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Cardiac physiology: electrical conduction
- – Sino-atrial node - pacemaker
- – Atrio-ventricular node - regulator
- – Bundle of His
- – Purkinje
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Contraction Phisilogy
- - electrical current
- - Ca released to sarcoplasm
- - interacts with troponin
- - actin-myosin coupling
- - contraction
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Action potential
- PHASE 0 - Fast sodium Channel
- PHASE1 - Mild repolarization
- PHASE2 - Slow calcium channel
- PHASE 3 - Repolarization (potassium exits the cell)
- PHASE 4 - Resting (sodium/potassium pump)
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FRANK-STARLING CURVE
- FS Law: Cardiac Output increases with pressure up to a point of congestive heart failure.
- Cardiac output (V pumped by H in 1 min) = Stroke volume (Vblood in one ventricle before systole) * heart rate.
- Systole=Contraction, Diastole=Resting
- Patients with CHF have low cardiac output, b/c heart lost its contractility => FS curve shifts down. When this occurs SV ⇓ and ⇑ preload (LEVP).
- Symptoms associated w/ CHF:
- 1. Edema: ♡ can't pump anymore => fluid is building up in lungs and lower extremities. Use Loop Diuretics, b/c too much fluid.
- 2. Shortness of breath and exercise intolerance.
- Cardiac glycosides shift the curve of the graph up
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Low output failure: treatment
- Congestive Heart Failure
- Treatment
- Diet - weight loss/
- low sodium/fat
- Diuretics: Loop and K+ Sparing
- Cardiac Glycosides
- ACE inhibitors
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CARDIAC GLYCOSIDE PHARMACOLOGY
- 1. Increase Contractility of ♡ (for longer and stronger contaction) (LOW DOSE)(↑ inotropic effect)
- Cardiac Glycosides decrease ability of myocardial cells to pump Ca++ out => Ca++ stays longer in the cell => longer and stronger contraction => ↑ CO
- 2. Decrease AV node conduction (in order to prevent V fib) (HIGH DOSE)
- – Decreased chronotropic effect (↓ heart rate)
- – Used in atrial fibrillation
- AV node prevent conduction of AP from atruim. Person can live with A-fib, but V-fib is fatal. In order to prevent V fib we use Glycosides. Glycosides ↓ AV node conduction => amount of electrical activity going to the ventricles is ↓
- Therapeutic index is narrow: ng/dL
- CHF dose: 1-2 ng/dL
- Afib: 1.5-2.5 ng/dL
- Toxic: >3 ng/dL
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EKG
- p - atrial contraction
- QRS- ventricular contraction
- T - repolarization (phase 3)
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Therapeutic monitoring
- 1. Apical PulseNurse should always measure apical pulse before administering drug. Do not administer drug if apical pulse <60, b/c patient may be toxic.
Cardiac glycosides work on AV node, they prevent conduction from atria. Higher dose => longer P-R interval (time btw atrial and ventricular conduction)=> 10 block has less ♡ beats=>WARNING: b/c patients apical pulse is <60 they could be in 10 block. If ignore warning => 30 block. - In 30 degree block the gate is completely closed, nothing goes through AV node (person is toxic with cardiac glycosides)
 - 2) Serum drug level
- Cardiac glycosides have a narrow therapeutic index. Easy to get toxic: ng/dL
- 3) Serum potassium- caution in hypokalemia
- We need K in phase 3 (repolarization), if person doesn't have enough K, he can't recover from phase 2 => toxic. Diuretics also ↓ K level
- 4) Serum Calcium- caution in hypercalcemiaCa found in phase 2(longer and stronger contraction), to much Ca, person can't get to phase 3.
- If patient doesn't have toxic blood level of cardiac glycosides, hypokalemia or hypercalcemia can make them TOXIC
5) EKG
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PHARMACOKINETICS
- • Five half lives leads to steady state
- • Loading Doses required
- • Toxicities - reversed by digoxin immune
- fab (Digibind®)
- • HALF LIFE
- – DIGOXIN - 24 HOURS
- – DIGITOXIN - 5 days
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BIOAVAILABILITY
• INTRAVENOUS - 100%
• INTRAMUSCULAR - 80%
• TABLET - 70%
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TOXICITIES
A-V BLOCK
SINUS BRADYCARDIA
ARRHYTHMIAS
YELLOW-GREEN HALO VISION
CNS: Headache, weakness, anorexia
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TOXICITY THERAPY
Discontinue Cardiac Glycoside
Digoxin immune fab (Digibind®)
Correct hypokalemia
Antiarrhythmic Agents
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THERAPEUTIC USES
CONGESTIVE HEART FAILURE
ADJUNCT THERAPY FOR ATRIAL FIBRILLATION
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