A Professional & Personal Networking Site for all People related to Cardiology

Cardiovascular Physiology/Pharmacology

1. Heart Muscle Mechanics - 3 concepts

A. TENSION (force) - Elements contributing:

1) Contractile element => Active tension

2) Elastic element (functional, not anatomic) => Resting tension

B. LENGTH of muscle fibers influences Tension

1) Starling's relationship (Tension (active & resting) vs Length)

2) Performance-wise this is PRELOAD effect

C. VELOCITY is influenced by Length and Tension

1) Calcium activation

2) Total calcium released

3) Sarcomere length alters calcium sensitivity

2. Cardiac Performance Cardiac output = HR x Stroke volume

A. Stroke Volume affected by

1) Preload

2) After load

3) Contractility

B. Law of La Place relates ventricular pressure and wall tension

1) T = Pr

2) 2h

3. The cardiac cycle

A. Isovolumetric ventricular contraction

B. Rapid ejection phase

1) Reduced ejection phase

C. Isovolumetric relaxation

D. Rapid filling phase

1) Slow filling period

2) (Atrial contribution (20-30% in failing heart))

4. Preload

A. Normal heart - increased venous return results in increased cardiac output

B. Failing heart - sarcomere length is already maximal; cardiac output increase requires increased contractility or heart rate

C. After load

D. Definition

E. Increased after load - increase in LVEDV and radius (=preload)

F. Anrep effect or homeometric autoregulation

G. Contractility - inotropic state of muscle

5. Indicators of Cardiac performance

A. Cardiac index = cardiac output/body surface area

B. LVEDP (or approximation)

1) mean left atrial pressure

2) mean pulmonary wedge pressure

3) pulmonary artery diastolic pressure

C. CI and LVEDP together are better indicators of contractility than either alone

D. Ejection fraction = stroke volume/end-diastolic volume

E. Fractional shortening - calculated from the diameter perpendicular to the midpoint of LV long axis

6. Coronary flow & myocardial O2 consumption

A. Very efficient oxygen extraction (70% oxygen utilization coefficient)

B. Coronary hemodynamics - Q = P/R

C. Viscous resistance

D. Autoregulatory resistance

E. Compressive resistance

F. Transmural gradient in myocardium - DPTI x HR = driving pressure

G. Myocardial oxygen consumption

H. Pressure work, contractility, heart rate, basal cell metabolism, electrical activation

CARDIOVASCULAR PHARMACOLOGY

7. Inotropes

A. Digitalis

1) Inhibit Na-K-ATPase - positive inotropic effect

2) Parasympathomimetic and anti-adrenergic mechanisms

3) Drug interaction - Quinidine, Verapamil, Amiodarone

4) Conditions that increase sensitivity

8. Inotropes, Vasoconstricting

A. Dopamine

1) Low doses - D1 receptors in renal vasculature

2) Increasing doses - b-1 receptors activated

3) High doses - a-adrenergic receptor activation

B. Epinephrine

1) Potent b and a effects

C. Norepinephrine

1) Potent alpha effects

9. Inotropes, Vasodilating

A. Dobutamine

1) Beta > alpha effect

2) Reduces LV filling pressures

3) Decreases afterload

B. Milrinone, Amrinone

1) Phosphodiesterase inhibitors

C. Isoproterenol

1) Inotropic (beta), chronotropic effects

10. Vasodilators & Vasoconstrictors

A. Vasodilators

B. Nitroprusside

1) Generalized vasodilatation

2) "Steal phenomena"

3) Indications - hypertension, acute heart failure

4) (thiocyanate toxicity - rare; with renal failure)

C. Nitroglycerine

1) General vasodilatation

2) Low doses - venous; high doses - arterial

3) Preload reduction and coronary vasodilation

4) Useful in management of ischemia

5) Decrease LVEDP and pulmonary vascular congestion

D. NO and Isoproterenol - pulmonary effects

E. Vasoconstrictors

F. Neosynephrine (pure alpha)

11. Calcium Antagonists

A. Mechanisms

B. Interference of Ca2+ - mediated smooth muscle contraction - coronary and peripheral smooth muscle relaxation

C. Selective Ca2+ channel inhibition

1) Treatment of angina pectoris / supraventricular tachycardia / hypertension

D. Agents

1) Verapamil

2) Nifedipine

3) Diltiazem

12. ACE Inhibitors

A. Mechanisms

1) Prevent conversion of Angiotensin I to Angiotensin II - vasodilation

2) Decreased Aldosterone secretion

3) Indication - hypertension, heart failure, prophylactically after MI

B. Agents

1) Captopril

2) Low cardiac output states - improvement in renal blood flow

3) Angioedema/cough/neutropenia/nephrotic syndrome

4) Increase in creatinine - RAS

C. Enalapril

1) Enalaprilat (liver) - delay - long duration

2) Less side-effects

13. Beta Blockers

A. Mechanisms

1) b-1 and b-2; cardioselectivity

B. Indications

1) Hypertension, angina pectoris, arrhythmias, prophylactically after MI

C. Adverse effects

1) Bronchospasm, Inhibition of myocardial contractility

D. Drug interactions

1) Lidocaine/Verapamil/Cimetidine/Diltiazem

E. Agents

1) Propanolol, metropolol, atenolol

2) Esmolol - very short half-life

14. Anti-arrhythmic Drugs and Their Actions Class Action Agents

Class	Action	Agents
IA	Inhibit Na+ transport	Quinidine
	Reduced dV/dT of action potential	Procainamide
IB	Slow dV/dT of phase 0	Disoprymadine
	Moderate prolongation of repolarization	Lidocaine
	Prolongs PR, QRS, and QT intervals	Phenytoin
	Limited effect on dV/dT of phase O	Mexiletine
	Shortens repolarization	Tocainide
	Shortens QT in clinical doses
	Elevates fibrillation threshold

15. Anti-arrhythmic Drugs and Their Actions

Class	Action	Agents
IC	Markedly slows dV/dT	Flecainide
	Little effect on repolarization	Ecainide
	Markedly prolongs PR and QRS
II	Beta-adrenergic blockers	Metoprolol
	Decrease nodal conduction	Atenolol
		Propanolol
III	Prolongs repolarization	Amiodarone
	Alters membrane response	Bretylium
IV	Calcium channel blockers	Verapamil
	Decrease nodal conduction	Nifedipine
		Diltiazem