Shock Flashcards
What is shock?
Clinical syndrome characterized by deceased tissue perfusion leading to impaired cellular metabolism. Begins as an adaptive response to injury / insult then progresses to multi-system organ failure
What are the three major classifications of shock?
1) Hypovolemic (Loss of volume)
2) Cardiogenic (Decreased contractility)
3) Distributive (Vasodilatory) –> Neurogenic, anaphylactic, septic
What are the 4 stages of shock?
1) Initial
2) Compensatory
3) Progressive
4) Refractory
What happens in the initial stage?
Nonspecific cellular changes but no clinical manifestations
What happens in the compensatory stage?
Compensatory mechanisms shunt blood to vital organs.
1) Nervous system compensation
2) Hormonal compensation
3) Chemical compensation
What is nervous system compensation?
SNS compensation:
Heart: Baroreceptors in aortic arch and carotid sinus increase HR, FOC, SV to increase CO and BP
Lungs: Increase RR, bronchodilation
Blood vessels: Constrict in skin, GIT, kidneys. Dilate in coronary arteries, skeletal muscles
Pupils: Dilate
Sweat glands: Increase activity
What is hormonal compensation?
Kidneys –> Decrease blood flow stimulates RAAS, Angiotensin II causes peripheral vasoconstriction. Adrenal cortex stimulated to release aldosterone increasing Na and H2O reabsorption
Adrenal medulla –> Release epinephrine, norepinephrine
Adrenal cortex –> Release aldosterone and glucocorticoids
Liver –> Secrete ACTH, leads to production of glucocorticoids (increases BG from glycogenolysis)
What is chemical compensation?
Lungs –> Decreased blood flow causes deadspace units, triggers chemoreceptors to increase RR. Causes resp alkalosis and eventually combined acidosis
Neuro –> Hyperventilation decreases CO2 causes cerebral vessels to constrict, decrease O2 to brain
Capillary –> Decreased CO causes cells to extract more O2
What happens in the progressive stage?
Ongoing compensatory mechanisms work against the pt, vasoconstriction causes adverse effects
1) Cellular function
2) Capillary dynamics
3) Systemic circulation
4) Specific organ systems
How is cellular function affected in the progressive stage?
Arteriolar vasoconstriction –> Decreased BF, decreased O2 and decreased ATP production. Cells switch to anaerobic metabolism, lactic acid produced which decreases FOC.
- -> Pt goes into metabolic acidosis.
- -> Impaired cellular function releases toxic substances accumulating in tissues and altering local environment
How are capillary dynamics affected in the progressive stage?
Acidic tissue environments from impaired cellular function causes pre-capillary sphincters to relax but post-capillary sphincters constrict. Histamine release further increases capillary permeability.
- -> Increased hydrostatic pressure, histamine, pt becomes edematous as fluid leads out of intra-vascular space, decrease CO, decrease CA perfusion, ischemia
- -> Blood becomes more viscous, increasing afterload, capillary sludging causes coagulopathy
What happens when blood becomes more viscous?
As fluid is lost, increased viscosity leads to:
Increased afterload Capillary sludging (aggregation of RBCs, platelets, large proteins) causing coagulopathy, DIC
How is the systemic circulation affected by the progressive stage?
Decreased perfusion to periphery causes distal ischemia of tissues. Pulses weaker, then absent, local ischemia progresses to necrosis and becomes infection risk
How are specific body organs affected by the progressive stage?
Damage due to acidosis and prolonged vasoconstriction:
Heart –> Increased O2 consumption with decreased perfusion, arrythmias
Brain –> Initially vasoconstriction due to SNS response, then SNS response is LOST leading to decreased HR and vasodilation
Kidneys –> Nephron hypoxia, acute kidney injury
GI –> Ischemia to interstitial lumen cells leads to hemorrhage and bacterial translocation
Liver –> Decrease in phagocytosis (Kuppfer cells) thus blood from GI tract cant get filtered. Impaired metabolism, detoxification, liver ischemia
Pancreas –> Release proteolytic enzymes and MYOCARDIAL DEPRESSANT FACTOR (increases splanchnic vasoconstriction, interferes with role of calcium?)
Lungs –> Pulmonary vasoconstriction increases CO2, acidosis leads to interstitial and alveolar pulm. edema, decreased surfactant production causes atelectasis and decreased compliance
What are the cycles of the refractory stage?
1) Cycle of cardiac failure
2) Cycle of acidosis
3) Cycle of cerebral ischemia
4) Cycle of blood clotting
What is the cycle of cardiac failure?
Decreased CO –> Decreased CA perfusion –> Ischemia –> Decreased FOC (worsened by acidosis and MDF) –> Arrythmias
What is the cycle of acidosis?
Decreased renal function –> Decreased resp function (increase CO2), decreased cellular function (Increase lactic acid) –> Mixed acidosis –> Decrease CO + Pre-capillary sphincters relax decrease circulating fluid
What is the cycle of blood clotting?
Decreased blood volume –> Clot formation –> Decreased blood flow + Sluggish capillary flow, DIC –> Cellular hypoxia –> Acidosis
What is the cycle of cerebral ischemia?
Decreased CO –> Cerebral ischemia –> Initially causes vasoconstriction due to SNS response, then SNS response is LOST leading to decreased HR and vasodilation –> BRAIN DEATH –> Cardiac arrest, resp arrest
How much volume needs to be lost for hypovolemic shock?
15-30%, 750 - 1500mls
What is the etiology of hypovolemic shock?
1) Internal losses (Third spacing, internal hemorrhage)
2) External losses (Whole blood loss, coagulation disorders, plasma, fluid loss)
What is pathophys of hypovolemic shock?
Decrease intravascular volume Decrease venous return Decrease filling pressures Decrease SV Decreased CO Decreased tissue perfusion
What is pulsus parodoxus associated with?
Hypovolemia (decreased preload and left side, decreased BP on inspiration)
Treatment of hypovolemic shock?
Fluid replacement –> Crystalloid / colloid / blood, should be warmed if large amount.
Inotropes / vasopressors
What are crystalloids?
NS, RL
Use isotonic solutions first, increase extracellular volume without altering electrolyte concentration of plasma. RL most compatible.
What are colloids?
Plasma proteins (FFP clotting factors, abumin). FFP MUST BE GIVEN COLD
What are blood products?
RBCs (improve O2 carrying capacity of blood), Cryoprecipitate (contains fibrinogens and other clotting factors)
What is the etiology of cardiogenic shock?
1) Coronary cardiogenic shock –> After acute MI decrease FOC
2) CA are fine but myocardium is sick decreasing FOC. Can be caused by viral infections, myocarditis, cardiomyopathies
What is 3 main pathophys of cardiogenic shock?
Systolic dysfunction, impaired LV contracility
Decrease tissue perfusion –> RAAS INCREASES AFTERLOAD
***Further decrease CO
Inadequate systolic emptying of LV
***Pulm. edema intra alveolar edema
Diastolic dysfunction, impaired LV compliance
Decreased preload, decreased CO
How does systolic dysfunction result in cardiogenic shock?
Impaired LV contracility Decrease SV, CO, BP Decrease tissue perfusion --> RAAS INCREASES AFTERLOAD Decrease CA perfusion Ischemia Decrease FOC ***Further decrease CO
Inadequate systolic emptying of LV Increase LV filling pressures, increase LAP Increase pulm. venous pressure Increase pulm. capillary pressure ***Pulm. edema intra alveolar edema
What is RV failure and what does it result in?
Caused with RV infarct, PE, pulm HTN, ARDS, sepsis. High RAP > 15 can result in:
RV ischemia
RV failure resulting in decreased LV filling
RV overload, tricuspid regurg and septal shift into LV
Decreased CO due to decreased LV filling pressures
What are clinical findings specific to RV failure?
Portal HTN, distended neck veins, chest may be clear as backflow is systemic
What are the key hemodynamic differences between RV and LV failure?
RVF: Increased RAP, decreased PADP, PCWP
LVF: Increased PADP, PCWP
What is treatment for LVF?
LVF causes fluid backup into lungs, pulmonary hydrostatic pressure pulm edema.
Treat: IDENTIFY CAUSE, INCREASE TISSUE PERFUSION
Dobutamine / Milrinone (FOC, decrease adterload)
Levophed
Diuretic (preload reduction)
Vasodilating agents once BP restored to decreased heart workload
Antiarrythmics
IABP (Can decrease afterload without decreasing MAP)
What is treatment for RVF?
RVF causes blood to backflow into systemic venous circulation causing portal HTN, peripheral and cerebral edema.
Treat: OPTIMIZE PRELOAD
Pulmonary vasodilators to decrease pulm htn
Inotropic agents (FOC)
Treat cause
How does the intra-aortic balloon pump work?
Sits in the aorta below left subclavian artery and above the renal vessels. Inflated with helium, works by COUNTERPULSATION.
IAB is inflated at the beginning of DIASTOLE and deflated in SYSTOLE. With inflation it displaces blood into the coronary and carotid arteries and distal systemic circulation, increases renal blood flow reducing RAAS. When deflated it creates potential space (Vacuum) in aorta which makes LV ejection easier.
***Improves CA perfusion and decreases LV workload
What is the overall theme of distributive shock?
Alterations in blood vessels leading to decreased peripheral resistance (SVR) and increased vascular capacity (vasodilation)
What is SIRS?
Systemic Inflammatory ResponseSyndrome
1) Temp > 38 or < 36
2) HR > 90
3) RR > 20 or PaCO2 <32
4) WBC > 12000 or < 4000
What is sepsis?
Life threatening organ dysfunction due to dysregulated host response to infection.
SEPTIC SHOCK is syndrome in which there are profound circulatory, cellular, and metabolic abnormalities that increase mortality >40%
What is SOFA?
Sepsis related organ failure assessment
1) PaO2 / FiO2 (Resp)
2) GCS (Neuro)
3) Platelets (Hem)
4) Creatinine (Renal)
5) Bilirubin (Liver)
6) HTN / Vasopressors (CV)
What is quick SOFA?
2/3 criteria warrant closer investigation:
1) Resp rate > 22
2) Altered mentation
3) SBP < 100
How to clinically identify septic shock?
Pt has been fluid resuscitated adequately and yet:
1) Require vasopressors to maintain MAP > 65
2) Serum lactate > 2
How do bacteria cause septic shock?
Release of endotoxins located in cell wall of bacteria, released on death of bacteria and creates biochemical changes
What is the pathophys of sepsis?
Excess of pro-inflammatory OR anti-inflammatory mediators cause harm to organs
1) Increased inflammatory response (Vasodilation, increased metabolic rate)
2) Increased coagulation (Decreased perfusion, DIC)
3) Decreased fibrinolytic activity (Traps platelets, further decrease in perfusion)
What are other pathophys changes seen in sepsis?
1) Decreased activated protein C (balances inflammatory process, coagulation, fibrinolysis)
2) Hormonal imbalance (Vasopressin and cortisol NOT released, worsening shock)
3) Multi-organ dysfunction
4) Myocardial depression
5) Massive systemic vasodilation, increased metabolic rate, vessel permeability, pt warm and flushed
What is the pathophys of cellular hypoxia and cell death in sepsis?
Pts have difficulty taking up or metabolizing available O2 despite normal delivery. Anaerobic metabolism occurs, lactic acid builds up, damage occurs to organs.
Lack of ATP redisposes NA/K pumps to fail, Na stays in the intracellular compartment drawing water in. Cellular organelles swell, energy production cannot be done, cells digestive organelles rupture and release digestive enzymes killing itself.
What are hemodynamics seen in septic shock?
Decreased RAP, PCWP, PAP
VERY LOW SVR
Increased SVO2
Increased CO/CI due to vasodilation (severe decrease in afterload)
Treatment for septic shock?
Measure lactate (goal to resus to normalize lactate)
Blood cultures
Broad spectrum antibiotic
Aggressive IV resus (30ml/kg IV crystalloid)
Vasopressors (Epi, Norepi, Vaso, Dobutamine) NO DOPAMINE
What is neurogenic shock?
Resulting from loss or suppression of sympathetic tone resulting in high CO however short lived
What is etiology of neurogenic shock?
Injury of spinal cord affecting sympathetic innervation to blood vessels, edema around spinal cord, high levels of spinal anaesthesia, vasomotor centre depression from drugs, hypoglycemia (lack of ATP to send out sympathetic outflow)
What happens with loss of SNS tone?
1) Inhibition of baroreceptors –> Brady –> Decreased CO
2) Peripheral vasodilation –> Decreased afterload, preload, decreased BP, CO
3) Impaired thermoregulation –> Assume room temp –> Decrease CO
What are the specific presentations of neurogenic shock?
CNS: Loss of reflexes below injury
Skin: Warm, pink, DRY (Vasodilated)
HR: Bradycardic
Temp: Inability to sweat
Treatment of neurogenic shock?
Treat cause Prevent CNS instability: Treat hypovolemia with fluid, treat arrythmias, hypotension Caution when suctioning, have atropine Maintain normothermia Monitor reflexes
What is anaphylactic shock?
Result of immediate hypersensitivity reaction with immunologic (Antigen-antibody) or non-immunologic activation of mediator releasing biochemical markers.
**Decreased tissue perfusion and shock
What is pathophys of anaphylactic shock?
Release of mediators
Peripheral vasodilation, increased cap permeability, smooth muscle constriction
Decreased BP, SVR, preload, coronary vasoconstriction
Decreased CO, tissue perfusion
Why is C-reactive protein tested for anaphylactic shock?
Measures degree of inflammatory response, assess if treatments are working
Treatment of anaphylactic shock?
Remove causative antigen
Epi, antihistamines (benadryl, ranitidine), steroids, IV fluids
