Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
59 Cards in this Set
- Front
- Back
|
Ventricular Dysfunction:
Systolic Dysfunction |
EF < 40%
CAD - Coronary Artery Disease - ischemic cardiomyopathy Nonischemic Cardiomyopathy - HTN -Valvular disease -Alcohol -Thyroid disease -Cardiotoxic drugs |
|
|
Ventricular Dysfunction:
Diastolic Dysfunction |
Impaired filling
Cardiomyopathies Elderly hypertensive women |
|
|
Major Manifestations of Heart Failure
|
Dyspnea on exertion
Orthopnea Paroxysmal nocturnal dyspnea Fatigue Fluid retention |
|
|
NYHA Classification: Class I
|
Class I:
No symptoms with ordinary activity |
|
|
NYHA Classification: Class II
|
Class II
Symptoms with ordinary activity; slight limitation |
|
|
NYHA Classification: Class III
|
Class III
Symptoms with LESS THAN ordinary activity; marked limitation |
|
|
NYHA Classification: Class IV
|
Class IV
Symptoms with any activity; also AT REST |
|
|
Physiologic goals of drug therapy:
Reduce Preload |
Reduce Preload
*Diuretics *Aldosterone antagonists *Venodilators |
|
|
Physiologic goals of drug therapy:
Reduce Afterload |
Reduce Afterload
*ACEIs *B-Blockers *Vasodilators |
|
|
Physiologic goals of drug therapy:
Increase Inotropy |
Increase Inotropy (contractility of myotrophy)
*Cardiac glycosides *Sympathomimetic amines *Phosphodiesterase inhibitors |
|
|
Clinical Management: Chronic CAD
|
Chronic CAD Management:
*B-Blockers *CCBs *Nitrates *Aspirin *Lipid-lowering agents |
|
|
Clinical Management: Unstable Angina, NSTEMI
|
Unstable Angina, NSTEMI Management
*Antianginal drugs *Heparin, ASA *GPIIb/IIIa antagonists *Thienopyridines (Antiplatelets) |
|
|
Clinical Management: STEMI
|
STEMI Management:
*Thrombolytics |
|
|
Stable Angina
|
A: ASA, antianginals
B: blood pressure, B-Blockers C: cholesterol, cigarettes D: diet, diabetes E: education, exercise |
|
|
Post-MI Management
|
ASA or clopidogrel if CI to ASA
B-blocker *Lipid-lowering agent (LDL<100) *ACEI if HF, LVEF<40%, HTN, DM, CKD *Aldosterone antagonist if LVEF <40% *Specific antiplatelet and anticoagulation recommendations for patients who undergo PCI |
|
|
Cardiac Conduction
|
Cardiac cell is polarized (negatively charged) compared to the outside.
|
|
|
Cardiac Conduction: Action Potential
|
Action Potential:
*Positive ions rush into cell *Causes depolarization, cardiac cell is now positive |
|
|
Cardiac Conduction: Electrical potential
|
Electrical potential flows from (-) to (+)
*cell to cell conduction of depolarization occurs through fast-acting sodium channels *Spread of action potential through gap junctions between cells *wave of electrical activity |
|
|
Cardiac Conduction: Depolarization
|
Depolarization
*positive ions rushing into the cardiac myocyte *contraction *occurs with both sodium and calcium ions at different stages |
|
|
Cardiac Conduction: Repolarization
|
Repolarization
*cardiac myocyte returns to negative charge *"resting" *occurs immediately after depolarization *slower process than depolarization; deflection is wider and lower magnitude *occurs with K+ ions |
|
|
Cardiac Conduction: Absolute Refractory Period & Relative Refractory Period
|
Absolute Refractory Period
*the period of time during which a cell or group of cells cannot be stimulated to fire *fast Na+ channels are closed *Phase 1, 2, part of 3 Relative Refractory Period *premature electrical impulses can be conducted in response to strong stimuli *End of Phase 3 |
|
|
Cardiac Conduction: Automaticity, Pacemaker Cells & Non-Pacemaker Cells
|
Automaticity
*ability to depolarize spontaneously in a rhythmic fashion Pacemaker Cells *possess automaticity *SA node, AV node, bundle of His, bundle branches and Purkinje fibers Non-Pacemaker Cells *Lack of automaticity *Atrial and ventricular myocytes |
|
|
Cardiac Conduction: SA Node
|
SA node is pacemaker
*greatest automaticity (ability to depolarize spontaneously) *generates first electrical impulse *depolarizes 60-100 times/min SA node ->atrial depolarization ->AV node ->bundle of His ->left and right bundle branches -> purkinje fibers -> ventricular depolarization Contraction follows depolarization |
|
|
Phases of Ventricular Action Potential
|
Phases of Ventricular Action Potential
Phase 0 *Fast Na+ channels open = ventricular depolarization Phase 1-3 *Fast Na+ channels inactivated = ventricular repolarization *plateau balanced by fluxes of K+ and Ca2+ Phase 4 *Na+, K+ ATPase pumps Na+ out of myocyte = resting potential |
|
|
Thiazides
|
Diuretic
HCTZ *MOA: competitive antagonism of Na-Cl transporter in distal tubule *Less effective if CrCl <30 *AE: hyperkalemia |
|
|
K sparing
|
Diuretics:
Triamterene, amiloride *MOA: Na channel blockade in collecting duct, increased K reabsorption *Often used with HCTZ *AE: hyperkalemia |
|
|
Loop
|
Diuretic:
furosemide, bumetanide, torsemide *MOA: inhibit Na-K-Cl cotransporter in loop of Henle *Alleviate congestive sxs of HF *AE: dose related ototoxicity, dec Mg, dec Ca, "sulfa" allergy *AE: Hypokalemia |
|
|
Aldosterone antagonist
|
Diuretics:
Spironolactone, eplerenone *MOA: competitive antagonist at aldosterone receptor; inhibits mineralcorticoid receptors *AE: Hyperkalemia |
|
|
Drugs with
HYPOKALEMIA Adverse Effects |
HCTZ
Furosemide (Lasix) |
|
|
Drugs with
HYPERKALEMIA Adverse Effects |
Spironolactone
Aliskiren (Tekturna) Lisinopril Losartan |
|
|
Nitroprusside
|
Vasodilator:
*Gives off NO -> arteriovenous dilation in smooth muscle *Renal and hepatic insufficency ->risk of cyanide toxicity *Available parenteral form *Used in HTN urgency/emergency |
|
|
Hydralazine
|
Vasodilator:
*Stimulates NO formation in endothelial cells -> arteriole dilation *AE: SLE *Rapid first-pass metabolism *Available parenteral form *Used in HTN urgency/emergency |
|
|
Fenoldopam
|
Vasodilator:
*D1 stimulation -> diuresis, natriuresis *Available parenteral form *Used in HTN urgency/emergency |
|
|
Minoxidil
|
Vasodilator:
*Used for alopecia as well as HTN *K+ channel openers *Active metabolite can cause hypotensive effects for 24 hours despite short half life |
|
|
JNC7: HF
|
JNC7: HF
Thiazide, BB, ACEI, ARB, aldosterone antag |
|
|
JNC7:MI
|
JNC7:MI
BB, ACEI, aldosterone antag |
|
|
JNC7:High CVD risk
|
JNC7:High CVD risk
thiazide, BB, ACEI, CCB |
|
|
JNC7:DM
|
JNC7:DM
thiazide, BB, ACEI, ARB, CCB |
|
|
JNC7:CKD
|
JNC7:CKD
ACEI, ARB |
|
|
JNC7:Recurrent Stroke
|
JNC7:Recurrent Stroke
thiazide, ACEI |
|
|
JNC7:Isolate systolic HTN
|
JNC7:Isolated systolic HTN
thiazide, CCB |
|
|
Diuretics
|
Drug Class: Diuretics
Indications: HF, systolic HTN CI:Gout |
|
|
B-Blocker
|
Drug Class: BBlocker
Indications: CAD, HF, Migraine, Tachyarrhythmias CI:Asthma, Heart Block |
|
|
Alpha- Blocker
|
Drug Class: Alpha -Blocker
Indications: BPH CI: Heart Failure |
|
|
CCBs
|
Drug Class: CCBs
Indications: systolic HTN CI: Heart Block |
|
|
ACEI
|
Drug Class: ACEI
Indications: Heart Failure, previous MI, diabetic nephropathy CI: RAS, pregnancy, hyperkalemia |
|
|
ARBs
|
Drug Class: ARBs
Indications: ACEI-assoc cough, diabetic nephropathy, HF CI: RAS, pregnancy, hyperkalemia |
|
|
Treatment Goal:
Reduce Preload |
Diuretics, aldosterone, antagonists, venodilators
|
|
|
Treatment Goal:
Reduce Afterload |
ACEIs, BB, vasodilators
|
|
|
Treatment Goal:
Increase Inotrophy |
Digoxin, sympathomimetic amines, PD inhibitors
|
|
|
Digoxin
|
*Narrow therapeutic index drug
*increases parasympathetic outflow |
|
|
Cardiac Conduction
|
Starts at 4 (bottom), spikes to 1 (with 0 as it spikes), then slides down to 2, 3 and back to the bottom at 4.
0= ventricular depolarization 1 = K+ out, Na+ gates closed 2 = Ca+ gos in, K+ closed (Absolute Refractory Period - no new AP fires) 3 = K+ out, Ca+ closed 4 = Na+/K+ ATP - pumps in -> Resting Potential |
|
|
Class 1a Antiarrhythmics
|
Class 1a Antiarrhythmics
Procainamide, Quinidine *Moderate open Na channel blockade *Decrease upstroke velocity *Prolong repolarization/QT *K+ blockade ->prolonged QT -> risk for TdP *Anticholinergic effects *AE's include lupus, thrombocytopenia, anemia, tinnitus *Prolongs AV node conduction/ PR |
|
|
Class 1b Antiarrhythmics
|
Class 1b Antiarrhythmics
Lidocaine, Mexilitine *Mild open and inactivated Na channel blockade *Not effective for SVT *Shortens repolarization |
|
|
Class 1c Antiarrhythmics
|
Class 1c Antiarrhythmics
Flecainide, propafenone *Decrease upstroke velocity *prolong repolarization / QT *Use w/ BBs produces additive negative inotropy *Prolongs AV node conduction / PR |
|
|
Class II Antiarrhythmics
|
Class II Antiarrhythmics
Beta Receptors *Known as BB *Esmolol is injectable with a fast onset and shortest duration of action *Negative inotropic effect *Slow conduction through AV node |
|
|
Class III Antiarrhythmics
|
Class III Antiarrhythmics
K+ Channels *Sotalol has Bblocking action *TdP is an AE of Ibutilide and Dofetilide due to prolongation of the refractory period *Dofetilide must be administered by a provider specifically certified by the drug company *Amidoarone has drug interactions with warfarin |
|
|
Class IV Antiarrhythmics
|
Class IV Antiarrhythmics
Ca++ Channels *Depolarization via blockade of Ca++ channel causing slowed SA node firing and slowed conduction through the AV node *The nonDHP CCBs are primarily used, such as Verapamil and Diltiazem which can not be used to treat ventricular tachycardia arrhythmias |
|
|
Which increase Risk of TdP by prolonging QT?
|
Quinidine, Procainamide, Ibutilide, Sotalol, Dofetilide
|
