Anti anginal drugs & heart failure drugs
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Transcript of Anti anginal drugs & heart failure drugs
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Josephus P. Sibal, MD
Anti Anginal Drugs & Heart Failure
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Objectives• Explain the pathophysiology of angina and
congestive heart failure • Discuss the kinetics, pharmacologic
actions, dosage, and interactions of – Anti anginal drugs – Heart failure drugs
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Types of Heart Failure:
Left-sided HF vs Right-sided HF
Systolic HF vs Diastolic HF (Heart failure with low EF vs Heart failure with preserved EF)
Acute HF vs Chronic heart failure
Low-output HF vs High-output HF
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Etiologies of Left-sided and Right-sided Heart Failure
Left-sided Heart Failure Right-sided Failure
LV end diastolic pressure (MI, CAD, dilated cardiomyopathy, valvular heart disease, AI, AS, hypertension) ↑ LA pressure (MS) Fluid overload (renal failure, iatrogenic)
Left-sided heart failure RV systolic overload (cor pulmonale, 1° PHPN, congenital HD with shunt anomaly) ↑ RA pressure (TS, TR)
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Differentiation of Systolic and Diastolic Heart FailureParameters Systolic Diastolic I. History: CAD ++++ + DM +++ + Valvular Heart Dse ++++ - II. Physical Examination: HPN ++ ++++ Jugular distention +++ + Cardiomegaly +++ + Soft Heart Sounds ++++ + S3 Gallop +++ + S4 Gallop + +++ Edema +++ +
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Differentiation of Systolic and Diastolic Heart FailureParameters Systolic Diastolic III. Chest X-ray: Cardiomegaly +++ + Pulm. Congestion +++ +++ IV. ECG: LVH ++ ++++ Q Waves ++ + V. Echocardiogram: Low ejection fraction ++++ - LV Dilatation ++ - LVH ++ ++++
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Pump failure = low CO
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CO = SV x HR
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Stroke Volume Preload Contractility Afterload
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Preload
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Afterload
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BP = SV x TPR
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Contractility Preload Afterload
Heart Rate Stroke Volume
Cardiac Output Total Peripheral Resistance
Blood Pressure
+ +
x
x
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Compensatory Mechanisms
•Cardiac •Neurohumoral
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Boyle’s Law
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Frank Starling
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LAPLACE LAWPressure x Radius 2 (Wall Thickness)Wall Stress =
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Model of Wall Stress
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SV
Ventricular end-diastolic volume
Ventricular massLaPlace
Frank-Starling
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Decreased BP
Sympa NS R-A system ADH
Contractility HR Vasoconstriction Circulating vol
Arteriolar Venous
Maintain BP
C.O.
S.V.
Venous return to heart ( preload)
(+)(+)
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Heart Failure
Failure of compensatory mechanisms
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Car
diac
Out
put
Left Ventricular End-Diastolic Volume!27
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Left
Vent
ricul
ar E
nd-D
iast
olic
Pre
ssur
e
Left Ventricular End-Diastolic Volume
hype
rtrop
hy
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SV
Ventricular end-diastolic
volume
Ventricular mass
La Place
Frank-Starlin
g
CHFAtrial Pressur
e
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Decreased BP
Sympa NS R-A system ADH
Contractility HR Vasoconstriction Circulating vol
Arteriolar Venous
Maintain BP
C.O.
S.V.
Venous return to heart ( preload)
(+)(+)
(-) Pulmonary congestion
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NYHA Classification of CHF:Functional
ClassDescription General Guide
I Dyspnea occurs with greater than ordinary physical activity.
Climbs ≥ 2 flights of stairs with ease
II Dyspnea occurs with ordinary physical activity.
Can climb 2 flights of stairs but with difficulty
III Dyspnea occurs with less than ordinary physical activity.
Can climb ≤ 1 flight of stairs
IV Dyspnea may be present even at rest.
Dyspnea at rest
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Signs and symptoms of Left-sided and Right-sided Heart Failure:
Symptoms of Left HF: Easy fatigability Exertional dyspnea Confusion Orthopnea PND Cough Signs of Left HF: Tachypnea Tachycardia Rales S3/4 Gallop Wheezes
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Signs and symptoms of Left-sided and Right-sided Heart Failure:
Symptoms of Right HF: Easy fatigability Early satiety RUQ discomfort Signs of Right HF: Elevated JVP Hepatomegaly Ascites Lower extremity edema
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Diagnostic Tests:
1. Chest X-ray 2. ECG 3. 2-D Echo
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What to do?
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Cardiac Drugs for HF, Classified According to Hemodynamic I Effects.
Mainly Preload Unloaders
(Venous Dilators)
Contractility Mainly Afterload Unloaders
(Arterial Dilators)
Diuretics Nitrates
Digoxin
Dobutamine
Dopamine
Ace-inhibitors Angiotensin-II Antagonists Hydralazine
Nitroprusside
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Congestive Heart Failure
Compensatory Responses
↑ Systemic vascular resistance (afterload) ↑ Blood volume (preload)
↓ Cardiac output ↑ LV end diastolic pressure
↑ Renin-angiotensin aldosterone system ↑ Sympathetic tone
↑ ADH release
• Vasodilators • Afterload unloader • Preload unloader
• Inotropic agents
• ACE inhibitors • ß blockers • Diuretics
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2. Treat all precipitating causes of CHF. Cardiac causes: • Non-compliance with medicines • Arrhythmia • Ischemia or infarction • Uncontrolled hypertension • RHD, myocarditis, valvular dse, MR • Endocarditis Non-cardiac causes: • Renal Failure (fluid overload) • Anemia • Pulmonary embolism • Infection • Delivery after pregnancy • Lifestyle
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3. Assess which of the following contributes to a decrease in cardiac output and must be corrected:
a. Increase in afterload b. Increase in preload c. Decrease in contractility d. Increase in heart rate
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4. If poor response to medical treatment:
a. Maximize medical treatment.
b. Consider a surgical option
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Diseases causing High Output HF:
• Anemia • Febrile disorders • Pregnancy • Beri-beri • Renal shunts • Arteriovenous fistulas • Thyrotoxicosis
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Usual Progression of Symptoms in Left-sided HF
• Dyspnea upon exertion • PND – Cardiac type: occurs 2-4 hrs after sleep – Pulmonary type: variable onset
• Orthopnea – Cardiac type: occurs after 5 mins – Pulmonary type: immediate onset
• Dyspnea at rest • Lower extremity edema
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Clinical Manifestations Based on Severity of Heart Failure:
• Early CHF (NYHA Class I): – May be asymptomatic
• Mild to Moderate CHF (NYHA Class II-III): – Mild, non-specific symptoms – PE may be normal
• Severe CHF (NYHA Class IV): – Signs and symptoms are obvious – Patients in marked distress: (orthopneic with distended
neck veins)
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Usual Cause of Death in Patients with CHF:
• Fatal ventricular arrhythmia (sudden cardiac death)
• Refractory heart failure
• Pulmonary embolism
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Precipitating Causes of Acute HF
Cardiac causes: • Non-compliance with medicines • Arrhythmia • Ischemia or infarction (superimposed) • Uncontrolled hypertension • RHD, myocarditis, valvular dse, MR • Endocarditis
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Treatment Options in Acute HF:
• Removal of precipitating cause • Morphine sulphate IV • Oxygen • Potent diuretics IV • Rapid digitalization • Rapid preload and afterload reduction • Intravenous titratable inotropic therapy • Rotating tourniquets • Intra-aortic counterpulsation • Cardiac surgery
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Precipitating Causes of Acute HF
Non-cardiac causes: • Renal Failure (fluid overload) • Anemia • Pulmonary embolism • Infection • Delivery after pregnancy • Lifestyle (stress)
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Basic Pharmacology of Drugs used in Heart Failure
• Digitalis – Purple foxglove (Digitalis purpurea) – Digoxin is the prototype – 65-80% absorbed after oral administration –Widely distributed in tissues – 2/3 is excreted unexchanged in the kidneys – Half life is 36-40 hours
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Digitalis• Inhibits Na+, K+, ATPase pump, or the
sodium pump • Increases contraction of the sarcomere by
increasing free calcium concentration • Done by: increase of intracellular sodium
via Na+, K+, ATPase inhibition, second, relative reduction in calcium expulsion
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Digitalis• Net effect is a distinctive increase in
cardiac contractility • Useful in dilated cardiomyopathy • Given at a slow loading dose of 0.125
-0.25 mg per day or rapid loading of 0.5 mg-0.75 mg q 8 hours for three doses
• Digoxin has no net effect on mortality but reduces hospitalization
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Effects of Digoxin of other Cardiac Tissues
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Effects in other organs• Since cardiac glycosides affect all
excitable tissues, smooth muscle and CNS effects are notable. – Nausea, vomiting, diarrhea, anorexia – Disorientation, hallucinations, visual
disturbances
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Interactions with K+, Ca++, Mg++
• Potassium and digitalis inhibit each other’s binding to Na+, K+, ATPase; therefore hyperkalemia reduces the enzyme binding of cardiac glycosides, where are hypokalemia reduces its actions.
• Hyperkalemia can precipitate bradycardia and hypokalemia can limit the effects of digitalis
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Interactions with K+, Ca++, Mg++
• Ca facilitates the effects of digitalis by overloading of intracellular calcium stores.
• Digitalis-induced abnormal automaticity
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Positive Inotropics• Bipyridines –Milrinone is a phosphodiestarase isoenzyme 3
inhibitor (PDE 3 inhibitor) – Increase myocardial contractility by increasing
calcium influx in the cardiac muscle during the action potential.
– Compared to inamrinone, milrinone is less likely to cause arrhythmias and can be used in acute heart failure or severe exacerbation of chronic heart failure.
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Positive Inotropics• Beta adrenoceptor stimulants – Dobutamine – Selective B1 agonist – Increases cardiac output by decreasing
ventricular filling pressure – Produce angina or arrhythmia – Given in mcg/kg BW –Maximum dose is 20 mcg/kg BW
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Positive Inotropics• Dopamine –May also be used in acute heart failure where
there is a need to increase the BP – It stimulates dopaminergic, beta, alpha effects
at different doses – Given in mcg/kg BW, max 20 mcg/Kg BW
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Drugs Without Positive Inotropic Effects
• Diuretics • ACE inhibitors • ARBs • Aldosterone antagonist • Beta blockers • Vasodilators
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Diuretics• Prototype: Furosemide • Mainstay of heart failure • No direct effect on cardiac contractility • Major action is to reduce venous pressure
and ventricular preload • Reduction in salt and water retention • Concomitant hypokalemia may develop • Usual dose: 40 mg IV or PO dose,
increased until signs of heart failure improve
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Diuretics• Thiazide type diuretics – Hydrochlorothiazide –May result to hyponatremia secondary to
potassium excretion – Usual dose 12.5 mg to 25 mg OD, in
combination with ARBs or ACEi • K+ sparing diuretics – Spironolactone or eplerenone – Aldosterone antagonist – Usual dose: 25-50 mg OD PO
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ACE Inhibitors• Blockade of RAAs • Given to patients with LV dysfunction • Reduction of preload (reduce salt & water
retention) and afterload (reduce peripheral resistance)
• Slow the progression of ventricular dilatation • Decrease long term remodeling of the heart
and vessels
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ACE Inhibitors• Prototype: captopril • Most commonly used: enalapril • Patient may benefit from asymptomatic to
severe heart failure • Usual dose: captopril 25 mg q 6, enalapril
10 mg OD,
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Angiotensin Receptor Blockers• Produce similar benefits as ACEi • Given to patients who are incessant to
cough. • Prototype: losartan • Usual dose: losartan 50 mg OD, eposartan
600 mg OD, candesartan 8 mg OD, irbesartan 150 mg OD, telmisartan 40 mg OD, olmesartan 20 mg OD
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Vasodilators• Nesiritide • Endogenous peptide (brain natriuretic
peptide) or BNP • Increases cGMP in smooth muscle cells
and reduces venous & arteriolar tone • Causes diuresis • Preload reducing agent
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Beta Blockers• Bisoprolol, carvedilol & metoprolol • Attenuate the high concentrations of
circulating cathecolamines • Decreasing heart rate, decrease
remodeling by reduction of the mitogenic activity of cathecolamines
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Antianginal drugs
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Pathophysiology of Angina
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Determinants of Coronary Blood Flow & Myocardial Oxygen Supply
• Coronary blood flow is directly related to: – perfusion pressure (aortic diastolic pressure) – Duration of diastole (vs tachycardia)
• Coronary blood flow is inversely proportional to the coronary vascular bed resistance
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Determinants of Vascular Tone• Increasing cGMP (dephosphorylation of
myosin light chains) – Nitric oxide
• Decreasing intracellular Ca2+ (calcium channel blockers which cause vasodilatation, decrease heart rate)
• Stabilizing or preventing depolarization of vascular smooth muscle cell membrane (increase the permeability of K+ channels
• Increasing cAMP (inactivation of myosin light chain kinase which causes vasodilatation) this mechanism is caused by beta blockers.
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• Vasodilate • Reduce rate
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Nitrates & Nitrites• Nitroglycerin – Prototype – Causes activation of guanylyl cyclase and an
increase in cGMP, the first step in smooth muscle relaxation
– Oral bioavailability is low – Sublingual dose eliminated first pass effect
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Nitrates• No effect on skeletal muscles • Direct effect of NTG is increased venous
capacitance and decreased ventricular preload
• Decreases platelet aggregation • Oral controlled release tablets, sublingual
tablets, buccal spray, transdermal patch & IV • Must NOT be taken with ED meds
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Nitrates• IV may be started at 0.5 mg/hr up to 5 mg/
hr • Oral preparations can be given 30 mg to
60 mg OD
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Calcium Channel Blockers• L-type calcium channel blocker • Dihydropyridines vs non dihydrophyridines • Reduces the frequency of opening in
smooth muscle content this gives decreased transmembrane content
• Decreased heart rate via dec sinus node pacemaker rate
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Calcium Channel Blockers• Tachyarrhythmias – Diltiazem & verapamil
HPN Amlodipine & nifedipine
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Beta blockers• Effects are due to dec HR, dec BP, dec
contractility • Effect would be decreased oxygen
demand at rest and exercise • Longer diastolic perfusion time
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Beta blockers• Contraindicated with: – Asthma – Severe bradycardia, AV dysfunction – Severe LV dysfunction – CHF NYHA IV
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Partial Fatty acid Oxidation (pFOX)
• Trimetazidine • metabolic mediators, inhibit the fatty
oxidation pathway in the myocardium
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Ivabradine• Activation of the If channel or the funny
bone channel • Decreases the heart rate without the effect
of hypotension
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Other Drugs• Sulfonylureas • thiazolidinediones
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