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Close window to return to IVIS Proceeding of the NAVC North American Veterinary Conference Jan. 8-12, 2005, Orlando, Florida Reprinted in the IVIS website with the permission of the NAVC http://www.ivis.org/ Published in IVIS with the permission of the NAVC The North American Veterinary Conference – 2005 Proceedings Close window to return to IVIS www.ivis.org NURSING MANAGEMENT OF THE ACUTE CONGESTIVE HEART FAILURE PATIENT resulting in increased stroke volume provides some degree of compensation for bradycardia. Harold Davis, BA, RVT, VTS (ECC) CONGESTIVE (BACKWARD) HEART FAILURE Congestive heart failure refers to heart failure that is accompanied by the backup of blood and fluid in tissues. Increased in pulmonary or systemic venous capillary pressure cause fluid to leak from capillary beds resulting in edema (pulmonary or peripheral) or effusions (pleural, peritoneal). Congestive heart failure can be characterized as right or left (Table 1) depending on whether systemic or pulmonary venous pressures are increased by heart disease. Veterinary Medical Teaching Hospital University of California, Davis, CA Heart failure is the inability of the heart to supply adequate blood flow to meet the metabolic demands of the body or to provide adequate blood flow at the expense of excessive increases in ventricular filling pressures. Heart failure exists in three forms congestive (backward) failure, low output (forward) failure or a combination of both. The veterinary technician may be called upon to provide nursing care of the acute congestive heart failure patient. An understanding of this disease process will aid the veterinary technician in providing nursing care. CARDIOVASCULAR ANATOMY AND PHYSIOLOGY The heart is a four-chambered pump. The tricuspid and mitral valve separates the atria from the ventricles and prevents back flow of blood when the ventricles contract. The pulmonic and aortic valves prevent the backflow from the pulmonary artery and aorta, respectively when the ventricles relax. Unoxygenated blood enters the right atrium from the anterior and posterior vena cavae. Blood is pumped into the pulmonary vasculature from the right ventricle. Oxygenated blood returns via the pulmonary vein into the left atrium. The left ventricle then pumps blood into the arterial system. Oxygenation of the heart muscle occurs through the coronary arteries. The heart generates electrical activity that induces mechanical contraction. Sympathetic stimulation increases heart rate, contractility, and conduction and contracts vascular smooth muscle. The sinoatrial node initiates electrical impulses, which causes atrial contraction. The electrical impulses travel down to the atrioventricular (AV) node, through the purkinje fibers, to the ventricular muscles, causing ventricular contraction. Cardiac output is the product of stroke volume and heart rate. It is the volume of blood pumped out of the heart per minute. Stroke volume is the amount of blood pumped out of the heart with each beat and there are three primary determinants of stroke volume: preload, contractility and afterload. Preload is the effective distending or filling volume of the ventricle as determined by the ventricular filling pressure and ventricular compliance. Preload affects myocardial fiber length and directly influences contraction: increased myocardial fiber length results in a more forceful contraction and greater stroke volume up to a physiological limit. Contractility refers to the ability of heart to contract independent of variations in preload and afterload. Afterload is the resistance the ventricle has to overcome in order to eject blood from the heart. As afterload increases, stroke volume decreases, and vice versa. Heart rate changes can cause rapid alterations in cardiac output. An increase in heart rate can cause a two to threefold increase in cardiac output. Excessive heart rates lead to increased myocardial oxygen demand and decreased ventricular filling time (causing decreased pre-load and stroke volume). A decrease in heart rate can cause a decrease in cardiac output. The increased time for ventricular filling Table 1 Partial list of causes of heart failure Dogs Left heart failure x Mitral regurgitation x Dilated cardiomyopathy x Infective endocarditis Right heart failure x Tricuspid regurgitation x Pericardial disease x Heartworm disease Biventricular heart failure x Dilated cardiomyopathy Cats x x x Hypertrophic cardiomyopathy Restrictive cardiomyopathy Cardiomyopathy secondary to hyperthyroidism LOW OUTPUT (FORWARD) HEART FAILURE Low output failure, is a form of cardiogenic shock especially when it is associated with hypotension. Low output failure occurs when the heart cannot pump sufficient oxygenated blood to the tissues. PATIENT ASSESSMENT It is important to remember that one of our goals is to minimize the patient’s stress or not aggravate the patient. If it appears that the patient can’t tolerate the physical examination, imaging or electrocardiography then such diagnostics should be postponed until the animal’s condition has improved. HISTORY / CLIENT COMPLAINT The patient may or may not present with a pre-existing history of heart disease. The most common owner complaint for pets with heart failure includes: tachypnea, dyspnea, weakness, collapse, and syncope. Additional complaints include coughing (mostly in dogs), weight loss, abdominal distention, and exercise intolerance. PHYSICAL EXAM Looking By looking at the patient we can assess mucus membrane (mm) color, capillary refill time (CRT), and jugular vein distention. The mm color should be pink and the CRT should be 1 - 2 seconds. Pale or white mm color suggests blood loss, anemia, or vasoconstriction. CRT is an indicator of peripheral perfusion and is a semi-quantitative evaluation of vasomotor tone. Vasoconstriction decreases tissue perfusion. Causes of prolonged capillary refill time include hypovolemia, poor cardiac output, hypoxia, hypothermia, 12 www.ivis.org Published in IVIS with the permission of the NAVC Veterinary Technician excitement, fear, pain and drugs. Anything that increases sympathetic tone can prolong capillary refill. A CRT that is faster than normal is due to vasodilation; in this instance the patient will have brick red mucus membrane. Causes of vasodilation include hyperthermia, sepsis, and vasodilator therapy. The jugular vein should be assessed with the patient standing and the head in a normal position. Jugular vein distention or pulses extending over one-third of the neck is suggestive of right heart problems, pulmonic stenosis, pericardial disease, or cranial vena cava obstruction. Listening Heart rate and rhythm can be determined by auscultation. Increase in heart rate (tachycardia) may be caused by hypovolemia (the tachycardia is a compensatory mechanism), fever, excitement, exercise, pain and drugs. Anything that increases sympathetic tone can cause tachycardia. Tachycardia is generally defined as a heart rate greater than 160 beats per minutes (bpm). Decrease in heart rate (bradycardia) may be caused by high vagal tone, severe electrolyte disturbances and atrioventricular conduction blocks. Bradycardia is generally defined as a heart rate less than 60 bpm. Auscultation of the heart may reveal murmurs or arrhythmias. Feeling Palpation of pulses is a way of assessing stroke volume, heart rate and rhythm. The height and width of the pulse waveform is determined by stroke volume. Large bounding (hyperkinetic) pulses usually indicate the rapid ejection of an increased volume of blood from the left ventricle. Bounding pulses may occur with exercise, fever, and cardiac disease associated with increased stroke volume. Small or weak (hypokinetic) pulses are due to diminished stroke volume and may be a result of advance mitral disease. When irregularities in heart sounds are heard, the heart rate should be compared to pulse rate and the difference in rates are called pulse deficits. Pulse deficits are indicative of arrhythmias. Hydration status can be assessed by checking skin turgor and gum moisture. When interstitial deficits occur, skin turgor will be decreased and gums will be tacky or dry. Cool extremities may indicate decreased peripheral perfusion. Imagining Radiography is useful in determining cardiovascular or pulmonary changes. Heart and vessel enlargement may be seen. The cardiac silhouette, takes on a soccer ball shape with pericardial effusions. Pulmonary findings include pleural effusions, and radiographic patterns suggestive of pulmonary edema. Ultrasonography is useful in determining chamber size, function of the valves, contractility and ejection fraction (percentage of the diastolic volume that is ejected form the heart during systole). This diagnostic tool is also useful for documenting, congenital defects, cardiac masses, pericardial effusions, hepatomegaly and possibly ascites. Imaging should not be performed at the expense of stressing the patient. Close window to return to IVIS www.ivis.org Electrocardiography The ECG reflects electrical activity of the heart; it does not measure mechanical activity. An arrhythmia is defined as an irregular heart rhythm. When assessing an ECG you should check the following: What is the heart rate? •Is the rhythm regular or irregular? •Is there a P wave for every QRS complex and is there a QRS complex for every P wave? •Is the P-R interval prolonged? •Is the QRS complex form normal in size and shape? •Are the T waves abnormally large? •Is there S-T segment depression? The heart rate defines the rhythm as a tachyarrhythmia or a bradyarrhythmia. Wide, bizarre QRS complexes may represent ventricular premature contractions (VPCs), right ventricular hypertrophy or right bundle branch block. VPCs are often not preceded by a P wave. Small but normal appearing QRS complexes may be due to pericardial effusion. Abnormally tall-tented T waves may be due to hyperkalemia, hypoxia, or dilation. S-T segment slurring or depression may be due to myocardial hypoxia. PATIENT MANAGEMENT The primary goal of therapy is to improve oxygen delivery. This goal is achieved by improving oxygenation, reducing effusion / pulmonary edema and optimizing cardiac output. Oxygen Therapy Maintaining oxygen saturation is one of the primary goals in maintaining blood oxygenation. If there is any question concerning a patient’s blood oxygenation, supplemental oxygen should be provided until assessment of arterial blood gases or hemoglobin saturation confirms that oxygen supplementation is not necessary. When this equipment is not available, assessment will have to be based on clinical dyspnea or auscultable abnormalities and clinical signs of hypoxia (cyanosis of the mucous membranes or dark colored blood, tachypnea, tachycardia, and anxiety). Individually, the clinical signs do not prove hypoxemia, but together they are suggestive of hypoxemia. There are a variety of methods of oxygen therapy. The method selected depends on the expected duration of therapy, the demeanor of the patient, and equipment availability. Available methods include facemask, oxygen bag (hood), oxygen cage, transtracheal, and nasal insufflation. In the case of acute heart failure it is perhaps best to use a technique that will be the least stressful to the patient. The ultimate goal of oxygen therapy is to provide adequate oxygen to the blood, using the lowest possible inspired oxygen concentrations. SEDATION When the patient is anxious or stressed it may benefit from sedation. Traditionally, morphine has been used in the dog. In addition to its anxiolytic affects it redistributes blood away from the lungs through venous vasodilation. Phenothiazine tranquilizers such as acepromazine may be used to produce similar effects. This drug can cause cardiovascular collapse in Boxers and probably should not be used in that breed. Reducing Pulmonary Edema and / or Effusion Pulmonary edema is seen in left heart failure because of an increase in pulmonary blood volume resulting in increased capillary pressures. Diuretics will decrease the blood volume and will decrease capillary pressures. Furosemide, a 13 www.ivis.org Published in IVIS with the permission of the NAVC The North American Veterinary Conference – 2005 Proceedings commonly used loop diuretic is used to treat pulmonary edema. It may be given intravenously or intramuscularly; using doses up to 8 mg/kg and 4 mg/kg every few hours in the dog and cat respectively. High dose administration is discontinued once the respiratory rate decreases and / or respiratory character improves. The patient is at risk for developing mild hypokalemia and dehydration secondary to high dose Furosemide administration. In dogs, this problem is usually corrected once the pulmonary edema is resolved and it resumes eating and drinking. Because cats do not readily eat and drink, fluids may be administered judiciously to correct dehydration. Cardiogenic pleural effusion in dogs is usually secondary to a combination of right and left heart failure. In the cat, left heart failure secondary to hypertrophic cardiomyopathy is the common cause for pleural effusion. Patients in respiratory distress with pleural effusion should benefit from a thoracentesis. The technician should be prepared to assist in the thoracentesis. The technician should be familiar with the indications, patient and procedure preparation, and performance of the procedure and associated complications. Ascites, secondary to severe right heart failure in the dog may require abdominocentesis. The ascites makes the patient feel uncomfortable and places pressure on the diaphragm causing breathing difficulties. Enough fluid should be removed to relieve the breathing difficulties and make the patient comfortable. The technician’s role in this procedure is similar to that in the thoracentesis. Vasodilator Therapy Vasodilating drugs are used to treat both congestive and low output heart failure. Nitroglycerin is a venodilator. Venodilators expands vascular capacity by dilating veins, which, reduces preload and venous pressure. Venodilation will reduce congestion but not improve cardiac output. Nitroglycerin is applied transdermally. Arterial vasodilators decrease systemic vascular resistance, which reduces afterload and improves cardiac output; in addition, it decreases the work of the heart. Hydralazine is an arteriolar dilator. It is used to treat severe mitral regurgitation. The drug is administered orally. The vasodilating effect occurs within 30 minutes to 1 hour and peaks in 3 hours. Nitroprusside is a potent veno and arteriolar dilator. It is reserved for severe fulminant heart failure. The drug has a short half-life and must be given as a constant rate infusion. Adverse effects include hypotension and cyanide toxicity. If the patient becomes hypotensive, the drug is reduced or turned off and its effects will dissipate within a few minutes. Cyanide toxicity, resulting from nitroprusside over-dosage, is characterized by hyperemia and dyspnea. Because these drugs are potent vasoactive substances blood pressure must be monitored. Close window to return to IVIS www.ivis.org ACE Inhibitors These drugs are balanced vasodilators, in other words they work on the venous and arterial side. They work by preventing the conversion of angiotensin I to angiotensin II. Reduction in angiotensin II is what leads to the vasodilation and ultimately the reduction in capillary pressure, edema formation and increased perfusion. Examples include Captopril and Enalapril. Positive Inotropes Positive inotropic drugs such as dobutamine increase stoke volume and ultimately cardiac output and blood pressure by increasing contractility. Dobutamine increases contractility without causing a significant increase in heart rate or vascular resistance. Dobutamine has a short half-life and must be administered as a constant rate infusion. It is indicated in cases where the patient is showing signs of congestion and diminished cardiac output. Monitoring Therapy Therapy should improve cardiac output or reduce pulmonary edema. With improvement of cardiac output, signs of increased perfusion should be evident. These signs include normal capillary refill, good pulse quality, warm extremities, and good urine production. More definitive assessments include reduction in blood lactate, increased venous oxygen tension or measured cardiac output. If therapy has been effective in resolving the pulmonary edema the patient’s attitude and mucous membrane color should improve and the animal may be able to lie down and sleep. If vasoactive drugs are utilized then blood pressure must be measured. CVP is useful in determining an endpoint for fluid administration or to measure the relative ability of the heart to handle the fluids being returned to it. Diuretic therapy should quickly produce increased urine production. A baseline body weight and palpation of the bladder should be performed to serve as a basis for comparison. Acute changes in body weight are usually due to fluid gains or losses. Electrolyte and acid base abnormalities can be caused by diuretic therapy; as a result these parameters should be measured. SUMMARY The veterinary technician may be called upon to provide nursing care of the acute congestive heart failure patient. An understanding of this disease process, rationale of therapy, and desired outcomes will aid the veterinary technician in providing nursing care. www.ivis.org 14