Sing special pops septic shock exam 2
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39 Terms
Q: What is shock?
A: Acute, generalized circulatory failure causing inadequate perfusion of cells/organs. SBP < 90 mmHg or MAP < 70 mmHg.
Q: Define MAP.
A: Mean Arterial Pressure: average arterial pressure during a single cardiac cycle.
MAP = CO × SVR.
Q: Define SVR.
A: Systemic Vascular Resistance — resistance the LV must overcome to circulate blood.
Q: Define DO₂.
A: Oxygen delivery to tissues. DO₂ = CO × CaO₂.
Q: Define VO₂.
A: Oxygen consumption by tissues. VO₂ = CO × (CaO₂ – CvO₂).
Q: Define CO.
A: Cardiac Output: amount of blood the heart pumps per minute. CO = HR × SV.
Q: Define SV.
A: Stroke Volume: amount of blood pumped per heartbeat.
Q: Define CaO₂.
A: Arterial oxygen content.
Q: Define CvO₂.
A: Venous oxygen content.
Q: Define SvO₂ and ScvO₂.
A: Mixed venous O₂ saturation (SvO₂) and central venous O₂ saturation (ScvO₂). SvO₂/ScvO₂ > 70% is adequate.
Q: What are the 4 shock syndromes?
A: Hypovolemic, Cardiogenic, Obstructive, Vasodilatory/Distributive.
Q: Examples of hypovolemic shock causes?
A: Trauma, hemorrhage, surgery.
Q: Cardiogenic shock causes?
A: Acute MI (80%), arrhythmias, valvular dysfunction, myocarditis.
Q: Obstructive shock causes?
A: Tension pneumothorax, cardiac tamponade, PE.
Q: Vasodilatory/distributive shock causes?
A: Sepsis (96%), anaphylaxis, spinal cord injury, pancreatitis, liver failure.
Q: What happens to preload, CO, afterload in hypovolemic shock?
A: ↓ Preload → ↓ CO → ↑ SVR (compensatory).
Q: What happens in cardiogenic shock?
A: ↓ CO from pump failure → ↑ preload (LV dilation) → ↑ SVR.
Q: What happens in obstructive shock?
A: ↓ Preload (tamponade, tension pneumo) OR ↑ afterload (PE) → ↓ CO.
Q: What happens in vasodilatory/distributive shock?
A: ↓ SVR (massive vasodilation) → ↓ preload → ↓ CO.
Q: Primary postsynaptic effect of:
α receptor: Vasoconstriction (↑ SVR).
β receptor: Inotropy/chronotropy (↑ CO).
D receptor: Renal/mesenteric vasodilation.
V receptor: Vasoconstriction + water retention (vasopressin).
AT receptor: Vasoconstriction (angiotensin II).
α receptor: Vasoconstriction (↑ SVR).
β receptor: Inotropy/chronotropy (↑ CO).
D receptor: Renal/mesenteric vasodilation.
V receptor: Vasoconstriction + water retention (vasopressin).
AT receptor: Vasoconstriction (angiotensin II).
Q: Common shock symptoms?
A: Dizziness, confusion, ↓ UO, hypotension, tachycardia, tachypnea, impaired capillary refill (>3 sec).
Q: Lab findings of shcok?
A: Lactate > 2 mmol/L, ↑ SCr/LFTs, INR >1.5, PLT <100k, ↓ H&H (hemorrhage), ↑ troponin (MI), UO <0.5 mL/kg/hr.
Q: Preferred diagnostic imaging for shock?
Echocardiography
Q: Goals of shock treatment?
A: Correct cause, maintain tissue perfusion (MAP ≥ 65), prevent organ damage, de-escalate therapies.
Q: What are the four phases of shock treatment?
A: Salvage, Optimization, Stabilization, De-escalation.
Q: Preferred IV access for fluids?
A: Large-bore peripheral IV x2.
Q: Preferred IV access for vasopressors?
A: Central venous catheter.
Q: Target MAP for most patients?
A: ≥ 65 mmHg.
Q: Exceptions for MAP?A: Elderly: 60–65 mmHg; chronic HTN: 80–85 mmHg; hemorrhagic shock: SBP 80–90 mmHg.
A: Elderly: 60–65 mmHg; chronic HTN: 80–85 mmHg; hemorrhagic shock: SBP 80–90 mmHg.
Q: Preferred fluids for shock?
A: Isotonic crystalloids (NS, LR).
Q: Colloids — when to use?
A: Controversial, theoretically for retained intravascular volume.
Q: Blood products — when indicated?
A: Hemorrhagic shock, Hgb ≤ 7 g/dL.
Q: Fluid dose for sepsis?
A: 30 mL/kg within 3 hours.
Q: Define vasopressor vs inotrope.
A: Vasopressor: ↑ SVR (vasoconstriction). Inotrope: ↑ CO (contractility).
Q: 1st line in septic shock?
A: Norepinephrine.
Q: Dopamine vs dobutamine?
A: Dopamine: mixed effects, less preferred. Dobutamine: strong inotrope for cardiogenic shock.
Q: Vasopressin use?
A: Add-on for septic shock not responding to norepinephrine.
Q: Corticosteroids role?
A: In refractory septic shock to help reduce vasopressor need.
Q: How to wean vasopressors/inotropes?
A: Slowly titrate down, monitor perfusion, avoid abrupt discontinuation.
Note 
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