CHF

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Author:
XQWCat
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246950
Filename:
CHF
Updated:
2013-11-30 23:31:08
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Pharm Tox
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Congestive Heart Failure in Pharm and Tox
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  1. 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
  2. cardiac function
    • four chambered pump (2 pumps)
    • Responsible for moving blood through vascular system.
    • Composed of myocardium, VERY strong, thick muscle
  3. 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
  4. diastole
    chamber filling
  5. systole
    chamber contraction
  6. stroke volume
    quantity of blood pumped by left ventricle into the aorta with each ventricular contraction
  7. Cardiac output
    • quantity of blood pumped by the left ventricle into the aorta each minute
    • stroke volume x heart rate
  8. ventricular preload
    • stretch of the walls of the left ventricle after passive filling and atrial contraction
    • Measured by left ventricular end diastolic volume (LVEDV)
  9. Left ventricular end diastolic volume
    volume of blood in the left ventricle at the end of diastole
  10. left ventricular end diastolic pressure
    pressure exerted on walls of left ventricle at the end of diastole
  11. 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
  12. Afterload
    resistance against which the left ventricle must eject its volume of blood during contraction (determined by aortic pressure, determined by PVR)
  13. 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
  14. 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
  15. 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
  16. pulmonary edema
    fluid in parenchyma of lungs
  17. pleural effusion
    fluid outside lungs, within thorax
  18. heart murmur
    turbulence in blood flow
  19. 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
  20. 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.
  21. 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
  22. 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
  23. 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
  24. Venous return
    • quantity of blood flowing from vena cava into right atrium each minute
    • Increase of venous return increases ventricular preload
  25. Ventricular preload
    • stretch of the walls of the left ventricle after passive filling and atrial contraction
    • Increased preload increases workload
  26. Myocardial consumption in CcHF
    • Myocardium gets inadequate blood flow
    • workload increases, O2 consumption increases
    • ischemia worsens heart failure
  27. 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
  28. Clinical signs of severe CHF
    • respiratory distress, dyspnea
    • severe exercise intolerance, collapse
    • profound muscle fatigue, no O2
    • marked ascites (cats, R side)
  29. Aims of therapy in CHF
    • inhibit compensation of body
    • improve contraction of left ventricle
  30. Positive inotropes
    • Cardiac (digitalis) glycosides
    • Pimobendan
    • Catecholamines (ER only)
  31. 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
  32. How Digoxin works
    • increases force of contraction without increasing HR
    • withdrawal of sympathetic tone decreases HR
    • Increases Ca in heart, increases contraction
  33. 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.
  34. 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)
  35. 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)
  36. 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.
  37. 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
  38. 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)
  39. 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
  40. Spironolactone
    • aldosterone receptor antagonist diuretic, potassium sparing
    • Useful in early aldosterone escape
    • lowers volume
    • lowers preload
  41. Diuretics and preload
    • increase volume of urine excreted
    • decrease plasma volume
    • decrease venous return
    • decrease ventricular preload
    • decrease third spacing.
  42. 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
  43. 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
  44. Prazosin
    • a-adrenergic receptor antagonist
    • vasodilator, increases CO and decreases preload
  45. 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
  46. 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
  47. 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
  48. 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
  49. 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
  50. ACE inhibitors in DCM
    use them early in disease to slow progression and delay heart failure (even asymptomatic)
  51. Aldosterone escape
    • at beginning of administration of ACE inhibitors, aldosterone is released anyway (another mechanism?)
    • Spironolactone
  52. 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.
  53. 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
  54. Class II heart disease
    • Exhibit clinical sings with mild or moderate exercise
    • ACE inhibitor (enalapril) and salt restricted diet
    • monitor renal function
  55. 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
  56. 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)
  57. 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.
  58. 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.
  59. 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.
  60. 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)
  61. orthopnea
    stretching neck out as far as possible in an effort to get a good breath.  Seen in CHF (class III)
  62. 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
  63. receptor down-regulation
    receptor up-regulation
    decreasing or increasing the numbers of receptors available
  64. 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.
  65. 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.
  66. 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
  67. Ca Channel blockers
    vasodilation, negative dromotrope and inotrope. Does not decrease sympathetic sensitivity, so BP stays the same and HR increases (diltiazem, amlodipine)
  68. Amlodipine
    Calcium channel blocker causing vasodilation.  Good for hypertension
  69. diltiazem
    calcium channel blocker used in feline HCM.  Vasodilator, relaxes heart, increases HR.  BP remains the same.
  70. Beta blockers in HCM
    • used usually in cats with systolic anterior motion of the mitral valve (controversial).  
    • Decrease ischemic disease
  71. 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.
  72. 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)
  73. 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.
  74. 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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