Hypotension & Shock Flashcards
shock - defined
*the physiologic state characterized by significant reduction of systemic tissue perfusion (blood flow), resulting in decreased tissue oxygen delivery
*if it persists, this imbalance b/w oxygen delivery & oxygen consumption → cell death, end organ damage, multi-system organ failure, and death
hypotension - defined
*systolic BP < 90 mmHg
*mean arterial pressure < 60 mmHg
*symptoms: light-headedness, dizziness, blurry vision
*lab findings (in acute settings):
-increased creatinine
-increased lactate/lactic acid
causes of hypotension (simple)
- decreased cardiac output
OR - decreased systemic vascular resistance
hemodynamic parameters obtained from Swan-Ganz catheter
*systemic vascular resistance (SVR)
*cardiac output (CO) - Fick equation
*mixed venous oxygen saturation (SvO2) - measured from the pulmonary artery
*pulmonary capillary wedge pressure (PCWP) - measured by blocking a pulmonary capillary
*central venous pressure (CVP) - measured in the right atrium
pulmonary capillary wedge pressure (PCWP)
*by occluding the pulmonary capillary (w/ Swan-Ganz catheter), the distal port measures the left atrial pressure, since the pressure from the capillary to the left atrium is almost the same
*left atrial pressure = LV diastolic pressure
types of shock
- cardiogenic
- hypovolemic
- distributive (septic, anaphylactic, neurogenic)
- obstructive
- combined/mixed
differentiating types of shock: HYPOVOLEMIC shock
*findings: low CO, low heart pressures (PCWP, CVP), high SVR
*decreased PCWP (preload; left atrial pressure)
*decreased cardiac output (pump function)
*increased systemic vascular resistance (afterload)
*decreased mixed venous oxygen saturation (tissue perfusion)
differentiating types of shock: CARDIOGENIC shock
*findings: low CO, HIGH heart pressures (PCWP, CVP, high SVR
*INCREASED PCWP (preload)
*decreased cardiac output (pump function)
*increased systemic vascular resistance (afterload)
*decreased mixed venous oxygen saturation (tissue perfusion)
differentiating types of shock: DISTRIBUTIVE shock
*findings: DECREASED SVR, INCREASED CO, decreased PCWP and CVP, increased mixed venous oxygen saturation
*decreased PCWP (preload)
*INCREASED cardiac output (pump function)
*DECREASED systemic vascular resistance (afterload)
*increased mixed venous oxygen saturation (tissue perfusion)
method for differentiating types of shock
1) look at cardiac output first:
2a) if CO DECREASED, look at PCWP (preload)
~decreased PCWP (preload) = HYPOVOLEMIC SHOCK
~increased PCWP (preload) = CARDIOGENIC SHOCK
2b) if CO INCREASED, look at SVR:
~decreased SVR (afterload) = DISTRIBUTIVE SHOCK
cardiogenic shock - overview
*systemic hypoperfusion secondary to severe depression of cardiac output & sustained systolic arterial hypotension with ELEVATED LEFT VENTRICULAR FILLING PRESSURE (i.e. elevated PCWP/INCREASED PRELOAD)
cardiogenic shock - etiologies
*ACUTE MYOCARDIAL INFARCTION/ISCHEMIA
*LV failure
*ventricular septal rupture (post-MI)
*papillary muscle/chordal rupture
*ventricular free wall rupture
*acute fulminant myocarditis
*valvular endocarditis
cardiogenic shock - pathophysiology
*systolic: myocardial injury/necrosis → decreased cardiac output → decreased systemic perfusion → compensatory vasoconstriction (INCREASED AFTERLOAD) → increasing dysfunction → shock/death
*diastolic: myocardial injury/necrosis → increased LV end-diastolic pressure (INCREASED PRELOAD) → pulmonary congestion → hypoxemia → ischemia → increasing dysfunction → shock/death
cardiogenic shock - clinical findings
*physical exam: elevated JVP, +S3 heart sound, rales, acute pulmonary edema
*hemodynamics: decreased CO, increased SVR, decreased SvO2, increased PCWP
*initial evaluation: hemodynamics (PA catheter), echocardiography, angiography
cardiogenic shock - 4 potential therapies
- pressors to maintain BP and improve CO (dobutamine, milrinone, dopamine, etc)
- intra-aortic balloon pump
- revascularization: coronary artery bypass/percutaneous coronary intervention (if CAD)
- fibrinolytics (only for STEMI)
*refractory shock: ventricular assist device, cardiac transplantation
hypovolemic shock - overview
*shock caused by decreased preload due to intravascular volume loss (~20% of blood volume)
*results in decreased CO
*SVR is increased in an effort to compensate
hypovolemic shock - etiologies
*hemorrhagic: trauma, GI bleed, hemorrhagic pancreatitis, fractures
*fluid loss induced: diarrhea, vomiting, burns
hemorrhagic hypovolemic shock - pathogenesis
*as blood is lost, venous return decreases and it is more difficult to maintain cardiac output
response mechanisms for hemorrhagic hypovolemic shock
*sympathetic system activated by hypotension: NE, vasopressin, and angiotensin-2 mediate arteriolar vasoconstriction
*post-capillary sphincters at site of bleeding constrict down due to decreased capillary pressure from bleeding
hypovolemic shock - treatments
*FLUIDS!!! (lots of fluids)
*once adequately volume-resuscitated, if still hypotensive, start pressors for further vasoconstriction
*blood products if needed
*control further blood loss (tourniquets, surgical intervention)
comparing hypovolemic vs. cardiogenic shock
*both have compromised cardiac outputs
*hypovolemic: no flow because NO BLOOD (DECREASED PRELOAD)
*cardiogenic: no flow because PUMP NOT WORKING (INCREASED PRELOAD)
note: PCWP is important for differentiation (high PCWP = cardiogenic; low PCWP = hypovolemic)
distributive shock - overview
*shock as a result of severely DIMINISHED SVR (extensive vasodilation)
*cardiac output is typically increased in an effort to maintain perfusion
*subtypes:
1. SEPTIC: secondary to overwhelming infection
2. ANAPHYLACTIC: secondary to a life-threatening allergic reaction
3. NEUROGENIC: secondary to a sudden loss of the autonomic nervous system function
stages of distributive shock
- “preshock” aka compensated/warm shock:
-body is able to compensate for decreased perfusion
-up to ~10% reduction in blood volume
-tachycardia to increase cardiac output & perfusion - “shock”
-compensatory mechanisms are overwhelmed
-see signs/symptoms of organ dysfunction
-about 20-25% reduction in blood volume - “end-organ dysfunction”
-leading to irreversible organ damage/death
distributive shock - pathogenesis
*sepsis/anaphylaxis/neurogenic → inadequate tissue perfusion → inadequate oxygen delivery to tissues →release of inflammatory mediators → further microvasculature changes, compromised blood flow, and further cellular hypoperfusion
*clinical manifestations: multiple organ failure & hypotension
