Critical Care Flashcards
Arterial O2 content equation
CaO2 = Hgb x 1.34 x O2 saturation + PO2 x 0.003
O2 delivery equation
O2 delivery = cardiac output x arterial O2 content x 10
MAP equation
MAP = cardiac output x systemic vascular resistance
cardiac index equation
cardiac index = cardiac output / BSA
stroke volume equation
stroke volume = LVEDV - LVESV
ejection fraction equation
ejection fraction = stroke volume / LDEDV
O2 consumption equation
VO2 = cardiac output x (arterial O2 content - venous O2 content)
mechanism of action milrinone
phosphodiesterase inhibitor (leads to increased cAMP), results in increased Ca flux and myocardial contractility, pulmonary vasodilation
mechanism of action of vasopressin
V1 receptor - vasoconstriction of vascular smooth muscles, V2 receptor (intrarenal) - water reabsorption at collecting ducts V3 receptors (extrarenal) mediate release of factor VIII and vWF
mechanism of action of dobutamine
beta1 (increases contractility mostly, tachycardia with higher doses)
mechanism of action of dopamine
low dose - dopamine receptor (renal), med dose beta / contractility, high dose alpha adrenergic vasoconstriction and increased BP
mechanism of action of phenylephrine
alpha1 (vasoconstriction)
mechanism of action of norepinephrine
beta1 (increased contractility) and alpha1/alpha 2 (splanchnic vasoconstriction)
mechanism of action of isoproterenol
beta1/beta2 increases HR and contractility, vasodilates; extremely arrythmogenic, can lead to hypotension
mechanism of action of nipride
arterial vasodilator, can lead to cyanide toxicity which you tx w/ amyl nitrite/sodium nitrite
mechanism of action of nitroglycerin
predominately venodilation with decreased myocardial wall tension from decreased preload, moderate coronary vasodilator
total lung capacity equation
TLC = forced vital capacity + residual volume
functional residual capacity equation
FRC = expiratory reserve volume + residual volume
Berlin definition of ARDS
1) within 1 week of insult or worsening symptoms 2) bilateral opacities not otherwise explained (effusion, ATX, mass), 3) resp failure not explained by HF/volume overload 4)PaO2/FiO2 <=300 – mild 200-300, moderate 100-200, severe <100
most common site of aspiration?
super seg of RLL
definition of SIRS
temp >38 or <36, HR > 90, RR >20 or PCO2 <32, WBC >12 or <4
methemoglobinemia O2 sat? treatment?
O2 sat reads 85%, tx w/ methylene blue
carbon manoxide - O2 sat? tx?
falsely increases O2 sat on pulse ox, binds to Hgb directly, tx w/ 100% O2 on ventilator, rarely need hyperbaric O2
mechanism of action of dexmedetomidine?
similar to clonidine - selective alpha 2 antagonist
mechanism of action of ketamine? limitations?
blocks glutamate NMDA receptors, limited by psychoactive effects
what is the benefit of CRRT in septic shock?
earlier use = filter inflammatory mediators, defined as within 8 hours of AKI onset, duration of RRT and LOS were shorter in early vs later, no difference in long term RRT needs, pt w/ increased IL8 increased risk of RRT dependence after hospital discharge (ELAIN trial in 2016)
free water deficit equation
( serum sodium - 140 ) / 140 x total body water – total body water is 50% of lean body mass in men, 40% in women – 50% is to be given over 24 hours
issue with treating hypernatremia too quickly?
cerebral edema – give 50% of deficient free water over 24 hrs (free water equation = serum sodium - 140 / 140 x total body water (weight * .5 men, .4 women)
normal cardiac output? cardiac index?
4-8 L/min, 2.5-4 L/min
normal SVR?
800-1400
normal pulmonary capillary wedge pressure? central venous pressure? pulmonary artery pressure?
PCWP 11+/-4, CVP 7+/-2, PAP 25/10 +/-5
Normal mixed venous O2 sat?
75+/-5
causes of increased SvO2?
increased SvO2 occurs with shunting or decreased O2 extraction (sepsis, cirrhosis, cyanide toxicitiy, hyperbaric O2, hypothermia, paralysis, coma, sedation)
causes of decreased SvO2?
decreased SvO2 occurs with increased O2 extraction or decreased O2 delivery – anything that decreases O2 saturation, cardiac output, malignant hyperthermia
symptoms of hypomagnesia?
similar to hypocalcemia = HYPERactive reflexes, muscle tremors, tetany, +Chvostek sign, severe deficiency can lead to delirium and seizures – also see prolonged QT
symptoms of hypermagnesia?
loss of tendon reflexes; respiratory/cardiac arrest
how to determine cause of metabolic alkalosis?
measure urine chloride, if low, means chloride responsive, is much more common in surgical patients and results from vomiting (GI loss of hydrogen ions), diuretics (GU loss of chloride), volume depletion (aldosterone stimulated hydrogen ion loss in urine); chloride resistant types (urine chloride >25), result form mineralcorticoid excess or potassium depletion
definition of hemorrhagic shock / classes
class 1 = up to 750 ml or <15% total blood volume, class 2 = 1500 ml or 30%, can have tachycardia, decreased pulse pressure; class 3 = 2000 ml or 40% decreased BP, class 4 = >2L or >40%, significantly decreased BP
general Swan-Ganz findings in sepsis – CVP? SVR? cardiac index? PCWP? SVO2?
CVP low (from loss of intravascular volume due to increased capillary permeability), SVR is low (due to toxins that produce vasodilation), cardiac index (usually elevated initially), PCWP (usually unaffected), SVO2 (usually high because tissues unable to extract O2 from blood for consumption)
acute treatment for hypermagnesia?
calcium chloride (cardiac protection), then dialysis if still elevated/persistent symptoms
effects of increased PEEP on - cardiac output, arterial oxygen content, pCO2
can decrease cardiac output due to increased intrathoracic pressure, can increased O2 content due to recruitment of collapsed/atelectatic lung, does not affect PCO2
most common organism involved with transfusion transmitted bacterial infection?
gram negatives (yersinia, pseudomonas – can grow at 4C
definition of intra-abdominal hypertension? abdominal compartment syndrome?
hypertension >= 12mm Hg; ACS is sustained pressures >20 w/ new end organ dysfunction
treatment of new VT (stable / unstable)?
stable - amiodarone, procainamide, sotalol; unstable defibrillation
characteristic findings in hepatorenal syndrome
relative hypovolemia, splanchnic and peripheral arterial vasodilation, intense vasoconstriction of the renal circulation – leads to azotemia, oliguria, very low urinary sodium, high urine osmolarity; type 1 is worse than type 2, associated with acute liver failure or EtOH cirrhosis
what is the pulmonary artery wedge pressure an indirect estimation of?
left atrial and left ventricular diastolic pressure
features of argatroban
direct thrombin inhibitor, used for HIT, monitored with aPTT, short half life (40-50 minutes), cleared by liver – drug of choice for pt w/ HIT and renal problems
features of lepirudin?
direct thrombin inhibitor, used for HIT, monitored with aPTT, 60-90 minute half life, cleared by renal metabolism, drug of choice for pt w/ HIT and liver problems
