PCCN Practice Quiz Questions and Answers

S1 - Mitral and tricuspid "lub" of "lub dub" S2 - Aortic and pulmonic "dub" of "lub dub" S3 - Ventricular Gallup. Beginning of diastole after S2. Too much volume S4 - Rare. Atrial Gallup. Resistance to filling. End of diastole 1/avl/V5/v6 - Lateral (Circumflex): AVL- High Lateral V6 Low Lateral Less common/ less severe II/III/avf - Inferior V1/v2/ v3/ v4 - Anterior V4R/ V5R - RV CO - HRXSV SV - Preload/ after load/ contractility SVO2 from central line - ~=70% Is increased SVO2 good or bad? - Bad- it means that the tissues are not up taking O2. This should be "used blood" so the number should be lower Parasympathetic response - Slows things down/ vagal response/ atropine blocks the vagas nerve and speeds up HR Betablockers - ⬇️HR ⬇️contractility=⬇️BP/ ⬇️myocardial O2 demand Used in acute coronary syndrome. Can cause HF. Look for crackles and S3 One of the first drugs we give with angina because it decreases myocardial O2 consumption Sympathetic response - Speeds things up/ epi/ dopamine Calcium Channel Blockers - ⬇️HR and contractility us in rapid rhythm. Don't use in ACS. Amlodapine, dilt, nicardipine Reduce afterload by lowering intracellular Ca+ which inhibits smooth muscle contraction. Decreases contractility Digoxin - Increase contractility= increased myocardial O2 demand. Takes 6 hrs to work. Don't use in ACS Pulse Pressure - Difference between Diastolic and Systolic pressures. Must be at least 40. <40 patient is not being filled properly (dry) or has vasoconstriction. Preload - Volume. Measured by CVP. How full in the ventricle before contraction. How to reduce Preload - Reduce volume (diuretics)/ vasodilation (when you cant get rid of volume: Nitro, dilt, morphine)/ dialysis Replace preload - Crystalloids: NS, isotonic, fluid bolus Colloids: Hetastarch, albumin, blood products:Expand intravascular volume. Use with caution in pulmonary edema Blood: ⬇️H&H, can increase afterload. Potential blood admin problems - Can increase afterload Hyperthermia and coagulopathy in massive transfusions Hyperkalemia (RBCs break) and hypocalcemia (preservative in blood binds with Ca+) Afterload - SVR (800-1200), resistance to ventricular ejection The more resistance the higher the myocardial O2 demand BP is indicator in tele How to reduce afterload - Reduce resistance: ACE, ARBs, Alpha agonists (prazosin, phentolamine, clonidine) Beta Blockers, Calcium Channel Blockers (Nicardipine, diltiazem) Negative Inotropes - Decrease HR and force of contraction: beta blockers, calcium channel blockers Positive inotropes - Whip the heart into shape. Increase Contractility: Digoxin, Dopamine, Dobutamine, Milrinone, Amrinone lactate Last choice, try to decrease pre & afterload first Drug commonly used for vasospasm - Calcium Channel Blockers Intended consequences of +Inotrope therapy - Increased SV, Increased EF, Increased CO, increased tissue oxygenation Unintended consequences of +inotrope therapy - Increased myocardial O2 demand- watch out for angina Unintended consequences of - inotrope therapy - Hypotension, HF (S3), Bracycardia What is nisiritide - Synthetic BNP- increases GFR thus urine output, increases calcium in myocardium. Creates a stronger contraction Pain: Cholecystitis - RUQ tenderness Pain: GERD - Associated with eating on at least 2 occasions, may be triggered by exercise Pain: Musculoskeletal - Persistent, associated with activity, does not increase with inspiration or changing position Pain: PE - Dyspnea, sudden onset or intermittent, no pulmonary symptoms Pain: Pericarditis - Sharp and goes away when patient leans forward, does not increase with inspiration. Global ekg changes Pain: Pleuritic - Sharp, Upper quadrant, worse with inspiration, Dyspnea Pain: Psychogenic - Unexplained, possible hyperventilation, inability to recall past episodes Pain: Aortic dissection - Hx hypertension, Family Hx, Severe tearing pain that can radiate to back, flank, abdomen Stable Angina - Predictable. With activity, goes away when activity is stopped. Unstable Angina - Unpredictable, doesnt go away when expected ***Prinzmetal's Angina - Vasospastic. ST Elevation. Dx in cath lab. TREATED WITH CALCIUM CHANNEL BLOCKERS! Relax smooth muscle to prevent vasospasm. MI - ***will always be STEMI in exam Treatment of unstable angina - MONA (Morphine, O2, Nitro, ASA) Anticoagulants Vasodilators: Nitro, MS04 (affects supply and demand) BetaBlockers (Supply and demand) ACE (demand only) ST depression in ALL leads - ischemia Causes of ST depression - Dig toxicity, Hypokalemia, right or LV hypertrophy, Intraventricular conduction abnormalities (BBB, WPW), Hypothermia, ST, Mitral valve prolapse, CNS disease Causes of Acute ST Elevation - Prinzmetal's Angina, Acute pericarditis (Global), Left ventricular aneurysm, Blunt trauma to chest, Hyperkalemia, Acute myocarditis, PE, Brugada Syndrome, Hypothermia, Infarction Leads for Anterior Wall MI - V1. V2, V3, V4 Anterior Wall MI affects...? - Left side , main pump, LAD Anterior wall MI symptoms - Pump failure, Pulmonary Edema, cardiogenic shock Anterior wall MI treatment - MONA, Diuretics, pre/post afterload reduction (Vasodilator ore ACE inhibitor, metoprolol (improves outcomes), pump assistance Arrhythmias associated with Anterior wall MI - VT, 2nd degree T2, 3rd degree Leads for Inferior wall MI - II, III, aVF Inferior Wall MI affects...? - RCA Inferior wall MI symptoms - Nausea, Bradycardia, 1st degree HB, JVD, Labile BP Inferior Wall MI treatment - Fluid, atropine Arrhythmias associated with Inferior Wall MI - Bradycardia, 1st degree, 2nd degree T1 RV MI Leads - R sided EKG V4R, V5R, V6R RV MI Symptoms - Neck vein distention, sudden drop in BP RV MI Treatment - Bolus, maintain contractility, avoid diuretics and vasodilators Lateral MI leads - I, aVL, V5, V6 Lateral MI affects...? - Circumflex Lateral MI symptoms - Heart blocks in some Septal MI leads - V1, V2 Septal MI affects...? - RCA Septal MI symptoms - Bundle branch blocks