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Cardiology Exam > Hypotension & Shock > Flashcards

Hypotension & Shock Flashcards

1
Q

shock - defined

A

*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

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2
Q

hypotension - defined

A

*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

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3
Q

causes of hypotension (simple)

A
  1. decreased cardiac output
    OR
  2. decreased systemic vascular resistance
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4
Q

hemodynamic parameters obtained from Swan-Ganz catheter

A

*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

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5
Q

pulmonary capillary wedge pressure (PCWP)

A

*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

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6
Q

types of shock

A
  1. cardiogenic
  2. hypovolemic
  3. distributive (septic, anaphylactic, neurogenic)
  4. obstructive
  5. combined/mixed
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7
Q

differentiating types of shock: HYPOVOLEMIC shock

A

*decreased PCWP (preload)
*decreased cardiac output (pump function)
*increased systemic vascular resistance (afterload)
*decreased mixed venous oxygen saturation (tissue perfusion)

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8
Q

differentiating types of shock: CARDIOGENIC shock

A

*INCREASED PCWP (preload)
*decreased cardiac output (pump function)
*increased systemic vascular resistance (afterload)
*decreased mixed venous oxygen saturation (tissue perfusion)

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9
Q

differentiating types of shock: DISTRIBUTIVE shock

A

*decreased PCWP (preload)
*INCREASED cardiac output (pump function)
*DECREASED systemic vascular resistance (afterload)
*increased mixed venous oxygen saturation (tissue perfusion)

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10
Q

method for differentiating types of shock

A

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

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11
Q

cardiogenic shock - overview

A

*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)

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12
Q

cardiogenic shock - etiologies

A

*ACUTE MYOCARDIAL INFARCTION/ISCHEMIA
*LV failure
*ventricular septal rupture (post-MI)
*papillary muscle/chordal rupture
*ventricular free wall rupture
*acute fulminant myocarditis
*valvular endocarditis

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13
Q

cardiogenic shock - pathophysiology

A

*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

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14
Q

cardiogenic shock - clinical findings

A

*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

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15
Q

cardiogenic shock - 4 potential therapies

A
  1. pressors to maintain BP and improve CO (dobutamine, milrinone, dopamine, etc)
  2. intra-aortic balloon pump
  3. revascularization: coronary artery bypass/percutaneous coronary intervention (if CAD)
  4. fibrinolytics (only for STEMI)

*refractory shock: ventricular assist device, cardiac transplantation

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16
Q

hypovolemic shock - overview

A

*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

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17
Q

hypovolemic shock - etiologies

A

*hemorrhagic: trauma, GI bleed, hemorrhagic pancreatitis, fractures

*fluid loss induced: diarrhea, vomiting, burns

18
Q

hemorrhagic hypovolemic shock - pathogenesis

A

*as blood is lost, venous return decreases and it is more difficult to maintain cardiac output

19
Q

response mechanisms for hemorrhagic hypovolemic shock

A

*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

20
Q

hypovolemic shock - treatments

A

*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)

21
Q

comparing hypovolemic vs. cardiogenic shock

A

*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)

22
Q

distributive shock - overview

A

*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

23
Q

stages of distributive shock

A
  1. “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
  2. “shock”
    -compensatory mechanisms are overwhelmed
    -see signs/symptoms of organ dysfunction
    -about 20-25% reduction in blood volume
  3. “end-organ dysfunction”
    -leading to irreversible organ damage/death
24
Q

distributive shock - pathogenesis

A

*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

25
Q

systemic inflammatory response syndrome (SIRS)

A

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%

26
Q

septic shock - overview

A

*hypotension secondary to sepsis (systemic inflammatory response to infection) that is resistant to adequate fluid administration and associated with hypoperfusion

27
Q

sepsis pathogenesis

A
  1. unbalanced immune reaction → tissue factor release → procoagulant state → microvascular thrombosis
  2. unbalanced immune reaction → release of inflammatory mediators → VASODILATION, capillary leak, and formation of ROS
28
Q

microcirculation in sepsis

A

*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

29
Q

septic shock - treatment

A

*AGGRESSIVE IV FLUIDS first!!!!
*antibiotics
*identify the source (cultures, CT, line & foley removal, surgical exploration)

30
Q

checkpoints to care in the septic patient

A

*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

31
Q

anaphylactic shock - overview

A

*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

32
Q

anaphylactic shock - pathophysiology

A
  1. antigen binds to IgE → activation of mast cells → degranulation/release of inflammatory mediators (esp. histamine)
  2. 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
33
Q

how epinephrine treats anaphylaxis

A

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

34
Q

treatment of anaphylaxis with epinephrine if a patient is on a beta blocker

A

*if on a beta-blocker, may consider glucagon (potentiates intra-cellular effects of epi by bypassing the blocked beta receptors) in addition to epinephrine

35
Q

obstructive shock - overview

A

*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

36
Q

obstructive shock - etiologies

A

*intrinsic: pulmonary embolism
*extrinsic:
-pericardial effusion → cardiac tamponade
-tension pneumothorax

37
Q

obstructive shock due to pericardial effusion - pathogenesis

A

*pericardial effusion → compresses RV during diastole → RV less blood in, less blood out → limits filling of left ventricle → less blood into aorta → tachycardia

38
Q

obstructive shock due to pulmonary embolism - pathogenesis

A

*pulmonary embolism → obstruction of pulmonary artery → pulmonary artery less blood in, less blood out → limits filling of left ventricle → less blood into aorta → tachycardia

39
Q

cardiac tamponade

A

*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

40
Q

comparing the treatment for cardiogenic, hypovolemic, and distributive shock

A

*hypovolemic & distributive: FLUIDS! (consider pressors [NE, phenylephrine, vasopressin] if still hypotensive after adequate fluid resuscitation)

*cardiogenic: pressors (dobutamine, milrinone, dopamine), NO fluids!

41
Q

common signs/symptoms associated with shock

A

*oliguria (decreased urine production)
*altered mental status
*cool/clammy skin
*lactic acidosis due to anaerobic metabolism (lack of oxygen)

Cardiology Exam (47 decks)

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