly due to hypertrophic cardiomyopathy. However, patients with preexisting concentric hypertrophy due to chronic hypertension who have a decrease in intravascular volume may develop dynamic aortic outflow tract obstruction with the classic findings of systolic anterior motion of mitral valve leaflet, increased ejection velocities signifying increased gradients across the aortic outflow tract, and cavity obliteration at end systole. This appears to occur most commonly in elderly patients with previously treated hypertension. Volume infusion to reverse intravascular hypovolemia may prevent left ventricular cavity obliteration and outflow tract obstruction and thereby reduce ventricular afterload. It is important to identify outflow tract obstruction as the cause of increased afterload because this cause of increased afterload is worsened by conventional afterload reduction therapy.
When afterload is reduced dramatically, or when intravascular volumes are expanded, the resulting high cardiac output state is sometimes called high-output cardiac failure. Actually, cardiac function still lies on a normal cardiac function curve, but the greatly increased venous return associated with low afterload results in high right- and left-side filling pressures with the appearance of right- and left-side congestion. This is particularly apparent in the presence of atrioventricular valvular stenosis, which previously may have been occult. Causes of high-output failure include anemia, arteriovenous fistulas, hepatic failure, Paget disease, thyrotoxicosis, pregnancy, carcinoid syndrome, and renal cell carcinoma.
Abnormal Heart Rate and Rhythm
Normally, heart rate and contractile states are matched to venous return and afterload to maximize the efficiency of the cardiovascular system. Even though heart rate is often of lesser importance in trying to increase cardiac output, excessively fast or excessively slow heart rates may limit cardiac output. Bradycardia is an important abnormal rhythm in a critically ill patient. Primarily, it is important to determine whether hypoxemia, drugs such as acetylcholinesterase inhibitors, or other reversible insults are the cause of bradycardia. In these cases, treatment consists of rapid reversal of the cause. In other cases in which bradycardia is due to primary cardiac disease, including myocardial infarction with involvement of the conducting system, therapy is directed at increasing heart rate by other means. Acutely, bradycardia may be treated with atropine and, if necessary, by isoproterenol or epinephrine infusion titrated to heart rate response. These temporizing measures allow placement of temporary or permanent pacemakers. In addition to the well-known indications for temporary pacing after myocardial infarction, it should be recognized that symptomatic bradycardia from any cause is an indication for pacing.
Tachycardia at sufficiently high rates results in an inadequate diastolic filling time, so stroke volume is reduced because adequate diastolic filling does not occur and the contribution to ventricular diastolic filling by the atria is less efficient, particularly in atrial fibrillation. An end-diastolic gradient across the mitral valve develops at fast heart rates. Hypoxemia and acidosis encountered in critically ill patients are frequently associated with ventricular and, even more commonly, supraventricular tachyarrhythmias. Hyperkalemia and hypokalemia, hypocalcemia, and hypomagnesemia are common electrolyte disturbances associated with increased incidence of ventricular arrhythmias. Accordingly, management of atrial and ventricular tachyarrhythmias involves correcting these potential contributing abnormalities.
Cardiac resynchronization therapy using biventricular pacing appears to improve cardiac function in patients having a decreased ejection fraction, bundle branch block, and New York Heart Association class III or IV heart failure.42,43 The role for resynchronization therapy in the critical care setting has not been fully defined.
Arrhythmias including atrial fibrillation, atrial flutter, and ventricular tachycardia should be immediately cardioverted if they are contributing to a shock state. Otherwise, rapid heart rate due to atrial fibrillation is slowed using β blockers or second-line agents including calcium channel blockers. Adenosine, verapamil, and maneuvers to increase vagal tone may be useful in the diagnosis of tachyarrhythmias and in treating paroxysmal supraventricular tachycardia.60 Multifocal atrial tachycardia responds to correction of underlying pulmonary disease and to verapamil.61 Ventricular dysrhythmias contributing to altered hemodynamic function must be treated. Specific management of ventricular arrhythmias is detailed in Chap. 24.
The valves regulate preload and afterload and are therefore important determinants of left ventricular pump function (see Chap. 29). In critically ill patients, the effect of preexisting valvular disease may change with altered hemodynamics, or the extent of valvular disease may change primarily. For example, aortic and mitral insufficiencies contribute to low cardiac output at high ventricular filling pressures in critical illness, and both respond quickly to afterload reduction. Moreover, mitral regurgitation may worsen acutely due to increased EDV and expansion of the mitral annulus. In contrast, mitral valve prolapse may worsen at low ventricular volumes due to hypovolemia. In high cardiac output states, previously insignificant mitral stenosis may result in a high Pla and pulmonary edema. The gradient across the stenotic aortic valve may increase in high-flow states and conversely decrease in low-flow states, so that, without considering the flow across the valve, an incorrect judgment of the functional significance of the valvular disease may be made. Dysfunction of prosthetic valves is important to identify and may be a surgical emergency.