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disease of the cardiovascular system

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Presentation on theme: "disease of the cardiovascular system"— Presentation transcript:

1 disease of the cardiovascular system


3 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

4 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

5 S3 Rapid filling of the heart Most common in horses
Best heard at heart rate slightly above resting

6 S4 Atrail contraction Also a sound

7 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

8 Two functional units of the cardiovascular system
Heart (pump) Vessels (ciruit)

9 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)

10 Heart failure

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

12 Causes of cardiovascular dysfunction
Cardiac arrhythmias Obstructed flow Regurgitant flow Contractile dysfunction (systolic failure) Inadequate filling (diastolic filling) Loss of blood

13 Other types of categorizing HF
Acute heart failure Chronic(congestive) heart failure Left H F Right H F Left and Right H F

14 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


16 right sided heart failure
Increase in right ventricular end diastolic pressure Results in right atrial pressure and jugular venous pressure Systemic venous distention


18 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)

19 Cardiac reserve and compensatory mechanism in HF
Capacity of the heart to increase output normally

20 Mechanism of sending blood to an organ
Increase in HR Increase in SV Redistribution of blood flow

21 Increase in HR Horses 6-7 times that of resting Cows 3-4
In HF beyond 120 in significant

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

23 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

24 Mixed venous oxygen tension
Increased extraction of oxygen in pump and circuit failure Blood redistribution

25 Autonomic nerve activity
Increasing HR Improving contrctility Regulating blood flow to vital organ

26 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)

27 Measurements of cardiac reserve
Heart rate Intensity Size of the heart Pulse characteristics Exercise tolerance

28 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

29 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

30 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

31 Right sided CHF

32 Left sided CHF

33 Clinical signs Prolonged time to return to normal \ Increase in HR
Evidence of cardiac enlargements

34 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

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

36 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

-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

38 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

39 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

40 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

41 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

42 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”

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

44 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)

45 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

46 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

47 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

48 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)

49 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

50 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)

51 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

52 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%

53 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

54 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

55 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, MR160 vs 87 days, DCM 143 vs 57 days (NS), 26% vs 9% in 6 mo., most benefit in 1st 2 mo.

56 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

57 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): ug/kg/min CRI in D5W

58 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)

59 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)

60 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

61 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)

62 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): ug/kg/min

63 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

-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

65 -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 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

66 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

67 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

68 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 ( mg/kg po q12h)

69 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)

70 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

71 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

72 Acute heart failure

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

74 Disorders of filling Percardial tamponade
Aortic and pulmonary artery rupture

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

76 bradycardia iatrogenic, Ca , xylazine & concentrated Kcl
Plant poisoning (taxus spp.)

77 Increased in workload Rupture of aortic valve Acute anaphylaxis

78 Arrhythmia and cardiac arrest in horses under general anesthesia

79 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

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

81 Clinical pathology Serum troponin I

82 Treatment Not usually possible Intracardiac injection of epinephrine
Pumping of the chest

83 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

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.

85 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

86 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

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

88 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

89 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

90 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

91 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

92 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

93 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

94 Atrioventriccular block
First degree AV block Second degree AV block Third degree AV block

95 1st degree AV block Detected by ECG
Delayed conduction at atrioventricular node Vagal tone waxing and waning No significance

96 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

97 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

98 Third degree Rarely in large animal Fatal
Atria and ventricles beat independently Atrial contractions are faster

99 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

100 Premature complexes(extrasystoles)
Discharges from myocardium Atrial, junctional , ventricular

101 Atrial premature beats
Discharges outside SA node Lower intensity in ven. Contraction P waves are sooner and abnormal in configuration QRS normal



104 Junctional premature beats (atrioventricular nodal premature complexes)
Discharges from the region of AV node or conducting tissue QRS usu normal but P wave opposite

105 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

106 VPC

107 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.

108 Arrhythmias with tachycardia
(an excitable focus within the myocardium may spontaneously …) 1- Paroxysmal tachycardia 2- Ventricular tachycardia

109 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

110 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




114 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

115 If uncorrected, ventricular tachycardia may lead to ventricular fibrillation and death

116 Treatment 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

117 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


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



122 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

123 Atrial Fibrillation in Horses
Horses with no heart disease Horses with heart disease

124 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

125 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

126 Atrial Fibrillation Most common clinical sign is a single episode of poor performance Deceleration suddenly during a race

127 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)

128 Atrial Fibrillation No Heart Disease

129 Atrial Fibrillation Treatment
Digoxin alone doesn’t work Quinidine sulfate

130 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

131 Quinidine Side Effects
Depression Weakness

132 Quinidine Toxicity HR > 100 QRS duration 2X pretreatment Diarrhea
Colic Nasal edema Laminitis Severe depression

133 Atrial Fibrillation With Heart Disease

134 Atrial Fibrillation With Heart Disease
Myocardial disease or scarring Valvular disease with heart enlargement (MI, TI, AI)

135 Atrial Fibrillation With Heart Disease
Increased heart rate Grade III or louder murmur consistent with MI, TI, or AI Atrial enlargement

136 Atrial fibrilation in cow
Secondary to myocardial disease or endocarditis resulting in atrial enlargement GI disease Metaboloic disease

137 Myocardial disease

138 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

139 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

140 Parasitic Toxoplasmosis, cysticercosis, sarcocystis, strongylous,

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

142 Clinical pathology LDH Creatine kinase Troponin I

143 treatment Primary cause

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

145 Cardiomyopathy Other causes Excess molybdenum High sulfates
Lymphosarcoma – neoplastic infiltration of myocardium Tumor infiltration

146 Cardiomyopathy Clinical signs – usually present with CHF Arrhythmias
Treatment – poor prognosis – treat CHF

147 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


149 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 ]

150 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)

151 Cor pulmonale Clinical signs Treatment Signs of CHF
Remove from high altitude Treat any primary lung disease Reversible if treated early

152 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

153 Valvular Disease in Horses
Degenerative thickening Bacterial endocarditis Ruptured chorda tendinae Myocardial disease with cardiomegaly Congenital malformation Valvulitis

154 Valvular Insufficiency Examination
Physical examination Auscultation Pulses Veins Echocardiography Doppler Laboratory testing

155 Valvular Insufficiency Examination
Intensity of murmur does not correlate with severity of insufficiency PMI commonly corresponds to location of valvular problem

156 Valvular Insufficiency Examination
MI radiates to heart base and can sound louder near AV MI commonly produces goose honk

157 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

158 Valvular Insufficiency Exam
TI leads to jugular pulsation

159 Consequence of Valvular Disease
Insignificant (Sometimes does devalue animal on prepurchase exam) Exercise intolerance Severe disease – heart failure

160 Doppler Estimates of Severity of Valvular Dysfunction

161 Consequences of Valvular Disease
Mild regurgitation may be insignificant or lead to exercise intolerance for horses performing at high levels

162 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

163 treatment No specific treatments

164 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

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

166 Vegetative endocarditis
Clinical signs Poor doing animal Exercise intolerance CHF Fluctuating fever Clinical pathology Severe leukocytosis Diagnostics Blood cultures Echocardiography

167 Vegetative endocarditis
Large cauliflower-like or small verrucous lesions on heart valves, or, Shrunken, scarred heart valves

168 Vegetative endocarditis

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

170 Congenital cardiac defects
Early detection important Expense Genetic implications

171 Congenital cardiac defects
Ventricular septal defect* Left to right shunt Tetralogy of Fallot Right to left shunt, cyanosis Ectopia cordis Patent foramen ovale PDA

172 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

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