Hemodynamic Shock Flashcards
Shock definition
potentially fatal physiologic reaction, state of acute circulatory failure, hypotension
Resulting from various conditions:
* Infection
* Injury
* Hemorrhage
* Dehydration
* Heart failure
Hypotension definition
SBP < 90 mmhg
or
↓ 40 mmHg from baseline
Shock characterization
↓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
Outcomes of shock
- Multi-organ system failure (MOSF)
- Death
CNS dysfunction
encephalopathy
cortical necrosis
Cardiac dysfunction
tachycardia, bradycardia
ventricular ectopy
MI, depression
Pulmonary dysfunction
acute respiratory failure
ARDS
Renal dysfunction
Pre-renal insults
AKI
Acute tubular necrosis
GI dysfunction
erosive gastritis
Ileus
pancreatitis
Hepatic dysfunction
ischemic hepatitis
cholestasis
shock liver
Metabolic dysfunction
hyperglycemia, glycogenolysis, gluconeogenesis, hypoglycemia (late)
hypertriglyceridemia
Immune system dysfunction
gut barrier fx
cellular/humoral immunity depression
Vital signs: CV organ compromise
Cardiac index <2.2 L/min/m2 (invasive)
SBP<90
or MAP < 65
Vital signs: tissue hypoperfusion
cold clammy mottled
Lactate
SCVO2<65 or SCO2<60
Vital signs: organ dysfunction
Encephalopathy, lethargy, confusion
UOP <0.5 ml/kg/hr
Liver dysfunction
Hemodynamic parameters
BP = CO x SVR
CO = HR x SV
SV
preload
intrinsic contractility
afterload
SVR
increases with vasoconstriction (cold skin)
decreases with vasodilation (warm skin)
MAP calculation
⅓ SBP + ⅔ DBP
MAP
cardiac output
vascular resistance
CO
heart rate x stroke volume
Monitoring Devices
CVC - subclavian
PAC - Swan ganz
Arterial line - radial artery
Central venous catheter (CVC)
Measures: Venous blood gas (SCVO2 >65%)
Administers: Fluids, Vasopressors, Antimicrobials, TPN
Pulmonary Artery Catheter (PAC)
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
Arterial Line
radial artery, continuous feedback
Measures MAP, SBP and DBP, ABG
Types of Shock
Hypovolemic - trauma
Cardiogenic - acute MI
Distributive - septic
Obstructive - PE, pulm HTN
Hemodynamic optimization
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
Optimizing preload
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
Hypovolemic Shock
1 cause of death in those <45 y/o (trauma/hemorrhagic shock)
Inappropriately low and sudden loss of intravascular volume
Hypovolemic - circulatory
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
Hemodynamic Shock Tx
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
Cardiogenic Shock
Failure of left ventricle to deliver blood due to impaired stroke volume or heart rate “pump failure”
Causes of cardiogenic shock
associated with CV disease
ACUTE MYOCARDIAL INFARCTION
Arrhythmias
Heart block, afib, vtach
End stage heart failure (ADHF)
Valve failure/disease
Dilated cardiomyopathy
etc
Cardiogenic - circulatory
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»_space; arterial
Cardiogenic Shock tx
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
Distributive Shock
Characterized by pronounced vasodilation – may have component of intravascular volume depletion// Not as much volume returning (lacks preload)
Distributive Shock Causes
- Septic shock - classic example
- Anaphylaxis
- Neurogenic, myxedema coma (thyroid insufficiency)
- Adrenal insufficiency, hepatic insufficiency
- Pancreatitis
Distributive - circulatory
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
Septic Shock
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
Obstructive shock
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
Obstructive - circulatory
backpressure = venous congestion
sympathetic overactivity = arterial vasoconstriction to maintain BP
Venous fluid > arterial
Common causes of distributive shock
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
Fluid therapy - shock states
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
starting vasoactive agents (vasopressors)
Start when MAP < 65 mmhg despite fluid admin
CVC req. for administration + arterial line for monitoring
Vasopressors/Inotropes
NE, EPI, DA (chronotropy), PE, ADH
Dobutamine
Norepinephrine (NE) MOA/effect
Alpha agonist
Increases MAP via peripheral vasoconstriction
+ b1 minimal fx on HR at lower doses
Norepinephrine (NE) use
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
Norepinephrine (NE) ADR
Major ADR: Significant vasoconstriction
Epinephrine (EPI) MOA/effect
Dose dependent activity
Low: b1 (↑ HR/SV), b2 vasodilation
High: a1 stimulation
Distribution of receptors in periphery determines pharmacologic effects
Epinephrine (EPI) use
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
Epinephrine (EPI) ADR
ADR: limits utility at higher doses - tachycardia, arrhythmias, cardiac ischemia, peripheral vasoconstriction, reduced RBF, hyperglycemia, hypokalemia
Dopamine (DA) MOA/effect
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
Dopamine (DA) use
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
Dopamine (DA) ADR
Major ADR
Tachycardia
Arrhythmogenesis
High dose: peripheral vasoconstriction
Phenylephrine (PE) MOA/effect
selective a1 agonist
High dose - may stimulate beta receptors
Peripheral vasoconstriction – purported reflex bradycardia
Phenylephrine (PE) use
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
Phenylephrine (PE) ADR
severe vasoconstriction
bradycardia
myocardial ischemia
Dobutamine (DB) MOA/effect
B1 inotrope
Inotropic action + vasodilation (BP effects depend on volume status)
Dobutamine (DB) use
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)
Vasopressin (ADH) MOA/effect
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
Vasopressin (ADH) use
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
Vasopressin (ADH) ADR
ADR: cardiac + mesenteric ischemia (w/ higher doses)
Giapreza (AGII) MOA/effect
Angiotensin II - peptide hormone of RAAS vasoconstriction + aldosterone release
Giapreza (AGII) use
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
