FCCN II: cardiac concepts Questions with solutions 2023

FCCN II: cardiac concepts Questions with solutions 2023 preload: what how wet/dry you are amount of fluid filling heart affected by dilating/constricting VEINS R heart -CVP L heart -PCWP (wedge pressure) preload: affected by VEINS constrict -- INCREASE dilate -- DECREASE Brainpower Read More Previous Play Next Rewind 10 seconds Move forward 10 seconds Unmute 0:05 / 0:15 Full screen preload: frank-starling principle giving fluid improves CO up to a certain pt preload: Tx low -crystalloids -colloids: albumin, hespan -blood: PRBCs, plasma preload: Tx high -diuretics: lasix -vasodilators: NTG, narector -dialysis: hemodialysis afterload: what resistance to heart ejecting blood L heart: systemic vascular resistance body = SVR R heart: pulmonary vascular resistance lungs = PVR afterload: affected by ARTERIES constrict -- INCREASE dilate -- DECREASE afterload: Tx low CONSTRICT ARTERIES -dopamine -norepinephrine -phenylephrine afterload: Tx high DILATE ARTERIES L heart (SVR) -nipride -ACE inhibitors -ARBs -apresoline R heart (PVR) -sildenafil -milrinone -isuprel -nitric oxide afterload: causes high L heart afterload -HF -dehydration -HTN R heart afterload -cor pulmonale -sepsis afterload: causes low ARTERIES DILATED -sepsis contractility: Rx to increase contractility = cardiac output -epinephrine 0.03-1.0 mcg/kg/min -milrinone 0.375-0.75 mcg/kg/min -dopamine 5-10 mcg/kg/min -dobutamine 2-20 mcg/kg/min MAP: equation MAP = CO x resistance only give vasopressors to Tx... DILATION O2 delivery: what affects Hgb x CO O2 load onto Hgb in lungs -- delivered to tissue via CO cardiac output = SV x HR SV = preload | afterload | contractility O2 demand vs consumption DEMAND -amount of O2 needed by tissues -CO x Hgb CONSUMPTION -amount of O2 used by tissues = O2 delivery - O2 returned (SvO2) healthy person increases delivery to meet need SvO2: what -shorthand O2 consumption -subtract from SaO2 to know how much O2 used -monitor trends NORMAL = 60-80% SvO2: problems DROP in SvO2: -delivering less O2: drop in Hgb or CO -consuming more: increased metabolic needs, pt can be restless shock: types -hypovolemic = preload -distributive = afterload -cardiogenic = contracility shock: compensation SNS -increased HR, contractility -clamp down, shunt blood to vital organs RAAS -angiotensin II: clamp down to shunt blood to vital organs -aldosterone: retain fluid hypovolemic shock: what PRELOAD: DECREASED -dehydrated -dilated veins -hemorrhage AFTERLOAD: INCREASED -SNS, RAAS SNS, RAAS = BAD RESULT == low CO hypovolemic shock: assessment -cool , clamped down -tachycardia -low UOP -thirsty, dry mucous membranes -narrowing pulse pressure hypovolemic shock: Tx -give fluid/blood -reverse compensatory mechanisms distributive (septic) shock: what PRELOAD: DECREASED -massive vasodilation -dilated veins -third spacing AFTERLOAD: DECREASED -dilated arteries SNS, RAAS = GOOD, but vasoconstriction doesn't happen CONTRACTILITY: DECREASED RESULT == high CO distributive (septic) shock: assessment -flushed, peripheral dilation -tachycardic -concentrated urine -hypotensive -high temperature distributive shock: Tx -ALWAYS give fluid FIRST -then clamp down w vasopressors -add inotrope PRN cardiogenic shock: what PRELOAD: INCREASED -aldosterone -fluid retention AFTERLOAD: INCREASED -RAAS, SNS SNS = BAD b/c increases HR, contractility, resistance == WORSENS RAAS = BAD b/c increases resistance, fluid retention == WORSENS CONTRACTILITY: DECREASED -MI, myopathy, etc cardiogenic shock: assessment -cool, clamped down -mottled -crackles, peripheral edema cardiogenic shock: Tx -block SNS, RAAS -decrease preload in L HF: lasix, dialysis -decrease afterload by dilating arteries: nipride, apresoline, ACE inhibitors, ARBs -increase contractility: inotropes hypovolemic shock: key pts cause: low preload (PCWP, CVP) == DRY afterload: INCREASES to compensate contractility: REDUCED d/t low fluid/"dry" BP: low to normal HR: high distributive (septic) shock: key pts cause: low preload d/t venous dilation + third spacing AND low afterload r/t arterial dilation contractility: CO INCREASES in early shock; decreases in LATE shock BP: low HR: high cardiogenic shock: key pts cause: low CONTRACTILITY d/t MI or HF preload: HIGH d/t vasoconstriction to retain fluid (compensatory mechanism) afterload: HIGH r/t vasoconstriction via SNS, RAAS (compensatory mechanism) BP: low HR: high