Hypotension

Sustained hypotension below the lower limit of blood flow autoregulation leads to organ dysfunction. However, autoregulatory limits vary from patient to patient and organ to organ and are altered by disease. The autoregulatory range is set to a higher level in chronic hypertension but may disappear entirely with critical illness, in which case organ blood flow becomes pressure dependent. However, if MAP is maintained at the expense of cardiac output, organ hypoperfusion may occur despite adequate blood pressure.

There are limited data concerning what constitutes an ideal blood pressure in critically ill patients. In one study of patients with septic shock, increasing MAP from 65 to 85 mmHg with norepinephrine did not improve markers of tissue perfusion or renal function.¹ In the absence of similar studies in cardiac surgical patients, a target MAP of more than 65 mmHg is a reasonable goal for most patients. Suggested blood pressure targets in different groups of cardiac surgery patients are listed in Table 20-2.

Table 20-2 Blood Pressure Targets in the First 48 Hours Following Cardiac Surgery

MAP, mean arterial pressure.

Low Cardiac Output and Tissue Hypoperfusion

Unlike blood pressure, cardiac output is not routinely measured in all patients, and clinicians often rely on clinical and biochemical markers of tissue hypoperfusion (Table 20-3). Unfortunately, clinical assessment of cardiac output is unreliable in the first few hours after cardiac surgery.² Cool peripheries are normal findings. Polyuria is common, even with evolving renal dysfunction. Tachycardia may be absent due to the inhibitory effects of cardiopulmonary bypass (CPB) and surgery on the cardiac conducting system. Lactic acidosis is suggestive of tissue hypoperfusion, but other causes (e.g., β₂-agonist drugs; see Table 31-3) may be responsible. Not uncommonly, low cardiac output occurs in the absence of lactic acidosis. A useful screening tool for low cardiac output is the oxygen saturation of blood drawn from the proximal port of a central venous catheter (i.e., from the superior vena cava; S_SVCO₂), which provides a close approximation of a true mixed venous oxygen saturation S_VO₂.³ Values above 65% are reassuring; values below 55% warrant further investigation. Other findings that demand further investigations include escalating inotropic support, a central venous pressure (CVP) above 15 mmHg, and unexplained metabolic acidosis (lactate >5 mmol/l, base deficit >6).

Table 20-3 Clinical and Biochemical Signs Consistent with Inadequate Cardiac Output

S_SVCO₂, superior vena cava oxygen saturation; S_VO₂, mixed venous oxygen saturation.

If low cardiac output is suspected—and the cause is not readily apparent on the basis of routine clinical assessment—cardiac output should be measured. Numerous devices may be used (see Chapter 8), but in cardiac surgery units, the pulmonary artery catheter (PAC) is the device most commonly employed. A PAC also allows measurement of pulmonary arterial pressure, pulmonary artery wedge pressure (PAWP), and S_VO₂. As with blood pressure, the normal value for cardiac output is ill defined. By convention, a lower limit of 2.2 l/min/m² is widely used; however, many “well” cardiac surgery patients have values below this figure.² Also, the appropriate cardiac output depends on the patient’s metabolic state. Thus, in a patient with a marked systemic inflammatory response to CPB, a cardiac output of 4 l/min/m² may be appropriate, whereas in a sedated, mildly hypothermic patient, a value of 2 l/min/m² may be satisfactory. As a simple guide, if filling pressures are normal (PAWP <15 mmHg, CVP <12 mmHg), and venous oxygen saturation is satisfactory (>65%), a cardiac output as low as 1.8 l/min/m² is probably acceptable.

Diagnosis and Treatment

Causes of hemodynamic instability in the early postoperative period are listed in Table 20-4. A stepwise approach to the diagnosis and initial treatment of hemodynamic instability is provided in Table 20-5. Important diagnostic clues can be obtained from the patient’s history and intraoperative course. The operation notes, angiograms, and echocardiograms should be reviewed. Examination should focus on the cardiovascular system, in particular the presence of any new murmurs. Specific diagnoses may be suggested on the basis of the electrocardiogram (ECG), CVP, and arterial pressure waveforms (see Chapter 8). If the ECG trace is abnormal, 12-lead and atrial ECGs should be obtained. Respiratory problems can cause hemodynamic instability, and a careful respiratory system examination, including checking the ventilator circuit and settings, should be performed. Chest drain bottles should be inspected for blood loss and bubbling. Important trends may be identified on the 24-hour ICU chart. Further blood tests, such as arterial blood gases, complete blood count, coagulation status, and troponin may be indicated, depending on the circumstances. Chest radiographs should be reviewed.

Table 20-4 Causes of Hemodynamic Instability in the Early Period Following Cardiac Surgery

LVOT, left ventricular outflow tract.

Table 20-5 A Stepwise Approach to the Diagnosis and Initial Treatment of the Hemodynamically Unstable Postoperative Cardiac Patient

ECG, electrocardiogram; MAP, mean arterial pressure; PAC, pulmonary artery catheter.

If the cause of hypotension or low cardiac output is not rapidly apparent, an echocardiogram should be performed. Pulmonary artery catheterization and echocardiography are complementary techniques: a PAC is preferred for measuring cardiac output, whereas an echocardiogram is preferred for diagnosing the cause of low cardiac output and hypotension. In the ICU, transesophageal echocardiography (TEE) offers significant advantages over transthoracic echocardiography (TTE) (see Chapter 7).

Diagnosis

Hypovolemia is usually obvious on the basis of clinical signs and invasive hemodynamic monitoring. However, in certain situations the clinical picture is confusing. Young patients with intact cardiovascular reflexes can have important hypovolemia without showing clinical indicators, whereas modest hypovolemia can cause profound hypotension in elderly patients who are mechanically ventilated and have blunted sympathetic tone. Hypovolemia frequently coexists with other causes of hemodynamic instability, complicating the diagnosis. The surrogates of preload, CVP and pawp, are often misleading (see Chapters 1 and Chapter 8).

Treatment

Hypovolemia may be treated with crystalloid or colloid solutions (see Chapter 32). Neither fluid has a protective benefit against pulmonary edema or is associated with improved patient outcome.⁹ With crystalloid fluid, approximately one and a half times the volume of a colloid must be administered to achieve the same clinical effect.⁹

In critically unwell patients, the PAWP associated with optimal stroke volume may cause pulmonary edema. Therefore a balance must be struck between gas exchange and cardiac output. In mechanically ventilated patients, modest increases in positive end-expiratory pressure (PEEP) (e.g., from 5 to 10 cm H₂O) may protect against pulmonary edema and allow a higher PAWP to be tolerated. Conversely, in the presence of intrapulmonary shunting, low cardiac output is associated with impaired gas exchange (see Chapter 27). Thus, in hypovolemic patients, fluid administration may improve oxygenation.

Diagnosis

The cardinal features of systemic vasodilation are hypotension and high cardiac output. Calculated systemic vascular resistance is low (see Eq. 1-5). Atrial pressures are normal or low, but enthusiastic fluid administration may lead to high filling pressures. Diastolic blood pressure is usually low (<50 mmHg) and pulse pressure is usually high (>50 mmHg).

Warm, dilatated peripheries are not a consistent finding in vasodilatated patients in the first few hours after surgery. If the cause of the vasodilatation is systemic inflammation, there may be signs of multiorgan involvement, particularly impaired gas exchange (with evidence of pulmonary edema on chest radiograph), fever, leukocytosis, abnormal liver function, and oliguria. Serum amylase may be mildly elevated.

The echocardiographic findings are similar to those of hypovolemia: ventricular function is vigorous and end-systolic area is reduced; however, in practice, this distinction is subtle.

Treatment

Concomitant hypovolemia must be corrected, but there is little gain in boosting atrial pressures to supranormal values. Hypotension should be treated with a norepinephrine infusion titrated to an appropriate MAP. If hypotension persists despite high-dose norepinephrine (>0.3 to 0.6 μg/kg/min), vasopressin (0.01 to 0.04 units/min) may be considered. The use of methylene blue (1.5 mg/kg over 5 to 10 minutes) has been reported, and in one small series it appeared to improve survival rates in postcardiac surgery vasoplegic shock.¹² As inadequate stress release of cortisol exacerbates vasoplegic shock, treatment with hydrocortisone (100 mg intravenously 8 hourly) may be considered.¹³ In a patient with a low ejection fraction, it is important to ensure that treatment with vasopressors does not precipitate a major fall in cardiac output.

Chronic

Chronic left ventricular systolic dysfunction results in remodeling (see Chapter 1), usually as a consequence of myocardial infarction, chronic ischemia (hibernating myocardium), or valvular heart disease. Ejection fraction is reduced and ventricular volumes are increased. A patient with compensated heart failure may have a normal cardiac output and left atrial pressure and, despite a low ejection fraction, may have good functional capacity. Such a patient often has an uneventful postoperative course. However, decompensation may occur if: (1) there is a further myocardial insult (e.g., myocardial stunning); (2) ventricular afterload is abruptly increased (e.g., after tracheal extubation or the withholding of usual vasodilator therapy); (3) there is a requirement for increased cardiac output (e.g., a severe inflammatory response to CPB).

Acute

Acute left ventricular systolic dysfunction occurs due to myocardial ischemia, acute infarction, myocardial stunning, drugs (e.g., β blockers), or systemic inflammation. Some degree of myocardial stunning occurs in all patients after cardiac surgery.¹⁴ However, severe postoperative stunning is likely when: (1) CPB is complicated or greatly prolonged; (2) severe myocardial ischemia was present preoperatively. With acute dysfunction, ejection fraction is reduced but ventricular volumes may be relatively normal. Cardiac output is reduced, left atrial pressure is increased, and there may be signs of pulmonary congestion and tissue hypoperfusion.

Myocardial ischemia must always be considered in any patient who develops new left ventricular systolic dysfunction. The patients at the highest risk for myocardial ischemia are those undergoing coronary revascularization (see Chapter 9), but ischemia can also occur in other situations, namely, the obstruction of a coronary ostium during aortic valve replacement; the kinking or obstruction of a coronary artery following its reimplantation during aortic root replacement; damage to the circumflex coronary artery during mitral valve surgery; and damage to the septal branch of the left anterior descending coronary artery as it runs in front of the pulmonary valve during the Ross procedure (see Chapter 10).

Diagnosis

Treatment

Preload, heart rate, and rhythm should be optimized. A heart rate of 80 to 100 beats per minute, using pacing if necessary, is appropriate for most patients. Inotropic support should then be commenced and titrated to effect. The choice of drug depends on the hemodynamic state. If cardiac output is low but blood pressure is satisfactory, an inodilator such as dobutamine or milrinone may be used. If both blood pressure and cardiac output are low, epinephrine or a combination of norepinephrine and milrinone (or dobutamine) may be used. If hemodynamic instability persists despite modest inotropic support (epinephrine 0.1 to 0.2 μ/kg/min or equivalent), insertion of an intraaortic balloon pump (IABP) should be considered (see Chapter 22). In patients with systolic ventricular dysfunction, high-dose norepinephrine can cause a precipitous fall in cardiac output and should be avoided unless cardiac output is being measured.

Combinations of inotropic drugs at high dosages (e.g., norepinephrine plus milrinone; or epinephrine/dopamine plus milrinone, and vasopressin) in conjunction with an IABP are sometimes required for severe postoperative myocardial stunning, and biventricular failure. If the hemodynamic state remains inadequate despite an IABP and combination high-dosage inotropic pharmacotherapy, and cardiac dysfunction is potentially reversible, placement of a ventricular assist device should be considered (see Chapter 22).

Severe acidemia (pH ≤7.0) exacerbates ventricular dysfunction and inhibits the actions of inotropic drugs^15,16; early institution of renal replacement therapy should be considered (see Chapter 33). Correction of the pH with sodium bicarbonate does not improve the hemodynamic state.^17,18

Weaning Therapy

Following a period of hemodynamic stability, weaning from cardiovascular support can commence. This should be done in a staged manner. Rapid, contemporaneous weaning of inotropic support, IABP, and mechanical ventilation can precipitate acute heart failure. Once inotropic support has been weaned to a modest level (epinephrine <0.1 μg/kg/min or the equivalent), it is appropriate to wean either ventilation or the IABP. If gas exchange is good and the patient is relatively intolerant of the endotracheal tube, mechanical ventilation may be weaned first. The disadvantage of this approach is the patient must be extubated lying relatively flat. If the patient cannot be weaned rapidly from mechanical ventilation or is agitated, he or she should be kept sedated and weaned from the IABP first (see Chapter 22). If the IABP can be removed and the patient extubated within 2 to 4 days, it is useful to leave the PAC in place until these events have occurred. Assuming renal function is intact and blood pressure is satisfactory, as inodilators are stopped, low-dosage ACE inhibitor therapy may be commenced to maintain a low afterload state.

Diagnosis

Right ventricular failure is manifested as a high CVP (with V waves) in association with a falling blood pressure and cardiac output. Pulmonary arterial pressure may be normal, high, or low, depending on the cause and on cardiac output. (Assuming pulmonary vascular resistance and left atrial pressure remain constant, a fall in cardiac output results in a fall in pulmonary arterial pressure; refer to Eq. 1-6.) With primary volume overload and right ventricular systolic dysfunction, pulmonary vascular resistance is not elevated; therefore, pulmonary arterial pressure is not increased. There is a small step-up in pressure between the CVP and mean pulmonary arterial pressure (<10 mmHg). By contrast, pulmonary arterial pressure is increased with pressure overload, reflecting increased pulmonary vascular resistance. The transpulmonary pressure gradient is elevated but PAWP may be normal or low.

Echocardiographic features include right ventricular dilation, impaired contractility, tricuspid regurgitation, leftward bowing of the interatrial septum, and characteristic changes in the shape and motion of the interventricular septum (see Fig. 7-15). With chronic pressure overload, right ventricular hypertrophy may be evident. With severe right ventricular dilation, the left ventricle may appear small and underfilled due to leftward displacement of the interventricular septum. In this situation, PAWP may be increased.

Treatment

Treating right ventricular dysfunction involves: (1) maintaining adequate preload; (2) maintaining right ventricular perfusion pressure; (3) reducing right ventricular afterload; and (4) augmenting contractility.

Traditionally, fluid loading has been advocated for patients with right ventricular infarction,^20,21 even though there is little evidence that this strategy improves cardiac output or blood pressure.^22,23 Furthermore, aggressive fluid administration reduces right ventricular perfusion pressure (by increasing right ventricular end-diastolic pressure); causes leftward displacement of the interventricular septum; and exacerbates tricuspid regurgitation. Only rarely does the CVP need to be greater than 15 mmHg.

Inotropes and vasopressors help to maintain right ventricular perfusion pressure and to augment contractility. Milrinone plus norepinephrine or dobutamine plus norepinephrine are good choices. For decompensated right ventricular pressure overload, maintaining right ventricular perfusion pressure, usually with norepinephrine, is critically important (see Chapter 24).

Afterload reduction is potentially beneficial. Simple measures such as avoidance of hypoxemia, hypercarbia, and acidemia are important. Airway pressure and PEEP should be kept as low as possible. The use of pulmonary vasodilators, such as inhaled nitric oxide, inhaled or intravenous prostacyclin, and milrinone (see Chapter 24), may reduce pulmonary vascular resistance and improve right ventricular function. However, they should be used with caution for the following reasons:

Gross Thoracic Edema

After prolonged cardiac surgery in which there has been massive blood product transfusion, severe edema of the thoracic structures (heart, lungs, mediastinum) can occur. Chest closure can result in severe hypotension, due primarily to right ventricular compression. If this occurs, the sternum may be left open at the end of surgery, the wound sealed with a dressing, and formal chest closure performed a few days later, once the edema has settled.²⁴ Similarly, sternal opening should be considered for intractable early postoperative right ventricular dysfunction.

Diagnosis

With echocardiography, systolic function is typically vigorous, with a normal or high ejection fraction and a low LVEDV. These findings are similar to those in hypovolemia, but in contrast to hypovolemia, the left atrium may be large and tense with abnormal rightward bowing of the interatrial septum, which is indicative of raised left atrial pressure. The transmitral Doppler waveform may show impaired relaxation and pseudonormal or restrictive filling (see Fig. 7-7). The E/Em ratio is usually higher than 15 (Chapter 7). PAWP is elevated and cardiac output is normal or low.

It is important to rule out other conditions before making the diagnosis of diastolic dysfunction. The finding of “normal” systolic function must be made in the context of inotropic therapy and the hemodynamic state. Severe right ventricular dilatation can impair the filling of the left ventricle, causing a high PAWP and a small, underfilled left ventricle. Similarly, a high PAWP and vigorous systolic function are also seen with dynamic left ventricular outflow tract (LVOT) obstruction, mitral regurgitation, and certain arrhythmias.

Treatment

There is no truly effective way to induce ventricular relaxation. The two goals of treatment are optimizing preload—while minimizing pulmonary congestion—and avoiding actions that worsen left ventricular filling. With a restrictive filling pattern (see Fig. 7-7), the majority of ventricular filling occurs in early diastole. Thus, modest tachycardia may improve hemodynamics. In contrast, with impaired relaxation a greater proportion of ventricular filling occurs late in diastole, and filling is more dependent than usual on atrial systole. Thus, tachycardia and loss of atrioventricular synchrony are poorly tolerated. A heart rate of 70 to 80 beats per minute may produce more favorable hemodynamics than a heart rate of 90 to 100 beats per minute. A slightly prolonged atrioventricular delay (e.g., 180 ms versus the usual 150 ms) may also augment cardiac output in patients who are sequentially paced. Atrial fibrillation and other tachyarrhythmias should be aggressively treated (see Chapter 21).

β-Adrenoreceptor agonists, by virtue of their chronotropic effect, may have an adverse effect on cardiac output. Phosphodiesterase inhibitors such as milrinone enhance early diastolic relaxation (lusitropy) by a direct myocardial action and by causing afterload reduction.²⁸ Thus, at least theoretically, they may improve early diastolic filling in patients with impaired relaxation; whether this effect is clinically important in the setting of normal systolic function and raised left atrial pressure is unknown. Probably the major benefit of milrinone in patients with impaired relaxation is that it does not cause tachycardia.

Diagnosis

Tamponade classically presents with hypotension, pulsus paradoxus, narrow arterial pulse pressure, and equally increased left and right atrial pressures. This constellation of clinical signs may develop in a patient who has a circumferential collection of unclotted blood. With echocardiography, unclotted blood appears as an echo-free (black) space around the heart (Fig. 20-1). The ventricular cavity typically appears small and underfilled—an echocardiographic sign termed “pseudohypertrophy”³⁰—and the venae cavae appear distended.

Figure 20.1 Echocardiogram showing tamponade due to unclotted blood around the heart. A transgastric, midpapillary short-axis view of the left ventricle is shown. The left ventricle (LV) is small, and a large pericardial collection (PC) is seen inferior and posterior to the heart. The right ventricle (RV) is only partially seen. A large strand of fibrin is seen in the pericardial collection (arrow).

When pericardial pressure exceeds the pressure in a cardiac chamber, collapse of that chamber occurs. This is manifested as atrial collapse during (ventricular) systole or ventricular collapse during diastole (the pressure in the ventricles is lowest in diastole and the pressure in the atria is lowest in ventricular systole).

In contrast to circumferential tamponade, regional tamponade is easily misdiagnosed. When clot overlies the right atrium or ventricle, CVP is usually high and PAWP usually low, mimicking right ventricular dysfunction; when clot lies behind the left atrium, PAWP is usually high and CVP is usually low, mimicking left ventricular dysfunction. Typical echocardiographic appearances of regional tamponade are shown in Figure 20-2. As clotted blood is echogenic, appearing gray or white, it may be difficult to delineate clot from myocardium, particularly in anterior collections. TEE usually provides far superior imaging than TTE.

Figure 20.2 Regional tamponade. Three common sites for localized pericardial clot formation are shown: (1) overlying the right atrial free wall; (2) behind the left atrium; (3) anterolateral to the right ventricle.

(Modified, with permission, from: Sidebotham D, Merry A, Legget M: In, eds. Practical Perioperative Transoesophageal Echocardiography. Fig. 6.2, p. 94. Philadelphia, Butterworth Heinemann, 2003.) LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Usually tamponade presents acutely within the first 24 hours after surgery. However, it can also present several days after surgery as a subtle deterioration in cardiorespiratory function (see subsequent material).

Treatment

The decision to reoperate for tamponade can be difficult to make. The degree to which a pericardial collection is responsible for hemodynamic instability depends not only on the size of the collection but also on the speed with which it has developed, the underlying ventricular function, the vascular tone, and the volume status. In patients with severely impaired ventricular function, even small collections can cause profound hemodynamic compromise. The decision to surgically drain a pericardial collection must be balanced against the increased risk for mediastinitis associated with reopening sternal wounds.³¹

The definitive treatment for tamponade is chest reopening. Less invasive procedures such as opening the lower end of the sternal wound or percutaneous placement of a pigtail catheter are not recommended for tamponade that develops within the first few hours after surgery. There are two reasons for this. First, an active source of bleeding must be sought and controlled. Second, regional tamponade may not be treated reliably unless the pericardial space is fully explored.

Medical treatment of tamponade is supportive. Fluid and inotropes should be given to optimize cardiac function and maintain blood pressure. CVP and PAWP may need to be high. PEEP should be kept to a minimum to avoid further obstruction of systemic venous return.³² Patients should be sedated and paralyzed. A common practice is “stripping” the drain tubing, either with a roller or manually, to remove clot from within the drains and to augment the negative intrapericardial pressure. Although there are few data supporting this practice,³³ it is occasionally dramatically effective in relieving pericardial tamponade.

Diagnosis and Treatment

Patients present with hypotension, low cardiac output, pulmonary hypertension, high PAWP, and signs of mitral regurgitation. Tachycardia is common. These findings may lead the clinician to assume the problem is left ventricular systolic dysfunction or primary mitral regurgitation and to commence inotropic therapy or place an IABP, which will exacerbate the problem.

With echocardiography the pathognomonic finding is systolic displacement of the anterior mitral leaflet into the LVOT (see Fig. 7-12). Additional echocardiographic findings include:

Treatment involves cessation of inotropic drugs, fluid loading, and administration of a vasoconstrictor such as phenylephrine. An IABP should be removed. Intravenous β blockers may be considered.

Sometimes LVOT obstruction is present but is not the primary cause of hemodynamic instability. For instance, SAM may be precipitated by hypovolemia, marked vasodilation (e.g., anaphylaxis) or cardiac compression (tamponade, tension pneumothorax). SAM is unlikely to be the cause of hemodynamic instability if there is no significant mitral regurgitation and the velocity in the LVOT is less than 2.5 to 3.5 m/sec.

Patient-Ventilator Dysynchrony

Patient-ventilator dysynchrony is common during awakening after cardiac surgery. Disorientation, biting the endotracheal tube, breath-holding, shivering, and inappropriate ventilator settings all contribute to patient-ventilator dysynchrony. Usually the diagnosis is obvious. However, sometimes the diagnosis is not immediately apparent: the patient may appear calm and sedated but there is a progressive rise in CVP and a fall in MAP. On close inspection, shivering or breath-holding may be apparent—but not always. Sedating or paralyzing the patient and seeing the blood pressure recover and the CVP fall confirms the diagnosis. Meperidine (25 mg intravenously) is useful for treating shivering.

Dynamic Lung Hyperinflation

In patients with obstructive lung disease, mechanical ventilation at relatively rapid breath rates may not provide enough time for full expiration to occur. Air trapping (auto-PEEP) develops, causing a progressive increase in intrathoracic pressure, which eventually obstructs venous return. Using the expiratory hold function on the ventilator (the patient must be heavily sedated or paralyzed), the finding of an end-expiratory pressure that is significantly higher than the level of applied PEEP confirms the diagnosis. In an emergency, the patient should be disconnected from the ventilator to allow full expiration to occur (Lazarus maneuver). When the hemodynamics improve, mechanical ventilation is reinstituted at a rate of 6 to 8 breaths per minute.

Tension Pneumothorax

Tension pneumothorax causes an obstruction of venous return because of high intrathoracic pressure and mediastinal shift. It may present with hemodynamic collapse or, rarely, with gradual cardiovascular decline. There may be unilaterally diminished breath sounds with tracheal deviation (away from the side of the pneumothorax) and quiet heart sounds. If the patient is sufficiently stable, an immediate chest radiograph may be obtained to confirm the diagnosis, but in the presence of a cardiac arrest or hypotension immediate needle thoracocentesis followed by tube thoracostomy (see Chapter 40) may be lifesaving.

Massive Hemothorax

Massive hemothorax (often involving the left chest because of bleeding from the left internal mammary artery bed after CABG surgery) usually presents with hypovolemia, anemia, and impaired gas exchange. Occasionally, direct compression of the heart can lead to mediastinal shift and impaired venous return, resulting in a tamponade-like clinical picture. The diagnosis is usually clear on the chest radiograph (see Fig. 6-26) or echocardiogram (see Fig. 7-16).

Severe Mitral Regurgitation

Mitral regurgitation may contribute to or (rarely) be the primary cause of hemodynamic instability. The diagnosis should be considered in the following circumstances:

Signs suggestive of mitral regurgitation include a (new) systolic murmur, pulmonary hypertension, and high PAWP with V waves. On the chest radiograph, there may be signs of chamber enlargement (left atrium and left ventricle) and pulmonary edema. The presence, severity, and mechanism of the mitral regurgitation should be assessed by echocardiography. Assuming the cause is not dynamic LVOT obstruction (see earlier material) and surgery is not indicated, treatment consists of diuretics, inotropic support, and vasodilation. Placement of an IABP may be appropriate.

Ventricular Rupture

Following myocardial infarction, rupture of the ventricular septum or free wall can occur. Patients present with profound shock, and mortality rates are high, even with rapid surgical intervention.

Hemodynamic Instability in the Presence of Vigorous Systolic Function

A patient may be hypotensive or have a low cardiac output and yet have vigorous left ventricular function on echocardiography: “The heart looks fine but the patient looks terrible.” It should be clear from the foregoing discussion that normal or supranormal left ventricular systolic function is seen in several causes of hemodynamic instability. They are listed in Table 20-8.

Table 20-8 Causes of Hemodynamic Instability in Which Left Ventricular Function May Appear Vigorous on Echocardiography

LVOT, left ventricular outflow tract.

Assessment of ventricular function must take into account loading conditions, the use of vasoactive drugs, and the patient’s metabolic rate as well as treatments such as an IABP and mechanical ventilation. Low preload (hypovolemia) and afterload (e.g., mitral regurgitation, low systemic vascular resistance) flatter ventricular function. Similarly, inotropic drugs, IABPs, and mechanical ventilation augment ventricular function. With normal ventricular function, inotropic drugs result in hyperdynamic wall motion, increased ejection fraction, and reduced ventricular volumes, particularly endsystolic volume. Even in patients with severely impaired systolic function, high-dose inotropic support imparts vigorous systolic wall motion, albeit with a characteristic “jerky” quality. Also, end-systolic volume remains elevated. Wall motion is hard to grade objectively in patients who are tachycardic.

With dynamic LVOT obstruction, stopping inotropic drugs and starting an infusion of phenylephrine is likely to improve the hemodynamic state. However, on echocardiography, systolic function will appear less vigorous and ejection fraction will appear reduced. (The increase in end-diastolic volume and the reduction in mitral regurgitation cause an increase in cardiac output despite a reduction in ejection fraction.) A similar phenomenon is seen with severe diastolic dysfunction.

Initial Resuscitation

When a cardiac arrest call is made, timely and appropriate intervention can be lifesaving. Assessment and treatment must occur simultaneously. The diagnosis is often made retrospectively after successful resuscitation.

An algorithm for the initial approach to a cardiac arrest call and the early treatment of near cardiac arrest is shown in Figure 20-3. Initial assessment and intervention center on confirming the presence of cardiac arrest and identifying and eliminating an airway, ventilation, monitoring, or drug-delivery problem. First, it should be established that the hypotension is real by palpating a central pulse. The arterial waveform, ECG, transducer, and infusion devices should be inspected. If necessary, transducers should be rapidly leveled, zeroed, and flushed. If a pulse can be palpated but the arterial waveform suggests cardiac arrest, blood pressure should be measured noninvasively. If the patient is being paced, it should be discontinued briefly to rule out underlying ventricular fibrillation. As soon as cardiac arrest or near cardiac arrest is confirmed, external chest compression should be commenced. An exception to this is in near cardiac arrest when the patient is still conscious and in cardiac arrest when the rhythm is VF/VT (see later discussion). Intubated patients should be disconnected from ventilators and ventilated with a manual resuscitator (see Fig. 28-1) using 100% oxygen. Extubated patients should receive mask-assisted ventilation, and intubation should be considered. Prolonged attempts at intubation must be avoided because they interfere with regular mask ventilation and can delay defibrillation. Chest movements should be inspected, the trachea palpated, and breath sounds auscultated. Infusions of hypotensive drugs should be discontinued. This initial period of diagnosis and treatment should be completed within 30 to 60 seconds.

Figure 20.3 Management algorithm for cardiac arrest and near cardiac arrest. DLHI, dynamic lung hyperinflation; ECG, electrocardiogram; ETT, endotracheal tube; MAP, mean arterial pressure; PAC, pulmonary artery catheter; TEE, transesophageal echocardiogram; TTE, transthoracic echocardiogram.

Rhythm-Specific Management

A rhythm-specific algorithm for managing cardiac arrest is shown in Figure 20-4.

Figure 20.4 Rhythm-specific management of cardiac arrest. ECC, external chest compressions; ICC, internal cardiac compressions; J, joules; PAC, pulmonary artery catheter; PEA, pulseless electrical activity; P-VT, pulseless ventricular tachycardia; VF, ventricular fibrillation; VT, ventricular tachycardia.

Specific Issues During Resuscitation

Personnel and Protocols

Within individual institutions, a protocol should be established to determine which personnel attend cardiac arrests in various parts of the hospital. In some ICUs cardiac arrests are managed in-house; in others, the hospital “crash” team attends. For all cardiac arrests, a structure should be established to determine who is responsible for running the arrest. In the ICU, it is commonly the on-call intensive care physician. This person should be in overall command and should be responsible for determining all treatments. If possible, the person running the arrest should not be involved in administering drugs or performing interventions.

All medical and nursing staff working within the ICU should be familiar with basic and advanced life support and be regularly recertified in these procedures. Staff should also be familiar with the emergency chest reopening protocol for their units.

During each arrest, one person should be responsible for documenting the time of the arrest, the dosages of all drugs that are administered, and the times of all interventions. In particular, the time to return of spontaneous circulation should be noted. Each cardiac arrest should be subject to postevent review as part of continuing quality assurance.