CMC certification Exam Questions And Answers With Complete Solution

CMC certification HIT (heparin induced thrombocytopenia) - Bivalirudin and Argatroban are direct thrombin inhibitors and alternatives for anticoagulation for patients with HIT. - HIT is an immune mediated adverse drug reaction caused by antibodies that develop after exposure to heparin, platelets become activated placing patients at risk for development of thrombosis pericarditis - inflammation of pericardial sac, chest pain-sharp,stabbing, dull, achy pain improved with sitting &leaning foward, pain worse with cough, positional changes and inspiration, pericardial friction rub, fever, Diffuse ST changes (depression of PR interval, concave ST segment in limb leads,st elevation in leads I and II Papillary muscle rupture - -associated with anterior or inferior wall MI - hemodynamic instability, new loud systolic murmur, acute mitral regurgitation, large V waves on PAOP waveform - treatment - hemodynamic support, Emergent surgical repair/valve replacement Ventricular septal rupture - -associated with septal wall MI -oxygen rich blood shunts to right side of heart from the left Symptoms of ventricular septal rupture - -acute SOB -S3 heart sound -crackles -holosystolic murmur - PA Catheter insertion-- falsely increaed CO, because CO reading is derived from the right ventricle, increased Svo2 due to left to right shunting, large V waves on CVP waveform, diagnosed by ECHO - treatement surgical repair cardiogenic shock - S3 pulmonary edema, tachycardia, dysrhythmias, signs of decreased perfusion (mottling), decreased UOP 0.5ml/kg/hr, hypotension, low CO/CI, elevated SVR often 1600 dynes/sec/cm, elevated RAP/CVP, PAOP 16 mmhg, decreased svo2 (65%) other diagnostics for cardiogenic shock - - cardiac catheterization if related to ischemia- PCI for reperfusion - ABG- mixed respiratory and metabolic acidosis:hypoxemia- lactic acidosis due to decreased perfusion and anaerobic metabolism -ECHO: decreased wall motion,reduced ejection fraction -Chestxray: pulmonary edema &congestion, may note opacity due to enlarged pulmonary vasculature, enlarge d heart, Kerley B lines in lower zones from interstitial edema, - BUN/CR- monitor for acute kidney injury - monitor other organs for dysfunction and failure supportive treatment for cardiogenic shock - -mechanical support (IABP,impella) -vasopressors to support blood pressure (use with caution as they increase SVR and workload of heart) -positive inotrope to improve contractility -diuretics afterload reduction / venous vasodilators cardiogenic pulmonary edema - -fluid in the alveolus due to increased alveolar hydrostatic pressures - impaired gas exchange, hypercapnia - hypoxemia- S3 heart sound, shortness of breath, crackles, pinky frothy sputum, anxiety Causes of cardiogenic pulmonary edema - myocardial infarction, heart failure, hypertensive crisis, mitral regurgitation, tamponade Treatment of pulmonary edema - -decrease preload -loop diuretics -nitroglycerin -morphine - CPAP or BIPAP - Positive inotrope to improve contractility Cardiac output (CO) - 4-8 L/min Cardiac index (CI) - 2.5-4 L/min/m2 Stroke volume (SV) - 50-100 ml/beat Stroke volume index - 35-60 ml/beat/m2 Right ventricular stroke work index (RVSWI) - 5-10 g/m2/beat Left ventricular stroke work index (LVSWI) - 50-62 g/m2/beat SVO2 - 60-75% Scvo2 - over 70% (70-85%) pulmonary artery pressure - 25/10 mmHG PAOP - 8-12 mmHG RAP/CVP - 2-8 mmHG SVR - 900-1400 dynes/sec/cm-5 SVRI - dynes/sec/cm-5/m2 PVR - 90-250 Dynes/sec/cm-5 LV pressure - 100 mmhg Cardiac output formula - CO=SVxHR MAP= - CO x SVR Cardiac output can be measures with - Pulmonary artery catheter, echocardiogram, indirectly via functional hemodynamics, noninvasive methods (bioreactance and continuous digit CO), fick equation in low output states patients compensate with - tachycardia, CO may be normal when the patient is tachycardic with lower SV Stroke volume formula - SV= end diastolic volume- end systolic volume SV=EDV-ESV Typical EDV - 120 ml amount of blood in the heart at the end of diastole Typical ESV - 50 ml amount of blood in the ventricles at end of ejection/systole Three measures that contribute to stroke volume - contractility, preload, afterload Preload - myocardial fiber length at the end of diastole - stretching of cardiac myocytes prior to ejection afterload - resistance the heart has to eject against during systole contractility - strength of myofibril contraction preload is indirectly measured on right side by - Central venous pressure or right atrial pressure 2-8 mmhg preload is indirectly measured on left side by - Pulmonary artery occlusive pressure (PAOP) - reflective of left atrial pressure - 8-12 mmhg PAOP is always lower than - PA diastolic conditions that cause an increase in preload: - Heart failure Hypervolemia Cardiogenic shock RV failure (Increased CVP) Ventricular septal defect (VSD) Pulmonary hypertension (increased cvp) tricuspid stenosis (increased cvp) mitral stenosis (increased PAOP) pericardial tamponade (increased cvp&paop) increasing PEEP on the ventilator (increased intrathoracic chest pressure ) IV fluids