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Shock
Widespread abnormal cellular metabolism that occurs when OXYGENATION and tissue PERFUSION needs are NOT MET
Patho is the same for all types of shock except cause is different
Pump (cardiogenic)
Pipes (distributive)
Plasma (hypovolemic)
Each P has a different associated shock
What are the three P’s of perfusion?
Adequate VOLUME of blood for the heart to pump (preload)
Effective PUMPING by the heart (CO)
Constriction and dilation of the VASCULATURE (SVR)
Unobstructed pathway for blood flow
What does adequate perfusion depend on (hemodynamics)?
CO = HR x SV
HR
SV = volume/beat
Preload = volume of blood available to be pumped
Afterload (SVR) = how much resistance the heart is beating against
Contractility = how strong each beat is
Control of peripheral circulation = dilation/constriction
MAP = indicator of perfusion of capillary beds
What are the hemodynamic terms?
((systolic + (2)diastolic))/3
How do you calculate MAP?
Blood FLOW (CO)
AMOUNT of hemoglobin available to carry oxygen (ex., anemia)
Percentage of arterial oxygen hemoglobin saturation (SpO2) (blood from ABG)
What does O2 delivery depend on?
O2 consumption
Represents the body’s demand for oxygen and is a reflection of the body’s metabolism
DECREASED in shock; magnitude of O2 consumption deficit has been correlated with mortality rates
Reduction in blood flow (hypovolemic, cardiogenic, obstructive)
Uneven distribution of blood (septic, anaphylactic, neurogenic)
Why does the body show decreased O2 consumption during shock?
The body normally provides 3-4 times more oxygen than needed for normal metabolism
Start CAB NOT ABC
Why is there some wiggle room before you give O2?
Volume
Not enough volume perfusing (ex. hemorrhage, dehydration, third spacing)
Wrong type of volume perfusing (ex. NS/LR)
Pump ineffective
Vasculature ineffective
Volume isn’t where it needs to be
Obstruction in the blood’s pathway
What are the possible causes of hypo-perfusion and hypoxia?
Hypovolemic (inadequate volume)
Cardiogenic (inadequate pump)
Distributive (ineffective vasculature)
Neurogenic
Chemical (anaphylaxis, sepsis, capillary leak)
(burns are a mix of distributive/hypovolemic)
What are the types of shock?
Initial
Nonprogressive/compensatory
Progressive
Refractory (irreversible)
What are the stages of shock?
MAP/SBP: Mild vasoconstriction
HR: Tachycardia (first sign something is wrong)
Respiratory status: Slight increase to retain more O2 (Kussmaul’s)
Skin: Pallor
UOP: Normal
Mentation: Normal, slight anxiety
Acid-base: Normal (still compensating)
What are the S/S of INITIAL shock?
MAP/SBP: Decreased 10-15 mmHg from baseline, hypotension
HR: Tachycardia (SNS stimulation)
Respiratory status: Increased RR, O2 sat decreased 2-5% from baseline
Skin: Cool, pale (vasoconstriction; body pulling blood away from vital organs)
UOP: Decreased; THIRST
Mentation: Anxious, restless
Acid-base: Mild acidosis, mild hyperkalemia
What do each of the body systems look like in NONPROGRESSIVE/COMPENSATORY shock?
MAP/SBP: Decreased >20 mmHg from baseline, hypotension
HR: Tachycardia
Respiratory status: Increased RR, O2 sat decreased 5-20% from baseline
Skin: Cool, cold, pale, DIAPHORETIC; anoxia to nonvital organs
UOP: Decreased to anuria
Mentation: altered, confused
Acid-base: metabolic acidosis, lactic acid production
What do each of the body systems look like in PROGRESSIVE shock?
MAP/SBP: SEVERE hypotension, MAP <65
HR: Blood is so acidotic and heart damaged that it could be any rate
Respiratory status: Respiratory FAILURE (intubation), pulse ox fails or is INACCURATE due to vasoconstriction
Skin: MOTTLED, dark, dusky (gray); very COLD to touch (no blood flow)
UOP: ANURIA, INCREASED BUN/Cr (kidney not filtering)
Mentation: COMA, loss of consciousness, SEIZURES
Acid-base: MIXED acidosis; hyperkalemia, lactic acid
CAN’T REVIVE
What do each of the body systems look like in REFRACTORY/IRREVERSIBLE shock?
HYPERKALEMIA AND HYPONATREMIA
What is the MAIN electrolyte imbalance that happens in shock?
Hypovolemic shock
Caused by a loss of whole blood, plasma, or interstitial fluids in such quantities that the body’s metabolic needs can no longer be met; low preload = low CO
Ex., dehydration, vomit/diarrhea, third-spacing, hemorrhage, diabetes (insipidus), burns
Decreased blood volume or plasma loss = decreased venous return (PRELOAD) = decreased STROKE VOLUME = decreased CO = decreased tissue PERFUSION
Decreased CO = ANAEROBIC metabolism and LACTIC ACID production = MYOCARDIAL DEPRESSION
Decreased CO = decreased CORONARY ARTERY perfusion
Decreased CO = inadequate cellular perfusion, which leads to an increased susceptibility to INFECTION and HEMORRHAGE = ORGAN DAMAGE
What is the PATHO for hypovolemic shock?
STAGE DEPENDENT (same as S/S shock)
Skin (least reliable indicator)
Cool, pale skin due to vasoconstriction
Decreased cap refill (>3)
Clammy, moist skin due to release of epinephrine and norepinephrine
Thirst
Activated due to increased serum osmolality
UOP
Decreased due to vasoconstriction and decreased GFR
ADH released to retain fluid
LOC
Hyper-alert initially, then decreased
TACHYCARDIA
Very early sign
SV decreases and HR increases to maintain CO
Increased RR (rate and depth)
Improve blood oxygenation levels
Blow off CO2 (Kussmaul’s)
Compensate for impending acidosis
Labs
What are the S/S hypovolemic shock?
H/H (depends on underlying cause)
Electrolytes (Hyperkalemia, Hyponatremia)
What do the LABS look like in hypovolemic shock?
CVP (preload)
2-6 mmHg
MAP
65-110 mmHg
SBP + (DBP x 2)/3
What are the hemodynamic parameters for hypovolemic shock?
Airway = assess and establish
Breathing = assess, assist
C = circulation
CAB for emergency pt.
What are the interventions for hypovolemic shock?
STOP THE LOSS
Restore circulating blood volume (most important intervention)
Replace what was lost (ex. fluid, blood, plasma, etc.)
Fluid replacement; ADMINISTER ENOUGH to correct problems (improve BP, UOP)
Secondary interventions
What is the intervention for circulation in hypovolemic shock?
Crystalloid solutions (LR, 0.9% NS)
Albumin
Hespan (hetastarch)
Plasma (FFP)
Blood
REPLACE WHAT WAS LOST
What is the fluid selection for hypovolemic shock?
ISOTONIC SOLUTION
Provides intravascular expansion
May or may not be all that is needed (depends on what is lost); not all that is needed in blood loss
DO NOT USE D5W
How do crystalloid solutions (LR, 0.9% NS) help in hypovolemic shock?
Glucose is metabolized, leaving behind water
Hypotonic fluid; leaves the blood vessels and is not in the circulating volume
Only causes edema
Why is D5W NOT used in hypovolemic shock?
Give if fluid loss is due to plasma (ex. BURNS)
Also given for clotting DO
How does plasma (FFP) help in hypovolemic shock?
Major blood losses should be replaced with blood products (ex. whole blood (trauma), packaged RBC (ED ICU), etc.)
How does blood help in hypovolemic shock?
Foot of bed elevated, may not be appropriate for all patients depending on oxygenation status and patient acuity
Increase blood flow back to heart
NOT in cardiogenic shock
What is the early positioning for hypotension?
CARDIOVASCULAR SUPPORT (if pump problem)
Contractility (LV function):
INOTROPIC agents (increase contractility)
DOBUTAMINE, MILRINONE, DIGOXIN
Preload:
Vasoconstrictors
NOREPINEPHRINE (LEVOPHED), NEO-SYNEPHRINE
Both:
DOPAMINE (Intropin) (EFFECTS ARE BASED ON DOSE)
What are the pharmacological interventions for hypovolemic shock?
Improve LV function, increase contractility of heart
What do inotropic agents do for cardiovascular support in hypovolemic shock?
Improve preload (after volume replaced)
What do vasoconstrictors/pressors or fluids do for cardiovascular support in hypovolemic shock?
Anaphylactic
What type of shock is Norepinephrine or Neo-synephrine NOT used?
Arterial line; continous ABG, BP, and MAP
What is important to monitor with vasopressors?
mcg/kg/min
How is dopamine titrated?
0.5-2 mcg/kg/min (low dose)
How much is dopamine given for renal and mesenteric (gut) dilation (increase blood flow)?
No
Does a patient with low UOP get dopamine?
2-10 mcg/kg/min
How much dopamine is given for inotropic effects (act on beta receptors in heart, increase contractility) to increase CO?
>10 mcg/kg/min
NOT GIVEN ABOVE 20 mcg/kg/min (severe)
How much is dopamine given for vasoconstriction (alpha receptors on blood vessels)?
Correct acid-base balance
Monitor for FVO; Rebound (over tx)
Meet nutritional needs
Provide emotional support
What are the secondary interventions for hypovolemic shock?
Cardiogenic shock
Caused whenever the heart’s pumping ability becomes impaired, resulting in decreased CO
S/S like HF but not about volume
Any condition that causes dysfunction of the LV, the RV or both due to ischemia, structural problems or dysrhythmias
What are the CAUSES of cardiogenic shock?
Decreased cardiac contractility
Decreased SV and CO leads to:
Pulmonary congestion
Decreased systemic tissue perfusion
Decreased coronary artery perfusion
Decreased coronary artery perfusion leads to a further decrease in cardiac contractility
What is the PATHO of cardiogenic shock?
Shock:
Acute issue
It is more about no oxygenation and perfusion, which causes the heart to reduce its contractility and ischemia to the heart.
HF:
More of a long-term issue and a pressure/congestion issue. Perfusion can be adequate.
Similarities:
S/S is are the same
How is cardiogenic shock different than HF?
CO/CI: Low
BP: Low (hypotension)
Peripheral pulses: Weak, decreased cap refill
Skin: cool, clammy
UOP: Low; not getting O2 to work correctly
LOC: impaired (alert → anxious → coma)
Heart failure S/S
Crackles
Tachypnea
Fatigue, confusion
Tachycardia
Systemic vascular congestion and peripheral edema
What are the S/S cardiogenic shock?
Initial cause: PUMP issue not plasma issue
S/S: Same except s/s HF
Collaborative interventions:
Hypovolemic: fluids
Cardiogenic: DIURETICS, INOTROPES
Expected outcome: better for hypovolemic
How do you differentiate when a patient arrives with a BP 76/30?
LISTEN TO LUNGS
Fluid overload = cardiogenic
Hypovol = Low CVP, preload, bleeding
How is cardiogenic shock different from hypovolemic shock?
Oxygenation
Increased CO (preload (CVP), afterload, contractility (SVR))
Decrease LV workload (diuretics)
Devices
What are the interventions for cardiogenic shock?
Correct any dysrhythmias
Correct any hypovolemia (or hypervolemia); monitor f/e
Meds: inotrope, vasopressor, and vasodilator (not at the same time as other)
How do you increase CO in cardiogenic shock?
Vasodilators to decrease AFTERLOAD (decreased workload on heart)
NITROGLYCERIN, NITROPRUSSIDE
Correct FLUIDS balance (hypo or hypervolemia); DIURETICS
How do you decrease LV workload in cardiogenic shock?
SBP >110
When do you use a VASODILATOR in cardiogenic shock?
Vasculature (circulatory) problem; pipes
What type of problem is distributive/circulatory shock?
Event (trigger)
Vasodilation (capillary beds)
Inflammatory response (leaky)
Misdistribution (everywhere else)
Decreased preload (doesn’t return to heart)
Decreased CO
Inadequate perfusion
What is the PATHO for distributive/circulatory shock?
Neural (neurogenic) (spinal cord)
Chemically
SEPSIS (infection)
ANAPHYLAXIS (allergy, antigen)
CAPILLARY LEAK (burns)
What are the two ways distributive/circulatory shock can be induced?
Neurogenic shock
Occurs due to massive VASODILATION as a result of loss of sympathetic tone
Spinal cord injury (T6 and above)
Spinal anesthesia
What are the CAUSES of neurogenic shock?
BP: Drops rapidly
HR: DECREASED; No sympathetic tone from severed spinal cord, so parasympathetic nervous system kicks in instead
Extremities: Warm/red initially (vasodilation); vessels will not send blood back to heart and eventully become cool/pale
Difficult thermoregulation
Compare and contrast neurogenic vs. hypovolemic shock S/S
Fluids (still hypovolemic and low CVP)
O2 (for all shock)
Vasoconstricting drugs
Norepinephrine (Levophed), Epinephrine
HIGHER MAP GOAL: 85-90 for the first 7 days after spinal cord injury
Increase perfusion to spinal cord
What are the interventions for neurogenic shock?
Acts as SNS, sending blood back to heart (preload) and increasing BP/MAP to improve perfusion
Why is vasoconstricting drugs used in treatment of neurogenic shock?
Anaphylactic shock
Sudden life-threatening hypersensitivity reaction to an antigen
Characterized by massive VASODILATION and INCREASED CAPILLARY PERMEABILITY
Not perfusing or oxygenating
Chemical mediators cause profound vasodilation, capillary permeability, bronchoconstriction, increased coronary permeability
What is the PATHO for anaphylaxis?
SEVERE HYPOEXMIA secondary to bronchoconstriction or from cardiovascular collapse
How does death result from anaphylaxis?
Rapid onset
Angioedema (airway edema)
Difficult breathing, dyspnea
Tachycardia
Hypotension
Dizziness or syncope (faint)
Anxiety
What are the S/S anaphylaxis?
Epi-pen (epinephrine)
O2, fluids
Benedryl
Steroids
Bronchodilators (albuterol)
Can give Epinephrine IV drip (vasoconstriction, increases BP, tx allergic reaction)
What is the TX for anaphylaxis?
Anaerobic metabolism
Brain: seizures, cerebral infarction, decreased LOC, coma, etc.
Kidneys: ACUTE TUBULAR NECROSIS, oliguria, BUN/Cr
Myocardium: dysrhythmias; place on EKG, tele, auscultate
Fluid shifts: distributive (edema)
Peripheral circulation: vasoconstriction; assess skin, cap refill, touch, turgor
GI: stress ULCERS, bowel infarction, ILEUS; assess septic shock, BOWEL SOUNDS
Hepatic system: JAUNDICE, DIC; assess ALT/AST, neuro
Glucose metabolism: HYPERGLYCEMIA (stress)
Lungs: ARDS
What are the body systems that are affected in all types of shock?
Inappropriate inflammation
Global inappropriate microcirculatory clotting (body uses up large amounts of platelets and clotting factors; loses ability to clot normally)
Paradoxical bleeding (excessive clotting and bleeding at the same time, seen everywhere in the body)
Lead to MODS
What is disseminated intravascular coagulation (DIC)?
Trauma
Shock
Sepsis
Toxin
Allergies
Cancer
(Don’t memorize, just know there are alot)
What are the CAUSES of DIC?
Check skin and others for bleeding
Check labs
Assess for clotting
Assess for organ dysfunction
How do you assess for DIC?
Platelets: low (all used up)
D-dimer: high (waste product of clotting)
PT: high (clotting factors used up)
PTT: high (clotting factors used up)
TT (thrombin time): high (clotting factors used up)
Fibrin: low (used up for inappropriate clotting)
FDP: high (waste product from clotting)
H/H: low with bleeding
JUST KNOW TRENDS
What are the LAB values in DIC?
Underlying cause
Correct secondary effects
Replace what’s missing
Volume
RBC
FFP
Clotting factors
HEPARIN therapy; stop clot, but STOP when bleeding
Monitor for bleed
What is the TX for DIC?:
Multiple organ dysfunction syndrome (MODS)
When 2 OR MORE organs separate from initial organ damaged after initial insult