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Flashcards in Shock & MODS Deck (15)
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1

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)

2

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

3

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)

4

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

5

Describe parameters for Quick Sequential Organ Failure Assessment (qSOFA)

1. Altered mental status (Glascow Coma Scale <15

2. RR>/= 22bpm (1st sign)

3. SBP =100 mmHg

Each criteria is worth 1 point, scores range from 0-3, a score of 3 = 75% chance of sepsis

6

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

7

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

8

 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

9

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%

10

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

11

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

12

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

13

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)

14

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)  

15

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