Left Ventricular Failure

Chapter 36 Left Ventricular Failure



Dennis E. Burkett, VMD, PhD, DACVECC



KEY POINTS



• Clinical signs of congestive left heart failure are most commonly tachypnea, dyspnea, and coughing secondary to pulmonary edema.

• Cats with congestive left heart failure commonly develop pleural effusion.

• The primary aim of managing heart failure is to prevent edema and effusion.

• Most patients with acute left heart failure are brought to the hospital in severe or fulminant left heart failure and require intensive therapy with oxygen and intravenously administered furosemide or nitroprusside, with or without dobutamine.


BASIC TERMINOLOGY



• Circulatory failure is present when the delivery of oxygenated blood is insufficient to meet the metabolic requirements of the body’s tissues. It may result from failure of any one or more of the various components of the circulation: the heart, the vascular bed, the blood volume, or the concentration of oxygenated hemoglobin (Hgb) in the blood.1

• Heart failure is the pathophysiologic state that results when the heart is unable to pump blood at a rate that will meet the metabolic demands of the tissues and maintain normal arterial or venous pressures at rest or with exercise.1

• Myocardial failure is heart failure caused by a defect in myocardial contractility (systolic pump failure). Myocardial contractility is depressed in dogs and cats with dilated cardiomyopathy, and this is the primary functional abnormality in these patients. Not all patients with heart failure, however, have decreased myocardial contractility. For example, dogs experiencing acute rupture of a chordae tendineae suffer heart failure even though myocardial contractility is normal. Other examples include pericardial effusion, constrictive pericarditis, and acute pulmonary thromboembolism.1

• Congestive heart failure is the clinical syndrome, not a disease, wherein abnormal cardiac function results in the accumulation and retention of sodium and water with the resulting signs of congestion and edema. Most, but not all, patients with heart failure develop systemic or pulmonary congestion. Congestive signs may be absent when heart failure develops suddenly and plasma volume is normal or reduced.1


LEFT VENTRICULAR FAILURE


Left ventricular failure is the classic type of cardiac dysfunction that clinicians usually think of when they think of heart failure. It can occur with or without signs of heart failure. Dogs with dilated cardiomyopathy apparently have left ventricular failure for years before showing clinical evidence of heart failure.2 Experimental cats live for years with taurine deficiency and mild to moderate left ventricular failure without signs of heart failure.3


Left ventricular failure without heart failure can be detected by echocardiography and is seen as an increase in end-systolic left ventricular diameter and decreased excursions of the left ventricular free wall and interventricular septum from diastole to systole (decreased wall motion). Left ventricular failure is always severe in dogs and cats with dilated cardiomyopathy when clinical signs become obvious. Left ventricular failure can occur secondary to other chronic diseases that affect the left ventricle, such as aortic regurgitation and patent ductus arteriosus.4



OTHER CAUSES OF LEFT VENTRICULAR FAILURE


Left ventricular failure frequently is absent in other left ventricular diseases, although the patient has clinical signs of heart failure. Feline hypertrophic cardiomyopathy is the classic example in veterinary medicine. Cats with this disease can have heart failure but apparently have normal myocardial contractility and enhanced left ventricular performance because of an increase in myocardial mass. Signs of heart failure occur in this disease because the heart muscle is extremely thick and therefore stiff, causing an increase in the left ventricular diastolic pressure.


Mitral regurgitation in small dogs is another example of a disease in which left ventricular failure is not the prevalent problem.5 In this disease the major factor leading to the signs of heart failure is massive regurgitation, or leakage, of blood into the left atrium rather than a decrease in myocardial contractility.


Patent ductus arteriosus does not result in clinically significant left ventricular failure in very young dogs but can cause signs of heart failure. Left ventricular failure develops if the lesion is left untreated for months to years.4


Signs of heart failure are divided into those referable to congestion and edema (congestive, or backward, heart failure), to inadequate blood flow (low-output, or forward, heart failure), or to markedly decreased blood flow and low blood pressure (cardiogenic shock).6,7 Cardiogenic shock is rare in patients with chronic heart failure, although it can occur in those that are treated vigorously with diuretics and that stop eating and drinking and become markedly dehydrated. It is identified more commonly in patients with acute heart failure4 (see Chapter 35, Cardiogenic Shock).



RIGHT-SIDED VERSUS LEFT-SIDED HEART FAILURE


In animals with heart failure, congestion develops as a consequence of excessive venous pressure caused by the combined effects of increased plasma volume (sodium and water retention) and decreased venous capacitance (venoconstriction). With impairment of the left side of the heart, pulmonary venous pressure increases, resulting in pulmonary edema (pulmonary capillary wedge pressure >25 mm Hg) and signs of respiratory distress (left-sided CHF). Conversely, with impairment of the right side of the heart, systemic venous pressures rise, resulting in hepatomegaly and ascites (central venous pressure >15 mm Hg, right-sided CHF).


Because the capacitance of the splanchnic veins and the systemic venous reservoir is large, a rather substantial increase in blood volume is required to raise pressures in this reservoir. As a result, right-sided congestive signs tend to develop slowly. By comparison, the capacitance of the pulmonary veins is small. Relatively small changes in blood volume or its distribution can cause a rapid rise in pulmonary venous pressure and resultant pulmonary edema. Sudden increase in sympathetic tone (with fear, anxiety, or exercise) constricts the splanchnic veins, causing a shift in the circulating blood volume from the systemic to the pulmonary venous reservoir. This is one reason for the often rapid onset of pulmonary edema in animals with left-sided heart failure.1



CONGESTIVE LEFT-SIDED HEART FAILURE


Congestion and edema in heart failure occur because of an increase in capillary hydrostatic pressure.6 In left-sided heart failure, increased diastolic pressure in the left ventricle (and consequently an increase in diastolic left atrial pressure, because the left ventricle and the left atrium are essentially one chamber during diastole when the mitral valve is open) or high systolic and diastolic pressures in the left atrium and pulmonary veins result in increased pulmonary capillary hydrostatic pressure, leading to pulmonary edema. Increased left ventricular diastolic pressure generally is caused either by a marked increase in blood volume and venous return to the left heart that overwhelms the ability of the heart to distend or by a stiff left ventricle that cannot accept a normal venous return at a normal pressure, or by both. Clinical signs of congestive left-sided heart failure are tachypnea, orthopnea, dyspnea, and coughing, usually secondary to pulmonary edema4 (see Chapter 21, Pulmonary Edema).


Poor cardiac output (blood flow into the aorta per unit time) results in poor tissue perfusion and can be caused by a myriad of abnormalities that affect the ability of the left ventricle to pump properly. Poor tissue perfusion caused by a decreased cardiac output causes clinical signs of fatigue, weakness, poor exercise tolerance, cold extremities, slow capillary refill time, poor mucous membrane color, and hypothermia.6 All of the signs except exercise intolerance will not become evident until heart failure becomes severe.


Laboratory evidence of left ventricular failure consists of a decreased cardiac output, a widened arteriovenous oxygen difference (arterial-venous oxygen content), a decreased venous oxygen tension in a patient that is not hypoxemic or anemic, and azotemia and lactic acidosis if the cardiac output is severely depressed.7 Decreased cardiac output results in decreased tissue oxygen delivery (tissue oxygen delivery = arterial oxygen content × cardiac output). Arterial oxygen content (ml O2/100 ml blood) is determined by the following relationship:



image



The calculated value indicates the number of milliliters of oxygen carried in a given quantity of blood.


If resting tissue oxygen consumption remains stable, the actively metabolizing cells in the body must extract more oxygen from the bloodstream to meet their needs when cardiac output is reduced. This results in a decreased amount of oxygen and partial pressure of oxygen at the end of a capillary bed and on the venous side. The oxygen tension at the end of the capillary bed is the critical factor that determines oxygen delivery to the mitochondria.8


In animals the normal value for end-capillary or venous oxygen tension is higher than 30 mm Hg.8 If oxygen delivery decreases enough at rest because of decreased cardiac output, it can result in the end-capillary tension or venous oxygen tension decreasing below a critical level of 20 to 24 mm Hg. When the end-capillary partial pressure of oxygen is less than 20 to 24 mm Hg, oxygen delivery to mitochondria becomes inadequate. At this stage, cells must start relying on anaerobic metabolism, resulting in lactic acid production.7–9


If the patient is exercising, lactic acid production in skeletal muscle results in the feeling of fatigue and forces the patient to stop. Therefore signs of left-sided heart failure are best identified in a patient that has mild or moderate heart failure either by exercising the patient and measuring blood lactate concentration or venous oxygen tension from blood draining working skeletal muscle or by obtaining a history of the patient’s exercise capabilities.10 Patients with severe heart failure may have evidence of left-sided heart failure at rest.

Related posts:

  1. Deteriorating Mental Status
  2. Hyperthermia and Fever
  3. Ventilator-Associated Lung Injury
  4. Allergic Airway Disease in Dogs and Cats and Feline Bronchopulmonary Disease

Stay updated, free articles. Join our Telegram channel
Tags:
Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Left Ventricular Failure

Full access? Get Clinical Tree
Get Clinical Tree app for offline access