Chapter 11 Shock, Sepsis, & Multiple Organ Dysfunction Syndrome Flashcards
Shock
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)
Multiple Organ Dysfunction Syndrome (MODS)
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
Components of Adequate Blood Flow
1) An effective pump
2) Adequate vasculature or circulatory system
3) Sufficient blood volume
(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
True
May develop rapidly or slowly
Any insult to the body can create a cascade of events resulting in poor tissue perfusion.
Common Physiological Changes to Shock
Hypoperfusion of tissues, hypermetabolism, & activation of the inflammatory response
SNS activation
What is the final pathway for all types of shock?
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
Cellular Changes During Shock
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
Cellular Changes During Shock: Glucose
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
Cellular Changes During Shock: Clotting Cascade Activation
. 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
Gluconeogenesis
The formation of glucose from noncarbohydrate sources such as proteins and fats
Vascular Responses to Shock
Autoregulation
Local regulatory mechanisms that vasodilate/vasoconstriction in response to biochemical mediators released by the cell communicating O2 & nutrient needs
Cytokine
Substance released by cell/immune cell (macrophage) that triggers action at cell site or travels to a distal site via bloodstream
Blood Pressure Regulation During Shock
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
Mean Arterial Pressure (MAP)
Average pressure at which blood moves through the vasculature
3 Major Components of Circulatory System
1) Blood volume
2) Cardiac pump
3) Vasculature
Formula for BP
Mean arterial BP = CO X Peripheral Resistance
Cardiac Output (CO)
Product of SV (stroke vol) & HR
- SV: Amount of blood ejected from LT ventricle during systole
When BP drops…
…catecholamines are released-> increase HR & cause vasocontriction-> restores BP
Ex) Epinephrine, norepinephrine
How do the kidneys regulate BP?
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
Renin
Potent vasoconstrictor released by the kidneys that converts angiontensin I -> angiotensin II
Antidiuretic Hormone (ADH) Function in BP Regulation
Causes the kidneys to retain water further in an effort to raise blood volume and BP
Phases of Shock
1) Compensatory
2) Progressive
3) Irreversible
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?
3 hours of identifying a shock state, especially septic shock
Compensatory Stage
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.
Clinical Findings Associated with the Compensatory Stage of Shock
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
Medical Management of the Compensatory Phase of Shock
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
By the time BP drops…
…damage has already been occurring at the cellular and tissue levels!
Patient must be assessed and monitored closely BEFORE the BP falls!
Progressive Stage of Shock
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
Systemic Effects of the Progressive Stage of Shock
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
Clinical Manifestations of the Progressive Stage of Shock
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
