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Cardiac disease
- Common in vet med, congenital or acquired (usu acquired)
- Southeast caused by Heartworm
- everywhere caused by vavular and myocardial disease (particularly mitral valve)
- Careful monitoring and cooperation and compliance of owner
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cardiac function
- four chambered pump (2 pumps)
- Responsible for moving blood through vascular system.
- Composed of myocardium, VERY strong, thick muscle
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Blood flow
Vena cava, right atrium, tricuspid valve, right ventricle, pulmonic valve, pulmonary artery, lungs, pulmonary vein, left atrium, mitral valve, left ventricle, aortic valve
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systole
chamber contraction
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stroke volume
quantity of blood pumped by left ventricle into the aorta with each ventricular contraction
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Cardiac output
- quantity of blood pumped by the left ventricle into the aorta each minute
- stroke volume x heart rate
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ventricular preload
- stretch of the walls of the left ventricle after passive filling and atrial contraction
- Measured by left ventricular end diastolic volume (LVEDV)
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Left ventricular end diastolic volume
volume of blood in the left ventricle at the end of diastole
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left ventricular end diastolic pressure
pressure exerted on walls of left ventricle at the end of diastole
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Peripheral vascular resistance
- impedance to blood flow through the systemic arteries determined by the tone of vascular smooth muscle and blood vessel diameter
- Increased by constriction of systemic arteries
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Afterload
resistance against which the left ventricle must eject its volume of blood during contraction (determined by aortic pressure, determined by PVR)
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Congestive Heart Failure
- Failure of the heart to pump sufficient blood to meet the metabolic needs of the body and/or prevent blood from pooling in pulmonary venous circulation
- Right CHF, fluid overload into vena cava, third-spacing into abdomen, ascites
- Left CHF, more common, fluid overload into lungs, pulmonary edema
- Sets off coping mechanism that makes things worse by retaining H2O and Na
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Dilated cardiomyopathy
- Dilated area in heart, lumen large and muscles thinner. Usually left ventricle to start. Myocardium weak, inadequate contraction, decreased stroke volume
- Acquired common in large and giant breed middle aged dogs (left and right sided dilation, left first most common, can be both)
- Ventricle can't pump properly, backflow into atrium, atrium stretches, can't pump properly, backflow causing CHF
- Was common in cats before taurine
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hypertrophic cardiomyopathy
- Common in cats
- myocardial walls (esp left ventricle) thick and stiff, decreased diastolic filling (DIASTOLIC DYSFUNCTION), increase in atrial backup and pressure lead to LA enlargement/dilation, hydrostatic pressure, pleural effusion and pulmonary edema
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pulmonary edema
fluid in parenchyma of lungs
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pleural effusion
fluid outside lungs, within thorax
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heart murmur
turbulence in blood flow
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Mitral insufficiency
- inadequate closure of mitral (left AV) valve. mostly seen in small, older dogs
- 50% of stroke volume regurgitated into left atrium during systole initially, can go to 75-90%
- Leads to left atrial dilation, decreased stroke volume, decreased CO, increased pressure, pulmonary edema, CHF
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Why do we see problems in left side of heart first?
Pulmonary veins can't take as much fluid overload before symptoms. Abdomen can take fluid before there's a problem.
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Problems with pulmonary edema
fluid in interstitial space increase diffusion distance, so less O2. May be increased CO2 because it is more soluble in water
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Decreased stroke volume causes...
- decreased CO
- CO x PVR = BP, so decreased BP
- reflex tachycardia and renin secretion
- aldosterone secretion retains water and sodium, making problem worse
- Baroreceptor reflex attempts to normalize BP, reflex tachycardia, heart enlarges, lower CO
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Compensatory mechanisms triggered by heart failure
- decreased CO leads to decreased blood flow to myocardium
- reflex tachycardia leads to lower CO (shortens filling time)
- Increased heart rate increases workload, increasing O2 consumption (necrosis/fibrosis/ischemia/attack)
- lowered BP causes increased sympathetic, vasoconstriction to increase BP, increases workload of heart.
- Renin-angiotensin system increases fluid retention, increases preload, increases workload
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Venous return
- quantity of blood flowing from vena cava into right atrium each minute
- Increase of venous return increases ventricular preload
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Ventricular preload
- stretch of the walls of the left ventricle after passive filling and atrial contraction
- Increased preload increases workload
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Myocardial consumption in CcHF
- Myocardium gets inadequate blood flow
- workload increases, O2 consumption increases
- ischemia worsens heart failure
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signs of mild to moderate heart failure
- tachycardia
- dyspnea +/- tachypnea (pulmonary edema, pleural effusion in cats)
- exercise intolerance
- mild-to-moderate ascites
- cough (enlarged heart presses on trachea, rare in cats)
- Dogs can have murmur, only 30% of cats do
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Clinical signs of severe CHF
- respiratory distress, dyspnea
- severe exercise intolerance, collapse
- profound muscle fatigue, no O2
- marked ascites (cats, R side)
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Aims of therapy in CHF
- inhibit compensation of body
- improve contraction of left ventricle
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Positive inotropes
- Cardiac (digitalis) glycosides
- Pimobendan
- Catecholamines (ER only)
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Cardiac (digitalis) glycoside, digoxin
- positive inotrope, increases CO, decreases dyspnea and HR (only one)
- increases contractile force of myocardium
- used in supraventriculartachyarrhythmias and myocardial failure. Not good for HCM, DCM, pericardial disease or tumors.
- Toxicity common, narrow TI
- Signs of toxicity: arrhythmias, electrolyte imbalance, anorexia, vomiting, lethargy, depression
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How Digoxin works
- increases force of contraction without increasing HR
- withdrawal of sympathetic tone decreases HR
- Increases Ca in heart, increases contraction
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Pimobendan (Vetmedin)
- positive inotrope, increase sensitivity of myocardial cells to Ca
- dilates arterioles and veins, decreases afterload, decreases PVR, decreases preload (pooling in veins), heart works less, less back pressure, less third-spacing.
- Only prolonged survival in DCM and mitral insufficiency (indications).
- Entire tablet must be used in one day if split, empty stomach, causes diarrhea.
- Contra in outflow obstruction, causes hypotension.
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catacholamines in CHF
- Crisis treatment, short-term
- dobutamine (increases force of contraction more than HR, drug of choice, indirect B1 increase)
- dopamine (for HF due to anesthetic ER or after cardiac resusitation, after the fact, dose-related modulation)
- Epi, Isoproterenol are arrhythmogenic. Epi for arrest/anaphalaxis, Iso in atropine refractory bradycardia (vagal bradycardia, unresponsive)
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Increase of CO, arterial dilation
- Arterial dilation lowers PVR to increase CO. Aortic pressure decreases, afterload decreases, stroke volume increases, cardiac output increases.
- Causes hypotension.
- Pimobendan (dilates V&A, increases survival)
- Prazosin (a1 block, dilates V&A)
- Hydralazine (dilates A, decreases afterload, inhibits movement of Ca, can't contract)
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venodilators and preload, and drug
- venodilators decrease preload
- dilation of vein increases capacitance, decrease venous return, decreases preload, decreases third spacing.
- Nitroglycerin (dynamite!), topical only.
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Nitroglycerin
- venodilator. CHF treatment in crisis and short-term. Decreases volume ASAP.
- applied topically to hairless skin (ears)
- dose determined by strip
- significant first pass biotransformation, metabolites 10x less potent
- wear gloves, cover site with tape
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Diuretic agents
- increase volume of urine secreted by kidneys (anti-aldosterone)
- Furosemide most common, interferes in loop of Henle, makes hypokalemia.
- spironolactone is an aldosterone receptor antagonist. Keeps potassium (hyperkalemia)
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Furosemide
- lasex. Intereferes with Na transport in loop of Henle. Diuretic. Secretes water, Na and K. Lasts 6 hours, very potent.
- Lowers volume, lowers preload
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Spironolactone
- aldosterone receptor antagonist diuretic, potassium sparing
- Useful in early aldosterone escape
- lowers volume
- lowers preload
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Diuretics and preload
- increase volume of urine excreted
- decrease plasma volume
- decrease venous return
- decrease ventricular preload
- decrease third spacing.
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Vasodilators, what they dilate and effect on heart (preload, afterload) (4)
- Pimobendan, V&A, decreases preload and afterload
- Prazosin, V&A, decreases preload and afterload
- Hydralazine, A only, decreases afterload
- Nitrogylcerine, V only, decreases preload
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Vasodilators and CO
- vasodilators increase CO and decrease preload
- a-adrenergic antagonists (prazosin)
- ACE inhibitors (enalapril, benazepril) balanced venodilators prevent angiotensin II which is an artery and venous constrictor
- Dilate arterioles and veins equally.
- arterial dialation - decreased PVR - decreased afterload - increased CO
- venodilation - decreased venous return - decreased preload - decreased pulmonary edema
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Prazosin
- a-adrenergic receptor antagonist
- vasodilator, increases CO and decreases preload
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enalapril
- Angiotensin Converting Enzyme (ACE) inhibitor, eliminated entirely in kidneys.
- balanced vasodilator (equal a and v)
- dilate arteries, decrease PVR, decrease AFTERLOAD, increase CO
- dilate veins, decrease veinous return, DECREASE PRELOAD, decrease pulmonary edema
- Makes people cough but not animals. Idiopathic
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Benazepril
- Angiotensin Converting Enzyme (ACE) inhibitor, eliminated in kidneys and bile
- balanced vasodilator (equal a and v)
- dilate arteries, decrease PVR, decrease AFTERLOAD, increase CO
- dilate veins, decrease veinous return, DECREASE PRELOAD, decrease pulmonary edema
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ACE Inhibitors in CHF
- Vasodilators of choice in CHF
- inhibit angiotensin converting enzyme (ACE), decreasing angiotensin II, which causes vasoconstriction, water/Na retention, aldosterone release and ADH release
- Improves survival time, but must monitor renal function (perfusion)
- Enalapril, benazepril
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Neural response to decreased stroke volume
- decreased SV = decreased CO = decreased arterial BP
- Reflex decreased parasympathetic and increased sympathetic = increased HR and increased arterial vasoconstriction = increased PVR, = increased AFTERLOAD
- Increases workload of heart, causing heart to enlarge and use more O2 it doesn't have, causing decreased ventricular contractility and more decreased CO
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hormonal response to decreased stroke volume
- decreased SV = decreased CO = decreased BP
- decreased BP in kidney = renin release = angiotensin pathway =
- angiotensin II = vasoconstriction (increased PVR), increased water and Na retention, increased aldosterone and increased ADH, all causing increased plasma volume = increased venous return = increased PRELOAD
- increasing workload of heart = enlargement and hypoxia = decreased ventricular contractility and decreased CO
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ACE inhibitors in DCM
use them early in disease to slow progression and delay heart failure (even asymptomatic)
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Aldosterone escape
- at beginning of administration of ACE inhibitors, aldosterone is released anyway (another mechanism?)
- Spironolactone
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Toxic effects of ACE inhibitors
- few.
- Initial steep decrease in arterial BP
- Potential for renal failure. Drops pressure in glomerular capillaries, decreases GFR, increases BUN and creatinine causing azotemia. Must decrease furosimide first, then ACE.
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Class I heart disease
- No clinical signs except with powerful exercise or severe CV challenges
- do not treat with drugs, just avoid high salt in diet
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Class II heart disease
- Exhibit clinical sings with mild or moderate exercise
- ACE inhibitor (enalapril) and salt restricted diet
- monitor renal function
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Class III heart disease
- Overt signs with mild exercise: cough, dyspnea, orthopnea, exercise intolerance, pulmonary edema, ascites in right sided disease
- Diuretics, ACE inhibitor, digoxin (tachyarrhythmias) or pimobenden, salt and exercise restriction
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Class IV heart disease
- Acute discompensation
- Require aggressive emergency therapy: vasodilators, IV diuretics, oxygen, inotropes. Add ACE inhibitors once stabilized (can't pill a sick dog)
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Propanolol
- non-selective IV B blocker, watch for asthmatics or breathing problems.
- Used in early CHF to decrease HR and renin release, decrease pathological changes in heart, increase contractile force of heart muscle. Seems worse for up to 3 months, but helps.
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Atenolol
- cardio-selective PO B blocker
- Used in cats with HCM or hyperthyroid (T4 causes sympathetic increase) while waiting for methimazole to work.
- Used in early CHF to decrease HR and renin release, decrease pathological changes in heart, increase contractile force of heart muscle. Seems worse for up to 3 months, but helps.
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Carvedilol
- cardio-selective PO B-blocker of choice in early CHF, decreasing ischemia and fibrosis.
- Used in early CHF to decrease HR and renin release, decrease pathological changes in heart, increase contractile force of heart muscle. Seems worse for up to 3 months, but helps.
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B blockers use in CHF
- Useful due to systolic dysfunction. decreased BP causes maximum sympathetic outflow and therefore excessive catecholamine release
- decreases available B1 receptors in heart, decreasing tachycardia/arrhythmias and pathological changes (ischemia, fibrosis, enlarged chambers)
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orthopnea
stretching neck out as far as possible in an effort to get a good breath. Seen in CHF (class III)
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Low dose B blockers effect in CHF
- decrease HR and renin release
- decrease pathological changes to heart (ischemia, fibrosis, enlargement or dilated chambers
- Increases contractile force of heart muscle
- Feel worse for up to 3 months, then better. Only use early in CHF when cardiac function is still okay
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receptor down-regulation
receptor up-regulation
decreasing or increasing the numbers of receptors available
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Effects of decreased diastolic filling
- Blood backs up into left atrium, eventual L atrial enlargement. Blood backs up into pulmonary circulation, increases hydrostatic pressure, pulmonary edema and/or pleural effusion
- decreased SV, decreased CO, insufficient CO to meet needs of body, CHF.
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feline HCM and diuretics
- Diuretics to decrease preload (furosimide)
- decreases plasma volume, decreases VR, decreases pressure in L atrium, decreases hydrostatic pressure in pulmonary capillaries, decreasing pulmonary edema and pleural effusion.
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Pharmacological therapy in feline hypertrophic cardiomyopathy
- Diuretics: decrease preload (Furosimide)
- Calcium channel blockers: vasodilation, neg inotrope and dromotrope (diltiazem)
- Beta Blockers: increases diastolic filling and relaxes heart
- ACE inhibitors: decrease angiotensin II
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Ca Channel blockers
vasodilation, negative dromotrope and inotrope. Does not decrease sympathetic sensitivity, so BP stays the same and HR increases (diltiazem, amlodipine)
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Amlodipine
Calcium channel blocker causing vasodilation. Good for hypertension
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diltiazem
calcium channel blocker used in feline HCM. Vasodilator, relaxes heart, increases HR. BP remains the same.
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Beta blockers in HCM
- used usually in cats with systolic anterior motion of the mitral valve (controversial).
- Decrease ischemic disease
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Clopidogrel bisulfate (Plavix)
- Platelet aggregation inhibitor
- Prevents thrombi in cats, not permanent like aspirin.
- Adverse include vomiting and anorexia, give with food.
- watch for bleeding.
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Low Molecular Weight Heparin
- Prevents thrombosis
- Preferentially inhibits Xa (regular heparin inhibits all).
- Only minimally inhibits thrombin and clotting time, so less risk of hemorrhage
- Must be given SQ (regular IV only)
- Acute emergency, concern of DIC.
- Enoxaparin (Lovenox), dalteparin (Fragmin)
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enoxaparin
- Low Molecular weight heparin
- Prevents thrombosis
- Preferentially inhibits Xa (regular heparin inhibits all).
- Only minimally inhibits thrombin and clotting time, so less risk of hemorrhage
- Must be given SQ (regular IV only)
- Acute emergency, concern of DIC.
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dalteparin
- Low Molecular weight heparin
- Prevents thrombosis
- Preferentially inhibits Xa (regular heparin inhibits all).
- Only minimally inhibits thrombin and clotting time, so less risk of hemorrhage
- Must be given SQ (regular IV only)
- Acute emergency, concern of DIC.
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