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56 Cards in this Set
- Front
- Back
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JNC7:
HTN Urgency |
*Diastolic pressure >120 with evidence of progressive end organ damage.
*Goal - decrease DBP to 100-105 within 24 hours *Clonidine |
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JNC7
HTN Crisis |
*Diastolic pressure >120 with evidence of end organ failure
*Goal - decrease DBP 100-105 ASAP *Nitroprusside, NTG, Labetalol, Fenoldopam |
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Diuretics
Indications & CI |
Indications: Heart Failure, systolic HTN
CI: Gout |
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B-Blockers
Indications & CI |
Indications: CAD, HF, migraine, tachyarrhthmias
CI: Asthma, heart block |
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a-blockers
Indications & CI |
Indications: BPH
CI: HF |
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CCBs
Indications & CI |
Indications: Systolic HTN
CI: Heart Block |
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ACEIs
Indications & CI |
Indications: HF, previous MI, diabetic nephropathy
CI: RAS, pregnancy, hyperkalemia |
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ARBs
Indications & CI |
Indications: ACEI-associated cough, diabetic nephropathy, HF
CI: RAS, pregnancy, hyperkalemia |
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Which class is down-regulation of sympathetic tone?
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B1-blockers
a1-blockers a2-agonists |
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Which classes are modulation of vascular smooth tone?
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CCB
K+ openers |
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Which class is reduction of intravascular volume?
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Diuretics
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Which classes are modulation of RAAS?
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ACEI
ARBs |
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Diuretics
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*decrease renal Na+ reabsorptionn which reduces water reabsorption
*Each class works in a different area of the nephron *Secreted and concentrated into tubule reaching higher concentrations than in blood (even as a PO med) *Non-renal AE are low |
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B-Blockers
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*antagonism of categcholamines at B-rc
*decreases CO by decreasing HR and contractility *initial compensatory increase in PVR *decreases peripheral resistance in long run by inhibition of B-receptors in kidney which decreases renin *produce resting bradycardia *reduction in exercise-induced tachycardia *avoid sudden withdrawal of agent |
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Vasodilators
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Vasodilation initiates compensatory responses - tachycardia, activation of RAAS, give with B-blockers and diuretics
*NO formation *K+ channel openers *D1 stimulation |
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Ventricular Dysfunction
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*Systolic dysfunction (EF <40%)
-CAD/Ischemic Cardiomyopathy -Nonischemic Cardiomyopathy *HTN *Valvular disease *Alcohol *Thyroid Disease *Cardiotoxic drugs *Diastolic dysfunction (impaired filling) -Cardiomyopathies -elderly hypertensive women |
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Major Manifestations of HF
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*Dyspnea
-on exertion -orthopnea -paroxysmal nocturnal dyspnea *Fatigue *Fluid retention |
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NYHA Classifications
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Class 1: no symptoms with ordinary activity
Class 2: symptoms with ordinary activity; slight limitation Class 3: Symptoms with less than ordinary activity; marked limitation Class 4: symptoms with any activity; also at rest |
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Physiologic goals of drug therapy
Reduce Preload |
*Diuretics
*Aldosterone antagonists *Venodilators |
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Physiologic goals of drug therapy
Reduce afterload |
*ACEIs
*BB *Vasodilators |
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Physiologic goals of drug therapy
Increase inotropy |
*Cardiac glycosides
*Sympathomimetic amines *Phosphodiesterase inhibitors |
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Diuretics
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*Distal tubule: 5-10% inc Na excretion
-Thiazides -Metolazone (Zaroxolyn) -K+-sparing aldosterone antagonists (spironolactone, eplerenone) -Lose effectiveness when CrCl<30ml/min *Loop diuretics: 20-25% increase Na excretion -inhibit Na+-K+-2Cl- cotransporter in loop of Henle -increase excretion of Na+, K+, H2O *Alleviate congestive symptoms *No evidence of mortality benefit with thiazide or loop diuretics *Thiazides less efficacious than loop |
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Aldosterone Antagonists
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*K+-sparing diuretic that acts as a competitive antagonist at aldosterone receptor.
*Decreases K+/Na+ exchange in distal tubule and collecting duct of nephron ***Mortality reduction *HYPERKALEMIA - do not use in patients with elevated K+ or renal dysfunction |
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ACEIs
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*Reverses vasoconstriction and volume retention that is caused by RAAS activation
*Reduces afterload which increases SV - increases GFR - increases natriuresis and diuresis *Reversal of aldosterone-related volume retention decreases preload *Statistically significiant mortality benefit |
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ARBs
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*Hemodynamic profile similar to ACEIs
*Lack of bradykinin-related vasodilation *Mortality benefit -use when ACEI is contraindicated -may be additive when used with ACEI *Routine combination of ACEIs, ARB, and aldosterone antagonist not recommended |
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BB
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*Benefit related to: inhibition of renin release, attenuation of cytotoxic and signaling effects of circulating catecholamines and prevention of ACS
*Do not use in acute decompensated HF ***Mortality benefit (bisoprolol, carvedilol, metoprolol ER) |
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Clinical Management of Chronic CAD
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*BB
*CCBs *Nitrates *Aspirin *Lipid-lowering agents |
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Clinical Management of Unstable Angina, NSTEMI
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*Antianginal drugs
*Heparin, ASA *GPIIb/IIIa antagonists *Thienopyridines |
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Clinical Management of STEMI
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*Thrombolytics
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Stable Angina - ABCDE
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A: ASA, antianginals
B: BP, BB C: Cholesterol, cigarettes D: diet, DM E: education, exercise |
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Post-MI Management
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*ASA or clopidogrel if CI to ASA
*BB *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 |
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Cardiac Conduction:
Action Potential |
Action Potential
*Cardiac cell is polarized (negatively charged) compared to outside *Positive ions rush into cell *Causes depolarization, cardiac cell is now positive |
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Cardiac Conduction:
Electrical potential flows from (-) to (+) |
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 |
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Cardiac Conduction:
Depolarization |
Depolarization
*Positive ions rushing into the cardiac myocyte *Contraction *Occurs with both Na+ and Ca++ ions at different stages |
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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 potassium ions |
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Cardiac Conduction:
Absolute 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 |
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Cardiac Conduction:
Relative refractory period |
Relative refractory period
*Premature electrical impulses can be conducted in response to strong stimuli *end of Phase 3 |
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Cardiac Conduction:
Automaticity, Pacemaker cells & Non-pacemaker cells |
Automaticity - ability to depolarize spontaneously in a rhythmic fashion
Pacemaker cells possess automaticity and SA node, AV node, bundle of His, bundle branches and Purkinje fibers Nonpacemaker cells lack automaticity - including atrial and ventricular myocytes |
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Cardiac Conduction:
The cycle of conduction |
*SA node is a pacemaker
-greatest automaticity (ability to depolarize spontaneously), generates first electrical impulse and depolarizes 60-100 times/minute *SA node -> atrial depolarization -> AV node -> bundle of His-> left and right bundle branches->Purkinje fibers->ventricular depolarization *Contraction follows depolarization |
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Phases of the Ventricular Action Potential
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Phase 0
*Fast Na+ channels open = ventricular depolarization Phases 1-3 *Fast Na+ channels inactivated = ventricular repolarization *Plateau balanced by fluxes of K+ and Ca++ Phase 4 *Na+ -K+ ATPase pumps Na+ out of myocyte = resting potential |
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Causes of Arrhythmias
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*Hypoxia
*Ischemia *Sympathetic stimulation (hyperthyroid, CHF, nervousness, exercise) *Drugs *Electrolytes (hypokalemia) *Stretch (enlargement and atrophy of atria) |
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Mechanisms of Arrhythmias
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Impulse Formation
*Altered automaticity *Triggered activity - early afterpolarization (TdP) -Delayed afterpolarization Impulse conduction *Re-entry *Conduction block *Accessory tract pathways |
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Sinus Rhythms
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*Every P wave is followed by a QRS complex
*Every QRS complex is preceded by a P wave *Normal PR interval - <.12 *Brady rhythms - HR <60 *Tachy - HR>100 |
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Bradyarrhythmias:
Sinus bradycardia |
Sinus bradycardia
*HR <60 *Treat if symptomatic *Treat if elderly/CHF/metal status changes |
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Bradyarrhythmias:
1st Degree AV block |
1st Degree AV block
*PR interval >0.2 seconds *Treatment - removing possible offending agents, BB, CCB |
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Bradyarrhythmias:
2nd degree AV block |
2nd degree AV block
*Type I (Wenckebach) -PR widens, widens, then drops a QRS - longer, longer, longer - drop *Type II - PR normal or prolonged -dropped QRS without notice/unknown timing |
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Bradyarrhythmias:
3rd degree AV block |
3rd degree AV block
*Widened QRS, heart waits for purkinje fibers to conduct *HR <40 ***Medical emergency *Patient needs pacing |
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Atrial Tachyarrhythmia:
Sinus tachycardia |
Sinus tachycardia
*HR >100 *Treat prolonged sinus tachycardia *Treat underlying cause |
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Atrial Tachyarrhythmia:
Paroxysmal supraventricular tachycardia (PSVT) |
Paroxysmal supraventricular tachycardia (PSVT)
*AV nodal reentry circuit *Accessory pathway mediated *Precipitating factors including: -caffeine -alcohol -recreational drugs -hyperthyroidism *Treatment -vagal/valsalva maneuvers -Adenosine -IV: BB, verapmil, diltiazem -Possibly other antiarrhythmics -Unstable: direct current cardioversion (DCC) -Long-term prevention - ablation |
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Atrial Tachyarrhythmia:
Atria fibrillation (Afib) |
Atria fibrillation (Afib)
*Irregularly, irreguar *No P waves (no atrial contraction) *Paroxysmal (self-terminating, <7days), persistent (not self-terminating, >7 days), permanent (failed cardioversion) *Treatment -Antiarrhythmics (BB, CC, amiodarone, digoxin) -Ablation -Cardioversion *Unstable:MI, hypotensive, altered mental status *Elective DCC for stable patients -Anticoagulants (Warfarin) |
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Atrial Tachyarrhythmia:
Atrial flutter |
Atrial flutter
*"Saw tooth" pattern *Irregular *Treatment -Antiarrhythmics (BB, CCB, amiodarone, digoxin) -Cardioversion *Unstable: MI, hypotensive, altered mental status *Elective DCC for stable patients |
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Ventricular Tachyarrhythmias:
Premature ventricular contractions (PVCs) |
Premature ventricular contractions (PVCs)
*Result from increased or abnormal ventricular automaticity *Antiarrhythmic agents increase mortality for PVCs post-MI *Precipitating factors: MI, hypoxia, anemia, HF *Treatment: -Asymptomatic - no treatment -Symptomatic - BB |
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Ventricular Tachyarrhythmias:
Ventricular tachycardia (VT) |
Ventricular tachycardia (VT)
*PVCs in succession *Precipitating factors: MI, CAD, HF, hypokalemia, hypomagnesemia *Treatment -Sustained VT (>30 sec) requires immediate intervention -Hemodynamically unstable patients with a pulse - DCC; without a pulse - defibrillation -Stable patients: Lidocaine (for patients with MI), procainamide, or amiodarone -History of VT: implantable cardioverter-defibrillator (ICD) |
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Ventricular Tachyarrhythmias:
Ventricular fibrillation (VF) |
Ventricular fibrillation (VF)
*Chaotic electrical activity in the ventricles leading to loss of synchronized ventricular depolarization (lack of pulse, CO and BP) *Treatment : DEFIBRILLATION -drugs to augment defibrillation: epi/vasopressin, amiodarone, lidocaine |
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Ventricular Tachyarrhythmias:
Torsades de Pointes |
Torsades de Pointes
*Polymorphic VT, prolongation of ventricular repolarization *Treatment: remove offending agent, magnesium -Hemodynamically unstable: DCC |
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Treatment of Arrhythmias
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*A particular type of arrhythmia can generally be caused by multiple mechanisms and it is often not possible to know which mechanism is causing an arrhythmia in a given patient
*Diagnosis is a matter of probability and a drug is selected which is believed to have the best chance of working *All drugs capable of stopping an arrhythmia are also capable of CAUSING an arrhythmia or making an existing arrhythmia worse *GOAL OF THERAPY -The goal of therapy will be different for every patient -The goal should be established prior to the beginning of therapy -Examples *Remove cause of arrhythmia (e.g. treat thyrotoxicosis, treat anemia, and correct electrolyte abnormalities: K+, Ca++, Mg+) *Prevent recurrence of arrhythmia *Control ventricular rate in the presence of AFib or AFlutter |
