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61 Cards in this Set
- Front
- Back
Positive SA node influence
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B-adrenergic
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Negative SA node influence
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Vagal
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His-Perkinje influence
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B-adrenergic causes increased automaticity
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3 things to slow pace of the heart?
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1. MDP more negative
2. Phase 4 depol. slower 3. Threshold more positive |
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EAD
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Early After Depolarization
-spon. depol. during phase 3 (muscle stretching, hypoxia) |
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DAD
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Delayed After Depolarization
-spon. depol. during phase 4 (B-adr, card. gly., extracellular ca) |
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1st degree AV block
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long PR interval, benign
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2nd degree AV block
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occasional missed beat
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Mobitz I AV block
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heart misses QRS-ventricular beat
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Mobitz II AV block
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QRS missed-at bundle of His
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3rd degree AV block
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atrial beats do not go through AV node, waves independent of each other
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Atrial flutter
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250-350 bpm, very rapid
**TX=propranolol, verapamil |
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Atrial fibrillation
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fibers stim too rapidly--no contraction
**TX=propranolol, anticoagulant |
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Supraventricular arrhythmia
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rapid premature contractions
TX: propranolol, verapamil ACUTE TX: adenosine |
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Ventricular tachycardia
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180 bpm, dangerous, may lead to ventricular fib.
TX: lidocaine |
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Ventricular fibrillation
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no effective pumping, extremely dangerous, requires defibrillation
TX: epinephrine |
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Automaticity
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cells spontaneously reach threshold and fire action potentials (SA node=normal)
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Excitability
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tendency to fire at a given stimulus
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Autonomic effects
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w/ drugs: change heart rate, stroke volume and total peripheral resistance
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Treatment goals of anti-arrhythmia drugs (1)
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1. Suppress abnormal automaticity (reduce ectopic pacemaking)
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Treatment goals of anti-arrhythmia drugs (2)
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2. Correct abnormal impulse conduction (prevent reentry of impulses)
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Type I drugs
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Block sodium channels
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Type II drugs
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Block sympathetic effects
(Beta blockers) |
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Type III drugs
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Prolong refractory period
(Potassium channel blockers) |
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Type IV drugs
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Block calcium channels
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Sodium channel blocker actions
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1. reduce automaticity
2. reduce excitability 3. reduce reentry |
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Beta blocker actions
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1. reduce automaticity
2. reduce excitability 3. reduce contractility 4. reduce reentry |
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IA Key
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inhibit sodium channels in active or damaged tissue
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IB Key
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have greater effects on damaged myocardium
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IC Key
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very slow off rates
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II Key
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block sympathetic effects through inhibition of b-ad receptors
***dizziness, ED |
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Potassium channel blockers
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1. increases refractory period
2. little or no effect on automaticity or excitability |
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III Key
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prevent repolarization of channels
***can induce arrhythmias |
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Calcium channel blockers
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1. reduce automaticity
2. minimal effects on excitability |
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IV Key
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targets SA and AV nodal pacemaking cells
***reflex tachycardia |
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Adenosine treatment
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PSVT, WPW syndrome
*causes no beat for a few seconds |
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CAST trial
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BAD: encainide, flecainide, moricizine
GOOD: beta blockers |
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CHF
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^ heart rate & O2 consumption
\/ stroke volume heart swells, fluid accumulation |
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Digoxin MOA
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^ intracellular Ca and contraction
**low K, high dig binding TARGET=sod/pot pump |
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Control HR-sympathetic
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cardiac B1-increases cAMP
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Control HR-parasympathetic
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cardiac M2-decreases cAMP
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RX for CHF
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inotropic agents w/ vasodilator w/ diuretic
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Angina
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chest pain caused by coronary blood flow that is inadequate to meet the O2 demands of the myocardium
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Angina RX goals
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improve heart blood flow and reduce myocardial O2 requirement
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RX classes for angina
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K channel openers
nitrates ca channel blockers ACE inhibitors beta blockers |
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potassium channel openers
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diminished contraction, vasodilate
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Nitric oxide
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crucial mediator of VSMC tone
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nitrates
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(generation of cGMP) relax arterial and venous smooth muscle
**can develop tolerance |
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calcium channel blockers-angina
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vasodilate-reduce afterload
**SE's: hypotension |
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ACE-I
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lower blood pressure
**SE's: cough (bradykinins in lungs), hypotension |
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ang II receptor blockers
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lowers blood pressure
** hypotension but no cough |
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beta blockers-angina
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takes work off heart by b1 and ang-ren system, decreases O2 req of heart
***do not use in diabetes, COPD |
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Hypertension def
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DBP is above 90 mmHg
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primary (essential) hypertension
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95% of cases
**worsened by obesity, smoking, and not enough exercise |
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secondary htn
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5% of cases
**OCP's, pregnancy, renal disease |
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complications of htn
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CHF, renal failure, stroke
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non-RX TX of htn
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lose weight, reduce salt, reduce alcohol, stop smoking, do exercise
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1st 3 RX's for HTN
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ACE, ARB, aldosterone antagonists
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2nd 3 RX's for HTN
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diuretics, ganglionic blockers, beta blockers
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3rd 4 Rx's for HTN
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alpha blockers, vasodilators, alpha 2 agonists in CNS, noradrenergic neuron blockers
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ganglionic blockers
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blocks autonomic system through nicotinic receptor
**used in emergency |