ACUTE HEART FAILURES

INTRODUCTION

Cardiac pump failure is an ominous sign in the critically ill patient that requires prompt recognition and management. Acute heart failure is not a single entity, but can involve the right or left side of the heart, or can occur during diastole or systole. The approach described here requires invasive monitoring with pulmonary artery catheters and centers on the mechanical problem rather than the specific illness.

HEMODYNAMIC MANIFESTATIONS

The diagnosis of heart failure begins with recognition of the early signs of heart failure, then identifies the phase of the cardiac cycle and the side of the heart involved.

EARLY RECOGNITION

The sequence of hemodynamic alterations is as follows :

1. The earliest sign of ventricular dysfunction is an increase in pulmonary capillary wedge pressure. The stroke volume is maintained at this stage because the ventricle is still preload-responsive (i.e., the Starling curve is still steep).

1. The next stage is marked by a decrease in stroke volume and an increase in heart rate. The tachycardia offsets the reduction in stroke volume, so that the cardiac output remains unchanged.

1. The final stage is characterized by a decrease in cardiac output. The point at which the cardiac output begins to decline marks the transition from compensated to decompensated heart failure. The decompensated phase of heart failure is characterized by peripheral vasoconstriction, which initially maintains peripheral blood flow but eventually causes a further reduction in cardiac output and peripheral flow.

Cardiac output may not be reduced in the early stages of heart failure. The early recognition of heart failure requires monitoring of the cardiac filling pressures and the ventricular stroke volume.

SYSTOLIC VERSUS DIASTOLIC FAILURE

Heart failure is not synonymous with contractile failure, and 40% of patients with newly diagnosed heart failure have normal systolic function. The problem in these patients is a decrease in ventricular distensibility, a disorder known as diastolic heart failure. In this type of heart failure, inadequate ventricular filling compromises cardiac output, while the force of ventricular contraction is normal. Common causes of diastolic heart failure in patients in the ICU include ventricular hypertrophy, myocardial ischemia, pericardial effusions, and positive-pressure mechanical ventilation.

The distinction between systolic and diastolic heart failure is important, because what would be appropriate management for one type of heart failure can aggravate the other.

Routine Hemodynamic Monitoring

Routine hemodynamic measurements are incapable of distinguishing diastolic from systolic heart failure. The upper curves in the figure are ventricular function curves relating ventricular end-diastolic pressure (EDP) and cardiac stroke volume. These curves demonstrate that heart failure of either type is associated with an increase in EDP and a decrease in stroke volume. The lower set of curves are diastolic pressure-volume curves, and these curves demonstrate that the increase in EDP in heart failure is associated with opposite changes in the end-diastolic volume (EDV) in the two types of heart failure; that is, the EDV is increased in systolic heart failure and decreased in diastolic heart failure. Therefore, monitoring cardiac filling pressures as an index of ventricular preload does not allow a distinction between systolic and diastolic heart failure.

END-DIASTOLIC VOLUME

The end-diastolic volume is thus the best measure for identifying systolic and diastolic heart failure. The EDV can be derived by the following relationship between the stroke volume (SV) and ejection fraction (EF):

EDV = SV/EF

The ejection fraction of the left ventricle can be measured with radionuclide ventriculography, and the ejection fraction of the right ventricle can be measured with a specialized pulmonary artery catheter with a fast-response thermistor. Because bedside radionuclide ventriculography is tedious, and expensive left-ventricular EDV is not a common bedside measurement.

RIGHT VERSUS LEFT HEART FAILURE

Right heart failure (which is predominantly systolic failure) is more prevalent than considered in patients in the ICU, and it may be particularly prominent in ventilator-dependent patients. The following measurements can prove useful in identifying right heart failure.

Cardiac Filling Pressures

The relationship between the central venous pressure (CVP) and the pulmonary capillary wedge pressure (PCWP) can sometimes be useful for identifying right heart failure. The following criteria have been proposed for right heart failure: CVP > 15 mm Hg and CVP = PCWP or CVP > PCWP. Unfortunately, at least one-third of patients with acute right heart failure do not satisfy these criteria. One problem is the insensitivity of the CVP; an increase in the CVP is seen only in the later stages of right heart (systolic) failure. Contractile failure of the right ventricle results in an increase in end-diastolic volume, and only when the increase in volume of the right heart is impeded by the pericardium does the end-diastolic pressure (CVP) rise.

Another problem with the CVP-PCWP relationship for identifying right heart failure is the interaction between the right and left sides of the heart. Both ventricles share the same septum, so enlargement of the right ventricle pushes the septum to the left and compromises the left-ventricular chamber. This interaction between right and left ventricles is called interventricular interdependence, and it can confuse the interpretation of ventricular filling pressures. In fact, as indicated by the diastolic pressures, the hemodynamic changes in right heart failure can look much like the hemodynamic changes in pericardial tamponade.

End-Diastolic Volume

The right-ventricular ejection fraction (RVEF) and end-diastolic volume (RVEDV), as determined with pulmonary artery catheters equipped with rapid-response thermistors, are the best measures for identifying right heart failure. A decrease in RVEF (normal RVEF is 45 to 50%) and an increase in RVEDV (normal RVEDV is 80 to 140 mL/m2) is expected in right heart failure. The response to volume infusion may be even more diagnostic. In one study, volume infusion resulted in a 30% increase in RVEDV in patients with right-ventricular dysfunction, while in other patients, there was no increase in RVEDV after a fluid challenge (14). In another study, volume infusion did not result in an increase in cardiac output if the RVEDV was in excess of 140 mL/m2.

Echocardiography

Cardiac ultrasound can be useful at the bedside for differentiating right from left heart failure. Three findings typical of right heart failure are (a) an increase in right-ventricular chamber size, (b) segmental wall motion abnormalities on the right, and (c) paradoxical motion of the interventricular septum.

MANAGEMENT STRATEGIES

The primary goal in managing heart failure is to maintain cardiac output, and the secondary goal is to decrease venous (capillary) pressure to limit edema formation. The strategies presented here are designed to achieve both of these goals.

LEFT HEART (SYSTOLIC) FAILURE

The approach to left-ventricular (systolic) failure presented here centers on the PCWP).

Suboptimal Wedge Pressure

Correction of inadequate filling pressures is the sine qua non of heart failure management. As stated by the cardiovascular physiologist, Carl Wiggers: “It is axiomatic that the heart can pump only as much as it receives.”

Condition: Low PCWP

Intervention: Volume infusion to optimal PCWP

The optimal wedge pressure is the highest pressure that augments cardiac output without producing pulmonary edema. This is shown in Figure 16.5 as the highest point on the lower (heart failure) curve that does not enter the hatched pulmonary edema region. The optimal PCWP is determined by the colloid osmotic pressure (COP) of blood. When the COP is normal (20 to 25 mm Hg), the optimal PCWP is 20 mm Hg.

Optimal Wedge Pressure

When the wedge pressure is optimal, therapy is dictated by the blood pressure (BP). The hemodynamic drugs recommended here are those given by continuous IV infusion.

Condition: Optimal PCWP, low BP

Intervention: Dopamine

Dopamine stimulates both b-receptors (cardio-stimulation and vasodilation) and a-receptors (vasoconstriction). The b effect increases the cardiac output, and the a effect raises the blood pressure. The a effect becomes evident at doses above 5 ug/kg/minute, and vasoconstriction is the predominant effect at doses above 10 ug/kg/minute.

Condition: Optimal PCWP, normal BP

Intervention: Dobutamine, amrinone

Dobutamine, a synthetic adrenergic agent that does not cause peripheral vasoconstriction, is widely regarded as the inotropic agent of choice for the acute management of (systolic) heart failure. Amrinone is a phosphodiesterase inhibitor that has both positive inotropic and vasodilator actions. This agent can serve as an effective alternative to dobutamine, or it can be added to dobutamine to enhance the overall effect.

Condition: Optimal PCWP, high BP

Intervention: Nitroprusside, nitroglycerin

Nitroprusside is a popular vasodilator in the critical care setting. However, cyanide accumulation is common during nitroprusside infusions (see Chapter 18), and the risk of cyanide toxicity should temper the use of nitroprusside. The risk of cyanide toxicity has led the Food and Drug Administration to recommend a maximum nitroprusside dose rate of 10 ug/minute for no more than 10 minutes. Nitroglycerin is a viable alternative to nitroprusside if administered in dose rates that exceed 50 ug/minute. Other vasodilators that can be given by continuous intravenous infusion, such as labetalol (a combined a-b blocker), esmolol (a short-acting b blocker), and trimethaphan (a ganglionic blocker) can decrease the cardiac output, and thus these agents are more appropriate for treatment of severe hypertension accompanied by an adequate cardiac output.

High Wedge Pressure

If the wedge pressure is high and the patient is at risk for hydrostatic pulmonary edema, the appropriate management is determined by the cardiac output (CO).

Condition: High PCWP, low CO

Intervention: Dobutamine, amrinone

Therapy with dobutamine and amrinone results in significant reductions in wedge pressure (5,19). Dopamine should be avoided when the wedge pressure is elevated because dopamine constricts pulmonary veins and can increase the wedge pressure further (19,20). Vasodilators can be detrimental in pulmonary edema because they increase shunt fraction and can aggravate hypoxemia (21).

Condition: High PCWP, normal CO

Intervention: Nitroglycerin, ? furosemide

A normal cardiac output in the face of a high PCWP suggests diastolic heart failure. Aggressive diuresis is not recommended as the first line of therapy in this setting because the high filling pressures help maintain cardiac output. Intravenous nitroglycerin (less than 100 ug/kg/minute) should be useful here because this agent reduces the wedge pressure while also reducing the arterial resistance to maintain cardiac output. Sublingual nitroglycerin can be given for immediate results. In the setting of pulmonary edema, nitroglycerin can increase shunt fraction and decrease the arterial PO2. Therefore, arterial gases should be monitored carefully when using nitroglycerin in pulmonary edema.

Furosemide

Intravenous furosemide is a popular therapy for acute pulmonary edema, and it is usually given with little regard for the effects on cardiac output. However, it is well established that intravenous furosemide often causes a decrease in cardiac output in patients with acute heart failure. A total of 169 subjects are included, and in 7 of 10 studies (involving 113 subjects, or 67% of the total study population) intravenous furosemide caused a significant reduction in cardiac output and/or stroke volume. This effect is the result of a decrease in venous return and an increase in systemic vascular resistance. The latter effect is due to the ability of furosemide to stimulate renin release and raise circulating levels of angiotensin, a vasoconstrictor. Considering the popularity of lowering angiotensin levels with angiotensin-converting enzyme inhibitors as a therapy in heart failure, the actions of furosemide to promote angiotensin formation seem to be counterproductive. This effect of furosemide should be considered carefully before the knee-jerk response of administering furosemide in acute heart failure is developed.

Because the diuretic effect of furosemide is more closely related to its urinary excretion rate than to its plasma concentration, continuous infusion furosemide has been advocated for more effective diuresis in patients with heart failure. Continuous infusion is usually recommended when more than 80 mg of intravenous furosemide is required to produce the desired diuretic effect. Dose rates range from 2.5 to 160 mg/hr.

LEFT HEART (DIASTOLIC) FAILURE

The optimal treatment for diastolic heart failure is unknown. Diuretic therapy should be avoided, and inotropic therapy should be ineffective. Although vasodilator therapy should carry a high risk of hypotension in diastolic heart failure (because a ventricle with normal systolic function should be unresponsive to changes in afterload), some vasodilator agents (e.g., calcium channel blockers and angiotensin converting enzyme or ACE inhibitors) may also have lusitropic actions that enhance myocardial relaxation. Verapamil has proven effective in idiopathic hypertrophic cardiomyopathies; however, there is evidence that calcium channel blockers do not improve myocardial relaxation in other conditions associated with diastolic heart failure. For now, the management of diastolic heart failure is similar to that for systolic heart failure, but careful hemodynamic monitoring is necessary to identify adverse effects in the management of diastolic heart failure.

RIGHT HEART FAILURE

Therapeutic strategies for right heart failure are similar in principle to those just described. The strategies below pertain only to primary right heart failure (e.g., acute myocardial infarction), and not to right heart failure secondary to chronic obstructive lung disease or to left heart failure. The PCWP and RVEDV are used as the focal points of management.

1. If PCWP is below 15 mm Hg, infuse volume until the PCWP or CVP increases by 5 mm Hg or either one reaches 20 mm Hg.

2. If the RVEDV is less than 140 mL/m2, infuse volume until the RVEDV reaches 140 mL/m2.

3. If PCWP is above 15 mm Hg or the RVEDV is 140 mL/m2 or higher, infuse dobutamine, beginning at a rate of 5 ug/kg/minute.

4. In the presence of AV dissociation or complete heart block, institute sequential A-V pacing and avoid ventricular pacing.

The response to volume infusion must be carefully monitored in right heart failure because aggressive volume infusion can overdistend the right ventricle and further reduce cardiac output through interventricular interdependence.

Dobutamine is an effective agent in right heart failure. Nitroprusside has been used in right heart failure, but it is not as effective as dobutamine.

MECHANICAL SUPPORT

A variety of devices are available that provide temporary mechanical support of the failing heart. Most of these devices are used after cardiac surgery, where about 5% of patients require postoperative mechanical assistance to support the cardiac output.

INTRAAORTIC BALLOON PUMP (IABP)

Intraaortic balloon counterpulsation has been the standard method of providing mechanical circulatory support for over 25 years. The IABP consists of a 30-cm polyurethane balloon attached to one end of a large-bore catheter. The device is inserted in the femoral artery at the groin, either percutaneously or via arteriotomy, with the balloon wrapped tightly around the catheter. Once inserted, the catheter is advanced up the aorta until the tip lies just beyond the origin of the left subclavian artery. When in place, the balloon wrapping is released to allow periodic balloon inflations. Correct placement does not require fluoroscopy, and the IABP can be placed successfully at the bedside.

Hemodynamic Effects

The intraaortic balloon is rapidly inflated with helium (35 to 40 mL capacity) at the onset of each diastolic period, when the aortic valve closes. The balloon is then rapidly deflated at the onset of ventricular systole, just before the aortic valve opens.

1. Inflation of the balloon increases the peak diastolic pressure and displaces blood toward the periphery. The increase in diastolic pressure increases the mean arterial pressure and thereby increases mean blood flow in the periphery. Coronary blood flow should also increase, because the bulk of coronary blood flow occurs during diastole. However, the IABP increases coronary flow only in hypotensive patients and does not promote coronary flow in normotensive patients.

2. Deflation of the balloon reduces the end-diastolic pressure, which reduces the impedance to flow when the aortic valve opens at the onset of systole. This decreases ventricular afterload and promotes ventricular stroke output.

Indications

The usual indications for the IABP include (a) cardiopulmonary bypass (before and after), (b) cardiac transplantation (before and after), (c) acute myocardial infarction with cardiogenic shock, (d) acute mitral insufficiency, and (e) unstable angina

Almost half of all balloon insertions occur in the immediate postoperative period following cardiopulmonary bypass surgery. The IABP has also gained increasing use as a bridge to cardiac transplantation.

Contraindications

The contraindications to the IABP include aortic regurgitation, aortic dissection, and a recently placed (within 12 months) prosthetic graft in the thoracic aorta.

Complications

The incidence of complications from the IABP ranges from 15 to 45%, with serious complications reported in 5 to 10% of cases (40). The most common complications are leg ischemia (9 to 22%) and septicemia (1 to 22%). Leg ischemia can occur in the ipsilateral or contralateral leg and can appear either with the device in place or soon after it is removed. When distal pulses disappear while the balloon is in place, removal of the device is often sufficient to restore flow without any further therapy. About 20% of patients require surgical interventions for lower leg vascular complications.

Weaning

Balloon assistance is usually withdrawn gradually, by either decreasing the frequency of balloon inflations per cardiac cycle (1:2, 1:3, etc.), or by reducing the inflation volume gradually to 10% of the original volume (40). The choice of weaning method is a matter of individual preference, and there is no evidence that one method is superior to the other. The weaning period is also a matter of individual preference and can range from 60 minutes to 24 hours.

VENTRICULAR ASSIST DEVICES

A ventricular assist device (VAD) is a nonpulsatile pump that is placed in parallel with either the right ventricle (RVAD), the left ventricle (LVAD), or both ventricles (BiVAD) (39,43,44). The pump is adjusted to provide a total systemic flow of 2.0 to 3.0 L/min/m2. These devices are placed intraoperatively in cases where the IABP fails to provide adequate circulatory support (usually after cardiopulmonary bypass surgery). After 24 hours of operation, attempts to wean pump support are usually initiated by decreasing the pump flow rate until right atrial pressure (RVAD) or left atrial pressure (LVAD) increases to 20 to 25 mm Hg. The duration of ventricular support is usually 1 to 4 days, but it can range from a few hours to longer than 10 days. Complications occur in over 50% of patients and most often include bleeding or systemic embolism. Most patients can never be weaned from pump support, but as many as one-third of patients survive the ordeal.

CARDIOPULMONARY BYPASS SURGERY

The immediate period following cardiopulmonary bypass surgery is often marked by hemodynamic instability. The following are some of the major hemodynamic concerns in the early postoperative period.

CARDIAC TAMPONADE

Cardiac tamponade occurs in 3 to 6% of patients undergoing open-heart surgery. It often appears in the first few hours after surgery, but can occur at a later time when the pacemaker wires are removed. The pericardium is open after cardiac surgery, and this prevents fluid from accumulating evenly around the heart. The most common cause of tamponade after surgery is a blood clot compressing the right heart.

Clinical Presentation

Cardiac tamponade often has an atypical presentation in the postbypass period. Two typical manifestations of cardiac tamponade may be absent.

1. Pulsus paradoxus (inspiratory drop in systolic blood pressure of at least 10 mm Hg) can be masked in patients receiving mechanical ventilation. Positive-pressure lung inflation can assist the left ventricle during systole and thereby augment the systolic blood pressure. The increase in systolic pressure produced by positive-pressure mechanical ventilation is called reverse pulsus paradoxus (see Chapter 26).

2. Equalization of diastolic pressures (CVP, pulmonary artery diastolic pressure, PCWP) may not be a feature of cardiac tamponade when a clot is compressing the right atrium. In this situation, the superior vena cava pressure (CVP) can increase while the pulmonary artery and wedge pressures decrease.

Diagnosis

Tamponade is often suspected on clinical grounds when there is a sudden decrease in blood drainage from mediastinal chest tubes followed by a rise in cardiac filling pressures and a progressive decline in cardiac output. The diagnosis is often uncertain (and is a source of much angst in cardiovascular surgeons) and requires repeat thoracotomy for verification and for ligation of bleeding sites. If available, transesophageal echocardiography can be a valuable tool for identifying compression of the right atrium and left-ventricular akinesis.

POST-BYPASS HEMODYNAMICS

The rewarming period after cardiopulmonary bypass is associated with a decrease in the compliance of the ventricles. The etiology is unclear, but myocardial edema from cooling and reperfusion may play a role. The peripheral vascular resistance can either increase or decrease in the immediate postoperative period. Systolic function is variable but seems to be well maintained in most patients. Acute infarction is reported in less than 10% of patients.

Management

The decrease in ventricular compliance during the rewarming period causes a decrease in EDV at any given EDP. This means that a normal wedge pressure in the early postoperative period represents a low EDV. Therefore, when cardiac output is low and the PCWP is not elevated, volume infusion is indicated until the PCWP is in the range of 20 mm Hg.

Drug therapy can be selected according to the systemic vascular resistance (SVR). The following scheme may be helpful:

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SVR Blood Pressure Intervention

High High Nitroprusside

High Normal Dobutamine

High Low Dopamine, IABP

Normal Normal Dobutamine

Normal Low Dopamine, IABP

Low Normal Dobutamine

Low Low Dopamine, epinephrine

The use of nitroprusside to treat postoperative hypertension carries a particularly high risk of cyanide accumulation after cardiopulmonary bypass surgery because of the depletion of thiosulfate associated with this procedure. Nitroglycerin is an effective alternative to nitroprusside, and I have been using trimethaphan (a ganglionic blocker) to treat severe hypertension in this situation.