Hemodynamic Shock Flashcards

Question

Arterial Line

Answer 1

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

Answer 2

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

Answer 3

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

Answer 4

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

Answer 5

#1 cause of death in those <45 y/o (trauma/hemorrhagic shock) Inappropriately low and sudden loss of intravascular volume

Answer 6

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

Answer 7

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

Answer 8

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

Answer 9

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

Answer 10

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 >> arterial

Answer 11

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

Answer 12

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

Answer 13

* Septic shock - classic example * Anaphylaxis * Neurogenic, myxedema coma (thyroid insufficiency) * Adrenal insufficiency, hepatic insufficiency * Pancreatitis

Answer 14

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

Answer 15

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

Answer 16

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

Answer 17

backpressure = venous congestion sympathetic overactivity = arterial vasoconstriction to maintain BP Venous fluid > arterial

Answer 18

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

Answer 19

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

Answer 20

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

Answer 21

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

Answer 22

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

Answer 23

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

Answer 24

Major ADR: Significant vasoconstriction

Answer 25

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

Answer 26

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

Answer 27

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

Answer 28

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

Answer 29

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

Answer 30

Major ADR Tachycardia Arrhythmogenesis High dose: peripheral vasoconstriction

Answer 31

selective a1 agonist High dose - may stimulate beta receptors Peripheral vasoconstriction – purported reflex bradycardia

Answer 32

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

Answer 33

severe vasoconstriction bradycardia myocardial ischemia

Answer 34

B1 inotrope Inotropic action + vasodilation (BP effects depend on volume status)

Answer 35

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)

Answer 36

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

Answer 37

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

Answer 38

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

Answer 39

Angiotensin II - peptide hormone of RAAS vasoconstriction + aldosterone release

Answer 40

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

Hemodynamic Shock Flashcards

(65 cards)