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PHM 703: Critical Care/Cancer > Hemodynamic Shock > Flashcards

Hemodynamic Shock Flashcards

1
Q

Shock definition

A

potentially fatal physiologic reaction, state of acute circulatory failure, hypotension
Resulting from various conditions:
* Infection
* Injury
* Hemorrhage
* Dehydration
* Heart failure

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2
Q

Hypotension definition

A

SBP < 90 mmhg
or
↓ 40 mmHg from baseline

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3
Q

Shock characterization

A

↓organ perfusion + inadequate O2 delivery = end organ dysfunction
Characterized by cellular dystonia
1. Diminished blood circulation
2. Inadequate o2 delivery (DO2) to tissues for given oxygen consumption (VO2)
3. Results in anaerobic metabolism

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4
Q

Outcomes of shock

A
  1. Multi-organ system failure (MOSF)
  2. Death
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5
Q

CNS dysfunction

A

encephalopathy
cortical necrosis

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6
Q

Cardiac dysfunction

A

tachycardia, bradycardia
ventricular ectopy
MI, depression

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7
Q

Pulmonary dysfunction

A

acute respiratory failure
ARDS

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8
Q

Renal dysfunction

A

Pre-renal insults
AKI
Acute tubular necrosis

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9
Q

GI dysfunction

A

erosive gastritis
Ileus
pancreatitis

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10
Q

Hepatic dysfunction

A

ischemic hepatitis
cholestasis
shock liver

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11
Q

Metabolic dysfunction

A

hyperglycemia, glycogenolysis, gluconeogenesis, hypoglycemia (late)

hypertriglyceridemia

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12
Q

Immune system dysfunction

A

gut barrier fx
cellular/humoral immunity depression

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13
Q

Vital signs: CV organ compromise

A

Cardiac index <2.2 L/min/m2 (invasive)
SBP<90
or MAP < 65

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14
Q

Vital signs: tissue hypoperfusion

A

cold clammy mottled
Lactate
SCVO2<65 or SCO2<60

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15
Q

Vital signs: organ dysfunction

A

Encephalopathy, lethargy, confusion
UOP <0.5 ml/kg/hr
Liver dysfunction

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16
Q

Hemodynamic parameters

A

BP = CO x SVR
CO = HR x SV

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17
Q

SV

A

preload
intrinsic contractility
afterload

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18
Q

SVR

A

increases with vasoconstriction (cold skin)
decreases with vasodilation (warm skin)

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19
Q

MAP calculation

A

⅓ SBP + ⅔ DBP

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20
Q

MAP

A

cardiac output
vascular resistance

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21
Q

CO

A

heart rate x stroke volume

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22
Q

Monitoring Devices

A

CVC - subclavian
PAC - Swan ganz
Arterial line - radial artery

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23
Q

Central venous catheter (CVC)

A

Measures: Venous blood gas (SCVO2 >65%)
Administers: Fluids, Vasopressors, Antimicrobials, TPN

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24
Q

Pulmonary Artery Catheter (PAC)

A

Measures :
* Pulmonary capillary wedge pressure
- Preload (LV end diastolic volume)
- Critical to assess volume status
* Cardiac output/cardiac index
* Mixed venous oxygen saturation (SVO2)
* Systemic vascular resistance (SVR)
- May get if vasodilated - generally not done or recorded

Not commonly used - several complications
Infections, ruptured pulmonary artery

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25
Q

Arterial Line

A

radial artery, continuous feedback
Measures MAP, SBP and DBP, ABG

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26
Q

Types of Shock

A

Hypovolemic - trauma
Cardiogenic - acute MI
Distributive - septic
Obstructive - PE, pulm HTN

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27
Q

Hemodynamic optimization

A

Assess volume status (preload)
Restore MAP ≥ 65 mmHg
Normalize lactate < 2 mmol/L
Venous oxygen saturation (VBG)
PA catheter: SVO2 > 60%
CVC: SCVO2 >65%
HR < 100 BPM

PCWP = 12-15 mmhg (swan gans/PAC)
Cardiac index >2.2 L/min/m2
Maintain oxygen delivery
* Hbg 7-9 gm/dL
* Arterial saturation > 88-92%
* SVO2/SCVO2 > 65%/70%
Reversal of oxygen dysfunction
* Lactate clearance to <2 mmol/L or normalization
Maintain urine output
* >0.5 ml/kg/hr
Reverse encephalopathy

28
Q

Optimizing preload

A

Fluid responsive = increased cardiac output
Blood pressure alone is not a reliable indicator of cardiac output
Stroke volume = amount of blood able to push out of heart
Preload = based on how much volume we have
Trend: drastically increase preload with increased SV
As you keep giving more volume, SV may not change as much→ overshooting can put someone in heart failure/acute MI (depress stroke volume by overextending LV) – would req diuresis

29
Q

Hypovolemic Shock

A

1 cause of death in those <45 y/o (trauma/hemorrhagic shock)

Inappropriately low and sudden loss of intravascular volume

30
Q

Hypovolemic - circulatory

A

Due to decreased preload (stroke volume) → HR increase
Increased afterload – Try to clamp down and shunt blood to brain/heart (SNS vasoconstriction to maintain BP)
Compensatory increase in SVR (BP/CO)

Venous = arterial

31
Q

Hemodynamic Shock Tx

A

Identify source of loss - surgical hemostasis may be required
Hemorrhage - replace blood
* Hgb: PRBCs
* May also need to give FFP and platelets
* Anticoagulation reversal (if AC cause of bleeding)
GI losses, burns, third spacing
* Fluid replenishment - titrate to target
* Crystalloids (check HR, SBP, MAP)
* Albumin - occasionally

32
Q

Cardiogenic Shock

A

Failure of left ventricle to deliver blood due to impaired stroke volume or heart rate “pump failure”

33
Q

Causes of cardiogenic shock

A

associated with CV disease
ACUTE MYOCARDIAL INFARCTION
Arrhythmias
Heart block, afib, vtach
End stage heart failure (ADHF)
Valve failure/disease
Dilated cardiomyopathy
etc

34
Q

Cardiogenic - circulatory

A

Failure to empty left ventricle
High venous pressure = fluid extravasation + edema
Tissue perfusion: pooling in extremities; venous O2 sat low
Preload: increases - unable to circulate volume
Cardiac output: decreased d/t mechanism of injury
Afterload: increases - senses lack of perfusion

Compensatory mechanism - vasoconstriction to maintain BP

Venous fluid&raquo_space; arterial

35
Q

Cardiogenic Shock tx

A

MI = Revascularization - cardiac catheterization or CABG
Arrhythmia = Try to achieve sinus rhythm (BB, CCB, antiarrhythmics)
Advance methods
* Left ventricular assist devices (LVAD)
* Impella
* HeartMate and Tandem Heart
ECMO

36
Q

Distributive Shock

A

Characterized by pronounced vasodilation – may have component of intravascular volume depletion// Not as much volume returning (lacks preload)

37
Q

Distributive Shock Causes

A
  • Septic shock - classic example
  • Anaphylaxis
  • Neurogenic, myxedema coma (thyroid insufficiency)
  • Adrenal insufficiency, hepatic insufficiency
  • Pancreatitis
38
Q

Distributive - circulatory

A

Vasodilation, hypovolemia = reduced SVR (preload)
Venous: Volume returning to the heart is reduced = Therefore, decreased preload

Arteries: capillary leak worses hypovolemia = edema

Compensation
Increase heart rate to maintain cardiac output (comp the low SV)
CO = HR x SV

39
Q

Septic Shock

A

Infection - release of proteins/inflammatory mediators → vasodilation
Early on - able to compensate (initial elevation CO and perfusion)
Later on - depressed CO and perfusion long term

40
Q

Obstructive shock

A

nonpharm mechanism
Results from critical decrease in left ventricular stroke volume or increase in left ventricle outflow obstruction – noncardiogenic

However, preload measurement will appear “elevated” due to ‘obstruction’ (increased intrathoracic pressure/LV)

Compensation: Increased afterload

41
Q

Obstructive - circulatory

A

backpressure = venous congestion
sympathetic overactivity = arterial vasoconstriction to maintain BP

Venous fluid > arterial

42
Q

Common causes of distributive shock

A

Pulmonary embolism = Treat with thrombolytic or remove mechanically
Severe pulmonary hypertension (RV artery – decreased flow)
Tension pneumothorax= Needle decompression
Pericardial tamponade
Manifestation of thrombolytic therapy, acute MI (pericardium fills with fluid, unable to pump)= Drain fluid

43
Q

Fluid therapy - shock states

A

Frank-starling curve theory = increases stroke volume, cardiac output, delivery O2
Use fluid asap to prevent need for vasopressors!

  • Crystalloid 30 ml/kg over 15-30 min (LR/NS) via central line
  • Then by 10 ml/kg boluses
  • Cardiogenic shock
  • 100-200 ml bolus

Optimize preload

44
Q

starting vasoactive agents (vasopressors)

A

Start when MAP < 65 mmhg despite fluid admin
CVC req. for administration + arterial line for monitoring

45
Q

Vasopressors/Inotropes

A

NE, EPI, DA (chronotropy), PE, ADH
Dobutamine

46
Q

Norepinephrine (NE) MOA/effect

A

Alpha agonist
Increases MAP via peripheral vasoconstriction
+ b1 minimal fx on HR at lower doses

47
Q

Norepinephrine (NE) use

A

septic shock #1
0.01 - 3 mcg/kg/min or 5-65 mcg/min
Downregulation of a receptor - higher dose req.
Improves RBF in fluid resuscitated patients

48
Q

Norepinephrine (NE) ADR

A

Major ADR: Significant vasoconstriction

49
Q

Epinephrine (EPI) MOA/effect

A

Dose dependent activity
Low: b1 (↑ HR/SV), b2 vasodilation
High: a1 stimulation
Distribution of receptors in periphery determines pharmacologic effects

50
Q

Epinephrine (EPI) use

A

0.05 - 2 mcg/kg/min
Increases MAP in septic shock secondary to ↑ HR/SV
2nd line for Sepsis

B2 skeletal muscle receptor stimulation = may increase aerobic lactate production (maybe don’t use lactate CL to guide resuscitation)

Useful for Anaphylactic shock

51
Q

Epinephrine (EPI) ADR

A

ADR: limits utility at higher doses - tachycardia, arrhythmias, cardiac ischemia, peripheral vasoconstriction, reduced RBF, hyperglycemia, hypokalemia

52
Q

Dopamine (DA) MOA/effect

A

EPI/NE precursor
Dose dependent pharmacology mcg/kg/min
< 5 = dopaminergic
* Vasodilation renal/mesenteric/coronary
* ↑RBF, GFR, Na excretion
5-10 = b1 adrenergic
* ↑ cardiac contractility, HR
* ↑ NE release
>10 = a1 adrenergic
* Arterial vasoconstriction
Maximum effects: 20 mcg/kg/min

53
Q

Dopamine (DA) use

A

Most effective: hypotensive w/ depressed cardiac function or cardiac reserve
Use if:
* Low risk for arrhythmia
* Significant bradycardia

Critically ill: may not respond in traditional dose-dependent fashion

54
Q

Dopamine (DA) ADR

A

Major ADR
Tachycardia
Arrhythmogenesis
High dose: peripheral vasoconstriction

55
Q

Phenylephrine (PE) MOA/effect

A

selective a1 agonist

High dose - may stimulate beta receptors
Peripheral vasoconstriction – purported reflex bradycardia

56
Q

Phenylephrine (PE) use

A

Usual: 0.5 - 9 mcg/kg/min
Lower dose for non-septic shock
Not for septic shock unless NE causes significant tachyarrhythmia, CO is high and BP persistently low, or other therapies are ineffective

57
Q

Phenylephrine (PE) ADR

A

severe vasoconstriction
bradycardia
myocardial ischemia

58
Q

Dobutamine (DB) MOA/effect

A

B1 inotrope

Inotropic action + vasodilation (BP effects depend on volume status)

59
Q

Dobutamine (DB) use

A

2 - 20 mcg/kg/min
Added to treatment of shock when cardiac output or ScO2/ScvO2 goals have not been achieved with vasopressor therapy

Often used for cardiogenic shock (pump failure)

60
Q

Vasopressin (ADH) MOA/effect

A

Released from pituitary - in response to ↓blood volume or ↑plasma osmolarity
V1: directly constricts smooth muscle + indirectly increases catecholamine release
V2: ADH activity
V3: increases ACTH release

61
Q

Vasopressin (ADH) use

A

Relative deficiency of ADH in septic shock
Low dose 0.01 - 0.04 units/min to increase MAP in catecholamine-resistant hypotension
Sepsis dose: 0.03 units/min not to be used as monotherapy in sepsis
Goal: reduce concurrent vasopressor doses

62
Q

Vasopressin (ADH) ADR

A

ADR: cardiac + mesenteric ischemia (w/ higher doses)

63
Q

Giapreza (AGII) MOA/effect

A

Angiotensin II - peptide hormone of RAAS vasoconstriction + aldosterone release

64
Q

Giapreza (AGII) use

A

Indicated for septic shock + distributive shock
Given by central line continuous infusion d/t short half life <1 min
* Titrated for MAP goal
* Add to standard therapy (NE)
* Used to reduce catecholamine vasopressor use

RISK: thromboembolism

65
Q
A

PHM 703: Critical Care/Cancer (17 decks)

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