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4  S1 : ventricular systole, synchronous with apex beat S1  Maximal audibility of the mitral valve(fifth in the horse and fourth in R)  For tricuspid valve on the right at 4 th intercostal space in the horse and costochondral level of 3 rd space for others

5  Closure of the aortic and pulmonary valve  Aortic component audible ventral to the horizontal line of shoulder at 4 th in H and 3 rd in other specie  Pulmonic component ventral and anterior to the aortic area 3 rd in the horse and 2 nd or 3 rd in others

6  Rapid filling of the heart  Most common in horses  Best heard at heart rate slightly above resting

7  Atrail contraction  Also a sound

8 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 Heart disease vs. Heart failure

9  Heart (pump)  Vessels (ciruit)

10  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)


12  Heart Failure results from:  1- defect in filling  2- electrical conductivity  3- contractile function  4- excessive workload  5- combination of two or more

13  Cardiac arrhythmias  Obstructed flow  Regurgitant flow  Contractile dysfunction (systolic failure)  Inadequate filling (diastolic filling)  Loss of blood

14  Acute heart failure  Chronic(congestive) heart failure  Left H F  Right H F  Left and Right H F

15  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


17  Increase in right ventricular end diastolic pressure  Results in right atrial pressure and jugular venous pressure  Systemic venous distention


19  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)

20  Capacity of the heart to increase output normally

21  Increase in HR  Increase in SV  Redistribution of blood flow

22  Horses 6-7 times that of resting  Cows 3-4  In HF beyond 120 in significant

23  1- ventricular distending pressure(end- diastolic pressure)  2-contrctility : adrenergic activity and catecholamines  3- increase in ejection fraction(afterload)

24 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 Heart disease vs. Heart failure

25  Increased extraction of oxygen in pump and circuit failure  Blood redistribution

26  Increasing HR  Improving contrctility  Regulating blood flow to vital organ

27  Primary defect in myocardial activity  In early course no problem B/C:  augmented ventricular filling pressure (increased venous return and increased blood volume)

28  Heart rate  Intensity  Size of the heart  Pulse characteristics  Exercise tolerance

29  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

30  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

31  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



34  Prolonged time to return to normal \  Increase in HR  Evidence of cardiac enlargements

35 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

36 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

37 Ways to challenge the function of the heart Systolic Pressure overloadDiastolic pressure overload -increased preload -results in increased filling pressures VOLUME OVERLOAD DIASTOLIC DYSFUNCTION -impedes the filling of the heart and results in an increased diastolic pressure for each given diastolic volume -forces the heart to generate high pressures during systole resulting in increased oxygen consumption and increased wall tension

38 CONGESTIVE HEART FAILURE Elevated Cardiac Filling Pressures -Valvular Insufficiency VOLUME OVERLOADDIASTOLIC DYSFUNCTION -Thick and Stiff Ventricular Walls -Abnormal Ventricular Relaxation -Ventricular Fibrosis -Pericardial Disease -Myocardial Failure -Moderate to Large L-> R shunt

39 PRESSURE OVERLOAD Valvular InsufficiencyMyocardial Failure Diastolic Dysfunction Concentric Hypertrophy Altered ventricular geometry Thickened Ventricular Walls Ischemia and Fibrosis Elevated Cardiac Filling Pressures CONGESTIVE HEART FAILURE

40 Myocardial Failure or Valvular Insufficiency SNS F-S Mech. RAS Activates Compensatory mechanisms Aldosterone Heart Rate Vasoconstriction Increased Venous Return and Increased Blood Pressure Augmentation of cardiac performance Angiotensin II Contractility Anti-diuretic Hormone Sodium and water retention

41 Reduced renal perfusion Reduced sodium delivery to kidneys Sympathetic Nervous System Release of Renin from Renal Juxtaglomerular cells Angiotensinogen Angiotensin I Angiotensin II Angiotensin converting enzyme (ACE)

42 Angiotensin II Vascular smooth muscle Renal efferent arteriole Proximal renal tubule Adrenal cortex Baroreflexes Central adrenergic activation, Ganglionic facilitation, Presynaptic receptors Constriction: increase PVR Constriction: maint. of GFR Increased Na + reabsorption Increased aldosterone secretion Withdrawal of vagal tone Increased release of NE

43 Ventricular Hypertrophy Eccentric Hypertrophy -response to increased diastolic wall tension -sarcomeres added in series -results in dilation of the chamber -a response to volume-overload Concentric Hypertrophy -response to increased systolic wall tension -sarcomeres added in parallel -results in thickening of walls -a response to Systolic pressure-overload Goal: to normalize myocardial wall tension A component of “Cardiac Remodeling”

44 Chronic activation of the compensatory mechanisms Progressive cardiac disease Progressive chamber enlargement Congestive Heart Failure

45 Elevated cardiac filling pressures Elevated venous pressures with venous distention (stage I) Elevated capillary pressures Leakage of fluid into the interstitium (stage II) Flooding of the alveoli (stage III) Decompensated Heart Failure Compensated Heart Failure

46 If the left side fails: Low output signsCongestive signs -Tachypnea and/or dyspnea -Coughing -Pulmonary crackles -Cyanosis -Tachypnea and/or dyspnea -Weak arterial pulses -Pale mucous membranes -Weakness, collapse, syncope Pulmonary Edema Reduced Cardiac Output If the left side fails:

47 If the right side fails: Low output signsCongestive 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

48 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 Prognosis

49 Therapy of 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) -increase survival time -reduce symptoms associated with heart failure Goals:

50 Therapy of Heart Failure Drugs used to treat heart failure Diuretics Vasodilators Positive Inotropes -Furosemide -Spironolactone -Thiazides Arterial -Hydralazine Venous -Nitroglycerin Mixed -ACE inhibitors -Nitroprusside Digoxin Dobutamine Pimobendan Beta-blockers: Carvedilol, Atenolol Metoprolol

51 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 ( mg in most cats)

52 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 hours

53 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%

54 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 hours

55 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

56 Mixed Vasodilators 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, MR  160 vs 87 days, DCM  143 vs 57 days (NS), 26% vs 9% in 6 mo., most benefit in 1 st 2 mo. RR=risk reduction

57 Mixed Vasodilators 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 RR=risk reduction

58 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

59 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: mg/kg po bid (dogs and cats)

60 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)

61 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) mg/kg po q 12 h (cats) 1/4th of a 2.5 mg tablet po sid

62 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): mg/kg PO q 12 hrs (cats): 1/4th of a mg tab PO q hrs)

63 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

64 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 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

65 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

66 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 mg po QD for 2 wks, then BID for 2 wks, and so on to a full dose of mg po q12h or the highest tolerated dosage

67 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 hours -Cage rest -IV catheter

68 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

69 Therapy of Heart Failure Chronic Heart 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 asymptomatic and primary problem is myocardial failure 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 ( mg/kg po q12h)

70 Therapy of Heart Failure Chronic Heart Failure 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) If asymptomatic and primary problem is valvular insufficiency ACEI (enalapril 0.5 mg/kg po sid) only if cardiomegaly and pulmonary venous congestion

71 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

72 Therapy of Heart Failure Chronic Heart Failure Patients with atrial fibrillation complicating MR or DCM Digoxin (dogs --> mg/kg po bid) +/- diltiazem (dogs --> 1 mg/kg po tid) Goal: to maintain a ventricular rate of bpm


74  Severe defect in filling  Failure of the heart as a pump  Sudden increase in workload

75  Percardial tamponade  Aortic and pulmonary artery rupture

76  Myocarditis (encephalomyocarditis virus, foot and mouth dis.)  Nutritional deficiency myopathy (Cu &Sel)  Plant poisoning(phalaris spp., white snake root)  Electrocondunction and lightening stroke

77  iatrogenic, Ca, xylazine & concentrated Kcl  Plant poisoning (taxus spp.)

78  Rupture of aortic valve  Acute anaphylaxis

79  Arrhythmia and cardiac arrest in horses under general anesthesia

80  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

81  Syndrome most common in horses  Diagnosis based on pulmonary hemorrhage and edema

82  Serum troponin I

83  Not usually possible  Intracardiac injection of epinephrine  Pumping of the chest

84  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

85  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.

86  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

87  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

88  Decrease HR due to decreased discharge from SA node  Highly trained fit animals  Abolishes by exercise or atropine  Diagnosed by ECG

89  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

90  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

91  Not heart disease  Increased vagal tone  Especially in H:  Sinus arrhythmia  Wandering pacemaker  Sinoatrial block  1 st and 2 nd degree atrioventricular block  Nose twitch in horse  If no sign of heart disease or abolished by exercise they are normal

92  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 

93  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

94  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

95  First degree AV block  Second degree AV block  Third degree AV block

96  Detected by ECG  Delayed conduction at atrioventricular node  Vagal tone waxing and waning  No significance

97  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

98  MOBITZ type 1 (wenkebach) 2 nd 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 6sECG_rdm.exe

99  Rarely in large animal  Fatal  Atria and ventricles beat independently  Atrial contractions are faster 

100 Premature beat  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

101  Discharges from myocardium  Atrial, junctional, ventricular

102  Discharges outside SA node  Lower intensity in ven. Contraction  P waves are sooner and abnormal in configuration  QRS normal



105  Discharges from the region of AV node or conducting tissue  QRS usu normal but P wave opposite

106  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


108  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.

109  (an excitable focus within the myocardium may spontaneously …) 1- Paroxysmal tachycardia 2- Ventricular tachycardia

110  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

111  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




115  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

116  If uncorrected, ventricular tachycardia may lead to ventricular fibrillation and death

117  Lidocaine (0.5-1 mg every 5 min for 4 treatment)  Quinidine sulfate (20 mg then 10 every 8 h)  Quinidine Gluconate (IV 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 every 12 h

118  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


120  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) /min  QRS normal in configuration, no pattern in Q_Q intervals



123  Horses predisposed to AF due to large atrial mass (size)  Autonomic imbalance during exercise (increased parasympathetic tone)  Myocardial disease  Atrial dilation

124  Horses with no heart disease  Horses with heart disease

125  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

126  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

127  Most common clinical sign is a single episode of poor performance  Deceleration suddenly during a race

128  Check for mitral regurgitation, tricuspid regurgitation, aortic regurgitation  Normal CBC and Chemistry  Normal heart rate (<60 normal)  Echocardiogram (normal size and FS)


130  Digoxin alone doesn’t work  Quinidine sulfate

131  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

132  Depression  Weakness

133  HR > 100  QRS duration 2X pretreatment  Diarrhea  Colic  Nasal edema  Laminitis  Severe depression


135  Myocardial disease or scarring  Valvular disease with heart enlargement (MI, TI, AI)

136  Increased heart rate  Grade III or louder murmur consistent with MI, TI, or AI  Atrial enlargement

137  Secondary to myocardial disease or endocarditis resulting in atrial enlargement  GI disease  Metaboloic disease


139  Myocarditis › 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

140  Bacterial › 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

141  Toxoplasmosis, cysticercosis, sarcocystis, strongylous,

142  May be incidental finding at necropsy  Treat primary condition – i.e., cow with mastitis  Arrhythmia  Sudden death

143  LDH  Creatine kinase  Troponin I

144  Primary cause

145  Toxicities: › Monensin, lasalocid › Gossypol › Cassia › Phalaris  Deficiencies › Vitamin E/Se (WMD or nutritional myodegeneration) › Copper deficiency › Copper/Cobalt deficiency in lambs

146  Other causes › Excess molybdenum › High sulfates › Lymphosarcoma – neoplastic infiltration of myocardium › Tumor infiltration

147  Clinical signs – usually present with CHF  Arrhythmias  Treatment – poor prognosis – treat CHF

148  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


150  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 ]

151  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)

152  Clinical signs › Signs of CHF  Treatment › Remove from high altitude › Treat any primary lung disease › Reversible if treated early

153  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

154  Degenerative thickening  Bacterial endocarditis  Ruptured chorda tendinae  Myocardial disease with cardiomegaly  Congenital malformation  Valvulitis

155  Physical examination › Auscultation › Pulses › Veins  Echocardiography  Doppler  Laboratory testing

156  Intensity of murmur does not correlate with severity of insufficiency  PMI commonly corresponds to location of valvular problem

157  MI radiates to heart base and can sound louder near AV  MI commonly produces goose honk

158  AI produces harsh diastolic murmur  Murmur sometimes cooing or buzzing  Bounding pulse with moderate to severe AI due to left volume overload

159  TI leads to jugular pulsation

160  Insignificant (Sometimes does devalue animal on prepurchase exam)  Exercise intolerance  Severe disease – heart failure


162  Mild regurgitation may be insignificant or lead to exercise intolerance for horses performing at high levels

163  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

164  No specific treatments

165  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

166  Lesions on valves are usually embolic in origin (chronic bacteremia)  Murmur  CHF may develop

167  Clinical signs › Poor doing animal › Exercise intolerance › CHF › Fluctuating fever  Clinical pathology › Severe leukocytosis  Diagnostics › Blood cultures › Echocardiography

168  Large cauliflower- like or small verrucous lesions on heart valves, or,  Shrunken, scarred heart valves


170  Treatment  Not highly successful › Cephalosporins/penicillin to calves with omphalophlebitis › Long term, broad spectrum antibiotics to cattle with vegetative endocarditis › Prognosis poor

171  Early detection important › Expense › Genetic implications

172  Ventricular septal defect* › Left to right shunt  Tetralogy of Fallot › Right to left shunt, cyanosis  Ectopia cordis  Patent foramen ovale  PDA

173  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

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