Dd&t2 Therapy Of Shock

Front 1

What are the 3 systemic effects of shock?

Back 1

Alterations in the serum pH (acidosis), endothelial dysfunction, stimulation of inflammatory and anti-inflammatory cascades

Front 2

What is the hallmark of shock?

Back 2

Hypotension (MAP < 60 mmHg)

Front 3

What are the 3 types of shock?

Back 3

Hypovolemic, cardiogenic, distributive

Front 4

What causes hypovolemic shock?

Back 4

Volume loss

Front 5

How is hypovolemic shock diagnosed?

Back 5

Low BP, tachycardia, skin is cool and clammy, neck veins are flat, evidence of massive blood or fluid loss, hypotension improves with IV fluid challenge

Front 6

What is the treatment plan for hypovolemic shock?

Back 6

1. Stablize the patient - fluid resuscitation, vasopressors and inotropes may be useful way as a temporizing measure to increase blood pressure. 2. Fix underlying cause.

Front 7

Low LVFP, Low CO, High SVR

Back 7

Hypovolemic shock

Front 8

What is the inciting factor for cardiogenic shock?

Back 8

Myocardial injury - something that causes loss of myocardial contractility

Front 9

Which has worse decreased CO, cardiogenic or hypovolemic shock? Why?

Back 9

Cardiogenic. Weakened heart has difficulties pumping blood through increased SVR

Front 10

How is cardiogenic shock diagnosed?

Back 10

Decreased BP, Tachycardia, skin cool and clammy, neck veins may be distended; EKG can alert to possible causes (AMI (ST elevation in 2 contiguous leads), Arrhythmias, Acute pericarditis (ST elevation in most EKG leads))

Front 11

What are the 4 causes of cardiogenic shock?

Back 11

Myocardial dysfunction, arrhythmias, mechanical problems, extracardiac abnormalities

Front 12

High LVFP, Low CO, High SVR

Back 12

Cardiogenic shock

Front 13

What pharmacologic treatments are used in cardiogenic shock?

Back 13

loop diuretics, inotropic agents, vasodilators

Front 14

What is an example of a loop diuretic used in treating cardiogenic shock?

Back 14

Furosemide

Front 15

MOA of furosemide

Back 15

Blocks sodium and water absorption in distal tubules => diuresis

Front 16

Furosemide route of administration

Back 16

IV preferred b/c of rapid onset of action and more reliable bioavailability. Furosemide is not well absorbed from edematous gut.

Front 17

Common side effect of loop diuretics

Back 17

electrolyte disturbances (K, Na, and Mg can be severely depleted)

Front 18

What are the 2 types of inotropic agents used in cardiogenic agents?

Back 18

Beta1 sympathomimetic agents (dobutamine) and milrinone

Front 19

MOA of furosemide Beta1 sympathomimetic agents

Back 19

Stimulate Beta1-adrenergic receptors, increased cAMP, increased Ca2+, increased force and velocity of myocardial contraction, increased CO

Front 20

MOA of milrinone

Back 20

Inhibitor of enzyme responsible for degradation of cAMP, increased cAMP, increased Ca2+, increased force and velocity of myocardial contraction, increased CO

Front 21

Dobutamine route of administration

Back 21

Continuous IV infusion

Front 22

Dobutamine side effects

Back 22

Tachycardia, ventricular arrhythmias, may make myocardial ischemia worse (angina)

Front 23

Milrinone route of administration

Back 23

Continuous IV infusion

Front 24

Milrinone side effects

Back 24

Tachycardia, ventricular arrhythmias, may make myocardial ischemia worse (angina), hypotension (vasodilatory effect on peripheral arteries)

Front 25

What are 2 non-pharmacologic treatments of cardiogenic shock?

Back 25

Intra-aortic ballon pulsation, left ventricular assist device

Front 26

What is the inciting factor for distributive shock?

Back 26

Infection

Front 27

How is distributive shock diagnosed?

Back 27

Decreased BP, Tachycardia, warm skin, collapsed neck veins

Front 28

Low LVFP, High CO, Low SVR

Back 28

Distributive shock

Front 29

2 steps to treating distributive shock

Back 29

Stabilize patient (IV fluids, vasopressors); diagnosed and treat underlying cause

Front 30

What are the 4 goals of therapy in distributive shock?

Back 30

Restore intravascular volume (CVP 8-12 mmHg), correct hypoperfusion of tissues (central venous oxygen saturation >70%), correct metabolic acidosis, maintain mean arterial pressure > 60 mmHg

Front 31

What is the pharmacologic treatment of distributive shock?

Back 31

Vasopressors (NE, dopamine, phenylephrine, vasopressin)

Front 32

What is the vasopressive affect of NE?

Back 32

Stimulates alpha1 receptors (potent vasoconstriction), stimulates beta1 receptors (increased CO)

Front 33

What are the vasopressive effects of dopamine?

Back 33

1-2 (dopaminergic 1 receptors in the renal arteries - selective vasodilatation), 5-10 (stimulates beta1 adrenergic receptors increase heart rate and CO), 10-40 (stimulates alpha adrenergic receptors, increased SVR)

Front 34

What is the MOA of phenylephrine as a vasopressor?

Back 34

Pure alpha-adrenergic vasoconstrictor

Front 35

What is the MOA of vasopressin?

Back 35

Antidiuretic hormone analogue

Front 36

What are the 2 types of distributive shock and their corresponding vasopressors?

Back 36

1. Hyperdynamic septic shock - low SVR and high CO (alpha adrenergic vasoconstrictor) 2. Hypodynamic septic shock - characterized by low to modestly reduced SVR and low CO (dopamine raises MAP without increasing SVR)