🌡️Shock Flashcards
Shock
the body can no longer meet cellular oxygen demands (anaerobic)
inadequate blood flow resulting in decreased perfusion
Shock Diagnosis
MAP <60 or evidence of organ hypoperfusion
Lactate = higher
ABD = higher
Bicarb = lower
Blood becomes acidotic
Shock - Initial Stage
Baroreceptors detect changes in volume –>
Decreased cardiac output
Decreased tissue perfusion
Shock - Compensatory Stage
body tries to self correct by SNS responses (neural, hormonal, chemical)
Neural compensation (4)
increase HR/contractility
arterial/venous vasoconstriction (clamping down peripheral)
shunting of blood to vital organs
catecholamines released
Hormonal compensation (3)
activate renin
stim anterior pituitary (1) and adrenal medula (2)
2(release ADH resulting in decreased sodium and water excretion)
2(catecholamines)
1(release glucocorticoids to increase blood sugar)
Chemical compensation
increase rate and depth of respirations to correct acidosis
Shock - Progressive stage
compensatory fails resulting in SIRS
now anaerobic metabolism produces large lactic acid
Progressive stage vascular effects (4)
increased vascular permeability
intravascular hypovolemia
tissue edema
decline in tissue perfusion
Progressive stage cellular effects (4)
apoptosis
Na+/K+ fails causes cells to swell/die
Mitochondria swells and ruptures
Cells cannot use o2
Progressive stage cardiac effects (4)
ventricular failure from release of myocardial depressant cytokines
microvascular thrombosis
lactic acidosis –> MASSIVE vasodilation
NEGATIVE inotropic effects –> weakened pump
Progressive stage pulmonary effects (4)
acute respiratory failure, respir distress, lung injury
increase cap membrane permeability
Acute respiratory distress syndrome
refractory hypoxemia leaving alveoli to drown in fluid/protein
Progressive stage neurologic effects (3)
microvascular thrombosis
↓
cerebral hypo perfusion (changes in orientation)
↓
SNS dysfunction (b1 +b2 depression, temp failiure, coma)
Progressive stage GI effects (4)
necrotic bowl/ liver/ pancreas
GI/hepatic/pancreatic failure
Progressive stage renal/hematologic effects (2)
quickest to be effected
Acute tubular necrosis –> DNR nephrons :(
DIC
Disseminated Intravascular Coagulation (DIC)
consumptive coagulopathy (blood is going from liquid to solid)
AEB: septic shock, trauma, OB emergency
DIC clinical manifestations (4)
decreased perfusion to tissues –> dusky/mottled
Occult (GI) and Overt (errrrwhere) bleeding
Petechiae and ecchymosis
Common lab findings for DIC:
Elevated PT, PTT
Decrease fibrinogen/platelets
Metabolic acidosis (decreased perfusion to tissue)
Elevated Fibrin degration product ( MOREEE BLEEEDING) 😝
+ D-dimer
What med is used to treat DIC?
HEPPARRRRIIINNNNNNNNNN🥰😎😎😎😎🤩
🤚🏼STOP body process to form clots
Shock - Refractory stage (3)
correction is difficult
cell hypoxia and death impending
multi-organ dysfunction syndrome
Hypovolemic shock causes
Decreased intravascular volume
Internal fluid shift
(GI bleed, ruptured spleen, hemothorax, third spacing, hemorrhagic pancreatitis)
Hypovolemic shock loss of (3)
WHOLE BLOOD –> hemorrhage
PLASMA –> burns/decubitus
BODY FLUID –> suctin v/d diuretic, DKA
Pathophys hypovolemic shock
Decreased intravascular volume
↓
decrease venous return (POOL IS ASSOCIATED WITH PRELOAD SO DECREASE DAWG)
↓
decrease ventricular filling ( how we gonna fill if we dont have volume)
↓
Decrease SV and cardiac output
IF WE CANT OUTPUT WHAT GONNA HAPPEN TO ORGANS💀💀☠️☠️☠️☠️💀☠️☠️☠️💀☠️☠️👽
Hypovolemic shock clinical manifestations (7)
No volume? DW we will just increase HR and RR 🤭😏🤪
Postural vitals >20 systolic >10 diastolic with position changes
Oliguria (kidneys be like 🖕🏼🖕🏼🖕🏼😡😡🤬🤬🤬🤬🤬🤯)
cool, pale, clammy skin
weak pulse
flat vein
decreased LOC
Hypovolemic shock diagnostic tests (5)
increased sodium (hypernatriemia
decreased HBG
ABG/Lactate/imagining relating to exam
Hypovolemic shock hemodynamic profile
DECREASED preload, CVP, PCWP, CO and BP
INCREASED AFTERLOADDDDD SVR HIGH ( we tryin to compensate)
🐭🐱(catecolamine (epi/norepi) and raas (fluid retention)= cats and rats)
Primary therapy for hypovolemic shock
🥄🧊🧊🧊🌊🌊🌊🌊💦💦💦💦💧💨💨💨💨💨💧💧💧💧💧
IV FLUIDS BBY!!!
Cardiogenic shock - cardiac etiology (4)
ischemia causing 40% or greater damage (usually caused by MI)
ventricular wall/pap muscle/septal rupture
cardiomyopathy
aortic stenosis
Cardiogenic shock - non-coronary etiology
usually can reverse
cardiac tamponade
restrictive pericarditis
PE
Pulmonary Hypertension
Tension pneumo
Cardiogenic shock clinical manifestations (noninvasive) (8)
rapid/thready pulse
narrow pulse pressure (120/105)
JVD
arrhythmia
angina
cool, pale, moist skin
oliguria
altered AxO
Cardiogenic shock clinical manifestations (pulmonary findings) (4)
dyspnea, tachypnea, crackles
ABG –> decreased Pa/Sa 02 decreased PaC02
Cardiogenic shock diagnostic tests (4)
cardiac enzymes(troponin/CKNB)
BNP
Echo (ejection fraction)
coronary angio
Cardiogenic shock hemodynamic profile
REMEMBER CARDIO = PUMP ISSUE
CO/CI and BP is LOW
PRELOAD is INCREASED (CVP/PCWP)
AFTERLOAD is INCREASED!!!!!!!!!!!!!!!!! SVR is high
Cardiogenic shock pharmacologic therapy (4)
POSITIVE inotropes (digoxin, dopamine, dobutamine)
Nitrates, diuretics, opioids –> BP IS LOW already so use with CAUTION
Vasopressors
Cardiogenic shock invasive treatment
early revascularization
IABP
LVAD
surg/transplant
Intra-aortic Balloon Pump
Goal: decrease myocardial workload to improve perfusion to corn air ie, reduce afterload
ALSO improves miss kidney’s R Ter IE
what is out of intra-aortic balloon pump’s scope of practice?
she cannot measure hemodynamic pressures (ASIDE FROM BP)
not a pacemaker
Nursing interventions for IABP (3)
HOB < 30 degrees (d/t hip flexion) can do reverse trendelenburg
monitor pedal pulses, LOC, U/O, bleeding
flush artery q1 hour (patency)
What treatment is appropriate for cardiogenic shock
POSITIVE INOTROPIC AGENT
nitroprusside, dobutamine
WE GOTTA PUMP IT UP!! GET YO PUMP ON! PUMP CITY BABY!
Distributive shcok
MASSIVE VASODILATION 🌫️🌫️🌫️🌫️
increase of vascular space for same volume of fluid which decreases venous return, SV, CO
either neurogenic, anaphylactic or septic
Neurogenic shock
DISTRIBUTIVE
loss of sympathetic tone by injury to spinal cord, spinal anesthesia, stress, severe pain, OD
Neurogenic shock clinical manifestations (3)
Hypotension
Bradycardia (nervous system cannot compensate)
Hypothermia
Neurogenic shock treatment (3)
remove cause
volume replacement
vasopressors
Anaphylactic shock
DISTRIBUTIVE
antigen/antibody
Anaphylaxis chemical response (2)
Histamine –> vasodilation, decreased SVR, decreased BP
Serotonin –> increased cap permeability, decreased volume, decreased BP
Anaphylactic shock causes (5)
drug, contrast, blood, bites/sting, food
Anaphylactic shock clinical manifestations (6)
pruritis
erythema
urticaria –> hives
angioedema
laryngeal edema
hypotension
Anaphylactic shock treatment(6)
PREVENTION, remove antigen
EPINEPHRINE
airway
corticosteroid
fluids
Positive inotropic agents
Sepsis
life threatening organ dysfunction
Septic shock
hypotension not responsive to fluid resuscitation –> perf abnormal
Sepsis clinical manifestations
Altered mental status (<15 GCS)
Tachypnea (>22)
Hypotension (<100 SBP)
QSOFA + IF ALL THREE
Tachycardia, fever, fatigue, nausea, increase WBC with left shift
Early recognition of sepsis
SIRS/qSOFA
Labs –> increased lactate, coags, liver/renal function, procalcitonin!!!!!!!!!!!
Diagnostic marker for septic shock
PROCALCITONIN
Systemic Inflammatory Response Syndrome Criteria
Temp > 38 degrees C
Heart rate > 90 beats/min
RR > 20 or PaCO2 <32
WBC >12,000 or >10% bands
2+ = sirs
Systemic Inflammatory Response Syndrome
inflammation, thrombosis and fibrinolysis
immune system is overwhelmed, feedback mech fails, process to protect is now harmful
SIRS pathophysiology
micro-organism invades body resulting in inflammation
sheds protein/releases toxins to activate cascades (fibrinolytic/platelets) –> results in increased cap membrane permeability, clotting, maldistribution of BF, 02 supply/demand imbalance
Sepsis vulnerable populations
young or old, immunosuppressant, trauma, addictive habits, invasive therapies
Sepsis bundle
The best treatment option
group of therapies that have extensive EBP to back them
Central line bundle
hang hygiene
barrier precautions
CHG
avoid femoral
review daily
record time/date of line placement
Sepsis diagnostics
Appropriate cultures (urine, sputum, wound)
Blood cultures (FROM TWO SPOTS TO ID POTENTIAL CONTAMINATION)
one percutaneous and one from each vascular access
Obtain cultures before:
antibiotics
One hour resuscitation bundle for sepsis (3)
LACTATE –> if >4 REPEAT THEN rapid crystalloid therapy
blood cultures PRIOR TO (you know this cmon now)
vasopressors to maintain map >65
Early septic shock clinical manifestations (5)
pink,warm, dry skin
CO normal/elevated (🐱🐱🐱🐱🐱)
decreased afterload
increase respirations
change mental status
Early septic shock hemodynamics (4)
preload decreased (CVP/Wedge follows)
afterload decreased (low SVR/BP)
HR increased
contractility normal/increased
Early septic shock therapy (3)
fluids, antimicrobial agents
cortiosteroids
supportive care –> DVT, hemodynamics, ventilation, electrolyte/glycemic control
Progression of septic shock
SIRS –> MODS
increase cap wall permeability –> leaves vasculature –> interstitial/intra-cellular edema
decrease volume
increase viscosity
compensatory failing, decreased perfusion, mitrocondrial change
Multi Organ Distress Syndrome
Failure 2+ separate organs
Hemostasis cannot be maintained without intervention
Late septic shock
hypodynamic “cold phase”
increased mortality
Late septic shock clinical manifestations (5)
cold, clammy skin, edema (anasarca), low CO, SEVERE HYPOTENSION
Late septic shock hemodynamic profile
Increased preload (CVP, PCWP)
Afterload increased (SVR)
Contractility decreased (BP/CO very low)
Late septic shock treatment (4)
supportive care
vasopressors
+ Inotropes
corticosteroids
Supportive measures for ALL stages of shock (4)
maintain airway/ventilation, CO
restore intravascular volume (albumin/NS)
improve acidosis
Therapy for low preload
POOLING ISSUE –> FILL IT UP WITH WATER
Position up if ventilation issue, position down if perfusion issue
Crystalloid aministration
electrolyte, hypo/hypertonic
need large fluid volume, overload is a risk
Colloid administration
usually albumin
keeps fluid in vascular compartment
Hydrostatic vs oncotic pressure
Hydrostatic SBP
Oncotic ( albumin pulls into vasculature)
Blood product administration
HGB <7.0
FFP for bleeding
Platelet if <5000 (30k for bleeding risk) (50k for surgery)
Patient positioning: Preload
low = flat HOB, modified trendelenberg
When preload is high you admin –>
diuretic, nitroglycerin, reduce fluid, patient positioning (elevate HOB)
specific to cardiogenic shock
When preload is low you admin –>
FLUID
alpha one med (norepi, dopamin, epi, phenylephrine, vasopressin)
AFTERLOAD IS LOW WITH which SHOCK
distributive
When afterload is high you admin –>
nitroprusside, ACE-I, CCB,
IF BP IS OK
WHEN CONTRACTILITY IMPAIRED YOU ADMIN
+ INOTROPIC AGENTS SUCH AS DOPAMINE, DOBUTAIN, MILRINONE, DIGOXIN
corticosteroids for septic shock
When require vasopressin after fluid resus (IV hydrocortisone)
**pt make have relative adrenal insufficency
