INTRODUCTION

Cardiogenic shock is defined as inadequate cellular metabolism secondary to cardiac dysfunction when there is adequate intravascular volume. It is a serious life-threatening emergency and must be recognized, diagnosed, and treated as soon as possible.

The etiology of cardiogenic shock is wide ranging and varied. Consequently diagnostic modalities, case management, and definitive therapy vary with the cause. Diagnosis is based on clinical demonstration of shock along with evidence of cardiac dysfunction. Ultimately, the aim of treatment is based on restoring cardiac output in order to normalize tissue perfusion and cellular metabolism.

PATHOPHYSIOLOGY

Shock is defined as inadequate cellular energy production. It can have multiple classifications, such as distributive, metabolic, hypoxic, or cardiogenic. Decreased tissue perfusion and subsequent inadequate metabolism and energy production at the cellular level will occur when cardiac output is reduced. This occurs most commonly as a result of inadequate intravascular volume or hypovolemic shock (classified under distributive shock). In the face of adequate intravascular volume, but reduced cardiac output from cardiac dysfunction, a patient has forward failure. When forward flow failure is sufficient to cause inadequate tissue perfusion despite an adequate intravascular volume, the patient has cardiogenic shock. Heart failure can be classified as forward or backward ventricular failure. Backward flow failure occurs secondary to elevated venous pressures, and left ventricular failure (forward flow failure) occurs secondary to reduced forward flow into the aorta and systemic circulation.

Cardiac output is a product of stroke volume and heart rate (SV × HR). A decrease in either stroke volume or heart rate can therefore lead to a reduction in cardiac output. The normal physiologic response to a decrease in stroke volume is a compensatory increase in heart rate (and systemic vascular resistance) to maintain cardiac output. This is due to a baroreceptor-mediated sympathetic stimulation to preserve blood pressure and tissue perfusion. A decrease in stroke volume that cannot be reciprocally compensated for by a further increase in heart rate will lead to reduced cardiac output and forward flow failure. Similarly, forward failure may result from a severe decrease in heart rate without a primary decrease in stroke volume. Cardiogenic shock will ensue if the forward flow failure leads to decreased tissue perfusion that does not meet cellular energy demands.

Stroke volume is determined by preload, afterload, and contractility. Cardiogenic shock can ensue from alterations in any of these. For the purpose of this chapter, the cardiac cycle will be split into systole and diastole, and compromise to either phase may result in a decreased stroke volume and cardiogenic shock.

In addition to the reflex increase in heart rate, strategies exist within the body to ensure normal tissue perfusion. In response to cardiac dysfunction–induced hypotension, neurohormonal mechanisms (e.g., renin-angiotensin-aldosterone system) increase the effective circulating volume (see Chapter 6, Hypotension). This increases preload, stroke volume, and therefore cardiac output and enables the animal to maintain a normal blood pressure. As a result, forward failure in patients with chronic cardiac conditions is rare. Most patients deteriorate secondary to the increase in preload and subsequent congestive (backward) heart failure and pulmonary edema. Examples of this include chronic valvular disease in dogs and hypertrophic cardiomyopathy in cats. Some patients may suffer from concurrent forward and backward failure (e.g., dogs with dilated cardiomyopathy).

Patients that demonstrate an acute decrease in cardiac output do not have time to compensate and, as a consequence, abruptly develop cardiogenic shock (e.g., acute pericardial effusion with cardiac tamponade). These animals commonly have signs consistent with cardiogenic shock (forward failure) but may also have evidence of right-sided backward failure (ascites).

A sustained decrease in cardiac output will eventually lead to organ dysfunction. Reduced coronary blood flow may result in arrhythmias or decreased contractility and will exacerbate existing cardiac dysfunction. Inadequate renal perfusion will lead to acute renal failure, and decreased gastrointestinal perfusion may cause hemorrhagic diarrhea.

CLINICAL SIGNS AND DIAGNOSIS

Cardiogenic shock is an extreme manifestation of forward failure and clinical signs will reflect this state. Diagnosis is based on signs consistent with shock and cardiac dysfunction. It is important to realize that there is overlap among different classes of shock and that a definitive diagnosis can sometimes be difficult to ascertain.

Clinical signs are consistent with global hypoperfusion. A patient with cardiogenic shock will have a change in mentation manifested as depression, unresponsiveness, or disorientation. Peripheral extremities will be cold and the mucous membranes pale, with a prolonged capillary refill time due to intense vasoconstriction. The patient will often be tachypneic because of concurrent congestive heart failure (CHF) (pulmonary edema) or may have a compensatory respiratory alkalosis in response to a lactic acidosis. Parenchymal or pleural space disease secondary to backward failure may result in dyspnea and cyanosis.

The heart rate should be elevated in animals with cardiogenic shock unless a primary bradycardia is the cause of the cardiogenic shock or the patient is moribund. The tachycardia will be due either to an appropriate sympathetic response to hypotension or concurrent CHF, or can be a malignant arrhythmia (ventricular or supraventricular tachycardia) that is not allowing adequate diastolic filling and is the primary cause of cardiogenic shock. Correction of the malignant tachycardia in the latter case will likely improve stroke volume and cardiac output, whereas treatment of the compensatory tachycardia is contraindicated. This distinction can sometimes be difficult, and careful evaluation of the electrocardiogram and patient’s volume status is necessary.

Careful auscultation of the heart and lungs should be performed. If the heart sounds are difficult to auscult, a pericardial effusion should be considered, although the clinician should not forget other causes of quiet heart sounds, including severe hypovolemia and obesity. If the patient has congestive heart failure, inspiratory crackles secondary to pulmonary edema may be heard on auscultation of the lungs, or the lungs may be quiet ventrally as a result of pleural effusion. A murmur or gallop may also be ausculted, and although extracardiac rule-outs for a heart murmur should be considered, this may provide further evidence for cardiac disease. “Synchronous” peripheral pulse palpation and cardiac auscultation should be performed to detect pulse deficits or arrhythmias.

Renal blood flow will be reduced with cardiogenic shock and may result in azotemia, with or without oliguria or anuria. Gastrointestinal tract perfusion will also be reduced and may lead to hemorrhagic diarrhea.

Venous blood gas analysis often reveals a metabolic acidosis. Inadequate cellular oxygenation may result in anaerobic metabolism and a lactic acidosis. Prerenal or renal azotemia may also contribute to the metabolic acidosis. The patient will usually have a compensatory respiratory alkalosis. If the patient has concurrent pulmonary edema the alveolar-arteriolar gradient (A-a gradient) will likely be increased on an arterial blood gas analysis (see Chapter 208, Blood Gas and Oximetry Monitoring).

An electrocardiogram should be performed on all patients that are in shock. Animals in cardiogenic shock may have a sinus tachycardia, bradyarrhythmia (e.g., AV block), or tachyarrhythmia such as atrial fibrillation or ventricular tachycardia. It is important to remember that patients with other causes of shock (e.g., distributive or hypoxic) can also have cardiac arrhythmias.

Chest radiographs should be performed when the patient is stable enough to withstand the stress of being held and may help to rule out cardiac disease as the primary cause of shock. There may be an abnormality in the cardiac silhouette and evidence of congestive or backward heart failure. Radiographic signs of CHF include enlarged pulmonary veins, an alveolar or interstitial pattern in the perihilar region (in dogs only; infiltrates are often patchy or diffuse in felines), or pleural effusion. However, it is important to remember that many animals in shock will have incidental cardiac disease that is not contributing to their morbidity. Information derived from radiographs and the electrocardiogram will not enable the clinician to definitively diagnose cardiogenic shock; rather, it should be interpreted in conjunction with clinical findings and results of other diagnostic tests.

Echocardiographic findings will vary depending on the underlying cause of cardiogenic shock. Congenital or acquired structural abnormalities, along with changes in cardiac chamber size or myocardial thickness, may be described. Pressure gradients, blood flow, and an assessment of systolic and diastolic function can be obtained. A diagnosis of cardiogenic shock may be made if there is evidence of systolic dysfunction in the presence of adequate end diastolic volume.

Even with advanced diagnostic imaging, the diagnosis of cardiogenic shock can still be difficult. A pulmonary arterial catheter (see Chapter 50, Pulmonary Artery Catheterization) can be placed to aid in both diagnosis and monitoring. A patient with cardiogenic shock will have a decreased cardiac output with an increase in the preload parameters of central venous pressure, pulmonary arterial pressure, and pulmonary arterial occlusion (wedge) pressure. This catheter can be helpful to obtain a diagnosis, guide therapy, and monitor the response to therapy.