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Emergency management of congestive heart failure
Patients with congestive heart failure are, unfortunately, common in small-animal practice. Some patients present with acute exacerbation of previously diagnosed and treated cardiac disease. Other animals may present with vague and nonspecific clinical signs and have no known history of cardiac problems.
Patients with congestive heart failure (CHF) are, unfortunately, common in small-animal practice. Some patients present with acute exacerbation of previously diagnosed and treated cardiac disease. Other animals may present with vague and nonspecific clinical signs and have no known history of cardiac problems.
Elisa M. Mazzaferro, MS, DVM, PhD
Depending on the primary cause and severity of the cardiac disease, clinical signs can vary from patient to patient and are by no means pathognomonic for cardiovascular disease. Clinical signs may include weakness and exercise intolerance, cough, lethargy, inappetence, vomiting, diarrhea, tachypnea, respiratory distress, syncope, or collapse. CHF is often presumptively diagnosed based on a patient's primary presenting complaints, signalment, a thorough history, and physical examination findings.
Important concepts to remember in managing any patient with CHF are to minimize patient stress and to do no harm. This discussion focuses on patients with CHF that present in cardiogenic shock and require emergency lifesaving treatment.
It's important to differentiate patients with cardiogenic shock from patients with hypovolemic shock because the treatment for cardiogenic shock (e.g. diuretics) can exacerbate hypovolemic shock. A careful physical examination is essential in diagnosing and treating a patient with CHF.1-4 If the animal is in severe distress, it should be placed in an oxygen cage or receive flow-by oxygen supplementation. The restraint for physical examination and diagnostic testing can sometimes push the most stressed patients over the edge. So initially observe the patient from afar. What is the respiratory rate and effort? Is fluid coming from the nares or mouth? Does the abdomen look distended? Is the patient able to stand or is it weak?
Next, approach the patient, and perform a systematic examination from head to toe. Are the mucous membranes pale pink or do they appear cyanotic? Is the capillary refill time prolonged? Look carefully at the thoracic inlet and jugular groove. Is there jugular venous distention or a jugular pulse? Is the heart difficult to hear during auscultation and are the heart sounds muffled? Is a murmur or a dysrhythmia present? Simultaneously palpate the inguinal region for a femoral pulse. Are the pulses strong or weak? Are they synchronous or asynchronous with the heart rate? Are the pulses absent in a patient with acute onset of respiratory distress and hindlimb or forelimb paralysis? Auscultate all lung fields to detect pulmonary crackles or wheezes. Palpate the abdomen to identify hepatomegaly and a fluid wave. Also palpate the distal extremities. Are they warm, or do they feel cold because of poor peripheral circulation? Finally, perform a rectal examination to check for bloody feces.
Patients with fulminant pulmonary edema from left-sided CHF may have blood-tinged fluid coming from the nares and mouth and have concomitant pulmonary crackles and a rapid restrictive respiratory pattern. A cardiac murmur is often present in cases of severe mitral insufficiency, but in some patients, the heart may be difficult to hear beyond harsh pulmonary crackles. Cardiac dysrhythmias may or may not be present. Weak pulses, pale mucous membranes, depressed mentation, prolonged capillary refill time, and cool peripheral extremities may indicate low output cardiac failure. Pulses may be absent in patients with severe low output failure or arterial embolism. Jugular venous distention and jugular pulses may be visible in patients with right-sided heart failure. Heart sounds may be muffled to absent in patients with pleural or pericardial effusion. Hepatomegaly and a fluid wave may be present on abdominal palpation in cases of right-sided heart failure. On rectal examination, hematochezia may be present secondary to poor mesenteric perfusion and splanchnic congestion from poor cardiac output.
Several diagnostic tests may be indicated when evaluating patients for CHF, including electrocardiography, radiography, echocardiography, blood pressure measurement, and oxygen saturation measurement.
Consider performing an electrocardiographic examination in all patients with clinical signs of CHF. Most standard electrocardiographic tracings are performed with animals in right lateral recumbency. However, if the patient is in severe respiratory distress and unstable, the electrocardiographic tracing can be performed with the animal in sternal recumbency or standing, although the results will need to be carefully interpreted, as standard measurements may not hold true.
Figure 1. A lateral thoracic radiograph of a cat with CHF. Note the increased cardiac sternal contact and perihilar and caudal edema.
A lead II electrocardiogram (ECG) may reveal changes consistent with cardiomegaly or dysrhythmia, but often the ECG may simply display a sinus tachycardia. A six-lead ECG may reveal axis deviation in cases of right-sided cardiomegaly.5 A left axis shift may be present, particularly in cats. Also, the presence of P mitrale or P pulmonale can help differentiate between the heart vs. the lung as the cause of dyspnea. Electrical alternans, an ECG abnormality in which the complexes alternate from large to small as the heart floats within the fluid in the pericardial sac, is most commonly associated with pericardial effusion. However, this abnormality may also be seen, though rarely, in cases of severe pleural effusion. Supraventricular and ventricular tachyarrhythmia and atrial fibrillation are common rhythm disturbances in cases of dilated cardiomyopathy. Depression of the ST segment may signal myocardial ischemia.
Figure 2. A lateral thoracic radiograph of a dog with chronic progressive CHF. Note the loss of the caudal thoracic cardiac waist, also known as the backpack sign.
Thoracic radiographs are one of the most important diagnostic tools in identifying CHF.6 Obtain lateral and dorsoventral radiographs once the patient is clinically stable. Increased perihilar interstitial to alveolar infiltrates are characteristic of pulmonary edema in dogs. Cats may demonstrate caudoventral alveolar infiltrates on thoracic radiographs (Figure 1). Left atrial enlargement may be observed as a loss of caudal cardiac waist, sometimes known as the backpack sign, on lateral thoracic projections (Figure 2). Right- or left-sided cardiomegaly may also be present in cases of valvular insufficiency. In cats, increased sternal contact and a classic valentine-shaped heart may be observed in cases of hypertrophic cardiomyopathy (Figure 3).
Figure 3. A dorsoventral thoracic radiograph of a cat with hypertrophic cardiomyopathy. Note the classic valentine shape of the heart.
Although not necessarily useful in the initial management of a patient with CHF, the vertebral heart size can be calculated to determine the degree of cardiomegaly in dogs and cats7:
1. Measure the long axis of the heart from the apex to the carina on the lateral view, and mark the distance on a sheet of paper. This is the long-axis heart dimension.
2. Measure the length of the long axis heart dimension in terms of vertebral bodies by placing the line below the vertebral column on the radiograph, and count vertebral bodies caudally, starting from the cranial edge of the fourth thoracic vertebra (T4).
3. Measure the short axis of the heart at the caudal vena cava, perpendicular to the long axis of the heart. This is the short-axis heart dimension.
4. Measure the length of the short axis heart dimension in terms of vertebral bodies as in Step 2.
5. Add the two vertebral numbers together to yield the vertebral heart size; a vertebral heart size greater than 10.5 is consistent with cardiomegaly.
In patients with acute pericardial effusion, the cardiac silhouette may appear normal in size or may appear enlarged and globoid, depending on the duration and volume of effusion within the pericardial sac. It may be difficult to distinguish between pericardial effusion and dilated cardiomyopathy on thoracic radiographs. Evaluating the pulmonary vasculature is helpful in differentiating pericardial effusion from dilated cardiomyopathy. Pericardial effusion, due to poor cardiac output and right heart incompetence, may be associated with hypoperfused lungs and small pulmonary vessels, whereas pulmonary venous congestion is usually noted in association with CHF due to dilated cardiomyopathy (Figure 4). Electrocardiography and echocardiography can be useful in distinguishing between the two entities.
Figure 4. A lateral thoracic radiograph of a dog with dilated cardiomyopathy and severe pulmonary edema.
In emergent patients with CHF, an emergency echocardiogram is often not warranted, particularly if there is radiographic evidence of left atrial enlargement, pulmonary venous distention, and perihilar edema. But echocardiography can help you distinguish between pericardial effusion and dilated cardiomyopathy, if radiographic changes are equivocal.8 M-mode, or motion mode, echocardiography is useful in determining left ventricular chamber size dimensions during systole and diastole, from which fractional shortening and ejection fraction can be calculated. The calculated fractional shortening is an approximation of myocardial function in patients with CHF.
Blood pressure measurement
Physical examination findings are largely subjective and by no means should be used to gauge therapy in patients with CHF. Knowing a patient's blood pressure is necessary to provide therapeutic intervention to improve preload, decrease afterload, and improve cardiac contractility. Knowing the blood pressure is also important to avoid deleterious drops in blood pressure because of certain medications used in treating CHF.
Arterial blood pressure can be measured directly or indirectly.9 The gold standard of arterial blood pressure measurement is through cannulation of an artery with a catheter connected to a pressure transducer. It is contraindicated to restrain unstable CHF patients in order to place the arterial catheter. In these critical patients, use indirect methods such as Doppler or oscillometric techniques to monitor blood pressure.
When using the Doppler technique, place the Doppler probe on the radial, dorsal pedal, or coccygeal artery. Place a cuff whose width is about 40% of the circumference of the peripheral extremity proximal to the Doppler probe, and use a sphygmomanometer to evaluate systolic blood pressure. Because of poor peripheral perfusion and peripheral vasoconstriction, using the Doppler probe may be difficult, particularly in patients with severe respiratory distress. Alternatively, you can place a cuff attached to an oscillometric monitor on the forelimb just above the carpus, on the hindlimb just proximal to the hock, or around the tail to measure systolic, diastolic, and mean arterial blood pressures.
Mean arterial blood pressure (MAP) should remain above 60 mm Hg at all times, with a target goal of 80 mm Hg, whenever possible. MAP is a function of cardiac output and systemic vascular resistance. Cardiac output is influenced by heart rate, preload, afterload, and contractility. Depending on the type of heart failure present, cardiac output can be adversely affected for many reasons, leading to hypotension, poor tissue perfusion, and impaired oxygen delivery. Left ventricular preload can be decreased because of pericardial effusion, right ventricular failure, or pulmonary hypertension. Afterload can be increased because of peripheral vasoconstriction. Dilated cardiomyopathy or chronic myocardial ischemia can cause impaired contractility.
Oxygen saturation measurement
Edema can cause severe pulmonary diffusion impairment and lead to hypoxia in patients with CHF. Oxygen saturation of hemoglobin can be measured by using arterial blood sampling or noninvasive pulse oximetry.10,11 A rule of thumb is to attempt to obtain the reading if it can be done without causing undue stress to the patient. When in doubt, administer oxygen and gauge the patient's oxygenation status by changes in its respiratory rate and effort and the resolution of pulmonary crackles on thoracic auscultation. Measuring oxygen saturation by arterial blood sampling or pulse oximetry can then be attempted when the patient is clinically more stable.
The gold standard for measuring a patient's oxygenation status is arterial blood sampling.12 However, the restraint required to obtain the sample is contraindicated in unstable patients. If an arterial blood gas can be performed without causing the patient untoward distress, samples can be obtained from the dorsal pedal or femoral arteries. Normal partial pressure of arterial oxygen (PaO2) is greater than 80 mm Hg in patients breathing room air. If the patient's PaO2 is less than 60 mm Hg and the partial pressure of arterial carbon dioxide (PaCO2) is greater than 60 mm Hg while the patient is receiving oxygen supplementation, mechanical ventilation should be strongly considered.
Pulse oximetry readings can be attempted on the tongue, ear pinna, toe web, prepuce, or vulva in cooperative patients. Severe hypotension, peripheral vasoconstriction, and patient movement secondary to respiratory distress may make obtaining an accurate pulse oximetry reading difficult in patients with CHF. Pulse oximetry readings less than 90% require intervention with supplemental oxygen. If the pulse oximetry reading is less than 80% in a patient receiving supplemental oxygen, consider more aggressive intervention in the form of mechanical ventilation.
Emergency treatment of patients with CHF consists of improving systemic oxygen delivery and minimizing patient stress. Oxygen delivery is a function of oxygen uptake by the respiratory system, cardiac output, and hemoglobin concentration. The mainstays of therapy for CHF are to provide supplemental oxygen and decrease fluid buildup within the lungs.
Administer flow-by oxygen in patients with CHF as the physical examination is taking place.13,14 Flow-by oxygen is well-tolerated and requires minimal physical restraint. Because flow-by is a relatively inefficient method of providing an increase in the fraction of inspired oxygen, use other methods such as oxygen hoods; oxygen cages; and nasal, nasopharyngeal, and tracheal oxygen insufflation for long-term therapy.
Oxygen hoods are available commercially or can be made in the hospital with a firm Elizabethan collar, white tape, and plastic wrap. Most patients tolerate oxygen hoods readily. But increased condensation and iatrogenic hyperthermia can develop, so monitor patients carefully.
Nasal or nasopharyngeal oxygen cannulae are well-tolerated for long-term oxygen supplementation.15-17 Measure a red rubber (5 to 8 F) catheter or Argyle infant feeding tube (Kendall) from the ramus of the mandible (nasopharyngeal) or from the medial canthus of the eye (nasal). Mark the tube, and lubricate the tip with lidocaine jelly. Insert the tube ventrally and medially, directing the nasal philtrum dorsally to facilitate passing the tube to the predetermined level. Humidified oxygen flow rates can be administered at 50 to 100 ml/kg/min. Nonhumidified oxygen can be used if a humidification source is unavailable, but this method is associated with dryness and irritation of the nasal mucosa and increased patient discomfort and intolerance of the nasal cannula.
Potential complications associated with placing a nasal or nasopharyngeal cannula include increased patient distress with restraint, epistaxis, and introduction of the tube through the cribriform plate, although this last complication is uncommon with careful placement. Nasopharyngeal catheters can allow for higher flow rates of supplemental oxygen and are my preferred method of oxygen supplementation.
Aside from oxygen supplementation, furosemide is one of the most important therapies for treating patients with CHF and cardiogenic pulmonary edema.18-21 Furosemide can be administered as a bolus (4 to 8 mg/kg intravenously or intramuscularly) or as a constant-rate infusion (0.66 to 1 mg/kg/hr intravenously) to promote diuresis and decrease pulmonary vascular overload and pulmonary edema. Subcutaneous administration and absorption of furosemide in patients with CHF is not dependable, given the degree of peripheral vasoconstriction, and, thus, is contraindicated. The goal of diuretic treatment is to repeat the therapy every 30 to 60 minutes until the patient's body weight has decreased by 5% to 7%. Loss of body weight typically corresponds with improvement of the patient's respiratory rate and effort as the pulmonary edema resolves. Once the patient's respiratory rate and effort have normalized, oral furosemide can be started. Repeated doses of furosemide can cause marked hypokalemia and metabolic alkalosis, particularly in cats, so potassium supplementation may be required in some patients.
Intravenous fluids: A cautionary note
Unless other drugs need to be administered by constant-rate infusion, the administration of intravenous supplemental fluids is contraindicated in patients with acute fulminant CHF. If intravenous fluids are necessary, a low-sodium fluid such as lactated Ringer's solution (130 mEq sodium/L), dextrose 5% in water, or half-strength (0.45%) saline solution should be considered at the lowest rate possible for drug administration.
Nitric oxide donors
Nitric oxide donors should be given as a primary initial therapy in any patient with fulminant CHF.22 Nitric oxide donors dilate the pulmonary and systemic vasculature, thereby reducing pulmonary vascular pressures. Nitroglycerine paste (0.25 in for patients < 10 kg [22 lb], 0.5 in for patients 10 to 20 kg [22 to 44 lb], 1 in for patients > 20 kg [44 lb] every eight hours) is absorbed readily across the skin and can be placed on the lateral body wall or the inner ear pinnae. If cardiac output is poor and the extremities, including the ear pinnae, are cool to the touch, nitroglycerine absorption may be poor. The axillary region or lateral thoracic wall would be a better site in these patients. Rotate the site at each treatment to improve absorption.
In a patient with refractory pulmonary edema not responding to traditional diuretic therapy, consider sodium nitroprusside, as long as the patient is not hypotensive. Sodium nitroprusside is a balanced arteriolar and venous dilator that decreases both pulmonary and systemic vascular resistance.23 The drug is administered as a constant-rate infusion (2 to 10 μg/kg/min intravenously, gradually increased to effect). Because of sodium nitroprusside's potent hypotensive effects, closely monitor arterial blood pressure throughout the infusion to reduce the risk of inducing organ hypoperfusion. When using sodium nitroprusside, start with the lowest dose possible (2 μg/kg/min), and gradually increase the dose to effect, checking blood pressures every five to 10 minutes. If the patient's blood pressure does not increase within 15 to 20 minutes, increase the dose in increments of 0.5 to 1 μg/kg/min to effect. Cyanide toxicosis has been suggested as a potential side effect with the use of nitroprusside for longer than 48 hours.
Morphine is an opioid agonist that can be used in patients with CHF. In dogs, low-dose (0.025 to 0.05 mg/kg intravenously every six to eight hours) morphine dilates the splanchnic vasculature and increases venous capacitance, allowing fluid drainage from the pulmonary parenchyma.24 Morphine also allows slower, deeper respirations and decreases anxiety in patients with CHF.
Dobutamine is a synthetic beta-adrenergic agonist that is sometimes useful in improving inotropic activity of the myocardium in severe cases of CHF, especially in patients with dilated cardiomyopathy. At lower dosages, dobutamine improves cardiac contractility with minimal effects on heart rate. This improves contractile function with minimal effects on myocardial oxygen demand. At higher dosages, however, dobutamine can be proarrhythmogenic, so carefully monitor the patient's ECG during the constant-rate infusion. To administer dobutamine (2 to 20 μg/kg/min), start with a low dose and gradually increase the dose until the desired effect is achieved. Potential side effects include tachyarrhythmias (at higher doses), facial twitching, and seizures.25,26 Cats are more at risk for complications associated with dobutamine infusion.
If pericardial effusion is diagnosed, pericardiocentesis can be a temporary lifesaving procedure until fluid reaccumulates or more definitive palliative therapy is performed. Before attempting pericardiocentesis, perform a prothrombin time to rule out pericardial hemorrhage secondary to vitamin K antagonist rodenticide intoxication.
To perform pericardiocentesis, place the patient in left lateral recumbency, and shave a 10-cm square caudal to the point of the elbow on the right lateral body wall. Aseptically scrub the clipped area, and, ideally, drape the area with sterile field towels. While wearing sterile gloves, infuse 1 mg/kg 2% lidocaine through the skin and intercostal muscles between the fifth and sixth intercostal space dorsal to the sternum to create an anesthetized subcutaneous tunnel through which the catheter can be inserted.
Monitor the patient's ECG throughout the procedure for potential life-threatening cardiac dysrhythmias. Make a small nick incision through the skin with a No. 11 scalpel blade, and insert a 16-ga, 5.5 in catheter (Abbocath-T—Abbott Laboratories) through the skin and intercostal muscles into the pleural space and pericardial sac.
A flash of blood will appear in the hub of the catheter as the catheter and stylet penetrate the pericardial sac. At this point, push the catheter off the stylet, and attach the hub of the catheter to a length of intravenous extension tubing, three-way stop-cock, and 60-ml syringe to remove the pericardial effusion. Place a small amount of the effusion into a red-topped tube, and monitor it for clots. Clots can form because of acute hemorrhage or iatrogenic puncture into the ventricular lumen. Removing even small amounts of pericardial fluid can drastically improve ventricular preload and cardiac output.
Irrespective of the underlying cause of CHF, affected patients must be treated carefully and aggressively after initial diagnosis. Supplemental oxygen, potent diuretics, and nitric oxide donors continue to be the mainstay of therapy in both cats and dogs during the initial treatment of CHF. Patients that do not respond to standard therapies may require additional therapies, including positive inotropic and intravenous vasodilatory drugs. Carefully monitor heart rate and rhythm, arterial blood pressure, respiratory rate and effort, and pulse oximetry or arterial oxygen saturation to evaluate a patient's response to therapy.
Elisa M. Mazzaferro, MS, DVM, PhD, DACVECC
Wheat Ridge Veterinary Specialists
3695 Kipling St.
Wheat Ridge, CO 80033.
Dr. Mazzaferro lectured on this topic at the 2005 Central Veterinary Conference. Her paper originally appeared in the conference proceedings.
1. Sisson DD, Ettinger SJ. The physical exam. In: Fox PR, Sisson D, Moise NS, eds. Textbook of canine and feline cardiology. Philadelphia, Pa: WB Saunders Co., 1999.
2. Wall RE, Rush JE. Cardiac emergencies. In: Murtaugh RJ, Kaplan PM, eds. Veterinary emergency and critical care. St. Louis, Mo: Mosby-Year Book, 1992.
3. Butson R. Treatment of congestive heart failure. J Small Anim Pract 2003;44:516.
4. Beardow AW. The diagnostic and therapeutic approach to the patient in acute congestive heart failure. Clin Tech Small Anim Pract 2000;15:70-75.
5. Kittleson MD. Pathophysiology and treatment of heart failure. In: Tilley LP, Owens JM, eds. Manual of small animal cardiology. New York, NY: Churchill Livingstone, 1985;307-332.
6. Root CR, Bahr RJ. The heart and great vessels. In: Thrall DR, ed. Textbook of veterinary diagnostic radiology. Philadelphia, Pa: WB Saunders Co., 1994.
7. Buchanan JW. Vertebral scale system to measure heart size in radiographs. Vet Clin North Am Small Anim Pract 2000;30:379-393.
8. Boon JA. Manual of veterinary echocardiography. Baltimore, Md: Williams & Wilkins, 1998.
9. de Laforcade AM, Rozanski EA. Central venous pressure and arterial blood pressure measurements. Vet Clin North Am Small Anim Pract 2001;31:1163-1174.
10. Hackett TB. Pulse oximetry and end tidal carbon dioxide monitoring. Vet Clin North Am Small Anim Pract 2002;32:1021-1029.
11. Proulx J. Respiratory monitoring: arterial blood gas analysis, pulse oximetry, and end-tidal carbon dioxide analysis. Clin Tech Small Anim Pract 1999;14:227-230.
12. Day TK. Blood gas analysis. Vet Clin North Am Small Anim Pract 2002;32:1031–1048.
13. Camps-Palau MA, Marks SL, Cornick JL. Small animal oxygen therapy. Compend Cont Educ Pract Vet 1999;21:587-598.
14. Manning AM. Oxygen therapy and toxicity. Vet Clin North Am Small Anim Pract 2002;32:1005-1020.
15. Drobatz K, Hackner S, Powell S. Oxygen supplementation. In Bonagura JD, ed. Current veterinary therapy XII small animal practice. Philadelphia, Pa: WB Saunders Co, 1995;175-179.
16. Dunphy EA, Mann FA, Dodam JR, et al. Comparison of unilateral versus bilateral nasal catheters for oxygen administration in dogs. J Vet Emerg Crit Care 2002;12:245-251.
17. Mann FA, Wagner-Mann C, Allert JA, et al. Comparison of intranasal and intratracheal oxygen administration in healthy awake dogs. Am J Vet Res 1992;53:856-860.
18. Goodwin JK, Strickland KN. The emergency management of dogs and cats with congestive heart failure. Vet Med 1998;93:818-822.
19. Sisson D, Kittleson MD. Management of heart failure: principles of treatment, therapeutic strategies, and pharmacology. In: Fox PR, Sisson D, Moise NS, eds. Textbook of canine and feline cardiology. Philadelphia, Pa: WB Saunders Co, 1999.
20. Ware WA, Bonagura JD. Pulmonary edema. In: Fox PR, Sisson D, Moise NS, eds. Textbook of canine and feline cardiology. Philadelphia, Pa: WB Saunders Co, 1999.
21. Adin DB, Taylor AW, Hill RC, et al. Intermittent bolus injection versus continuous infusion of furosemide in normal adult greyhound dogs. J Vet Intern Med 2003;17:632-636.
22. Laste NJ. Cardiovascular pharmacotherapy: hemodynamic drugs and antiarrhythmic agents. Vet Clin North Am Small Anim Pract 2001;31:1231-1252.
23. Proulx J, Dhupa N. Sodium nitroprusside: uses and precautions. In: Bonagura JD, ed. Current veterinary therapy XIII small animal practice. Philadelphia, Pa: WB Saunders Co, 2000;194-197.
24. Green JF, Jackman AP, Parsons G. The effects of morphine on the mechanical properties of the systemic circulation in the dog. Circ Res 1978;42:474-478.
25. Knight DH. The efficacy of inotropic support of the failing heart. Vet Clin North Am Small Anim Pract 1991;21:879-904.
26. Goodwin JK, Strickland KN. Managing arrhythmias in dogs and cats with congestive heart failure. Vet Med 1998;93:823-829.