Recognition

The bedside diagnosis of low cardiac output can be divided into clinical and measured parameters.

The clinical diagnosis of low cardiac output resolves around signs and symptoms of organ hypoperfusion. The primary systems which we use to evaluate this state are the skin, the kidney and the brain. When cardiac output is low, skin perfusion is dramatically reduced. Therefore, the skin becomes cold and clammy. In addition, a drop in cardiac output significantly reduces kidney perfusion with the resultant rapid decrease in urine output. And finally, low cardiac output dramatically affects cerebral perfusion with resultant decreased consciousness.

Direct measurements of cardiac output can be obtained by the following: utilizing the Swan-Ganz catheter and the thermodilution computer. In addition arterial blood gas analysis showing the development of metabolic acidosis should alert one to the potential of low output state with resultant lactic acidosis. Finally, analysis of blood obtained from the distal port of the Swan-Ganz catheter showing a low mixed venous oxygen saturation should again suggest the diagnosis of low output state.

Treatment

The treatment of a low cardiac output revolves around the understanding of the variables controlling cardiac output. Mathematically, cardiac output is equal to cardiac stroke volume times heart rate. Stroke volume itself is determined by preload, afterload and myocardial contractility. Hence manipulation of the patient's heart rate, his preload, his afterload or his myocardial contractility will allow one to adjust the overall cardiac output. Problems in heart rate and rhythm

It is not uncommon for postoperative patients to experience problems with significant bradycardia. In addition, many patients, particularly those with surgery around the tricuspid valve, have problems with heart block. In both of these conditions the treatment of choice is atrial, ventricular, or atrial-ventricular pacing. AH postop cardiac patients have either ventricular, atrial or atrial and ventricular pacing wires in place. Therefore the initial treatment for these conditions is external pacemaking. In addition, patients who are ventricularly paced can have a drop in cardiac output due to the fact that they have lost their atrial component of ventricular filling. Therefore, switching these individuals to atrial-ventricular pacing may significantly improve their cardiac output. In those individuals where pacing wires are either not present or have been removed, or are not capturing, pharmacologic manipulation of heart rate is indicated. The primary drugs of choice used are atropine and isoproterenol. Finally, in those individuals where a particular dysrhythmia adversely affects the cardiac output, treatment (see section on dysrhythmias) of the underlying dysrhythmia may significantly improve the deteriorating output state. Treatment of inadequate preload

Preload may be defined as the ventricular fiber length at the end of diastole. Hence preload is closely related to the ventricular end diastolic pressure which can be approximated by measurement of the pulmonary capillary wedge pressures or the pulmonary artery diastolic pressure. Problems in preload arise when one or two conditions develops. The first is hypovolemia. Hypovolemia occurs due to blood loss, plasma loss, significant venodilation, or to inadequate volume replacement. Under these conditions, the appropriate treatment would be to replace the missing component. In conditions where significant blood loss has occurred and the hematocrit demonstrates a loss of red cell mass, transfusions of packed red blood cells would be appropriate. In conditions where significant plasma loss has occurred the hematocrit itself may be high but the pulmonary capillary wedge pressure would be low demonstrating a depleted intravascular space. Under these conditions, fluid replacement is in order. On our service it is preferred that a colloid-type agent be used so that the replacement remains in the intravascular space. It is our preference to use 5% albumin or Hespan when volume replacement is required.

The other problem with preload is impaired filling. Impaired ventricular fll-ing occurs when conditions such as cardiac tamponade, tension pneumothorax, or excessive positive pressure breathing interferes with the normal return of blood to the heart. The treatment of impaired ventricular filling revolves around the

elimination of the agent causing the impairment. In the case of tamponade a return to the operating room to drain the mediastinum would be appropriate. In the presence of tension pneumothorax a chest tube will quickly relieve the problem. Finally, in situations where positive pressure breathing may be interfering with blood return, a diminution of the end expiratory pressure may be necessary. Treatment of problems in afterload

Afterload may be defined as the pressure that the heart must overcome in order to open the aortic valve successfully and eject its ventricular volume. More simply, it is the aortic impedance to ventricular ejection. Problems develop in afterload when either the systemic vascular or pulmonary vascular resistances are either increased or decreased. An increase in afterload usually occurs post-bypass and when the patient experiences significant pain. This is due to excessive circulating catecholamine levels produced by the bypass technique or by postoperative pain. Increased pulmonary vascular resistance may occur secondary to chronic pulmonary vascular changes or secondary to a pulmonary embolus. The treatment of increased afterload therefore revolves around the use of vasodilatory drugs. The drug of choice used on our service is Nitroprusside. The drug is given by continuous IV infusion, with close observation of blood pressure and cardiac output. It is our first choice because it has an immediate onset of action and its effects are quickly terminated upon discontinuation of infusion. In situations where afterload is significantly decreased secondary to marked vasodilation due to either drugs or sepsis, the treatment is vasoconstriction of the distal arteriolar beds. Drugs such as Neo-Synephrine may be utilized for this purpose. In conditions where sepsis is the underlying cause, treatment of the septic process remains the primary means of correcting the afterload situation.

Treatment of inadequate myocardial contractility

Myocardial contractility is defined as the inotropic state or contractile state of the heart. Mathematically, it is the velocity of ventricular contraction when afterload and preload are kept constant. Problems in postoperative contractility occur when patients have had:

1) pre-existing ventricular dysfunction

2) inadequate intraoperative myocardial protection

3) coronary air or particulate embolism

4) residual, uncorrected cardiac defects

5) acute myocardial infarction

6) pharmacologic myocardial depression

7) hypoxemia

8) acid base imbalance

9) septic or prolonged hypovolemic shock

10) fever or tachycardia

11) allergic reaction

12) hypocalcemia

Treatment of contractility is inotropic stimulation to the heart. It must be remembered that when problems in cardiac output occur that we manipulate first heart rate, second the preload, third the afterload and finally, and only then, the

contractility. Evidence of myocardial contractile failure occurs when all other parameters have been correctly stabilized yet cardiac output remains low and ventricular end diastolic filling pressures or pulmonary capillary wedge pressures remain high. Then inotropic drugs should be given. The primary drug used for this purpose on our service is Dopamine. Dopamine is given as an IV infusion, starting at around 2 to 5 mcg/kg/min. It may be increased as needed. In addition, Dobutamine may also be utilized as a primary agent or to supplement a patient already on Dopamine. Isoproterenol, another very potent inotropic drug, may also be utilized in patients with failing myocardial contractile function.

Cardiac Care

Hypotension

This discussion will define hypotension as the systolic blood pressure less than 90 mmHg. It is recognized that some patients have a blood pressure which normally runs around 90 systolic, and in these cases nothing need be done. Also, in elderly patients blood pressures much higher than 90 may be required. However, for the average patient a blood pressure of less than 90 systolic in combination with signs and symptoms of tissue hypoperfusion or low cardiac output requires intervention. The causes of hypotension are many and must each be recognized and treated independently. Hypovolemia

The hypovolemic patient presents with low central venous pressure and low pulmonary capillary wedge pressure. This individual needs expansion of his in-travascular volume. This may be done with colloid-type agents. If the hematocrit is low, replacement with packed blood cells is the treatment of choice. When the hematocrit is high and the circulating intravascular volume low, replacement with agents such as 5% albumin or Hespan become the treatment of choice. Immediately postop and during the first few postoperative days patients have significant third space fluid accumulations. Therefore, mannitol or 25% albumin, which shifts fluid from the third space to the intravascular space, is frequently used on our service.

Perioperative myocardial infarction

Diagnosis of postoperative myocardial infarction can usually be made with EKG changes, increases in the left ventricular end diastolic filling pressures, decrease in cardiac output, and an increase in the CPK MB fraction. The standard treatment for a myocardial infarction should be initiated. Dysrhythmias

Various dysrhythmias seen in the postoperative course can lead to problems of hypotension. The treatment of the particular dysrhythmia causing the problem should therefore be initiated (see section on dysrhythmias for appropriate management).

Massive transfusion of blood products

It is well recognized that massive transfusion of blood products is complicated by excessive unbound citrate contained within the blood product to prevent coagulation. The citrate abruptly decreases the ionized circulating calcium level and

can lead to severe myocardial depression. Therefore, whenever blood products are given in massive rapid infusions, it is important to give calcium chloride via central vein. Medications

Various medications can cause postoperative hypotension. It is not uncommon for the infusion of nitroglycerin or Nitroprusside or the oral administration of inderal or nifedipine to cause significant hypotension. It is important to recognize these agents as the cause and to discontinue their use as indicated. Tension pneumothorax

A tension pneumothorax may develop at anytime in the postoperative period. It may occur secondary to injury to the lung at the time of surgery or to rupture a pulmonary bleb due to excessive positive end expiratory pressures. It is important to recognize this problem and to treat it with placement of a chest tube.

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