Shock & MODS Flashcards
Impaired Cellular Metabolism: Oxygen Use
Shift from aerobic to anaerobic. It leads to increased lactate which is an ACID!! Leads to metabolic acidosis. And if you remember oxygen affinity curve, more acidotic, the less oxygen is bound to hemoglobin
Sodium Potassium pump just fails, so sodium in the cell stays in the cell. THis leads to intracellular fluid and less circulatory volume
Decreased volume and edema leads to inflammation and clotting!
Release of lysosomal enzymes further disrupt cellular processes (Lysosomal enzymes are digestive enzymes)
Impaired Cellular Metabolism: Glucose Use
Impaired due to impaired delivery or impaired re-uptake
MASSIVE glycolysis and gluconeogenesis. Glycolysis is breaking glucose to pyruvate and gluconeogenesis is production of glucose just in case if people needed a refresher!!
Proteins used in gluconeogenesis so not available for maintaining cellular structure, function, repair, and replication
Know parameters for SIRS
System Inflammatory Response Syndrome (SIRS): systemic inflammatory response to pathologic insult (burns, trauma, pancreatitis, infection)
At least 2 or more of the following:
Temp >38 or <36
HR >90
RR or PaCO2 <32mmHg
WBC >12,000, <4,000; or >10% bands (immature cells)
Describe risk factors and symptoms for septic shock
Increased risk in elderly, males, patients with chronic diseases (especially immunocompromised); invasive procedures or devices
Most common source-respiratory infection
30-40% mortality rate
Each new organ system affected adds 15-20% to mortality rate above baseline; causative organism not good predictor
Culture and sensitivity does not always demonstrate a causative organism
Increased or very low WBCs
Tachypnea
Fever in 60% (commonly not present in those with advanced age, renal failure, or those taking anti-inflammatory medications)
Hypothermia (ominous sign)
Hypoxia
Hypotension
Tachycardia (nearly universal except those taking medications such as beta-blockers or those with cardiac abnormalities)
Elevated lactate levels=increased mortality
Describe parameters for Quick Sequential Organ Failure Assessment (qSOFA)
- Altered mental status (Glascow Coma Scale <15
- RR>/= 22bpm (1st sign)
- SBP =100 mmHg
Each criteria is worth 1 point, scores range from 0-3, a score of 3 = 75% chance of sepsis
Describe differences in effects between low, moderate, and high quantities of inflammatory mediators
Inflammatory mediators (used to fight off infection and maintain homeostasis)
In sepsis, there is a high amount of inflammatory mediators
Describe effects of septic shock on organ systems
Respiratory
75% of patients will require mechanical ventilation for average of 7-10 days. ½ of patients will develop ARDS
Work of breathing increased (increased airway resistance)
Ventilator demands increased (lactic acidosis)
Circulatory
Impaired vascular tone, circulatory leak lead to hypotension
Myocardial contractility decreased, can mimic cardiogenic shock
Renal
Oliguria and creatinine elevations common, but fewer than 15% progress to overt renal failure
Metabolic
Lactic acidosis due to multiple and poorly understood mechanisms
GI
Splanchnic blood flow shunted to other organs, impairs function, increase GI bleed risk
Coagulation
100% have elevated D-dimer levels, 90% have reduced protein C levels, DIC occurs in 30%, strong correlation with mortality
Understand changes in D-dimer and protein C in septic shock
D-Dimer: fibrin degradation product, contains 2 cross-linked D fragments of the fibrinogen protein. Used to look for DVT, PE, DIC
Protein C: vitamin K dependent protease that regulates blood coagulation by inactivating factors Va and VIIA
Describe parameters, risk factors for cardiogenic shock
Inability of the heart to deliver oxygen and nutrients to tissues in the presence of adequate circulating volume
Hemodynamic Criteria:
SBP <90mmHg for at least 30 mins
Cardiac index <2.2 (normal 2.5-4.2 L/min/meter2)
Pulmonary artery capillary wedge pressure (PCWP) >15mmHg (indirect measure of L atrial pressure, normal 8-10)
Other presenting S/S: poor tissue perfusion demonstrated by delayed capillary refill, decreased urine output, alteration in mental status, cool and mottled extremities
Epidemiology:
Most commonly due to large MI
Other causes: acute mitral regurgitation, ventricular septal rupture
Those most likely to develop: elderly, females, diabetes, anterior infarct, larger infarct
Mortality rate 50-60%
Understand the effect of different doses of dopamine on the body
(Don’t need to know exact doses, just know what’s considered high or low)
Low dose (2-5 mcg/kg/min): binds D1 receptors, dilating blood vessels of renal and coronary arteries – diuretic effects
Intermediate doses (5-10 mcg/kg/min): positive inotropic and chronotropic effect through beta-1 receptor activation. Will increase CO and BP
High dose (10-20 mcg/kg/min): “pressor” dose. Increases SVC and BP through alpha-1 receptor activator, but risk constriction of renal vessels
Describe diagnostic criteria, causes, and symptoms of anaphylactic shock
Diagnostic Criteria: can occur within minutes; peak symptoms within 1 hour of exposure
Observations of skin and mucosal tissue symptoms
Respiratory distress
Hypotension
Possible: GI symptoms
Cause: allergies, insect bites, chemicals
Activation of mast cells and basophils by igE due to exposure to:
Foods: shellfish, nuts, eggs, milk
Drugs: PCN, anesthetics, insulin, sedatives/analgesics (IV), streptokinase, vancomycin, radiocontrast dye
Inset venom, snake venom
Latex
Ultimately lead to vasodilation, peripheral pooling, and relative hypovolemia
Effects On Systems:
Cutaneous
Flushing, urticaria, angioedema, rash
Oral
Pruritus of lips, tongue, palate; edema of lips; metallic taste in mouth
Respiratory
Larynx: Tightness in throat, dysphagia, dysphonia, cough, stridor
Airway obstruction is most common cause of death
Bronchospasm; wheezing
Neurologic:
AMS with hypotension; anxiety, impending sense of doom
Cardiovascular
Syncope, chest pain, dysrhythmia, vasodilation leading to hypotension
Compensatory tachycardia
Capillary leakage causing volume depletion
Within 10 minutes, as much as 50% of intravascular fluid can leak into extravascular space
Gastrointestinal
Abdominal pain, nausea, vomiting, diarrhea
Eyes:
Itching, excess lacrimation
Note: There is a risk for a second peak response to occur several hours after first-anyone with a severe anaphylactic response should be monitored overnight
Understand medications used to treat anaphylaxis
Epinephrine 1st line drug!!!! Alpha and beta agonist. Increases vascular resistance, reduced permeability, produces bronchodilation, increase CO.
Can be given SubQ or IV
Note: patients on beta-blockers may not respond appropriately and may need norepinephrine and dopamine
Antihistamines
Corticosteroids: not immediate acting but will shorten duration of symptoms and help prevent return
Inhaled bronchodilators
Fluids
Note: there is risk for a second peak after 1st –pts w severe shock should be monitored overnight
Signs and symptoms of hypovolemic shock
Hypotension, tachycardia, cool and clammy skin, weak and thready pulses, decreased capillary refill, altered mental status (restlessness and agitation early, progressing to coma if continues)
Causes and symptoms of neurogenic shock (also referred to as vasogenic shock)
Massive vasodilation that results from an imbalance between parasympathetic and sympathetic stimulation of vasculature smooth muscle; “relative hypovolemia”
Causes: trauma to spinal cord or medulla, conditions that deprive the medulla of glucose (insulin reactions), depressive drugs, anesthetic agents, severe emotional stress, pain
Symptoms:
Clinical hallmark is low SVR with bradycardia
Bradycardia may cease when compensatory mechanisms kick in
Ejection fraction remains normal
Warn, dry extremities
Priapism (persistent and painful erection)
Understand causes of MODS, and describe the 2-step process of MODS development
Common Causes of MODS:
Sepsis, multiple trauma, burns, ARF, pancreatitis, gastric aspiration, ischemia necrosis, ischemia-reperfusion, ARDS, severe hemorrhage, delayed or ineffective shock resuscitation, etc.
Primary MODS:
Organ injury directly associated with specific insult (ischemia or impaired perfusion from an episode of shock or trauma, thermal injury, soft tissue necrosis, invasive infection)
Stress response initiated
Neutrophils and macrophages “primed” by cytokines, which can be activated by a secondary insult resulting in….
Secondary MODS
Progressive organ dysfunction as a result of excessive inflammatory reactions in organs distant from the site of initial injury
Often the second insult is mild but produces an immense and disproportionate response due to the previous priming of leukocytes
Interaction of injured organs leads to self-perpetuating inflammation
After secondary MODS and aggressive resuscitation for 24 hours, patient develops low-grade fever, tachycardia, tachypnea, dyspnea, AMS, hyperdynamic and hypermetabolic state
Lungs begin to fail and ARDS appears in 24-72 hours
Days 7-10: Hypermetabolic and hyperdynamic state intensifies; bacteremia with enteric organisms common; signs of hepatic, intestinal, renal failure develop
Days 14-21: Renal and liver failure more severe. Hematologic and myocardial failure manifest. Encephalopathy can occur at any time.
Sequence CAN evolve rapidly with death occurring b/w days 14-21, or can evolve over weeks
