Critical Care Flashcards
Hypovolemic Shock
GI bleed, hemorrhage
Low CI
Low PCWP
High SVR (reflex)
Treat with fluid resuscitation
Blood products if Hgb <7 or actively bleeding
Pressors if hypotension not improved after fluids
Cardiogenic Shock
Acute MI, ADHF, valvular injury
Low CI
High PCWP (impaired blood flow causes congestion)
High SVR (reflex vasoconstriction)
Treat based on acute cardiovascular diseases
Obstructive Shock
Massive PE, Tamponade
Low CI
Low PCWP, if tamponade
High PCWP, if massive PE, aortic stenosis)
High SVR
Treat obstruction to reverse shock
PE: thrombectomy or thrombolytics
Tamponade: remove fluid
Fluids & vasopressors may improve symptoms but not outcomes
Distributive Shock
Sepsis
Early:
High CI
Low PCWP
Low SVR
Late:
Low CI
High PCWP
Low SVR
Antibiotic & fluid resuscitation in first hour
Sepsis
life-threatening end organ dysfunction caused by dysregulated response to infection
Do not use qSOFA as only screening tool
Septic shock
subset of sepsis
profound circulatory, cellular, and metabolic abnormalities are associated with greater mortality risk than sepsis alone
criteria: vasopressor need for MAP >65 and lactate > 2 despite fluid resuscitation
Surviving Sepsis Campaign 1 hour bundle
1) Baseline lactate
2) Obtain blood cultures prior to antibiotics
3) Administer broad spectrum antibiotics
4) 30mL/kg crystalloid infusion (LR may be > NS)
5) Initiate vasopressors if hypotensive during or after fluids for MAP > 65
6) Reassess if persistent arterial hypotension
Vasopressor extravasation
Get central venous access ASAP but may start peripherally to not delay administration
If extravasation occurs, stop immediately and switch to another site
Inject phentolamine (alpha receptor antagonist) around site ASAP to reduce tissue necrosis
Alternatives in shortage: nitroglycerin ointment or SC terbutaline
Vasopressor treatment cascade
1) DOC: Norepinephrine
2) Vasopressin may be added if needed at 0.03 units/minute
3) Epinephrine can be added if inadequate MAP on norepi + vasopressin
Alternative: Dopamine
Phenylephrine
Norepinephrine vs Dopamine
No difference in 28-day mortality
Dopamine associated with higher risk of arrhythmia, more days on vasopressor therapy, and needed another pressor.
Norepi does not improve mortality but is safer and more effective.
Norepinephrine (dose, receptors, info)
0.01-3 mcg/kg/min
alpha»_space; B1
No activity at B2 or DA
Decrease renal perfusion
Increase SVR, MAP
No change or increase CO
May cause peripheral ischemia
Can induce tachyarrhythmia & Myocardial ischemia
Vasopressin (dose, receptors, info)
0.03-0.04 unit/min - no titration
No adrenergic activity at alpha, B1, B2, or DA
V1 agonism = peripheral vasoconstriction
No adrenergic activity = effective during acidosis & hypoxia
High dose = coronary vasoconstriction, peripheral necrosis
Epinephrine (Dose, receptors, info)
0.04-1mcg/kg/min
alpha»_space;>B1=B2
No activity at DA
low doses = beta adrenergic
Positive inotrope/chronotrope = tachyarrhythmia & myocardia ischemia
May increase lactate (type B lactic acidosis) and blood glucose
May reduce splanchnic circ = gut ischemia
Used in refractory hypotension
Phenylephrine (dose, receptors, info)
0.5-8 mcg/kg/min
alpha only (no B1, B2, DA) - minimal cardiac activity
Reduce renal perfusion
Increase SVR, MAP
Primarily used to raise BP. Can rapidly inc SBP, DBP which may cause bradycardia = reduction in CO.
Low dose dopamine (dose, receptors, info)
1-3 mcg/kg/min = lower inotropic dose
+/- alpha
+ B1
+/- B2
++++ DA
Causes renal, coronary, mesenteric, and cerebral arterial vasodilation & natriuretic response
Do not use for renal protection. No evidence to support
Complements vasoconstrictive effects of norepi
May induce arrhythmia. May cause endocrine changes.
Immediate precursor to norepi. Prolonged infusion can deplete norepi stores = loss of vasopressor response
Moderate dose dopamine (dose, receptor, info)
3-10 mcg/kg/min
+ alpha
++ B1
0 B2
++ DA
May increase contractility and SVR
Can induce arrhythmia. Can cause endocrine changes.
Immediate precursor to norepi. Prolonged infusion can deplete norepi stores = loss of vasopressor response
High dose dopamine (dose, receptors, info)
10-20 mcg/kg/min
alpha +++
B1 ++
B2 0
DA +
Vasodilatory effect on renal blood flow may be lost due to predominant alpha1 vasoconstrictive effects
Can induce arrhythmia. Can cause endocrine changes.
Immediate precursor to norepi. Prolonged infusion can deplete norepi stores = loss of vasopressor response
Dobutamine (dose, receptor, info)
2-20 mcg/kg/min
B1»_space;> alpha = B2
0 DA
Positive inotrope = increased CO
B2 stimulation = possible hypotension
Higher doses can cause tachyarrhythmia and changes in BP which may cause myocardial ischemia
Milrinone (dose, receptor, info)
50 mcg/kg load over 10 min, then 0.375-0.75 mcg/kg/min
*Load often omitted due to increased risk of vasodilation - vasodilation can cause hypotension, arrhythmia
Nonadrenergic
PDE type 3 inhibitor
Positive inotrope = increased CO
Renally adjust
Angiotensin II (dose, receptor, info)
10-80 ng/kg/min then 1.25-40 ng/kg/min
Nonadrenergic
Causes smooth muscle contraction & vasoconstriction
Increased thrombotic risks
May cause increased HR, LA, infections, delirium
ACE-I = exaggerated response
ARB = reduced response
Antibiotic cascade in SSC
Broad spectrum abx initiated within an hour (septic shock) after 2 sets of blood cultures and other cultures obtained
Each 1 hour delay = increase risk of mortality by 7.6%
Infuse broadest antibiotic first as rapidly as possible
Limit empiric antibiotic to 3-5 days
SSC steroid recommendation
Hydrocortisone 200mg/day
Unsure if mortality benefit, but has short term benefits
Do not use corticotropic stimulation test
Initiate when norepinephrine needs of > 0.25mcg/kg/min for at least 4 hours
Ascorbic acid in septic shock
Possible anti-inflammatory, antioxidant properties
2021 guidelines recommend against use of ascorbic acid
Metabolic acidosis
pH <7.35
pHCO3 <22
Compensation: increase RR to decrease pCO2
Metabolic alkalosis
pH > 7.45
pHCO3 > 26
Compensation: decrease RR to increase pCO2
Respiratory acidosis
pH < 7.35
pCO2 > 45
Compensation: increase HCO3 (kidneys regulate this)
Respiratory alkalosis
pH > 7.45
PCO2 < 35
Compensation: decrease in HCO3 (kidneys regulate this)
Anion gap calculation
Na - [Cl + HCO3]
Normal: 6-12
>12: primary metabolic acidosis
For every 1 decrease in albumin less than 4, AG decreases by 2.5-3
Respiratory acidosis causes
Think - Decreased respirations
Bronchospasm
Cardiac arrest
CNS depression
PE
Pneumonia
Pulmonary edema
Spinal cord injury
Sedatives
Stroke
Respiratory acidosis treatment
Correct cause
Invasive/noninvasive ventilation
Respiratory alkalosis causes
Think - increased respirations
Anxiety, pain
CNS tumor
Stroke
Head injury
Hypoxia
Stimulants
Reduced oxygen-carrying capacity
Reduced alveolar oxygen extraction
RR stimulation
Extracorporeal removal
Respiratory alkalosis treatment
Correct cause
O2 supplement
Invasive/noninvasive ventilation
Hypoventilation
Sedation