Shock and Resuscitation

Question 1

Hypovolemic Shock

Answer 1

Tachycardia, orthostatic HOTN progresses to supine HOTN w/ severe

Extremities cold and clammy with sluggish cap refill

Narrowed pulse pressure due to low BP and increased SVR

Question 2

Triad of Death

Answer 2

Coagulopathy

Metabolic acidosis

Hypothermia

Question 3

Shock and Lactic Acidosis

Answer 3

Used to determine if tissues are undergoing anaerobic respiration

Anion gap metabolic acidosis if so

High return CO2 to the heart - abnormal value

Question 4

Cardiogenic Shock

Answer 4

Heart failure causing ischemia of tissues

High SVR and filling pressures with low CO -> narrow pulse pressures

Chest pain, orthopnea/PND, JVD, peripheral/pulmonary edema

S3 gallop heart on auscultation

Question 5

Distributive Shock

Answer 5

Commonly septic shock

Decrease in SVR causing loss of fluid into 3rd space - widened pulse pressures (high CO, at least initially)

Can also be caused by anaphylactic shock or adrenal crisis (give steroids)

Question 6

Obstructive Shock

Answer 6

Impaired cardiac filling - tamponade, pericarditis, tension pneumo, PE

High filling pressures and SVR, low CO - narrowed pulse pressures

Pulsus paradoxus, friction rub

Question 7

Beck’s Triad

Answer 7

Indicates acute cardiac tamponade

Low arterial BP

Distended neck veins (JVD)

Distant, muffled heart sound

Question 8

Catecholamine Receptors

Answer 8

Beta 1 - 1 heart: increases cardiac contractility

Beta 2 - 2 lungs: induces smooth muscle vasodilation

Alpha 1: arterial vascular smooth muscle contraction

D1/D2: vasodilation of renal/splanchnic vasculature

Question 9

Transfusion parameters

Answer 9

Goal of hgb >7 unless cardiac ischemia

Question 10

Frank-Starling Law

Answer 10

SV increases in response to an increase in the volume of blood filling the heart

-Increased stretch increases contractility

Question 11

Norepinephrine (Levophed)

Answer 11

Primarily an alpha-1 agonist

Causes vasoconstriction w/o impacting CO or HR

First line for septic shock

May be toxic to cardiac myocytes - cause apoptosis

Question 12

Vasopressin (Pitressin)

Answer 12

Anti-diuretic hormone (ADH)

Acts on V1 (vasculature) - cause smooth muscle contraction

Acts on V2 (renal) - increase water resorption at collecting ducts

Increase sensitivity to NE

No affected by acidosis or hypoxia

Question 13

Dopamine

Answer 13

Natural NE precursor

Dose determine which receptors affected

• 3-10 ug/kg/min - B1 (NE release)
• 10-20 ug/kg/min - alpha 1 (vasoconstriction)

Higher risk of tachyarrhythmias

Question 14

Dobutamine

Answer 14

Beta 1 and Beta 2 (3:1) receptor agonist

Also binds alpha 1 - mild vasodilation

Used for cardiogenic shock and sepsis-induced cardiogenic dysfunction

Increases myocardial oxygen demand

May be pro-arrhythmic

Question 15

Epinephrine (Adrenalin)

Answer 15

Affinity for beta 1&2 and alpha 1 receptors

-beta @ low dose, alpha @ high dose

Used for cardiac arrest - “atomic bomb” of vasoconstriction

Improves coronary blood flow

Can cause cardiac toxicity

Question 16

Infusion Rate

Answer 16

Directly proportional to catheter length

-peripheral short catheters are preferred for shock resuscitation due to short, fat length

Question 17

Central Access and When to Place

Answer 17

Internal Jugular

Subclavian

Femoral vein

Place when you need:

• rapid med delivery
• peripheral veins inadequate
• need to monitor CVP/ScVO2