CARDIOVASCULAR MONITORING

Assessing physiologically unstable patients requires both simple and sophisticated monitoring techniques to: 1) evaluate current and changing cardiorespiratory and cardiovascular status; 2) detect impending problems; 3) alter therapies; and 4) recognize improving trends. These tests are most useful when used systematically in conjunction with a cogent history, detailed patient evaluation, and complete data base.

Electrocardiography. Heart rate and rhythm are essential data. A 10 lead ECG provides information about cardiac chamber enlargement, may detect severe pericardial or pleural effusion, and can help assess certain suspected systemic and metabolic disorders (e.g., marked disturbances of potassium or calcium, ischemia, infarction). Arrhythmias which are intermittent are not discovered from short rhythm strips but require continuous ECG monitoring, an event recorder, or 24 hour (Holter) recording. The later, performed before and after therapy, helps to assess efficacy.

Radiography. The radiograph yields valuable information to: 1) confirm disease suspected from the history and physical examination, 2) assess disease severity, 3) help distinguish between cardiac and respiratory disease, 4) confirm tube/catheter placement, 5) screen for unsuspected conditions, 6) discover complications, and 7) monitor (from repeated studies) response to therapy.

Echocardiography. Two-dimensional, M-mode, and Doppler echocardiography often provides useful diagnostic information. It assists cardiac examination when the heart is obscured by severe pleural effusion. It is a rapid and safe method to diagnosis pericardial effusion; provides quantitative assessment of cardiac structure (valves; chamber dimensions, wall thickness, and integrity) and pathology; assesses systolic (contractile) and diastolic function and gradients; detects disturbances of blood flow; detects intracavitary masses (clots, tumors); and helps characterize congenital and acquired heart diseases.

Noninvasive Monitoring of Oxygen (Pulse Oximetry). The saturation of hemoglobin with oxygen in arterial blood (SaO₂) is a useful indicator of hypoxemia. Pulse oximetry is a noninvasive technique to allow continuous monitoring of arterial oxyhemoglobin saturation. As such, it is useful for any pet who is at risk for the development of hypoxemia.

Noninvasive Blood Pressure Monitoring. Hypertension may predispose certain "target" organs to injury, particularly the eyes, kidneys, and cardiovascular and neurovascular systems. Hypotension is a common consequence of shock, dehydration, and certain drug toxicities. Techniques for non-invasive blood pressure include Doppler, oscillometric (Dinamap^TM), plethysmography, and auscultatory methods. These utilize a cuff to constrict a peripheral artery (on front leg, hind leg or tail) and a transducer or microphone placed distal to the cuff to detect blood flow or arterial wall motion once the blood pressure overcomes the pressure of the cuff. Systolic blood pressure >160 suggests hypertension; SBP>200 mmHg recorded on 2 occasions at least 24 hours apart indicate hypertension unless the animal was excited. End-organ injury provides supportive evidence of hypertension. SBP <90 indicates hypotension.

Central Venous Pressure (CVP). CVP directly measures pressure in the great thoracic veins as blood returns to the right heart. Serial or continuous CVP measurement helps assess right heart function and intravascular volume status. Evaluation of the direction of change in CVP measurements over time is more relevant than basing diagnostic/therapeutic changes on isolated measurements. The central venous catheter also provides central intravenous access that can be used to administer medications, fluids, and electrolyte solutions, draw blood samples, and provide an emergency route for temporary pacemaker insertion. CVP generally decreases as venous return decreases. Low CVP measurements suggest hypovolemia. CVP generally increases as venous return increases. Elevated CVP measurements suggest either right ventricular failure or intravascular volume overload.

ARRHYTHMIA DIAGNOSIS AND THERAPY

Tachyarrhythmias may depress cardiac output, cause hemodynamic impairment or hypotension, and result in organ ischemia. Shortened diastolic filling decreases coronary blood flow, reduces myocardial oxygen supply, causes ischemia and results in more serious arrhythmias. Certain tachyarrhythmias may deteriorate by becoming electrically unstable. Hemodynamic impact of tachyarrhythmias are influenced by factors related to underlying cardiac disease and the particular type of arrhythmia (i.e., (a) loss of synchronized atrial systole, (b) altered ventricular activation sequence, (c) rapidity of ventricular rate, (d) timing of ectopic beats relative to preceding P-QRS-T complexes, (e) background vasomotor tone, (f) cardiac effects of antiarrhythmic drugs, and (g) underlying cardiac function or health. Cardiac output is the product of heart rate x stroke volume. With sustained paroxysmal atrial tachycardia (i.e., >300/sec), stroke volume decreases and arterial pressure may rapidly decline.

Electrical instability is increased by rapid ventricular rates and multifocal impulse origination. Additional factors include timing of the ectopic impulse (i.e., the earlier the premature complex relative to the preceding T wave, the greater electrical liability). Depolarizations occurring within the preceding T wave are extremely dangerous. The underlying state of ventricular function, systemic and metabolic alterations, and concurrent drug or anesthetic agents influence electrical stability.

Tachycardia occurs when the ventricular rate >240bpm in cats; > 180bpm in small breed dogs; > 160bpm in large breeds, and >220bpm in puppies.

Sinus Tachycardia is a narrow complex tachyarrhythmia common with increased sympathetic discharge (e.g., pain, fright, systemic disease, heart failure, hypovolemia, shock) and therefore, may be persistent in critical patients. Vagal maneuvers may gradually slow the rate by inhibiting SA nodal discharge but the tachycardia returns to the previous rate when carotid massage is discontinued.

Atrial Tachycardia (AT) is a regular, generally narrow complex arrhythmia (probably due to reentry circuits in the atrium, AV node, or accessory pathways). When terminated it ends abruptly. The P wave contour is different from that of sinus initiated P waves. When due to digitalis toxicity, 1st and 2nd degree AV block may be present. At rapid rates the distinction between atrial tachycardia with block and atrial flutter can be blurred. Tachycardia of sudden onset that changes from sinus rhythm to tachycardia in one beat (e.g., precipitated by an APC) is termed "paroxysmal." In contrast, tachycardia with gradual onset and termination, is termed "nonparoxysmal." AT occurs most commonly in structural heart disease with left atrial enlargement. Treatment is usually directed toward reducing congestive signs, increasing contractility, and slowing the ventricular rate. The latter includes digitalis glycosides and calcium entry blockers.

Av Junctional Tachycardia (AVJT) generally causes a regular, narrow complex tachycardia with P waves difficult discern. The mechanism in many cases relates to reentry sustained within the AV node. Atrial depolarizations may be hidden in the QRS complexes or occur just after the QRS. Diagnosis is facilitated by response to vagal maneuvers. Treatment is similar to atrial tachycardia.

Atrial Flutter classically displays P waves in a "saw-toothed" pattern at a rate between 250-350bpm. Most animals have physiologic AV block that protects the ventricle from rapid stimulation (e.g., 2:1 or 4:1 atrial to ventricular conduction). Animals having atrial flutter with 2:1 AV block and ventricular response of 150-160 may fool the clinician into diagnosing atrial tachycardia. In this setting, carotid sinus massage (Vagal Maneuver) may temporarily increase AV block and allow flutter waves to become more evident. Enhanced AV nodal conduction or AV nodal bypass connections can lead to more rapid ventricular response, often 1:1. These situations are dangerous. Atypical atrial flutter (termed fib-flutter) may not display the classic "saw-toothed" pattern but instead, transcribe irregular and chaotic atrial activity.

Atrial Fibrillation (AF) results when the atrial myocardium continuously discharges in a chaotic, rapid manner resulting in ineffective, 'quivering,' atrial contraction. This produces irregular, low voltage fibrillatory waves on the ECG. Most impulses encounter the AV node during refractory periods and are blocked from further conduction. Those passing through the AV node find it and the ventricles in different states of repolarization. This results in irregularly irregular R-R intervals and QRS complexes with varying degrees of aberrant conduction (widening). AF usually results from extreme atrial dilation caused by cardiomyopathies or volume overloads. Treatment strategies include: 1) digitalization followed by adding diltiazem--or a beta-blocker--to slow the ventricular rate if not already slowed by the digoxin, or 2) simultaneous digoxin and diltiazem administration.

Ventricular Tachycardia arises distal to the His bundle in the specialized conduction system or ventricular muscle. The rate typically varies from about 100-300 (rates from 60-100 are called idioventricular tachycardia or enhanced ventricular rhythm. Diagnosis is based upon three or more wide, bizarrely shaped premature ventricular complexes, often of large amplitude, with the ST-T segment pointing opposite the major QRS deflection, and whose duration generally exceeds 60-65msec in the dog and 45msec in the cat. The R-R intervals are often regular but may also vary. The tachyarrhythmia may originate at multiple sites (multifocal) or at the same site. The atria can display independent activity; P waves are unassociated with QRS complexes, or may be depolarized by the ventricle retrogradely. Fusion complexes and capture beats may be evident. Initial antiarrhythmia therapy includes lidocaine, procainamide, Beta-blockers, and treatment of the underlying condition.

Ventricular Fibrillation is a terminal arrhythmia characterized by chaotic, irregular, deformed, coarse or fine deflections without recognizable P-QRS-T deflections; abrupt loss of consciousness from lack of cardiac output, and death. Immediate defibrillation and basic life support is required.

Complete (3^rd Degree) AV Block or high grade 2^nd degree AV block are bradyarrhythmias which usually result in weakness, collapse, and sometimes, CHF. Implantation of a permanent pacemaker is the most commonly required and effective therapy.

CARDIAC TAMPONADE

A number of diseases may cause pericardial effusion including neoplasia, inflammation, hemorrhage, and heart failure. In some instances, acute or chronic pericardial fluid accumulation raises intrapericardial pressure to exceed RV filling pressures. In such cases ventricular underfilling occurs and pericardial tamponade is said to be present. Affected animals may display weakness, distended jugular venous pulses, pleural and/or abdominal effusion, muffled heart sounds, tachycardia, low QRS voltage (ECG), and shock. Diastolic collapse of the RA and/or RV is usually evident by echocardiography. Pericardiocentesis is the only treatment that reduces intrapericardial pressure. Diuretics are not effective to reduce pericardial fluid and should be avoided in acute settings.

HYPERTENSIVE EMERGENCY

Systemic hypertension accompanied by acute clinical evidence of end-organ injury usually require urgent treatment. Emergency therapy is indicated particularly in cases of systolic blood pressure > 250mmHg accompanied by acute blindness or central nervous system signs (stupor, seizures, coma). Aggressive therapy utilizes a constant rate infusion of sodium nitroprusside. A less risky agent is oral hydralazine (used particularly in dogs). In all cases, close blood pressure monitoring is essential.

ACUTE CONGESTIVE PULMONARY EDEMA (CONGESTIVE HEART FAILURE)

Acute pulmonary edema in dogs most commonly results from chronic degenerative valvular disease (severe mitral regurgitation) or dilated cardiomyopathy. In cats, pulmonary edema most frequently accompanies decompensated hypertrophic and restrictive cardiomyopathy. In cases where severe pleural effusion is present, therapeutic thoracocentesis is advised before additional testing is accomplished. Urgent treatment for acute, severe pulmonary edema involves a number of possible drug treatment plans. The basic initial therapy generally involves the use of FON--i.e., furosemide, oxygen, and nitroglycerin ointment. FON-H adds oral hydralazine, a potent arteriolar dilator. Hydralazine is often added as a 'salvage agent' in cases of fulminant pulmonary edema caused by severe mitral insufficiency. The potent vasodilator, sodium nitroprusside, is an alternative to hydralazine but must be given by constant rate infusion with close monitoring of arterial blood pressure. FON-D involves the addition of the inotrope, dobutamine (constant rate infusion), when severe myocardial failure or cardiogenic shock is present (e.g., dilated cardiomyopathy). FON-Dig adds digoxin when CHF is accompanied by atrial fibrillation, as can occur with DCM or mitral regurgitation. Antiarrhythmic therapy is added as appropriate for prevailing supraventricular or ventricular arrhythmias.

MYOCARDIAL FAILURE (CARDIOGENIC SHOCK, DILATED CARDIOMYOPATHY)

Dilated cardiomyopathy is the most common cause of systolic (pumping) failure in dogs. Doberman pinschers are particularly affected and may present with such poor cardiac output that cardiogenic shock (forward output failure) is present. Most of these dogs have fulminating pulmonary edema. Therapy is directed to rapidly remove edema fluid (intravenous furosemide), thereby increasing oxygenation, and supporting global cardiac systolic function (dobutamine, constant rate infusion. ACE inhibitors, and digoxin are generally added. Arrhythmias are prevalent and diltiazem is usually administered to control heart rate when atrial fibrillation is present. Severe ventricular arrhythmias are treated acutely with lidocaine constant rate infusion.