Chapter 11 Shock, Sepsis, & Multiple Organ Dysfunction Syndrome

Question 1

Shock

Answer 1

A life-threatening condition that results from inadequate tissue perfusion

Tissue hypoperfusion prevents adequate oxygen delivery to cells, leading to cell dysfunction and death.

Disease Progression: Neither linear/predictable, especially septic shock (the most life-threatening form of sepsis)

Question 2

Multiple Organ Dysfunction Syndrome (MODS)

Answer 2

The presence of altered function of 2 or more organs in an acutely ill patient such that interventions are necessary to support continued organ function may ensue
- Often resulting in patient death

Occurs if shock is not effectively treated

MODS may be a complication of any form of shock but is most commonly seen in patients with sepsis

Question 3

Components of Adequate Blood Flow

Answer 3

1) An effective pump
2) Adequate vasculature or circulatory system
3) Sufficient blood volume

Question 4

(T/F) True or False: Shock affects all body systems. During shock, the body struggles to survive, calling on all its homeostatic mechanisms to restore blood flow

Answer 4

True

May develop rapidly or slowly

Any insult to the body can create a cascade of events resulting in poor tissue perfusion.

Question 5

Common Physiological Changes to Shock

Answer 5

Hypoperfusion of tissues, hypermetabolism, & activation of the inflammatory response

SNS activation

Question 6

What is the final pathway for all types of shock?

Answer 6

Failure of compensatory mechanisms to effectively restore physiologic balance is the final pathway of all shock states and results in end-organ dysfunction and death

Question 7

Cellular Changes During Shock

Answer 7

In shock, cells lack adequate blood supply & don’t have adequate oxygen/nutrients-> anaerobic metabolism to produce energy

1) Anaerobic metabolism results in low-energy yields from nutrients and an acidotic intracellular environment

2) Normal cell function stops
- Cells will swell & membrane becomes permeable-> electrolytes & fluid seep out of & into the cell

3) Sodium potassium pump is impaired-> mitochondria is damaged->cell death occurs

Question 8

Cellular Changes During Shock: Glucose

Answer 8

In stress states, catecholamines, cortisol, glucagon, and inflammatory cytokines are released, causing hyperglycemia and insulin resistance to mobilize glucose for cellular metabolism.
- Promotes gluconeogenesis
- Glycogen that has been stored in the liver is converted to glucose through glycogenolysis to meet metabolic needs, increasing the blood glucose concentration

Continued activation of the stress response-> depletion of glycogen stores, resulting in increased proteolysis and eventual organ failure

The deficit of nutrients and oxygen for normal cellular metabolism causes a buildup of metabolic end products in the cells and interstitial spaces

Question 9

Cellular Changes During Shock: Clotting Cascade Activation

Answer 9

. With significant cell injury or death caused by shock, the clotting cascade is overproductive, resulting in small clots lodging in microcirculation

This upregulation of the clotting cascade further compromises microcirculation of tissues, exacerbating cellular hypoperfusion

Cellular metabolism is impaired, and a self-perpetuating negative situation is activated

Question 10

Gluconeogenesis

Answer 10

The formation of glucose from noncarbohydrate sources such as proteins and fats

Question 11

Vascular Responses to Shock

Question 12

Autoregulation

Answer 12

Local regulatory mechanisms that vasodilate/vasoconstriction in response to biochemical mediators released by the cell communicating O2 & nutrient needs

Question 13

Cytokine

Answer 13

Substance released by cell/immune cell (macrophage) that triggers action at cell site or travels to a distal site via bloodstream

Question 14

Blood Pressure Regulation During Shock

Answer 14

Tissue perfusion and organ perfusion depend on mean arterial pressure (MAP)

MAP must exceed 65 mm Hg for cells to receive the oxygen and nutrients needed to metabolize energy in amounts sufficient to sustain life

BP is regulated by baroreceptors located in the carotid sinus & aortic arch
- Monitor circ vol & regulate neural & endocrine activities

Question 15

Mean Arterial Pressure (MAP)

Answer 15

Average pressure at which blood moves through the vasculature

Question 16

3 Major Components of Circulatory System

Answer 16

1) Blood volume
2) Cardiac pump
3) Vasculature

Question 17

Formula for BP

Answer 17

Mean arterial BP = CO X Peripheral Resistance

Question 18

Cardiac Output (CO)

Answer 18

Product of SV (stroke vol) & HR
- SV: Amount of blood ejected from LT ventricle during systole

Question 19

When BP drops…

Answer 19

…catecholamines are released-> increase HR & cause vasocontriction-> restores BP

Ex) Epinephrine, norepinephrine

Question 20

How do the kidneys regulate BP?

Answer 20

Releasing renin: This stimulation of the renin–angiotensin mechanism and the resulting vasoconstriction indirectly lead to the release of aldosterone from the adrenal cortex, which promotes the retention of sodium and water (i.e., hypernatremia)

Hypernatremia then stimulates the release of antidiuretic hormone (ADH) by the pituitary gland.

These secondary regulatory mechanisms may take hours or days to respond to changes in BP.

The initiation os shock depends on the effectiveness of the primary & secondary mechanisms to restore BP

Question 21

Renin

Answer 21

Potent vasoconstrictor released by the kidneys that converts angiontensin I -> angiotensin II

Question 22

Antidiuretic Hormone (ADH) Function in BP Regulation

Answer 22

Causes the kidneys to retain water further in an effort to raise blood volume and BP

Question 23

Phases of Shock

Answer 23

1) Compensatory
2) Progressive
3) Irreversible

Question 24

Current evidence suggests that the window of opportunity that increases the likelihood of patient survival occurs when aggressive therapy begins within how many hours of identifying a shock state?

Answer 24

3 hours of identifying a shock state, especially septic shock

Question 25

Compensatory Stage

Answer 25

BP remains stable

Vasoconstriction, increased heart rate, and increased contractility of the heart contribute to maintaining adequate cardiac output
- Results from SNS stim and subsequent release of catecholamines

Patients display the often-described “fight-or-flight” response

The body shunts blood from organs such as the skin, kidneys, and gastrointestinal (GI) tract to the brain, heart, and lungs to ensure adequate blood supply to these vital organs.

As a result, the skin may be cool and pale, bowel sounds are hypoactive, and urine output decreases in response to the release of aldosterone and ADH.

Question 26

Clinical Findings Associated with the Compensatory Stage of Shock

Answer 26

BP: WNL
HR: >100 bpm Tachycardic

Respiratory Status: More than or equal to 22 breaths per min, PaCO2 < 32mmHg

Skin: Cold, clammy
Cap Refill is less than or equal to 3.5 s

Urinary Output: Decreased
Mentation: Confusion/agitation

Acid-base Balance: Respiratory alkalosis

Question 27

Medical Management of the Compensatory Phase of Shock

Answer 27

Directed toward identifying the cause of the shock, correcting the underlying disorder so that shock does not progress, and supporting those physiologic processes that thus far have responded successfully to the threat.

Fluid replacement, supplemental oxygen, and medication therapy must be initiated to maintain an adequate BP and reestablish and maintain adequate tissue perfusion

Question 28

By the time BP drops…

Answer 28

…damage has already been occurring at the cellular and tissue levels!

Patient must be assessed and monitored closely BEFORE the BP falls!

Question 29

Progressive Stage of Shock

Answer 29

In the second stage of shock, the mechanisms that regulate BP can no longer compensate, and the MAP falls below normal limits.

Patients are clinically hypotensive; this is defined as a systolic BP of 100 mm Hg or lower, or a decrease in systolic BP of 40 mm Hg from baseline.

The patient shows signs of declining mental status

Question 30

Systemic Effects of the Progressive Stage of Shock

Answer 30

1) Overworked heart cannot meet increased O2 demands-> ischemia-> HF

2) Microcirculation regulation fails-> increased permeability-> interstitial edema

3) Need for energy prompts anaerobic metabolism-> acidosis-> disordered cell function

4) Reversal of cause is not enough, cycle ensues

Question 31

Clinical Manifestations of the Progressive Stage of Shock

Answer 31

BP: Systolic is < or equal to 100 mmHg; MAP is < or equal to 65 mmHg
- Fluid resuscitation to support BP
HR: >150 bpm

Respiratory status: Rapid shallow breaths, crackles
- PaO2: < 80 mmHg
-PaCO2: >45 mmHg
Skin: Mottling, petechiae
- Cap refill: > or equal to 3.5 secs

Mentation: Lethargy
Acid-Base Balance: Metabolic acidosis