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
systemic inflammatory response syndrome (SIRS)
defined by an acute change from baseline in TWO out of the four criteria:
*temperature > 38 or < 36
*HR > 90
*RR > 20 or PaCO2 < 32
*SBC > 12 or < 4 or bands < 10%
septic shock - overview
*hypotension secondary to sepsis (systemic inflammatory response to infection) that is resistant to adequate fluid administration and associated with hypoperfusion
sepsis pathogenesis
- unbalanced immune reaction → tissue factor release → procoagulant state → microvascular thrombosis
- unbalanced immune reaction → release of inflammatory mediators → VASODILATION, capillary leak, and formation of ROS
microcirculation in sepsis
*sepsis leads to:
-microthrombi in capillaries
-slow flow/no flow in capillaries
-capillary dysfunction
-leaky capillaries
*areas with an affected capillary have:
-less oxygen
-less venous return
-less flow
-buildup of lactate
septic shock - treatment
*AGGRESSIVE IV FLUIDS first!!!!
*antibiotics
*identify the source (cultures, CT, line & foley removal, surgical exploration)
checkpoints to care in the septic patient
*CVP > 8 mmHg indicates adequate fluid resuscitation
*early ABX (broad-spectrum)
*MAP > 65 mmHg helps to ensure that all organs are getting the pressure they need to perfuse
*SvO2 > 70% ensures that tissues are getting adequate oxygenation and CO
anaphylactic shock - overview
*shock secondary to a severe allergic reaction (mostly IgE mediated)
*top causes of anaphylaxis:
-food (peanuts, shellfish, milk, red meat)
-stinging insects (bees, ants)
-meds (penicillins)
-radiocontrast media
anaphylactic shock - pathophysiology
- antigen binds to IgE → activation of mast cells → degranulation/release of inflammatory mediators (esp. histamine)
- histamine leads to:
-bronchoconstriction/tongue swelling
-VASODILATION → plummet in SVR and reflex tachycardia
-increased vascular permeability → fluid leaves vascular space through leaky capillaries → decreased vascular volume
how epinephrine treats anaphylaxis
epinephrine is an agonist for beta1, beta2, and alpha 1 receptors:
*beta1: increases heart rate & contractility → INCREASED CARDIAC OUTPUT
*beta2: inhibits mast cells from releasing more histamine & bronchodilation
*alpha1: vasoconstriction & decreased capillary leak → increased systemic vascular resistance
*overall: increasing CO & SVR helps to restore BP; inhibition of mast cells addresses the source of the shock
treatment of anaphylaxis with epinephrine if a patient is on a beta blocker
*if on a beta-blocker, may consider glucagon (potentiates intra-cellular effects of epi by bypassing the blocked beta receptors) in addition to epinephrine
obstructive shock - overview
*with obstructive shock, there is either intrinsic or extrinsic obstruction that limits cardiac output (no problem with heart muscle itself)
*common features: tachycardia & increased SVR
obstructive shock - etiologies
*intrinsic: pulmonary embolism
*extrinsic:
-pericardial effusion → cardiac tamponade
-tension pneumothorax
obstructive shock due to pericardial effusion - pathogenesis
*pericardial effusion → compresses RV during diastole → RV less blood in, less blood out → limits filling of left ventricle → less blood into aorta → tachycardia
obstructive shock due to pulmonary embolism - pathogenesis
*pulmonary embolism → obstruction of pulmonary artery → pulmonary artery less blood in, less blood out → limits filling of left ventricle → less blood into aorta → tachycardia
cardiac tamponade
*increased fluid collection around the heart → compression of the heart
*pressure in the pericardium exceeds venous pressure, which means that the pericardial effusion is squeezing the right heart during most of diastole
*requires emergent pericardiocentesis (drains fluid from the pericardial space)
note: do NOT drain pericardial effusion if it is caused by an ascending aortic dissection
comparing the treatment for cardiogenic, hypovolemic, and distributive shock
*hypovolemic & distributive: FLUIDS! (consider pressors [NE, phenylephrine, vasopressin] if still hypotensive after adequate fluid resuscitation)
*cardiogenic: pressors (dobutamine, milrinone, dopamine), NO fluids!
common signs/symptoms associated with shock
*oliguria (decreased urine production)
*altered mental status
*cool/clammy skin
*lactic acidosis due to anaerobic metabolism (lack of oxygen)
