Cardio Flashcards
Mechanisms of Arrhythmias
- Abnormal automaticity
- Triggered acitivity (EADs, DADs)
- Re-entry
Abnormal automaticity
non-pacemaker cells take on pacemaker AP and fire faster than SA node
Early Afterdepolarizations (EADs)
Prolonged AP
Slow HR
Delayed afterdepolarizations (DADs)
Ca overload
Re-entry
Impulse persists to reactivate the myocardium instead of dying out
Classes of anti-arrhythmics
Class 1: Na channel blockers
Class 2: B-blockers
Class 3: K channel blockers
Class 4: Ca channel blockers
Class 1 Anti-arrhythmics
Block fast Na channels
Class 1a anti-arrhythmics
quinidine
procainamide
Class 1b anti-arrhythmics
lidocaine
mexiletine
Class 2 anti-arrhythmics
Propanolol
Atenolol
esmolol
(block b-receptors)
How to class 2 anti-arrhythmics work?
Decrease HR and contractility
Why must class 2 anti-arrhythmics be titrated?
Up regulate B receptors
Propanolol
Non-selective B blocker
Atenolol
B1 cardioselective
Esmolol
B1 cardioselective
Class 3 anti-arrhythmics
K channel blockers
Sotalol, amiodarone
Sotalol
non selective
Amiodarone
Class 1, 2, 3, 4, and a1 blocker
Long half life
Limited use
Side effects (turns people BLUE)
Class 4 anti-arrhythmics
Ca channel blockers
Diltiazem, Amlodipine
Furosemide
Loop diuretic
CHF and pulmonary edema
Always use with ACE inhibitor
Loop diuretics
Furosemide
Torsemide
Hydrochlorothiazide
Thiazide diuretic
Distal convoluted tubule
Sprionolactone
K-sparing
Distal tubule and collecting duct
Arteriodilators
Relax smooth muscle of arterioles
Reduce AFTERLOAD
Venodilators
Relax vein smooth muscle
Reduce PRELOAD
Balanced or mixed vasodilators
act at both arteries and veins
Nitrates
Venodilators
NO formation and reduction of Ca
Nitrogylcerin
Nitroprusside
Sodium nitroprusside
Balanced vasodilator (both arteries and veins)
Side effects of nitrates
Hypotension
Rebound hypertension
Cyanide poisoning
Arteriodilator drugs
Nitroprusside
Amlodipine
Hydralazine
Hydralazine
decreases cGMP
Sildenafil
treats pulmonary hypertension
ACE inhibitors
Enalapril
Benazepril
Given to patients with CHF to blunt effects of RAAS
Mechanism of positive inotropic drugs
Increase amount of Ca available to increase contractility
“Cost” of positive inotropes
Myocardial ischemia and monocyte death (due to increase oxygen consumption)
Classes of inotropes
- Cardiac glycosides
- B adrenergic agonists (synthetic catecholamines)
- phosphodiesterase inhibitors
- calcium sensitizing agents
Cardiac glycosides
Plant extracts (purple foxglove) Digoxin
How do cardiac glycosides work?
Inhibit Na/K ATPase pump -> increase intracellular Na
Na exchanges for Ca
When are cardiac glycosides used?
Systolic myocardial failure
Atrial fibrillation
Synthetic catecholamines are used for ____ inotropic support
Acute (half life is minutes)
Examples of synthetic catecholamines (b1 agonists)
Dopamine
Dobutamine
Dopamine
Act on alpha, b1, and dopaminergic receptors
(Low doses: vasodilation, DA receptors
Higher doses: positive inotropy, B1
Very high doses: vasoconstriction, a)
Dobutamine
B1 effects
Mechanism of Phosphodiesterase inhibitors
inhibit breakdown of cAMP
Examples of phosphodiesterase inhibitors
Amrinone
Milronone
Mechanism of Calcium sensitizing agents
Increases AFFINITY of troponin C for calcium during systole and diastole
Enhances contractility without increasing O2 consumption
Examples of calcium sensitizing agents
Pimobendan
Levosimendan
Pimobendan
“Inodilator”: positive inotrope AND systemic pulmonary vasodilator
Beta receptors found in cardiac muscle
B1
Beta receptors found in bronchial and vascular smooth muscle
B2
Effects of beta blockade
Decrease HR (decrease SA node firing)
Improved myocardial perfusion
Slows AV nodal conduction
Decrease myocardial contractility (less O2 consumption)
Use of beta blockers
anti-arrhythmics
HCM
CHF
First generation beta blockers
Propanolol
Sotalol
(nonselectively inhibit both B receptors)
Second generation beta blockers
Atenolol
esmolol
(b1 receptors only)
Third generation beta blockers
additional vasodilatory properties
B2 stimulatory properties
added alpha blockade