Shock Flashcards
What is shock?
Occurs when the CV system fails to adequately perfuse cells, tissues & organs –> impairment of cellular metabolism and tissue function
What constitutes shock?
Decreases oxygen delivery and/or increased tissue demand for oxygen
Types of shock (x4)
Cardiogenic
Hypovalemic
Obstructive
Distributive
What determines O2 delivery? (x5)
- Blood pressure (keeps blood moving)
- Systemic vascular resistance (no resistance = can’t generate BF)
- Cardiac output (SV regulated by pre/afterload & contractility)
- Stroke volume
- O2 content (partial pressure of O2 - conc gradient, hemoglobin levels, respiratory disorders)
What increases O2 demand? (x4)
- Increased basal metabolic rate: regulated by TF (hyperthyroidism = increased O2 demand)
- Infection/fever: active immune cells
- Increased work of organs: O2 is needed to generate ATP to keep ion pumps running
- Agitation/pain: increased HR & respiratory rate (clenching skeletal muscle)
Cellular alterations in shock
Shift from aerobic –> anaerobic respiration
36 ATP per glucose vs 2 ATP per glucose
ATP is used more quickly than replenished –> cells run down
What happens when there is tissue hypoxia? (shock)
Switches to anaerobic respiration
Buildup of LA –> pH drops –> metabolic acidosis –> cardiac depression
Stages of shock (x4)
- Initial: cellular alterations due to decreased O2 –> no clinical signs except elevated LA
- Compensatory: includes neural, hormonal + chemical responses to improve tissue perfusion
- Progressive: multi-organ failure
- Refractory: permanent damage to myocardium, no longer able to maintain CO (point of no return)
What compensatory mechanisms are in place? (x3)
Neural
Hormonal
Chemical
Neural compensatory mechanism
*Immediate response
Baroreceptors sense the decrease in BP
Increased sympathetic drive –> increases PVR, HR, myocardial contractility, CO and BP
Reduced BF to kidney, GI tract (non-essential stuff)
Hormonal compensatory mechanism
Adrenal medulla releases norephinephrine & epinephrine –> increases sympathetic drive
Posterior pituitary releases ADH which increases renal water reabsorption –> increased blood volume… also causes vasoconstriction –> increases BP
Reduced BF to kidneys = renin release
Angiotensin II induces vasoconstriction (binds to receptors on vascular SM)
Aldosterone promotes sodium + water reabsorption –> increases blood volume
Chemical compensatory mechanism
Hypoxemia + acidosis stimulates an increase in respiratory depth & rate –> improves blood oxygenation to blow off CO2
Breathing out more CO2 = less protons in the blood = less acidic
Cardiogenic shock
Due to failure of the pump (heart attack etc.) + vasoconstriction
Reduced SV/HR
Sweating (sympathetic output)
Obstructive shock
Obstruction to BF which impedes the filling/emptying of the heart (pulmonary embolism, anything related to lungs, cardiac tamponade)
Blood doesn’t pass through the lungs to get oxygenated
Hypovolemic shock
Reduction in total blood volume (bleeding, dehydration)
Reduced preload (due to loss of BV, less filling of the heart)
Shunting of blood away from non-essential organs (peripheral pulses are not palpable)
