Hemodynamics CCRN Latest Update with Certified Solutions

Hemodynamics CCRN Latest Update with Certified Solutions Cardiac output equation CO = HR x SV Components of stroke volume Preload Afterload Contractility Preload components CVP (right ventricular) - central venous pressure PAOP (left ventricular) - pulmonary artery occlusive pressure Afterload components PVR (right ventricular) - pulmonary vascular resistance SVR (left ventricular) - systemic vascular resistance Normal cardiac output 4-8L/min CI -Cardiac index -take into account body surface area and is a more meaningful value than CO Normal cardiac index (CI) 2.5-4.0L/min/m2 CO and HR -As heart rate increases -Cardiac output increases up to a point -Extreme bradycardia results in low CO and hypotension -Increase in HR first sign of compensation for a low CO Definition of stroke volume -How many mL pr beat the left ventricle ejects Stroke Volume and CO -As stroke volume increases, cardiac output increases Normal SV (stroke volume) 50-100 mL per beat Define preload -Preload is the volume/pressure in the ventricle at the end of DIASTOLE after the AV valves close, just prior to ejection -As preload increases, SV and CO will increase up to a point -Too high of a preload may lead to heart failure -Preload will seldom be elevate if the heart is without disease and there are no metabolic abnormalities What pressures reflect the right ventricle preload? -Right atrial (RA) -Central venous pressure (CVP) What pressure reflects the left ventricle preload? -Pulmonary artery wedge pressure (PAOP) Define afterload -Afterload is the pressure (resistance) against which the ventricle must pump to open the valve (pulmonic and aortic) How is afterload measured for the right ventricle? -Pulmonary Vascular Resistance (PVR) How is afterload measured for the left ventricle? -Systemic Vascular Resistance (SVR) Afterload and CO -As afterload increases, SV and CO decrease Define contractility -Is the contractile force of the myofibrils independent of preload and afterload -As contractility increases, SV and CO increase Stroke Index 25-45 ml/beat/m2 Right Atrial pressure (RAP) 2-6 mmHg 3-8 cm H20 Pulmonary Artery Pressure (PAP) 20/8-30/15 Mean: 20 Pulmonary Artery Wedge Pressure (PAOP) 8-12 mmHg Systemic Vascular Resistance (SVR) 800-1200 dynes/s/cm Pulmonary Vascular Resistance (PVR) 50-250 dynes/s/cm Coronary Artery Perfusion Pressure (CAPP) 60-80 mmHg Mixed Venous Oxygen Saturation (SvO2) 60-75% *Direct measurement from pulmonary artery Central Venous Oxygen Saturation (ScvO2) 70% *Direct measurement from superior vena cava Arterial Oxygen Saturation (SaO2) 95-99% Arterial Oxygen Content (CaO2) 12-16 mL/dl Oxygen Delivery (DO2) 900-1100 Oxygen Consumption 250-350 mL/min Tx to increase preload -Volume expanders (crystalloids/colloids) -Pressors Tx to decrease preload -Diuretics -Dilators (nitrates, nitroprusside, morphine) Tx to increase afterload -Norepinephrine -Phenylephrine -High dose dopamine -Epi drip Tx to decrease afterload -Nitroprusside -ACE inhibitors -Hydralazine -Calcium channel blockers -IABP -Nitroglycerin Tx to increase contractility -Dobutamine -Dopmaine 5-10 mcg/kg/min -Primacor -Epi drip Tx to decrease contractility -Beta blockers -Calicum channel blockers -Metabolic problems (met acidosis, endotoxins of sepsis) Most sensitive indicator of cellular oxygenation Mixed venous Oxygen Saturation (SvO2) 60-75% Oxygen parameter used to measure therapy for septic shock -ScvO2 70% What will decrease Do2 (Oxygen delivery) -Pump problems (heart) Oxygen consumption is (low or high) in septic shock LOW Increased SvO2 75% Septic shock** Hypothermia** Paralysis Decreased SvO2 60% Low cardiac output Decreased PaO2 Increased O2 demand (fever, shivering, seizures, increased WOB) If SvO2 is decrease, assess for... -hypoxemia -hypotension -hypovolemia -hemoglobin drop -fever -arrhthymias Acute Mitral Valve Insufficiency and PAOP waveform changes -Giant V waves -Indicate mitral valve insufficiency (regurgitation) -Often association with acute inferior wall myocardial infarction/papillary muscle dysfunction/rupture Square Wave Test -Dynamic response test -Performed to assess the accuracy of the hemodynamic monitoring system Overdampened wave response -Reults in falsely decreased systolic pressure and false high diastolic pressure -Diminshed or absent dicrotic notic -May be due to air or blood in the system, loose connections, loss of air in the pressure bag, or kinking of the catheter/tubing system Underdampened wave response -Results in false high systolic pressures, possible false low diastolic pressures and "ringing" artifacts on the waveform -May be due to pinpoint air bubbles in the system, add on tubing, or defective transducer Dopamine 5-10 mcg -stimulates beta-1 receptors -increases contractility Dopamine 10 mcg -stimulates alpha receptors -vasoconstriction -increases afterload Dobutamine -stimulates beta-1 receptors -increases contractility Nitro -causes venodilation and results in a decrease in preload Norepinephrine -potent vasoconstrictor -increases afterload Beta blockers -Block beta-1 receptors -results in decreased contractility and decreased in the heart rate Nitroprusside -decrease preload, decrease afterload ACE inhibitors -decrease in afterload -Block the conversion to angiotensin II - angiotensin II is a potent vasoconstrictor Furosemide -potent loop diuretic and Venodilator -reduces preload Fluid bokus -increase preload Milrinone -increases contractility Morphine -decreases preload Hypovolemic Shock characteristics -low CVP -low PAOP -high SVR (compensation to hypovolemia) Cardiogenic shock characteristics -elevated PAOP -low CI -elevated SVR Acute right ventricular failure characteristics -high CVP -low PAOP (due to poor RV output) -CI low Septic shock characteristucs -low SVR (massive dilation) -increased CI -decreased preload and afterload Sign of improved right HF -decreased RA pressures Signs of improved left HF -decreased PAOP