Shock - Hesi - Nclex Review

Front 1

Describe Shock.

Back 1

Widespread, serious reduction of tissue perfusion (lack of O2 and nutrients), which, if prolonged, leads to generalized impairment of cellular functioning.

Front 2

Arterial pressure is the driving force for blood through the organs.

What is it dependent on?

Back 2

CO

Peripheral tone to return blood to heart

Amount of circulating blood

Marked reduction - HYPOTENSION

Front 3

Who is at risk for development of shock? Clients with...

Back 3

very young/very old

post-MI

severe dysrhythmia

adrenocortical dysfunction

history or recent hemorrhage or blood loss

burns

massive infection

Front 4

What are the early signs of shock

Back 4

agitation, restlessness with severe hypoxia

Front 5

Describe Hypovolemic Shock

Back 5

R/t external or internal blood loss (most common cause of shock)

Front 6

Describe Cardiogenic Shock

Back 6

R/t ischemia/impairment in tissue perfusion from myocardial infarction, serious arrhythmia, or CHF. All of this results in decreased CO

Front 7

Describe Vasogenic Shock

Back 7

R/t allergens, spinal cord injury, or peripheral neuropathy, all resulting in venous pooling and decreased blood return to the heart, which decreases CO over time

Front 8

Describe Septic Shock

Back 8

R/t to endotoxins released from bacteria, which cause vascular pooling, diminished venous return and CO.

Front 9

HESI HINT: Cardiogenic shock

Back 9

If cardiogenic shock exists with the presence of pulmonary edema (pump failure), position the client to REDUCE venous return further to the left ventricle

Front 10

What are the stages of hypovolemic shock?

Back 10

Stage I - Initial
Stage II - Compensatory
Stage III - Progressive
Stage IV - Irreversible

Front 11

S/S of Stage I

Back 11

Apprehension and restlessness (first signs of shock)

Increased HR

Cool, pale skin

Fatigue

Front 12

Clinical Description of Stage I

Back 12

Arteriolar constriction

Increased production of ADH

Arterial pressure is maintained

CO usually normal for healthy people

Selective reduction of BF to skin and muscle beds

Front 13

S/S of Compensatory Stage

Back 13

Flattened neck veins and delayed venous filling time

Increase pulse and respirations

Pallor, diaphoresis, cool skin

Decreased UO

Sunken soft eyeballs
Confusion

Front 14

S/S of Progressive Stage

Back 14

Edema

Increased blood viscosity

Excessively low BP

Dysrhythmia, ischemia, and MI

Weak, thready, or absent peripheral pulses

Front 15

Clinical Description of Compensatory Stage

Back 15

Marked reduction in CO

Arterial pressure decline (despite compensatory arterial vasoconstriction)

Massive adrenergic compensatory response resulting in: tachycardia, tachypnea, cutaneous vasoconstriction, and oliguria

Decreased cerebral perfusion

Front 16

Clinical Description of Progressive Stage

Back 16

Rapid circulatory deterioration

Decreased CO

Decreased tissue perfusion

Reduced blood volume

Front 17

S/S of Irreversible Stage

Back 17

Profound hypotension, unresponsive to vasopressor drugs

Severe hypoxemia, unresponsive to O2 administration

Anuria, renal shut down

Heart rate slows, BP falls, with consequent cardiac and respiratory arrest

Front 18

Clinical Description of Irreversible Stage

Back 18

Cell destruction so severe that death is inevitable

MOD Failure

IT THE NURSE'S RESPONSIBILITY TO RECOGNIZE THE S/S OF SHOCK. EVERY EFFORT SHOULD BE MADE TO PREVENT THE DEVASTATING CLINICAL COURSE THAT THE PROGRESSION OF SOCK CAN TAKE.

Front 19

HESI HINT: Severe Shock

Back 19

Severe shock leads to widespread cellular injury and impairs the integrity of the capillary membranes.

Fluid and osmotic proteins seep into the extravascular spaces, further reducing CO. A viscious cycle of decreased perfusion to ALL cellular level activities ensues.

All organs are damaged, and if perfusion problems persist, the damage can be permanent.

Front 20

What is the goal of the medical treatment for shock?

Back 20

Quick restoration of cardiac output and tissue perfusion.

Front 21

How do you restore CO and tissue perfusion?

Back 21

Rapid infusion with volume-expanding fluids (but if the shock is cardiogenic, then you could create pulmonary edema)

Central venous OR pulmonary artery catheters to monitor if shock is cardiogenic vs hypovolemic

Serial measuremnts of CVP, UO, HR, and mental states q 15 min

Follow immediately to improve perfusion, attention is directed towards the underlying condition

Administration of drugs is usually withheld until circulating volume has been restored

Give O2

Front 22

What are volume-expanding fluids/substances?

Back 22

Whole blood, plasma, plasma substitutes (colloid fluids)

Note that whole blood is acceptable volume expander, it is rarely used due to high risk transfusion reactions.

Front 23

What are isotonic solutions?

Back 23

They are electrolyte intravenous solutions like Lactate Ringer's and Normal Saline

Front 24

If shock is cardiogenic in nature, what are things you want to do to help prevent or decrease pulmonary edema?

Back 24

Resotration of cardiac function should take priority

Give cardiotonic drugs (digitalis) may increase cardiac contractility

Other drugs that enhance contractility include dopamine (Dopram)

Vasoconstricting agents like dopamine and norepinephrine (Levophed) may be used as vasoconstrictors in cardiogenic shock

Front 25

Vitals of a patient in shock...

Back 25

Tachycardia

Tachypnea

Blood pressure decreased (<80)

Front 26

Early mental status in a patient with shock

Back 26

Restless

Hyper-alert

Front 27

Late mental status in a patient with shock

Back 27

Decreased alertness

Lethargy

Coma

Front 28

Skin changes in a patient with shock

Back 28

Cool, clammy (warm with vasogenic and early septic shock)

Diaphoresis

Pale

Front 29

Fluid status in a patient with shock

Back 29

UO decreases or imbalance between IO

Abnormal CVP (<4 cm H2O)

Urine specific gravity >1.020 (hypovolemia)

Front 30

How much urine do you want to maintain in a shock patient per hour?

Back 30

30 mL

Less represents decrease renal perfusion = permanent renal damage = CALL DOCTOR

Front 31

What measures can be taken to help the patient increase their level to a good level of CVP?

Back 31

Bllod

Colloids

Electrolyte Solutions

Front 32

The HCP may order fluids to elevate the CVP to ...

Back 32

16 to 19 cm H2O to compensate for decreased CO

Front 33

What are the vasopressors you give?

Back 33

Epinephrine

Dopamine

Dobutamine

Norepinephrine

Isproterenol

Front 34

What are the nursing interventions when you give vasopressors?

Back 34

Administer through volume-controlled pump

Monitor BP q 5-15 min

Watch IV site for extravasation and tissue damage

Ask HCP for target BP (usually 80-90 systolic)

Front 35

What are the vasodilators you give? Why?

Back 35

Hydralazine

Nitro

Hydrochloride

They counteract vasopressors

Front 36

If the drop in BP occurs and you are prescribed vasodilators and vasopressors...what do you do?

Back 36

Decrease vasodilator infusion rate first

Increase vasopressors

Front 37

If the rise in BP occurs and you are prescribed vasodilators and vasopressors...what do you do?

Back 37

Decrease rate of vasopressors

Increase vasodilators

Front 38

MAP

Back 38

Mean Arterial Pressure

Pressure in the central arterial bed measured indirectly by BP measurement

Adults usually measure 100 mmHg

Measure through arterial catheter insertion

Front 39

How do you calculate MAP?

Back 39

CO X SVR

or

(SBP + 2DBP)/3

Front 40

CO

Back 40

Volume of blood ejected by the left ventricle per unit of time

Stroke Volume x HR

Normal is 4-6 L/min

Front 41

SVR

Back 41

systemic vascular resistance

Resistance to blood flow offered by the vessels in the peripheral vascular bed

Front 42

CVP

Back 42

Central Venous Pressure

Pressure within the right atrium

Normal is 4-10 cm of H2O

Front 43

HESI HINT: Plasma

Back 43

A common volume expanding substance is plasma and possibly whole blood