TEST 3: Shock Flashcards
Basic principles of shock
(Lecture, p. 1557)
-Inadequate tissue perfusion—> decreased oxygen and nutrient delivery —> impaired cellular metabolism
-Can have increased oxygen demand and nutrients (hyper metabolic state)
-Can have decreased removal of cellular waste
Cellular changes in shock
(Lecture, p.1558)
BLUEPRINT
Main problem of shock at the cellular level:
-We switch from aerobic to anaerobic metabolism (d/t overconsumption of oxygen)
When anaerobic metabolism starts:
-Increased lactate, metabolic acidosis, increase in the oxy-hgb dissociation
-Next, protein metabolism increases, causing increased muscle wasting( decreased real and cardiac muscle strength) decrease immunoglobulin (will decrease your immune response) and increased cellular edema (inflammatory response that activates the clotting cascade)
-Lastly, decreased ATP, which increase intracellular Na/ water, decreased circulating volume, and can also trigger the clotting cascade
Metabolic changes in shock
(Lecture)
1559
- Increased glucose (from catecholamine, cortisol, and growth hormone release; BUT insulin resistance) which causes:
Increased protein breakdown, increased pyruvate, increased lactate (also increases insulin resistance) - Inability to use glucose/increased insulin resistance causes:
Increased gluconeogensis and glycogenolysis (which deplete energy store and increase cell failure), also increase Lipolysis (so you increase the amount of free fatty acids and triglycerides).
INTERESTING: except in the liver, kidneys and muscles, the body’s cells have extremely limited stores of glycogen. The total body stores can fuel the metabolism for only about 10 hours. Though depletion of fat and glycogen stores is not considered organ failure, but contributes considerably to Cellular failure.
General shock management
(Lecture)
-Consider patient history, risk factors, clinical situation
-Tx: address under lying cause, improve tissue perfusion, improve oxygen delivery, support metabolic demands and manage hyperglycemia
Stages of shock
(Lecture)
- Compensated:
Where the body is still able to compensate for relative or absolute fluid loss (patient is able to maintain adequate BP and cerebral perfusion)
—-vasoconstriction, increased HR & contractility maintain CO, activation of RAAS - Decompensated:
Late phase of shock where body’s compensatory mechanisms are unable to maintain adequate perfusion to the brain and vital organs
—-vascular collapse, decreased CO (all the predictable symptoms) - Irreversible:
Rapid deterioration of the cardiovascular system and the compensatory mechanisms have failed—> MODS–> DEATH
Cardiogenic Shock etiology & characteristics
(Lecture, p. 1567)
Results from the inability of the heart to pump adequate blood to the tissues and organs
3 primary etiologies:
-Decreased contractility (pump failure): from MI, sepsis, contusion, dysrythmia, papillary muscle rupture
-Impaired diastolic filling: arrhythmias
-Obstruction: PE, tamponade, valve disorders, tumors, wall defects
-Caused by extensive myocardial damage and aggravated by inflammatory response
Defining characteristics: hypotension and hypoperfusion despite adequate LV filling pressure & intravascular volume
-Also results in metabolic acidosis and is often fatal
Cardiogenic shock compensatory mechanisms
(Lecture, p. 1567)
2 main mechanisms
- Decreased CO = Activates RAAS and stimulates ADH (which increases volume) —> preload, SV, HR increase—> causes systemic and pulmonary edema (causing dyspnea)
- Decreased CO = activates catecholamine compensatory release—>
Causing increased SVR, preload, SV, HR—>which increases myocardial oxygen requirements (worsening the failure/ shock)—> leading to decreased CO/ EF
—> worsened tissue perfusion, low BP
—> ischemia, impaired cell metabolism, worsening myocardial dysfunction
Cardiogenic shock manifestations/ treatment
(Lecture, p. 1567)
-Caused by inadequate perfusion to the heart and lungs
Manifestations:
-CP, dyspnea, faintness, impending doom
-Tachycardia, tachypnea, hypotension, JVD, low CO
-Signs of poor perfusion: mottling, cyanosis, low UO
-Extra heart sounds, pulm edema, hypoxemia
-Elevated end organ lab values (LFT/ BUN/ Creat)
-Treatment: support the pump, remove the obstruction/ PCI to open coronary arteries, IABP, impella, ECMO
Hypovolemic Shock
(Lecture, p. 1568)
-Caused by reduced intravascular volume (preload) from loss of whole blood (hemorrhage), plasma (burns), or interstitial fluids (diaphpresis, DM, emesis, diuretics) in large amounts, which reduces CO.
-Symptoms occur with 15% of intravascular volume loss
Etiologies:
-Whole blood: hemorrhage
-Plasma: burns
-Interstitial fluids: diaphoresis, DM, DI, emesis, diarrhea, diuretics
Defining characteristics: compensatory mechanisms up to a certain point and then they fall off a cliff
Hypovolemic shock compensatory mechanisms
(Lecture, p. 1569)
Decreased volume causes decreased CO= interstitial fluid shift into intravascular spaces, aldosterone and ADH to increase fluid reabsorption, and splenic discharge (disgorges stored rbc’s and plasma)
Decreased volume caused decreased CO= catecholamine release—> increase SVR /HR/ contractility (which increases CO)
Note, if loss continues, compensatory mechanisms fail and tissue perfusion is further decreased
Prompt control of hemorrhage is main goal
Hypovolemic shock manifestations/ treatment
(Lecture, p. 1568)
-High SVR: pallor and cool extremities
-Thirst
-Oliguria
-Low Preload (RA/ CVP) and tachycardia
Treatment:
Fluid/ blood replacement
Neurogenic shock (aka vasogenic)
(Lecture, p. 1566)
-Widespread, massive vasodilation that results from an imbalance between the parasympathetic and sympathetic nervous system stimulation of vascular smooth muscle
-Etiologies (anything that stimulates parasympathetic activity and inhibits sympathetic activity) :
-Trauma: spinal cord or medulla
-Conditions that deprive medulla of oxygen or glucose
-Depressive drugs, anesthetic agents, severe emotional distress, pain
Defining characteristics: hypotension with bounding peripheral pulses and flash cap refill/ bradycardia
GEM hallmark sign of neurogenic shock is very low SVR (hypotension) as well as bradycardia
Neurogenic shock compensatory mechanisms
(Lecture)
-Really no body compensatory mechanisms IN the body WE have to do something (Ie vasopressin)
Imbalance between sympathetic and parasympathetic stimulation= massive vasodilation—> causing decreased vascular tone—> causing decreased SVR—> leading to inadequate CO and decreased tissue perfusion—> leads to impaired cellular metabolism
Anaphylactic Shock
(Lecture, p. 1565)
-Is the outcome of a widespread inflammatory and vasodilatory reaction to an allergic antigen (usually a protein)
-Etiologies: exposure to allergic antigen
-Anaphylactoid type— cold, exercise, and medication contaminants (not IgE mediated, non immunologic)
Defining characteristics: similar to neurogenic shock with vasodilation, peripheral pooling, and tissue edema/
Bronchoconstriction
Mediators:
Histamine, kinins, prostaglandins, complement, leukotrienes, serotonin
Anaphylactic shock compensatory mechanisms
(Lecture)
-The second type of shock that doesn’t have internal compensatory mechanisms WE must intervene to treat
Antigen exposure—> trigger inflammatory response—> mild to severe response (usually more extreme)
Anaphylactic Shock manifestations/ treatment
(Lecture, p.1566)
Manifestations:
-CV: hypotension, diaphoresis, pallor
-Resp: SOB, cough, rhinorrhea, throat tightening, wheezing,
-GI: N/V/D, abdominal pain
-Cutaneous: erythema, pruritis, urticaria, angioedema
OMINOUS: anxiety, confusion, impaired mentation (sign of worsening shock)
Treatment:
-Epi to stop mast cell degranulation, fluid resuscitation, antihistamines, steroids
Septic shock
(Lecture, p. 1560)
-Is the endpoint of a physiologic state of hypoperfusion with profound underlying circulatory, cellular, and metabolic abnormalities (subset of sepsis)
-Etiology: Infection
-Gram negative and positive bacteria, virus, or fungus related
-can be anywhere: PNA, bloodstream, intravascular catheter, intraabdominal, urosepsis, surgical wound.
Overview of shock categories
(P.1560)
Distributive > septic + anaphylactic + neurogenic
Cardiogenic
Hypovolemic
Obstructive
Note— initial management for all is to discover, diagnose and correct/ remove underlying cause
The sepsis spectrum
(Lecture)
SIRS —>sepsis —>septic shock—> MODS
Obstructive shock
(P.1569)
-Associated with a mechanical obstruction to and/ or from the heart (generally within the great vessels of the heart) that causes inadequate cardiac output
-Commonly combined with cardiogenic shock
-Usually due to PE, tension pneumo, or cardiac tamponade
-Potentially life threatening due to hemodynamic instability
SIRS
(Lecture)
-Reaction to anything that stimulates the inflammatory response (can be both infectious and non infectious)
Cause: infection, trauma, pancreatitis, burns etc.
CARS (compensatory Anti-inflammatory response syndrome)
-SIRS Criteria:
Temp >38 or <36
HR > 90
RR > 20 or PaC02 <32
WBC > 12,000 or <4000, or > 10% bands
Sepsis
(Lecture)
-Life threatening organ dysfunction caused by a deregulated host response to infection
Defining characteristics— systolic hypotension <90 and organ dysfunction
SOFA Score
(Lecture)
Sequential organ failure assessment score :
-P/ F ratio (with or without mechanical ventilation)
-Platelet count (heme function)
-Glasgow coma score (neuro, anything less than patients normal is positive)
-Bilirubin (liver function)
-MAP (cardio function)
-Creatinine (kidney function)
*Considered positive if score increases two points= organ dysfunction due to hypoperfusion (aka positive sofa score)
-Quick SOFA score (qSOFA)
Used on patients not in the icu
-RR> 22
-GCS < 15
SBP < 100
If 2/3 are true, considered positive for sepsis organ dysfunction (best measure outside of icu ie clinic)
How bacteremia works
(Lecture)
Bacteremia—> gram negative bacteria release endotoxins or gram positive bacteria release exotoxins, which both cause—> release of pro inflammatory cytokines, which causes activation of—> complement system, coagulation system, kinin system, neutrophil, endothelial, and monocyte-macrophage cell activity, which then —> anti inflammatory cytokine release —> endothelial cell dysfunction, ultimately resulting in—> capillary leak, micro vascular thrombus, cell adhesion, tissue hypoxia, apoptosis, impaired vascular tone, free radical damage
–Inadequate to diagnose sepsis especially without organ dysfunction (1563)
Sepsis manifestations
(Lecture)
General:
-Hypo/hyperthermia, tachycardia, tachypnea, AMS, edema, hyperglycemia, cyanosis, mottling
Inflammatory:
-Leukocytosis or leukopenia, bandemia, elevated CRP, elevated procal
Hemodynamic:
-SBP< 90/Map <70, or an SBP decrease >40
-SvO2>70
-Cardiac index > 3.5L/min
Organ dysfunction:
-PF ratio <300, oliguria, creatinine increase, coagulopathy, ileus, thrombocytopenia, hyperbilirubinemia
Tissue dysfunction: lactic acidosis, decreased cap refill
1562-1563
Septic shock
(Lecture)
-Subset of sepsis with profound circulatory, cellular, metabolic abnormalities (greater risk of mortality)
*Defining characteristics— vasopressors to maintain MAP > 65, low SVR and vasodilation, lactic > 2, without hypovolemia
1563
MODS
Definition
Causes
Risk Factors
Prognosis
Progressive dysfunction of 2 or more organ systems resulting from an uncontrolled inflammatory response to a severe illness or injury.
Causes:
Sepsis/septic shock MOST COMMON CAUSE
severe trauma, major surgery, burns, circulatory shock, acute pancreatitis, ARF, ARDS, Blood transfusion, Heat stroke, Liver failure, mesenteric ischemia, propofol infusion syndrome, DIC, and tissue necrosis.
Risk:
Elderly, significant tissue injury, pre-existing conditions
Prognosis:
2 systems fail 54% mortality
5 systems fail 100% mortality
1570
Primary MODS
Organ injury directly associated with a specific insult, generally ischemia, or decreased perfusion from shock or trauma, burn, soft tissue necrosis, or invasive infection.
Localized tissues/organs
GENERALIZED HYPOPERFUSION IN PRIMARY MODS USUALLY CANNOT BE DETECTED CLINICALLY
The insult does create a stress response initiating hormones, especially catecholamines. This response is “PRIMED” not active.
1570
Secondary MODS
Progressive organ dysfunction from excessive inflammatory reaction after a latent period following an initial injury, in organs distant from the original injury.
Thought to be triggered by the second (often mild) insult not the primary injury, but produces an immense and disproportionate response secondary to being “primed” resulting in self perpetuating inflammation
1570
Pathophysiology of secondary MODS
- macrophages trigger inflammatory cytokines->endothelial damage-> neutrophils -> more tissue damage-> more inflammation-> nitric oxide (vasodilation)-> microvascular thrombi-> DIC!!
-Stress response-> catecholamines->hypermetabolism-> high O2 consumption-> catabolic state-> LOW SVR
-Neutrophils activated-> inflammation-> ROS -> damage endothelium.
Complement, kallikrein-kinin, coagulation and fibrinolytic cascades are ALL activated.
-Hyperinflammatory, hypercoagulable state that contributes to vasodilation, vasopermeability, cardiovascular instability, endothelial dysfunction, and clotting abnormalities!! OOF
-Bacterial translocation (gut hypothesis), maldistribution of blood, hypermetabolism, myocardial depression, supply-dependent oxygen consumption (demand exceeds supply), if O2 restored reperfusion injury.
1171-1175
High and Low metabolism pathways
High: increased metabolic rate attempt to compensate for lack of energy but leads to accelerated depletion of energy stores and exacerbates cellular damage.
Low: cells slow their metabolism due to lack of substrates & O2, functionality is reduced, energy deficiency and repair/growth/maintenance are impaired
RESULT: dysfunctional ion pumps cause increase in Na & water -> cellular swelling possibly lysis
-toxic metabolites accumulate, acidosis, enzymes alter protein functions, increasing cellular injury and death.
organizer
SIRS vs Sepsis
SIRS:
can be infectious or non-infectious in nature
Systemic inflammatory signs with no confirming infection
Sepsis:
always a dysfunctional response to infection
infection root cause of organ dysfunction
Sepsis vs Septic Shock
Sepsis:
organ dysfunction from infection response
Septic Shock:
progression of sepsis with sustained hypotension despite fluid resuscitation, evidence of tissue hypoperfusion (elevated lactic)
Septic Shock vs MODS
Septic Shock:
Acute circulatory failure requiring immediate intervention
MODS:
Longer term progression of organ failure, often following septic shock, where multiple organ systems are now impaired due to prolonged hypoperfusion and inflammation
MODS timeline
Initial: 0-24hrs
Fever, tachycardia, dyspnea, AMS, hypermetabolic state
Intermediate: 24-72hrs
ARDS
Progressive: 7-10 days
Persistent hypermetabolic & hyperdynamic state, bacteremia, multisystem organ failure (liver, kidney, GI)
Late: 14-21 days
Worsening Organ failure, potentially evolving to death
Chronic: 21+ days
Lingering symptoms, gradual improvement or DEATH
