Key CC Concepts Flashcards
(41 cards)
Define shock.
A severe imbalance between O2 supply and demand, leading to inadequate cellular energy production, cellular death, and multi-organ failure.
What are mechanisms that can lead to shock? Which is most common?
- Decrease in oxygen delivery (DO2) relative to oxygen consumption (VO2) - most common
- Hypovolemic shock - loss of intravascular volume
- Distributive shock - maldistribution of vascular volume
- Obstructive shock - obstruction to diastolic filling
- Cardiogenic shock - failure of the cardiac pump - Metabolic disturbances
- Cytopathic hypoxia
- Hypoglycemia
- Toxic exposures - Decreased arterial oxygen content
- Severe anemia
- Pulmonary dysfunction
- Methemoglobinemia/carbon monoxide poisoning
What are the consequences of shock?
Inadequate cellular energy production leads to:
1. Cell membrane ion pump dysfunction (Na-K ATPase)
2. Intracellular edema
3. Leakage of intracellular contents extracellularly
4. Inability to regulate intracellular pH
This ultimately leads:
1. Systemic acidemia
2. Endothelial dysfunction
3. Activation of inflammatory and antiinflammatory cascades
Describe the pathophysiology of hypovolemic shock?
- Loss of intravascular fluid volume causes inadequate organ perfusion and therefore insufficient oxygen delivery
2.Insufficient oxygen delivery causes a shift from aerobic to anaerobic metabolism
3.Anaerobic metabolism leads to the accumulation of lactate, hydrogen ions, and oxygen free radicals. - Damage associated molecular patterns (DAMPs) respond to damaged or dying cells. DAMPs activate the innate immune system by interacting with pattern recognition receptors (PARs) and triggering a pathologic systemic inflammatory response.
- Prolonged oxygen deprivation ultimately causes cellular necrosis, apoptosis, followed by end-organ damage and multiple organ dysfunction.
What are the compensatory mechanisms triggered in hypovolemic shock?
- Baroreceptors
- Peripheral chemoreceptors
- Central chemoreceptors
- Activation the RAAS system
- +/- Osmotic effects of hyperglycemia
How do baroreceptors function in hypovolemic shock?
- Baroreceptors communicate with the brain via the glossopharyngeal nerve (CN IX) and vagus nerve (CN X) to the nucleus of the solitary tract in the brainstem.
- There is a decrease in impulse firing to the medulla oblongata in response to low pressure or stretch in the carotid sinuses or aortic arch.
- This enables (disinhibits) sympathetic activation while inhibiting parasympathetic activation.
- The resultant response to shock-induced hypotension includes increased arteriolar and venous tone, cardiac contractility, and heart rate.
How do peripheral chemoreceptors function in hypovolemic shock?
Central chemoreceptors located in the respiratory center of the medulla oblongata sense an increase in CO2 or decrease in pH of the cerebrospinal fluid and cause an increase in respiratory rate and tidal volume.
What effect does hypotension have on catecholamines and endorphins?
Severe hypotension increases circulating catecholamines and endorphin release, which reduces perception to pain.
What is the compensatory mechanism of hyperglycemia in hypovolemic shock?
Hyperglycemia’s osmotic effect may contribute to intravascular volume replacement during shock.
What is the compensatory mechanism of the renin-angiotensin-aldosterone system in hypovolemic shock?
Reduced renal blood flow activates the RAAS system and leads to:
1. Increase in norepinephrine and angiotensin II-mediated vasoconstriction
2. Sodium and water retention via the release of both aldosterone and antidiuretic hormone
What are the subclassifications of hypovolemic shock?
- Hemorrhagic shock - acute drop in circulating red blood cells causing tissue hypoxia
- Hypovolemic shock without hemorrhage
- severe imbalance between fluid intake and fluid loss (ex. vomiting/diarrhea, uncompensated renal losses, large volume fluid sequestration). - Traumatic hemorrhagic shock
- acute drop in circulating red blood cells causing tissue hypoxia; further complicated by inflammatory response of soft tissue injury, resulting in worsening microvascular dysfunction, endothelial injury, and vasomotor tone derangements - Traumatic hypovolemic (nonhemorrhagic) shock
- large surface burns and deep skin lesions
What are the four major classifications of shock?
- Cardiogenic
- Hypovolemic
- Distributive
- Obstructive
Define distributive shock. What are the subcategories of distributive shock?
Distributive shock refers to a state of relative hypovolemia due to the pathologic redistribution of fluid caused by changes in vascular tone or increased vascular permeability.
Subcategories of distributive shock include septic, anaphylactic, and neurogenic shock.
Define sepsis.
Sepsis is defined as life-threatening organ dysfunction in response to infection.
Define septic shock.
Life-threatening organ dysfunction in response to infection, with persistent hypotension requiring vasopressor therapy.
How does sepsis lead to distributive shock?
Sepsis results in cytokine-mediated endothelial dysfunction, which causes both increased endothelial permeability and vasodilation. The result is both a relative decrease in vascular filling and a shift of volume from the intravascular to the interstitial space.
How does neurogenic shock meet criteria for distributive shock?
Vasodilation seen in neurogenic shock (typically traumatic brain or spinal cord injury) results from abnormally low sympathetic tone and unopposed parasympathetic stimulation of vascular smooth muscle.
Define obstructive shock. List examples of obstructive shock.
Obstructive shock is the result of the compression of the heart or a great vessel, compromising venous return, diastolic filling, and cardiac preload.
Ex.)
- Gastric dilation (with or without volvulus) which decreases preload
- Tension pneumothorax or cardiac tamponade, which reduces diastolic filling.
- High positive end-expiratory pressure ventilation, which negatively affects venous return and cardiac output.
Define cardiogenic shock.
Systolic or diastolic cardiac dysfunction resulting in hemodynamic abnormalities that include increased heart rate, decreased stroke volume, decreased cardiac output, decreased blood pressure, increased peripheral vascular resistance, and increased right atrial, pulmonary arterial, and pulmonary capillary wedge pressures.
These pathologic changes
result in diminished tissue perfusion and increased pulmonary venous pressures, resulting in pulmonary edema and increased respiratory effort.
What are some characteristics of a well-perfused patient?
- Central venous pressure between 0 and 6 cm H2O
- Urine production of at least 1 ml/kg/hr
- MAPs between 70 and 100 mm Hg
- Normal body temperature
- Normal heart rate
- Normal heart rhythm
- Normal respiratory rate
- Pink moist, CRT < 2 seconds
What are signs associated with compensated shock?
- Mild to moderate mental depression
- Tachycardia
- Normal or prolonged capillary refill time
- Cool extremities
- Fair to moderate pulse quality
- Tachypnea
- Normal blood pressure
What are signs of decompensated shock?
- Pale mucous membranes
- Poor peripheral pulse quality
- Depressed mentation
- Hypotension
What are signs associated with the hyperdynamic phase of sepsis or SIRS (aka vasodilatory shock):
- Tachycardia
- Fever
- Bounding peripheral pulse quality
- Hyperemic mucous membranes (secondary to cytokine-mediated peripheral vasodilation)
Hard to recognize in cats
