disease of the cardiovascular system Vet-student.mihanblog.com
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Special examination of the cardiovascular system S1 : ventricular systole, synchronous with apex beat Maximal audibility of the mitral valve(fifth in the horse and fourth in R) For tricuspid valve on the right at 4th intercostal space in the horse and costochondral level of 3rd space for others vet-student.mihanblog.com
S2 Closure of the aortic and pulmonary valve Aortic component audible ventral to the horizontal line of shoulder at 4th in H and 3rd in other specie Pulmonic component ventral and anterior to the aortic area 3rd in the horse and 2nd or 3rd in others vet-student.mihanblog.com
S3 Rapid filling of the heart Most common in horses Best heard at heart rate slightly above resting vet-student.mihanblog.com
S4 Atrail contraction Also a sound vet-student.mihanblog.com
Heart disease vs. Heart failure HEART DISEASE- any structural abnormality of the heart (may or may not result in heart failure) HEART FAILURE- when the heart does not provide a cardiac output that is sufficient to meet the metabolic and hemodynamic needs of the body vet-student.mihanblog.com
Two functional units of the cardiovascular system Heart (pump) Vessels (ciruit) vet-student.mihanblog.com
Each may fail independently so we have 2 forms of circulatory failure: Heart failure(fails as a pump) Circuit failure(fails to return blood to the heart or decreased circulatory blood volume) vet-student.mihanblog.com
Heart failure vet-student.mihanblog.com
Heart Failure results from: 1- defect in filling 2- electrical conductivity 3- contractile function 4- excessive workload 5- combination of two or more vet-student.mihanblog.com
Causes of cardiovascular dysfunction Cardiac arrhythmias Obstructed flow Regurgitant flow Contractile dysfunction (systolic failure) Inadequate filling (diastolic filling) Loss of blood vet-student.mihanblog.com
Other types of categorizing HF Acute heart failure Chronic(congestive) heart failure Left H F Right H F Left and Right H F vet-student.mihanblog.com
Left sided heart failure Increase in left ventricular end diastolic pressure Increase in left atrial pressure and pulmonary venous pressure Can result in interstitial edema If severe , results in pulmonary edema, dyspnea and death vet-student.mihanblog.com
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right sided heart failure Increase in right ventricular end diastolic pressure Results in right atrial pressure and jugular venous pressure Systemic venous distention vet-student.mihanblog.com
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Circuit failure Decrease of effective blood volume (hypovolumic shock) Pooling of blood in peripheral vessels and increased capillary permeability(maldistributive shock) Results in incomplete filling of the heart Reduction in heart output(although no pump defect). The effects are the same as CHF (less nutrient and waste removal) vet-student.mihanblog.com
Cardiac reserve and compensatory mechanism in HF Capacity of the heart to increase output normally vet-student.mihanblog.com
Mechanism of sending blood to an organ Increase in HR Increase in SV Redistribution of blood flow vet-student.mihanblog.com
Increase in HR Horses 6-7 times that of resting Cows 3-4 In HF beyond 120 in significant vet-student.mihanblog.com
Stroke volume 1- ventricular distending pressure(end-diastolic pressure) 2-contrctility : adrenergic activity and catecholamines 3- increase in ejection fraction(afterload) vet-student.mihanblog.com
Heart disease vs. Heart failure Signs of Heart disease: heart murmur abnormal heart rhythm abnormal heart sounds jugular pulses Signs of Heart failure: tachypnea and/or dyspnea coughing collapse, syncope, and/or weakness abdominal distention associated with ascites vet-student.mihanblog.com
Mixed venous oxygen tension Increased extraction of oxygen in pump and circuit failure Blood redistribution vet-student.mihanblog.com
Autonomic nerve activity Increasing HR Improving contrctility Regulating blood flow to vital organ vet-student.mihanblog.com
Cardiac reserve in cardiac insufficiency Primary defect in myocardial activity In early course no problem B/C: augmented ventricular filling pressure (increased venous return and increased blood volume) vet-student.mihanblog.com
Measurements of cardiac reserve Heart rate Intensity Size of the heart Pulse characteristics Exercise tolerance vet-student.mihanblog.com
Cardiac enlargement Hypertrophy (concentric hypertrophy) : in response to pressure load, individual fibers and total muscle mass Dilatation (eccentric hypertrophy): in response to volume load and fiber rearrangement vet-student.mihanblog.com
Chronic (congestive) HF Valvular disease Myocardial disease Congenital defects producing shunts Hypertension, (pulmonary [high altitude]or systemic) Pressure load Volume load Pumping defect (leukosis) Filling defects: pericardial temponade vet-student.mihanblog.com
pathogenesis Reduced cardiac reserve , normal at rest but not in exercise . CHF develops when these compensatory mechanism reach their limit. Most signs are associated with congestion or edema vet-student.mihanblog.com
Right sided CHF vet-student.mihanblog.com
Left sided CHF vet-student.mihanblog.com
Clinical signs Prolonged time to return to normal \ Increase in HR Evidence of cardiac enlargements vet-student.mihanblog.com
HEART FAILURE Several ways to describe heart failure: -congestive heart failure -forward heart failure -backward heart failure -low output heart failure -high output heart failure -right sided heart failure -left sided heart failure vet-student.mihanblog.com
HEART FAILURE CARDIAC OUTPUT = STROKE VOLUME X HEART RATE Determinants of Stroke volume: -level of contractility -afterload -preload -valvular competence -atrioventricular synergy Determinants of heart rate: -balance of parasympathetic and sympathetic tone -sinus node function -presence of an ectopic focus -conduction system vet-student.mihanblog.com
Diastolic pressure overload Ways to challenge the function of the heart Diastolic pressure overload Systolic Pressure overload VOLUME OVERLOAD -forces the heart to generate high pressures during systole resulting in increased oxygen consumption and increased wall tension -increased preload -results in increased filling pressures DIASTOLIC DYSFUNCTION -impedes the filling of the heart and results in an increased diastolic pressure for each given diastolic volume vet-student.mihanblog.com
CONGESTIVE HEART FAILURE -Thick and Stiff Ventricular Walls -Abnormal Ventricular Relaxation -Ventricular Fibrosis -Pericardial Disease -Myocardial Failure -Valvular Insufficiency -Moderate to Large L-> R shunt VOLUME OVERLOAD DIASTOLIC DYSFUNCTION Elevated Cardiac Filling Pressures CONGESTIVE HEART FAILURE vet-student.mihanblog.com
Cardiac Filling Pressures OVERLOAD Concentric Hypertrophy Thickened Ventricular Walls Altered ventricular geometry Myocardial Failure Valvular Insufficiency Ischemia and Fibrosis Elevated Cardiac Filling Pressures Diastolic Dysfunction CONGESTIVE HEART FAILURE vet-student.mihanblog.com
Activates Compensatory mechanisms Myocardial Failure or Valvular Insufficiency Activates Compensatory mechanisms SNS Anti-diuretic Hormone RAS Angiotensin II Aldosterone Vasoconstriction Sodium and water retention Increased Venous Return and Increased Blood Pressure Heart Rate F-S Mech. Contractility Augmentation of cardiac performance vet-student.mihanblog.com
Angiotensin II Reduced renal perfusion Release of Renin from Renal Juxtaglomerular cells Reduced sodium delivery to kidneys Sympathetic Nervous System Angiotensinogen Angiotensin I Angiotensin converting enzyme (ACE) Angiotensin II vet-student.mihanblog.com
Increased aldosterone Angiotensin II Vascular smooth muscle Constriction: increase PVR Renal efferent arteriole Constriction: maint. of GFR Proximal renal tubule Increased Na+ reabsorption Increased aldosterone secretion Adrenal cortex Baroreflexes Withdrawal of vagal tone Central adrenergic activation, Ganglionic facilitation, Presynaptic receptors Increased release of NE vet-student.mihanblog.com
Ventricular Hypertrophy Goal: to normalize myocardial wall tension Eccentric Hypertrophy Concentric Hypertrophy -response to increased diastolic wall tension -sarcomeres added in series -results in dilation of the chamber -a response to volume-overload -response to increased systolic wall tension -sarcomeres added in parallel -results in thickening of walls -a response to Systolic pressure-overload A component of “Cardiac Remodeling” vet-student.mihanblog.com
Chronic activation of the compensatory mechanisms Progressive cardiac disease Progressive chamber enlargement Congestive Heart Failure vet-student.mihanblog.com
Compensated Heart Failure Elevated cardiac filling pressures Compensated Heart Failure Elevated venous pressures with venous distention (stage I) Elevated capillary pressures Leakage of fluid into the interstitium (stage II) Decompensated Heart Failure Flooding of the alveoli (stage III) vet-student.mihanblog.com
Reduced Cardiac Output If the left side fails: If the left side fails: Low output signs Congestive signs -Tachypnea and/or dyspnea -Weak arterial pulses -Pale mucous membranes -Weakness, collapse, syncope -Tachypnea and/or dyspnea -Coughing -Pulmonary crackles -Cyanosis Reduced Cardiac Output Pulmonary Edema vet-student.mihanblog.com
Reduced Cardiac Output If the right side fails: Low output signs Congestive signs -Pitting edema -abdominal distention (ascites) -tachypnea and/or dyspnea -Tachypnea and/or dyspnea -Pale mucous membranes -Weakness, collapse, syncope -Weak arterial pulses assoc. with reduced LV preload Ascites or pleural effusion Reduced Cardiac Output vet-student.mihanblog.com
Prognosis In people: -renal function is predictive of mortality in patients with chronic CHF -chronic diuretic therapy is associated with poor clinical outcomes and high resource utilization in patients with and without renal insufficiency -poor LV function predicts higher mortality -Anemic patients with CHF have increased mortality vet-student.mihanblog.com
Therapy of Heart Failure Goals: -increase survival time -reduce symptoms associated with heart failure -normalize tissue perfusion -improve the pumping function of the heart -maintain normal blood pressure -prevent the accumulation of edema or effusions -blunt the deleterious effects of chronic activation of the compensatory mechanisms (RAS, SNS, ALD, etc) vet-student.mihanblog.com
Therapy of Heart Failure Drugs used to treat heart failure Diuretics Vasodilators -Furosemide -Spironolactone -Thiazides Arterial -Hydralazine Venous -Nitroglycerin Mixed -ACE inhibitors -Nitroprusside Positive Inotropes Digoxin Dobutamine Pimobendan Beta-blockers: Carvedilol, Atenolol Metoprolol vet-student.mihanblog.com
Diuretics Furosemide (Lasix ®) -loop diuretic (thick ascending limb of the loop of Henle) -most potent of the commonly used diuretics-first line diuretic for CHF therapy -inhibition of the Na/K/CL cotransporter resulting in loss of sodium, potassium and chloride and the prevention of the formation of the hypertonic medullary interstitium -side effects: dehydration and azotemia, hypovolemia, hypokalemia, hyponatremia, hypochloremia -Dosage (dogs): 2-6 mg/kg PO, IM or IV (depending on whether being used in the emergency or chronic management of CHF) (cats): 1-2 mg/kg PO, IM, or IV (6.25-12.5 mg in most cats) vet-student.mihanblog.com
Diuretics Spironolactone (Aldactone ®) -Weaker potassium-sparing diuretic -Distal tubule and collecting duct -Aldosterone antagonist -in humans, use of this drug in class IV heart failure increased survival times (most likely associated with the reduction of myocardial fibrosis secondary to increased aldosterone) -side effects: hyperkalemia (esp. when combined with ACEI), dehydration -Dosage (dogs): 1-2 mg/kg po q 12-24 hours vet-student.mihanblog.com
Aldosterone Deleterious Effects: -myocardial fibrosis -catecholamine potentiation -ventricular arrhythmias -endothelial dysfunction -potassium and magnesium loss The Trials: -RALES (Randomized Aldactone Evaluation Study) Spironolactone increased the probability of survival in heart failure by 30% in patients with moderate to severe heart failure compared with placebo -EPHESUS (eplerenone post MI efficacy and survival study): decreased relative risk of total mortality by 15% compared with placebo and decreased the risk of sudden cardiac death by 21% vet-student.mihanblog.com
Diuretics Thiazide diuretics hydrochlorothiazide (hydrodiuril®) chlorothiazide (diuril®): -weak diuretics affecting the distule tubule -never used as primary diuretic -used in combination with spironolactone and furosemide Dosage (dogs): 1-2 mg/kg po q 12-24 hours vet-student.mihanblog.com
Mixed Vasodilators Angiotensin Converting Enzyme Inhibitors (ACEI) Enalapril (Vasotec ®, Enacard ®) Benazepril (Lotensin ®) -modest vasodilators used primarily for their ability to blunt compensatory mechanisms activated in chronic heart failure (decreases AgII) -may cause azotemia and hypotension -first line therapy for patients with myocardial dysfunction (eg., dilated cardiomyopathy) -currently the only group of drugs that increase survival time in dogs with CHF vet-student.mihanblog.com
Mixed Vasodilators ACEI trials RR=risk reduction ACEI trials -IMPROVE: MR and DCM dogs improved heart failure class, faster pulm. edema resolution, increased mobility after 20 days -COVE: MR and DCM dogs 32% vs 15% finished the study, DCM improved faster than MR in all clinical indices -LIVE: (dogs from above studies) overall 157 vs 77 days, MR160 vs 87 days, DCM 143 vs 57 days (NS), 26% vs 9% in study @ 6 mo., most benefit in 1st 2 mo. vet-student.mihanblog.com
Mixed Vasodilators ACEI trials BENCH: MR and DCM dogs (benazepril) RR=risk reduction ACEI trials BENCH: MR and DCM dogs (benazepril) 44% decrease RR in treatment failure overall, no diff with DCM, 51% decrease in RR in endpoint for MR 46% decrease in RR in endpoint for class II No RR in endpoint for class III Survival not different SVEP: CKCS with MR (enalapril) class I and II NYHA No change in RR for onset of CHF No difference in time to onset of CHF vet-student.mihanblog.com
Mixed Vasodilators Nitroprusside (Nipride ®) -very potent mixed vasodilator -requires CRI and monitoring of BP -can be used in combination with dobutamine in severe cases of CHF and low output failure -short term use only; tolerance and toxicity may develop with prolonged use (greater than 72 hrs) -rarely used in veterinary medicine due to expense and high maintenance monitoring Dosage (dogs): 1-10 ug/kg/min CRI in D5W vet-student.mihanblog.com
Venodilators -Nitroglycerine (Nitro-bid®, Nitrol®) -primarily used in the emergency therapy for CHF -topical administration -tolerance develops if used for greater than 72 hours Dosage: 1/8-1 inch topically q 6-8 hours -Isosorbide dinitrate (Isordil ®) -direct acting venodilator -rarely used in veterinary medicine Dosage: 0.2-1.0 mg/kg po bid (dogs and cats) vet-student.mihanblog.com
Arterial vasodilators Hydralazine -direct acting potent arterial vasodilator -can be used to reduce afterload in the setting of severe mitral regurgitation -may cause reflex tachycardia secondary to hypotension -dose must be titrated to effect (at least a 20 mmHg decrease in mean BP) Dosage (dogs): 1-3 mg/kg po bid (titrated to effect) vet-student.mihanblog.com
Arterial vasodilators Amlodipine (Norvasc®) -Calcium channel blocker (1,4 dihydropyridine family) -predominantly used in the treatment of systemic hypertension -may be used for afterload reduction in patients with MR or DCM Dosage: (dogs) 0.05-0.2 mg/kg po q 12 h (cats) 1/4th of a 2.5 mg tablet po sid vet-student.mihanblog.com
Positive Inotropes Digoxin (Cardoxin ®) -mild to modest positive inotrope -inhibits the Na/K ATPase -centrally increases vagal tone -restores baroreflex function -also used as an antiarrhythmic agent for supraventricular tachycardias -RADIANCE and DIG trials in humans -side effects: cardiac (arrhythmias), gastrointestinal (anorexia, vomiting, diarrhea), neurologic (lethargy, depression) -clinically used for: atrial fibrillation, myocardial failure, and chronic CHF Dosage (dogs): 0.005-.01 mg/kg PO q 12 hrs (cats): 1/4th of a 0.125 mg tab PO q 12-48 hrs) vet-student.mihanblog.com
Positive Inotropes Dobutamine (Dobutrex ®) -synthetic beta-1 agonist -positive inotropic effects -positive chronotropic effects at higher dosages -indicated for severe myocardial failure -may be used in combination with nitroprusside -requires CRI administration and continuous ECG monitoring Dosage (dogs): 3-20 ug/kg/min vet-student.mihanblog.com
Positive Inotropes Pimobendan - new phosphodiesterase inhibitor -sensitizes the myofilaments to calcium -positive inotrope and vasodilator (“inodilator”) -increases inotropic state without increasing oxygen consumption -not currently available in US -0.1-0.6 mg/kg po q12h at least 1 hour before food Milrinone and Amrinone -both positive inotropic and vasodilator effects -potent phosphodiesterase inhibitors -rarely used in veterinary medicine -assoc. with an increase in mortality in people in the PROMISE trial vet-student.mihanblog.com
LANDMARK HUMAN Beta-blocker TRIALS -US Carvedilol Heart Failure Trials Program: placebo decreased the probability of event-free survival by 65% compared to carvedilol -MERIT-HF trial: metroprolol decreased cumulative mortality by 34% compared to placebo -CIBIS-II: survival was decreased 35% with placebo compared to bisoprolol -COPERNICUS: survival was decreased 35% with placebo compared with carvedilol vet-student.mihanblog.com
-protection from catecholamine toxicity in the heart and kidney Beta blockers: -protection from catecholamine toxicity in the heart and kidney -reversal of cardiac remodeling -blockade of renin release and lowering of Ag II levels -decrease of arrhythmias. -effective in mild to moderate and moderate to severe disease Carvelilol (CoReg®) -non-selective beta-blocker with alpha-1 blocking activity as well as free radical scavenging/anti-oxidant activity and decreases endothelin release -1.56-3.125 mg po QD for 2 wks, then BID for 2 wks, and so on to a full dose of 12.5-25 mg po q12h or the highest tolerated dosage vet-student.mihanblog.com
Therapy of Heart Failure acute heart failure -Oxygen therapy -Furosemide 2-6 mg/kg IV q 2-6 hours based on respiratory rate trend -Nitroglycerine topical q 6-8 hours for 36-48 hours -Cage rest -IV catheter vet-student.mihanblog.com
If the underlying process involves severe valvular insufficiency Therapy of Heart Failure Acute Heart Failure If the underlying process involves myocardial failure Dobutamine CRI (3-20 ug/kg/min) If the underlying process involves severe valvular insufficiency Hydralazine 1-3 mg/kg PO bid titrated to effect (reduction of mean BP by at least 20 mmHg) Or Nitroprusside 1-10 ug/kg/min CRI in D5W with invasive blood pressure monitoring vet-student.mihanblog.com
Therapy of Heart Failure Chronic Heart Failure If asymptomatic and primary problem is myocardial failure ACEI (enalapril 0.5 mg/kg po sid) Carvedilol (titrated to highest tolerable dosage) +/- Digoxin (0.005 mg/kg po bid) +/- Antiarrhythmics as needed +/- Spironolactone (1-2 mg/kg po q12-24h) If symptomatic and primary problem is myocardial failure ACEI (enalapril 0.5 mg/kg po sid-bid) Digoxin (0.005 mg/kg po bid) furosemide (2-6 mg/kg po bid-tid) +/- Carvedilol (as above) +/- Spironolactone (as above) Pimobendan (0.1-0.3 mg/kg po q12h) vet-student.mihanblog.com
Therapy of Heart Failure Chronic Heart Failure If asymptomatic and primary problem is valvular insufficiency ACEI (enalapril 0.5 mg/kg po sid) only if cardiomegaly and pulmonary venous congestion If symptomatic and primary problem is valvular insufficiency ACEI (enalapril 0.5 mg/kg po sid-bid) Furosemide (2-4 mg/kg po sid-tid) +/- digoxin (0.005 mg/kg po bid) +/- cough suppressant +/- Carvedilol (1.56 mg po qd titrated to highest tolerable dosage +/- Spironolactone (1-2 mg/kg po q12-24h) vet-student.mihanblog.com
Therapy of Heart Failure Chronic Heart Failure Refractory patients with MR and/or myocardial failure -ACEI (enalapril) -Digoxin -Furosemide -Spironolactone + hydrochlorothiazide (1-2 mg/kg po sid-bid) +/- cough suppressant* -Moderate sodium restriction *cough suppressants only if pulmonary edema has been ruled out as the cause of the coughing -butorphanol -hydrocodone vet-student.mihanblog.com
Therapy of Heart Failure Chronic Heart Failure Patients with atrial fibrillation complicating MR or DCM Digoxin (dogs --> 0.005 mg/kg po bid) +/- diltiazem (dogs --> 1 mg/kg po tid) Goal: to maintain a ventricular rate of 100-150 bpm vet-student.mihanblog.com
Acute heart failure vet-student.mihanblog.com
Severe defect in filling Failure of the heart as a pump Sudden increase in workload vet-student.mihanblog.com
Disorders of filling Percardial tamponade Aortic and pulmonary artery rupture vet-student.mihanblog.com
Tachyarrhythmia Myocarditis (encephalomyocarditis virus, foot and mouth dis.) Nutritional deficiency myopathy (Cu &Sel) Plant poisoning(phalaris spp., white snake root) Electrocondunction and lightening stroke vet-student.mihanblog.com
bradycardia iatrogenic, Ca , xylazine & concentrated Kcl Plant poisoning (taxus spp.) vet-student.mihanblog.com
Increased in workload Rupture of aortic valve Acute anaphylaxis vet-student.mihanblog.com
Arrhythmia and cardiac arrest in horses under general anesthesia vet-student.mihanblog.com
Clinical findings Commonly during excitement or activity Dyspnea Staggering and falling and death Pallor No pulse and heart sounds Sudden unset of respiratory distress in horses with rupture of aortic or mitral valve and atrial fibrillation vet-student.mihanblog.com
Syndrome most common in horses Diagnosis based on pulmonary hemorrhage and edema vet-student.mihanblog.com
Clinical pathology Serum troponin I vet-student.mihanblog.com
Treatment Not usually possible Intracardiac injection of epinephrine Pumping of the chest vet-student.mihanblog.com
Arrhythmias Electrocardiography Recording the action potential based electrical activity at body surface Positive and negative electrodes (upward and downward deflection). ECG in large versus small animals Base-apex lead system vet-student.mihanblog.com
SERUM CARDIACTROPONIN I CONCENTRATION excellent cardiac biomarker in large animals sensitive and persistent indicator of cardiac injury. In horse below 0.11 ng/mL using the human immunoassay. Healthy neonatal foals have cardiac troponin I concentrations of less than 0.49 ng/mL. Healthy cattle cardiac troponin I concentrations below 0,04 ng/mL. vet-student.mihanblog.com
Arrhythmias (dysrrhythmias) Variation in cardiac rate and rhythm include : tachycardia, bradycardia, arrhythmia and gallop Autonomic influence Myocardial disease Acid-base and electrolyte imbalance Treatment of the underlying disease vet-student.mihanblog.com
Sinus tachycardia Increase in heart rate Pain , excitement , hyperthermia … Initiated by the SA node Detectable on ECG and origin is SA(tachycardia on auscultation with detectable cause) Not about 120 Usually above 48 in H and 80 in cow vet-student.mihanblog.com
Sinus bradycardia Decrease HR due to decreased discharge from SA node Highly trained fit animals Abolishes by exercise or atropine Diagnosed by ECG vet-student.mihanblog.com
Bradycardia occurs Space occupying lesions of cranium Pituitary abscess Increase in blood pressure Hyperkalemia Hypothermia Hypoglycemia Alpha-2-adrenergic agonists (xylazine) Vagus indigestion and hernia in cattle Food restriction In young R by forceful tail elevation BSE vet-student.mihanblog.com
Rarely resting heart rate below 22 in H and 44 in cow Rates below this (22 in H, 44 in Cow) are suggestive of pathological bradicardia, hypothermia, hypothyroidism or an intrinsic heart problem vet-student.mihanblog.com
Physiological arrhythmia Not heart disease Increased vagal tone Especially in H: Sinus arrhythmia Wandering pacemaker Sinoatrial block 1st and 2nd degree atrioventricular block Nose twitch in horse If no sign of heart disease or abolished by exercise they are normal vet-student.mihanblog.com
In foals arrhythmias occurs B/C of hypoxemia Occurrence of cardiac irregularities after exercise is indicative of serious heart disease In foals arrhythmias occurs B/C of hypoxemia Cardiac arrhythmias in dairy cattle B/C of GI disorders vet-student.mihanblog.com
Sinus arrhythmia Normal physiological arrhythmia occurs at slow resting heart beat associated with variation in the rate of discharge from SA node resulting from variation in the intensity of vagal tone Correlated with respiration ( during inspiration) Tame sheep and goat, dogs, young of all species Abolished by atropine or exercise Detected by variation in P-P interval with or without variation in P-R interval Associated with difference in the site of discharge from SA node Induced by hypercalcemia during treatment for MF vet-student.mihanblog.com
Sinoatrial block Sinus node fail to discharge Complete absence of heart sound and pulse No P, QRS, and T Twice distance between pre and postblock P waves Common in normal fit racing horse Induced by increasing vagal tone Normal if disappears during exercise vet-student.mihanblog.com
Atrioventriccular block First degree AV block Second degree AV block Third degree AV block vet-student.mihanblog.com
1st degree AV block Detected by ECG Delayed conduction at atrioventricular node Vagal tone waxing and waning No significance vet-student.mihanblog.com
2nd degree AV block (partial heart block) Periodic interference with conduction at AV node Randomly of regular pattern No s1 and s2 and pulse Forth sound in horse :du LUBB DUPP, du…,du LUBB DUPP Atrail jugular impulse seen Intensified postblock first sound Complete QRS and T absence vet-student.mihanblog.com
MOBITZ type 2 : P-Q interval remain unchanged Normal in horses MOBITZ type 1 (wenkebach) 2nd degree AV block : grdual increase in P-Q interval up to block MOBITZ type 2 : P-Q interval remain unchanged Normal in horses Upper lip twitch More common in thouroughbred and stanardbred horses in 20% race horses Abolished by atropine or exercise 6sECG_rdm.exe vet-student.mihanblog.com
Third degree Rarely in large animal Fatal Atria and ventricles beat independently Atrial contractions are faster vet-student.mihanblog.com
Premature beat and complex Detected by auscultation , palpation of an artery Visual insp. Of jugular vein A beat is always assocaited with complex Premature complex Electrical event detected on ECG A complex can be unaccompanied by a beat vet-student.mihanblog.com
Premature complexes(extrasystoles) Discharges from myocardium Atrial, junctional , ventricular vet-student.mihanblog.com
Atrial premature beats Discharges outside SA node Lower intensity in ven. Contraction P waves are sooner and abnormal in configuration QRS normal vet-student.mihanblog.com
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Junctional premature beats (atrioventricular nodal premature complexes) Discharges from the region of AV node or conducting tissue QRS usu normal but P wave opposite vet-student.mihanblog.com
Ventricular P B Focus within ventricular myocardium Interruption of the normal beat by an earlier beat The heart sound decreased but the following heart sound increased Bizarre QRS complexes vet-student.mihanblog.com
VPC vet-student.mihanblog.com
P B,s are indicative of myocardial disease Atrial P B in cattle indicative of GI disease Atrial premature complexes can progress to atrial fibrillation in these cases where there is excessive vagal tone. vet-student.mihanblog.com
Arrhythmias with tachycardia (an excitable focus within the myocardium may spontaneously …) 1- Paroxysmal tachycardia 2- Ventricular tachycardia vet-student.mihanblog.com
Paroxysmal tachycardia From an irritant focus within the atria or ventricles (more common in farm animal) The increase and fall to normal is abrupt HR is elevated to a rate far excess of normal vet-student.mihanblog.com
Ventricular tachycardia May produce a regular or irregular HR and rhythm Ventricular tachycardia with atrioventricular dissociation (ven. Focus exceeds SA node ) : Regular QRS Abnormal amplitude and duration of QRS and T, T oriented opposite QRS P waves maybe detectable but no relationship with QRS Evidence of severe cardiac disease vet-student.mihanblog.com
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V T Primary myocarditis, nutritional cardiomyopathy,or myocardial neoplasia secondary to valvular disease and myocardial ischemia. Ventricular arrhythmias are common in certain plant poisonings and other toxicities, and in severe electrolyte and acid-base disturbance, and commonly occur in the final stages of heart failure vet-student.mihanblog.com
If uncorrected, ventricular tachycardia may lead to ventricular fibrillation and death vet-student.mihanblog.com
Treatment Lidocaine (0.5-1 mg every 5 min for 4 treatment) Quinidine sulfate (20 mg then 10 every 8 h) Quinidine Gluconate (IV 0.5-2.2 every 10 min to 12 mg ) Phenytoin sodium in H (initial dose of 20 mg/kg every 12 hours for 4 doses, then maitenance oral 10-15 every 12 h vet-student.mihanblog.com
Ventricular fibrilation Not observed clinically Occurs in terminal stages of fatal conditions (lightening stroke, plant poisoning, overdose with anesthetics, severe toxemia and terminal phase of acquired heart disease ) Complete absence of pulse and heart sounds Blood pressure falls Animal become unconscious and die vet-student.mihanblog.com
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Atrial fibrilation Atrial depolarization is characterized by numerous independent fronts of excitations that occurs continuously and haphazardly Not possible to establish any basic rhythm by tapping out No atrial contractions Passive ventricle filling No S4 Accentuated S3 No P waves Multiple waveforms (f waves) 300-600 /min QRS normal in configuration, no pattern in Q_Q intervals vet-student.mihanblog.com
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Atrial Fibrillation in Horses Horses predisposed to AF due to large atrial mass (size) Autonomic imbalance during exercise (increased parasympathetic tone) Myocardial disease Atrial dilation vet-student.mihanblog.com
Atrial Fibrillation in Horses Horses with no heart disease Horses with heart disease vet-student.mihanblog.com
Atrial fibrillation Horses w/o Heart Disease Poor performance and exercise intolerance most commonly in horses performing at a high level (race horses, cross country, polo ponies, Grand Prix Jumpers) Exercise intolerance less common in show horses, pleasure horses, dressage horses vet-student.mihanblog.com
Atrial fibrillation w/o heart disease Cardiac output at rest is normal in most horses with atrial fibrillation Maximal cardiac output during exercise is limited because atrial contribution to filling needed at high heart rates Atrial pressure already high during intense exercise is increased with atrial fibrillation vet-student.mihanblog.com
Atrial Fibrillation Most common clinical sign is a single episode of poor performance Deceleration suddenly during a race vet-student.mihanblog.com
Atrial Fibrillation - Examination Check for mitral regurgitation, tricuspid regurgitation, aortic regurgitation Normal CBC and Chemistry Normal heart rate (<60 normal) Echocardiogram (normal size and FS) vet-student.mihanblog.com
Atrial Fibrillation No Heart Disease vet-student.mihanblog.com
Atrial Fibrillation Treatment Digoxin alone doesn’t work Quinidine sulfate vet-student.mihanblog.com
Quinidine Regimes for Atrial Fibrillation Most common treatment is quinidine sulfate via nasogastric tube at 22 mg/kg every 2 hours to a cumulative dose of 88 to 112 mg/kg Alternative regimens if horse toxic vet-student.mihanblog.com
Quinidine Side Effects Depression Weakness vet-student.mihanblog.com
Quinidine Toxicity HR > 100 QRS duration 2X pretreatment Diarrhea Colic Nasal edema Laminitis Severe depression vet-student.mihanblog.com
Atrial Fibrillation With Heart Disease vet-student.mihanblog.com
Atrial Fibrillation With Heart Disease Myocardial disease or scarring Valvular disease with heart enlargement (MI, TI, AI) vet-student.mihanblog.com
Atrial Fibrillation With Heart Disease Increased heart rate Grade III or louder murmur consistent with MI, TI, or AI Atrial enlargement vet-student.mihanblog.com
Atrial fibrilation in cow Secondary to myocardial disease or endocarditis resulting in atrial enlargement GI disease Metaboloic disease vet-student.mihanblog.com
Myocardial disease vet-student.mihanblog.com
Myocardial disease Myocarditis Cardiomyopathy Inflammation of the myocardial wall (bacterial, viral, parasitic) Cardiomyopathy Diseases where myocardial damage is the prime manifestation Dilated cardiomyopathy is the only form of clinical significance in large animals vet-student.mihanblog.com
Myocarditis Bacterial Viral Staph, Clostridium, 2º to bacteremia or septicemia, pericarditis, endocarditis, from navel-ill, following strangles, tuberculosis (esp. horse), Histophilus Somni, Viral FMD, AHS, EIA, E herpes virus, Bluetongue in sheep vet-student.mihanblog.com
Parasitic Toxoplasmosis, cysticercosis, sarcocystis, strongylous, vet-student.mihanblog.com
Myocarditis May be incidental finding at necropsy Treat primary condition – i.e., cow with mastitis Arrhythmia Sudden death vet-student.mihanblog.com
Clinical pathology LDH Creatine kinase Troponin I vet-student.mihanblog.com
treatment Primary cause vet-student.mihanblog.com
Cardiomyopathy Toxicities: Deficiencies Monensin, lasalocid Gossypol Cassia Phalaris Deficiencies Vitamin E/Se (WMD or nutritional myodegeneration) Copper deficiency Copper/Cobalt deficiency in lambs vet-student.mihanblog.com
Cardiomyopathy Other causes Excess molybdenum High sulfates Lymphosarcoma – neoplastic infiltration of myocardium Tumor infiltration vet-student.mihanblog.com
Cardiomyopathy Clinical signs – usually present with CHF Arrhythmias Treatment – poor prognosis – treat CHF vet-student.mihanblog.com
Cor pulmonale Pulmonary hypertension, brisket disease, high altitude disease, or high mountain disease Cor pulmonale reflects effect of lung dysfunction on heart, therefore, heart disease is secondary vet-student.mihanblog.com
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Cor pulmonale Alveolar hypoxia Destruction of pulmonary vascular bed Chronic interstitial pneumonia Chronic obstructive pneumonia Pimelea spp. Toxicosis Chronic severe elevation in pulmonary venous pressure Persistent pulmonary hypertension of the neonate (PPHN) [endothelin I ] vet-student.mihanblog.com
Cor pulmonale Pathophysiology: Pulmonary hypertension right heart hypertrophy, dilatation or failure Underlying cause is hypoxic vasoconstriction caused by High altitude dwelling (> 6,000 feet) Pulmonary disease (bronchopneumonia or lungworms) vet-student.mihanblog.com
Cor pulmonale Clinical signs Treatment Signs of CHF Remove from high altitude Treat any primary lung disease Reversible if treated early vet-student.mihanblog.com
Valvular Disease in Horses Stenotic lesions congenital and extremely extremely rare in horses Acquired valvular incompetency common (endocarditis, rupture of cordae tenneae), blood cyct in cattle Affects aortic, mitral, and tricuspid valves Cattle tricuspid, mitral, aorta vet-student.mihanblog.com
Valvular Disease in Horses Degenerative thickening Bacterial endocarditis Ruptured chorda tendinae Myocardial disease with cardiomegaly Congenital malformation Valvulitis vet-student.mihanblog.com
Valvular Insufficiency Examination Physical examination Auscultation Pulses Veins Echocardiography Doppler Laboratory testing vet-student.mihanblog.com
Valvular Insufficiency Examination Intensity of murmur does not correlate with severity of insufficiency PMI commonly corresponds to location of valvular problem vet-student.mihanblog.com
Valvular Insufficiency Examination MI radiates to heart base and can sound louder near AV MI commonly produces goose honk vet-student.mihanblog.com
Valvular Insufficiency Exam AI produces harsh diastolic murmur Murmur sometimes cooing or buzzing Bounding pulse with moderate to severe AI due to left volume overload vet-student.mihanblog.com
Valvular Insufficiency Exam TI leads to jugular pulsation vet-student.mihanblog.com
Consequence of Valvular Disease Insignificant (Sometimes does devalue animal on prepurchase exam) Exercise intolerance Severe disease – heart failure vet-student.mihanblog.com
Doppler Estimates of Severity of Valvular Dysfunction vet-student.mihanblog.com
Consequences of Valvular Disease Mild regurgitation may be insignificant or lead to exercise intolerance for horses performing at high levels vet-student.mihanblog.com
Consequences of Valvular Disease Moderate to severe regurgitation leads to volume overload and exercise intolerance and sometimes heart failure Acute death can result from rupture of a major valve chordae vet-student.mihanblog.com
treatment No specific treatments vet-student.mihanblog.com
Vegetative endocarditis Arcanobacter pyogenes or α-hemolytic strep, micrococcus and staph spp., mycoplasma and cl. chauvoei in cattle, erysipelothrix or strep in swine Actinobacillus equuli, strp. Spp., pasteurella, pseudomonas spp., and migrating strongylus in the horse vet-student.mihanblog.com
Lesions on valves are usually embolic in origin (chronic bacteremia) Murmur CHF may develop vet-student.mihanblog.com
Vegetative endocarditis Clinical signs Poor doing animal Exercise intolerance CHF Fluctuating fever Clinical pathology Severe leukocytosis Diagnostics Blood cultures Echocardiography vet-student.mihanblog.com
Vegetative endocarditis Large cauliflower-like or small verrucous lesions on heart valves, or, Shrunken, scarred heart valves vet-student.mihanblog.com
Vegetative endocarditis vet-student.mihanblog.com
Vegetative endocarditis Treatment Not highly successful Cephalosporins/penicillin to calves with omphalophlebitis Long term, broad spectrum antibiotics to cattle with vegetative endocarditis Prognosis poor vet-student.mihanblog.com
Congenital cardiac defects Early detection important Expense Genetic implications vet-student.mihanblog.com
Congenital cardiac defects Ventricular septal defect* Left to right shunt Tetralogy of Fallot Right to left shunt, cyanosis Ectopia cordis Patent foramen ovale PDA vet-student.mihanblog.com
Ventricular Septal Defect Most common congenital abnormality Effects depends on size Small hole pressure differential adequate - no effect Large hole - can die of congestive heart failure in first few days of life vet-student.mihanblog.com