Hypotension/Shock Flashcards

1
Q

What should always be started with hypotension?

A

Small fluid bolus to check fluid responsiveness

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2
Q

What is shock?

A

Physiologic condition of inadequate systemic tissue perfusion–decreased O2 delivery–cellular hypoxia and metabolic malfunction

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3
Q

What determines systemic tissue perfusion?

A

Mean Arterial pressure (which equals CO x SVR)

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4
Q

What influences SVR

A

Vessel length and diameter and blood viscosity

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5
Q

Ways to assess adequate global perfusion

A
Mental status
UOP
Serum lactate/acidosis
Peripheral perfusion assessment
(not all pts with hypotension are in shock)
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6
Q

Stages of shock

A

Pre-shock
Shock
End organ dysfunction

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7
Q

What is pre-shock?

A

Warm shock or compensated shock

Tachycardia, peripheral vasoconstriction, hypotension

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8
Q

Shock as a stage

A

Compensatory mechanisms overwhelmed and s/s of organ dysfunction appear
Tachycardia, dyspnea, metabolic acidosis, oliguria, confusion, cool clammy skin

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9
Q

Categories for the etiologies of shock

A
Hypovolemic
Cardiogenic
Obstructive
Neurogenic
Distributive
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10
Q

Lines used in resuscitation

A

Arterial line
Central line
Swan Ganz (pulm artery) catheter

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11
Q

Arterial line in shock

A

Radial/ brachial/ femoral
Invasive arterial BP monitoring (recurrent ABGs)
Don’t use for meds!!

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12
Q

Indications for central line

A

Delivery of caustic or critical meds and measurement of CVP (triple lumen, double lumen, dialysis catheters, Swan-Ganz catheter, PICC line-peripherally inserted central line)

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13
Q

Normal value of central venous pressure

A

5-15 mmHg

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14
Q

What is central venous pressure?

A

Pressure near right atrium
Correlates to preload or overall volume status
Can be obtained with any central line
*trend it

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15
Q

Normal value of pulmonary capillary wedge pressure (hemodynamic parameter)

A

5-15 mmHg

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16
Q

Normal value for cardiac output (hemodynamic parameter)

A

4-8 L/min

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17
Q

Normal value for SVR (hemodynamic parameter)

A

1000-1500 dynes/sec/cm5

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18
Q

When to monitor hemodynamics

A

If cause of shock is unclear

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19
Q

Most appropriate to monitor hemodynamics in cardiogenic shock

A

Swan-Ganz catheters

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20
Q

What is used to monitor hemodynamics in all other types of shock?

A

Central lines (include PICC lines) to determine vol status (CVP) and resuscitation

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21
Q

Presentation of all types of shock

A

Hypotension (SBP<90 or decrease SBP >40)
Tachycardia and tachypnea
Oliguria
Mental status changes (confusion, lethargy)
Metabolic acidosis
Cool clammy skin
Later: multi organ failure and coagulopathy

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22
Q

What shock has a decreased HR?

A

Neurogenic shock

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23
Q

What shock has flushed and warm skin?

A

Early distributive and neurogenic shock

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24
Q

Why can pregnant pts present differently with shock?

A

Can compensate for a while b/c increased CO

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25
Q

What is hypovolemic shock?

A

Inadequate intravascular volume leads to decrease CO and decreased O2 delivery

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26
Q

Etiology of hypovolemic shock

A
Blood loss/hemorrhagic (TRAUMA, GI bleeding, internal hemorrhage, post-surgical)
Fluid loss (dehydration-n/v/d, burns, acute pancreatitis)
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27
Q

What happens in hypovolemic shock?

A

Switch from aerobic to anaerobic metabolism
Decreased BP from baroreceptors activates SNS and vasoconstriction
Blood shunted and redistributed

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28
Q

Hemodynamic parameters of hypovolemic shock

A

CVP down <5
CO down <4
SVR up >1500

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29
Q

What does the presentation of hypovolemic shock depend on?

A

Amount of loss (small can be tolerated)

Rate of loss (slow allow for time to compensate)

30
Q

Presentation of hypovolemic shock

A

Hematemesis, hematochezia, melena
N/v/d
Abd pain, evidence of trauma
Post-op

31
Q

PE of hypovolemic shock

A

Dry oral mucosa
VS: hypotension, tachycardia/pnea, decreased JVP/ CVP/ urine output
Cool and clammy with decreased turgor
Confused

32
Q

Diagnostic studies for hypovolemic shock

A
CBC, CMP, PT/INR
Lactate
ABG
CXR/ CT
Abd x-ray/ CT
33
Q

Lactate in hypovolemic shock

A

Lactate increases during anaerobic metabolism, derangements affecting O2 utilization and decreased hepatic clearance
Increased mortality!

34
Q

Management for hypovolemic shock

A
Tx underlying problem
Replace vol (crystalloid-normal saline, colloid-albumin, blood)
Monitor response (urine output, perfusion, mentation)
35
Q

Vasopressors in hypovolemic shock

A

Must remember that best thing to do replace vol b/c thats the problem!
If dire situation (SBP<70) can use while replacing vol

36
Q

What is cardiogenic shock?

A

Decreased CO secondary to pump failure

37
Q

Etiology of cardiogenic shock

A

Ischemia (MI, cardiomyopathy)
Valvular heart disease
Arrhythmias
OBSTRUCTIVE (extracardiac- massive PE, cardiac tamponade, tension pneumo)

38
Q

Pathophys of cardiogenic shock

A

Pump failure- activate SNS
Hypotension and decreased CO so decreased renal perfusion (sodium and fluid retention)
Increase filling pressure-vol overload in lungs
Increase SVR to compensate for decreased CO

39
Q

Hemodynamic parameters of cardiogenic shock

A

CVP increased >5 (preload)
PCWP increased >5
CO decreased <4
SVR increased >1500 (Afterload)

40
Q

Presentation of cardiogenic shock

A

Chest pain, dyspnea, palpitations, fatigue

41
Q

PE for cardiogenic shock

A

VS: tachycardia, tachypnea, hypotension
Cool and clammy
Cardiac: increased JVP, muffled heart sounds, new murmur
Pulm: trachea deviated, lungs depend on pathology (crackles if pulm edema)

42
Q

Studies for cardiogenic shock

A

CBC, CMP
Cardiac enzymes
ABG, EKG, CXR, echo
CT chest

43
Q

Management for cardiogenic shock

A
Treat underlying probs
Cardiology consult (preserve function and perfusion)
Fluids but be cautious
Inotropes (to enhance contractility)
Diuresis, anti-arrhythmias, HF meda
44
Q

How to treat underlying cause of cardiogenic shock

A

MI: O2, cath lab
Vtach/fib: ACLS
Tension pneumo: decompression
Cardiac tamponade: pericardiocentesis

45
Q

First line inotrope for cardiogenic shock

A

Dobutamine

46
Q

Last line management for cardiogenic shock

A

Assist devices (LVAD, RVAD, total artificial heart)
ECMO
Heart transplant

47
Q

What is distributive (vasodilatory) shock?

A

Decreased SVR (vasodilation)

48
Q

Etiologies of distributive shock

A
SEPSIS
Adrenal insufficiency
Liver disease
Anaphylaxis
Drugs/meds
(SALAD)
and neurogenic
49
Q

What is septic shock?

A

Inadequate tissue perfusion and cellular hypoxia from increased O2 demand from tissues to combat systemic infection and septic endotoxins

50
Q

Etiology of septic shock

A

Any kind of infection (UTI, pneumonia, bacteremia)

51
Q

Pathophys of early septic shock

A

Initial response to meet increased demand for O2 by cells is vasodilation
Decrease SVR and hypotension
Detect low BP and increase HR and CO
Start to see signs of organ impairment (due to endotoxins)
*associated with hyperdynamic response-well compensated but difficult to maintain

52
Q

Pathophys of late septic shock

A

Capillary leakage and loss of vascular tone so relative hypovolemic and hypotension
Stimulate SNS more
Increased HR and SVR (vasoconstriction aggravates cellular hypoxia)

53
Q

PE for septic shock

A

VS: fever, hypotension, tachycardia and tachypnea
Extremities: warm early and cool late
Confused

54
Q

Common initial physiologic response to septic shock

A

Tachypnea

55
Q

When to suspect septic shock in elderly or immunocompromised

A

Unexplained hypotension, mental status changes or signs of organ system dysfunction

56
Q

Hemodynamic parameters of early (warm) shock

A

Decrease CVP
Increased CO
Decreased SVR

57
Q

Hemodynamic parameters of late (cold) shock

A

CVP +/- usually decreased
Decreased CO
Increased SVR

58
Q

Studies for septic shock

A

CBC, CMP
Lactate
Cultures (blood x2, urine, sputum)
ABC, CXR

59
Q

Management of septic shoc

A
Goal directed therapy
Panculture before abx then empiric
Fluid resuscitation
Vasopressors
Ventilator if needed
60
Q

First line vasopressor for septic shock

A

NE

61
Q

What causes anapylaxis?

A

Sudden release of mast cell mediators into systemic circulation (IgE usually)

62
Q

Sxs of anaphylaxis

A

Skin/mucosa: hives, rash, itch, edema, conjunctival swell
Resp: discharge, congestion, voice quality, throat swelling, stridor, SOB, wheeze
GI: n/v/d, abd pain
CV: syncope, dizzy, tachycardia, hypotension

63
Q

Most often death from anaphylaxis

A

Usually due to asphyxiation due to upper or lower airway obstruction or from CV collapse/shock

64
Q

Tx for anaphylaxis

A
IM Epi 1:1000 (.01 mg/kg IM)
Oxygen, airway
Fluid bolus
H1 antihistamine (diphenhydramine)
Maybe steroids (methylprednisolone)
65
Q

What is neurogenic shock?

A

Loss of sympathetic tone, leading to vasodilation and hypotension (bradycardia + hypotension)

66
Q

Etiology of neurogenic shock

A

Spinal cord injury (disruption b/w brain and spinal cord)

Closed head trauma (injury to brain stem)

67
Q

Pathophys of neurogenic shock

A

Sympathetics travel down cervical spinal cord etc
Release epi and NE to increase HR, contraction and vasoconstriction
Disruption of SNS results in unopposed PNS action
Hypotension with decreased SVR and normal to decreased HR

68
Q

PE for neurogenic shock

A

VS: HR normal or decreased and hypotension
Altered LOC, para/quadriplegic, senses affected based on lesion, absent or hyperreflexia, warm extremities
Decreased sphincter tone

69
Q

Hemodynamic parameters of neurogenic shock

A

CVP normal or decreased <5
CO normal or decreased <4
SVR decreased <1500

70
Q

Studies for neurogenic shock

A

CBC, CMP
X-rays (C spine to clear )
Head CT (structural lesions or hernation)
Spinal CT/MRI

71
Q

Management of neurogenic shock

A

Co-existing probs
Fluids for relative hypovolemia
Neurosurgery consult!