CPR Flashcards
What is target PaCO2 following achievement of ROSC?
Dog: 32-44 mmHg
Cat: 26-36 mmHg
Examples of static fluid responsive markers
CVP
MAP
IVC diameter
LVED (EED) area
- May have confounding factors to limit precision
Dynamic Markers of fluid response
- Try to determine patient’s location on curve by inducing short term change in preload (fluid bolus) & measuring magnitude of response
** Not volume status but fluid response!
LA:Ao, CVCd, CVCci
Type A hyperlactemia
(MC) occurs with clinical evidence of a relative (exercise, tremors, seizures) or absolute (hypoperfusion) tissue oxygen deficiency (more likely lactate >6 mmol/L)
Type B hyperlactemia
occurs in absence of clinical evidence of decreased O2 delivery–> Defective mitochondrial oxidative function and abnormal carbohydrate metabolism but adequate O2 delivery to tissues; usually associated with more mild to moderate increases in lactate (3-6mmol/L)
B1 : assd with underlying disease (Sepsis - A and B , SIRS, Shock)
B2: assd with drugs or toxins (prednisone, ethylene glycol, propylene gylcol -act charcoal, epinethrine)
B3 assd with congenital or hereditary metabolic defects
D Lactate
- Need specialty lab to measure
- Present in 1%-5% of L lactate
- In cats, DKA, propylene glycol intoxication and EPI with bacterial dysbiosis, cats with GI disease
- Consider a rare but possible cause for high anion gap in metabolic acidosis - once through whole checklist of acidosis and can’t find anything
What are the main neurohormonal compensatory mechanisms in shock states?
- Baroreceptor reflexes:
- Carotid sinus (IX) and aortic Arch (X) → NTS in Medulla (cardioregulatory and vasomotor centers)
- Decreased firing (due to dec BP) → decreases PSNS, increases SNS - Chemoreceptor reflexes
- Carotid bodies (IX) & Aortic Arch (X) → NTS of medulla
- Centrally sense pH and PaCO2; Peripherally pH and PaO2
- Decreased PaO2, increased PaCO2 and/or decreased pH → increased SNS to cardiac and vessels, decreased PSNS - Renin-angiotensin-aldosterone system
- ADH
- Counter-regulatory hormones
WHat is SvO2 vs ScvO2?
- SvO2: mixed venous hemoglobin saturation
SvO2 is reflective of the entire body’s oxygen utilization - ScvO2: central venous hemoglobin saturation
ScvO2 is reflective of the cranial portion of the body (head/neck) oxygen utilization - In health state; ScvO2 is greater thanSvO2 due to the increased oxygen utilization of the cerebrum
However, in shock states the relationship becomes reversed and ScvO2 is greater than Svo2 due to splanchnic hypoperfusion
What is coronary Perfusion Pressure?
CPP = aortic diastolic pressure - right atrial diastolic pressure
- higher compression rates improve CPP< HR above 120 decreases due to decreased time in decompressive phase
- Majority of myocardial perfusion happens during decompression phase of chest compressions & determined by coronary perfusion pressure (CPP). Higher CPP = better success of CPR
- takes 60 sec of continuous compressions before CPP reaches maximum
Well performed compressions only provide _______% of normal CO
30
Appropriate respirations for CPR
- 10 breaths/min
- inspiratory time of appx 1 sec
- tidal volume 10 ml/kg
- Avoid hyperventilation → dec arterial CO2→ cerebral vasoconstriction → dec cerebral blood flow
- Avoid high tidal volume: increased PPV→ dec venous return → decreased CPP
Epi dose for CPR
- Low dose (0.01 mg/kg) every other cycle = higher rates of survival to discharge. Recommended initially
- High dose epi (0.1 mg/kg IV) After prolonged CPR - higher rates of ROSC
- ET admin: 10x dose and dilute 1:1 with sterile water; administer with red rubber
*𝛂1: most beneficial during CPR, vasoconstrict periphery, but spare myocardial and cerebral vasculature
Vasopressin CPR
- 0.8 U/kg IV every other cycle of CPR
- Efficacious in acidic environments when 𝛂1 receptors unresponsive
- No 𝛃1 effects → no chronotropic or inotropic effects (which may worsen myocardial ischemia in epi cases)
**V1 receptors
WHen to use alkalinizing agents in CPR?
- CPA >10-15 minutes → acidemia
- Na bicarb 1 mEq/kg once dilutes IV may be considered if prolonged CPA and pH >7 of metabolic origin
**Acidosis usually resolves with ROSC
When should defibrillate in CPR?
- Treatment for Pulseless V tach and V fib
- VF >4 min: one full cycle of CPR prior to defibrillating; this allow blood flow and O2 delivery to myocardial cells → generates ATP and restore normal membrane potentials → more likely to respond positively to defib
** VF less than 4 min –> IMMEDIATE defibrillation
- Biphasic: 2-4J/kg
- Monophasic: 4-6J/kg
** May increase dose by 50% up to 10, recommend doing this only once