Shock Flashcards

1
Q

Metabolic changes

A

Increase in glucose, increase in protein breakdown, converts to increase pyrurate, and converts to increase lactate
Increase in catecholamines, cortisol, growth hormones
Increase in Lipo lysis, increase in gluconeogenesis, glycogenolysis, increase in triglycerides and fatty acids, which are inflammatory, insulin resistance

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2
Q

Three phases of shock

A

Compensated-absolute and relative fluid loss, still able to maintain adequate blood pressure, cerebral perfusion, vasoconstriction chance to Brain and vital organs
Decompensated -late, no longer perfusion of Brain and vital organs
Irreversible -rapid deterioration of cardiovascular system, compensatory mechanisms, fail result in death

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3
Q

What is shock?

A

In adequate tissue perfusion, decreased oxygen in nutrient delivery causes impaired, cellular metabolism causes decrease remove our cellular waste

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4
Q

Anaerobic metabolism

A

Produce lactic acid
Results of metabolic, acidosis, oxyhemoglobin, disassociation, hemoglobin, releasing more oxygen, do to more consumption, feedback loop

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5
Q

Protein metabolism

A

Increased, as serum protein breaks down and is lost, increase muscle wasting, causing respiratory and cardiac failure
Decrease in immuno globulin levels and decrease immune response
Increase in cellular edema as osmotic pressure causes fluid shift due to decreased albumin and increases Edema, clotting cascade activated, lysosome activity, production increases cells, cannot take on the process, and they take more nutrients and oxygen

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6
Q

ATP

A

Production is decreased, increased in intracellular, sodium and water, decreased circulating, water, activation of clotting, cascade, lysosome, enzyme production increases in the cycle continues

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7
Q

Anaphylactic shock

A

Inflammatory and vasa dilatory reaction to an allergic antigen
Allergy antigen, anaphylactoid type can be due to cold, exercise, meds, contaminants
Similar to neurogenic with vasodilatation, peripheral pooling, tissue, edema, bronchoconstriction of smooth muscle
Antigen, antibody, IgG, E, mass cell activation, activation of compliment, histamine, release, Kinin activation, prostaglandins, increase, capillary, permeability, peripheral vasodilation, smooth muscle constrict, including bronco, and laryngospasms, DIC
Hypotension, diaphoresis, pallor, shortness of breath, cough, rhinorrhea, throat, tightness, wheezing, nausea, vomiting, diarrhea, abdominal pain, erythema, pruritis, hives, angioedema, anxiety
Treatment is Epi, fluids, anti-histamines, steroids

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8
Q

Neurogenic shock

A

Stimulation of parasympathetic and inhibition of sympathetic activity, a.k.a. muscle tone, causing a relative hypovolemia
Due to trauma cord or medulla, conditions to private medulla of oxygen and glucose, such as depressive drugs, anesthetic agents, severe, emotional stress and pain
Imbalance between sympathetic and parasympathetic stimulation body has no compensation for this causes, massive, vasodilation, decrease, vascular, tone, decrease, systemic, vascular, resistance, inadequate, cardiac output, decrease tissue, perfusion, an impaired cellular metabolism
Massive vasodilation due to imbalance in parasympathetic and sympathetic nervous system. Most of the blood is peripheral. Exhibit hypotension, bounding, pulse, flash, capillary, refill, and bradycardia.
Treatment is supportive

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9
Q

Cardiogenic shock

A

And ability of the heart to pump blood to tissues and organs
Caused by decrease contractility, due to MI, cardiomyopathy, sepsis, myocarditis, pericarditis, aneurysm, dysrhythmias, contusion, metabolic abnormalities, papillary, muscle rupture, impaired, diastolic, feeling due to dysrhythmias, such as SVT, obstruction, due to pulmonary embolism, Tamponade, valve disorders, tumor, wall defects
Hypotension, hypo, perfusion, despite left ventricular filling, and intravascular volume pre-load is OK
Decreased cardiac output, causes body to compensate with RAAS, causes increase in volume, but this is not the problem result in an increase preload
Stroke volume and heart rate cause increase systemic and pulmonary edema, cause shortness of breath or catecholamine release cause increase in systemic, vascular resistance, causing increase in freeload, stroke, volume and heart rate increase in pulmonary and systemic edema, shortness of breath, increase and preload and stroke, volume and heart rate, while decrease of cardiac output and ejection fraction, hypotension, decreased tissue, perfusion ischemia Impaired cellular metabolism and impaired myocardial dysfunction, goal is to decrease, systemic, vascular resistance
Inadequate perfusion to heart, lungs, and organs
Chest pain, shortness of breath, faintness, Impending Doom, tachycardia, tachypnea, hypertension, JVD, decreased cardiac output, cyanosis, Mottling, cool extremities, low, urine output, extra heart, tones, S3 and S4, pulmonary edema, hypoxemia, elevated organ labs, such as LFTs, creatinine bun
Treatment is support heart, improve relaxation, and remove obstruction

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10
Q

Hypovolemic shock

A

Lots of whole blood, plasma, interstitial, fluid, and large amounts about 15%
Whole blood hemorrhage, plasma, Burns, interstitial fluid loss, due to diaphoresis, diabetes mellitus, and insipidus, emesis, diarrhea, diuresis
Body compensate until cannot
Decrease intravascular, volume causes, decreasing cardiac output, shift of interstitial fluid causes aldosterone and ADH to release causes splenic or liver. Discharge result in an increase volume or increase in catecholamine release, cause increase in heart rate, and contact Silletti and systemic vascular resistance. If cardiac output increases and more volume is lost, and then decreases cardiac output, decrease in systemic and pulmonic pressures, decrease tissue, perfusion, impaired cellular metabolism, decrease tissue, perfusion, and impaired cellular metabolism.
Increase in systemic, vascular resistance, causes cool, pale extremities, thirst, oliguria, decrease, preload, and central venous pressure, tachycardia
Treatment of fluid replacement, or blood replacement

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11
Q

Septic shock

A

Progressive organ dysfunction, due to infection, can be gram-negative or positive bacteria, viral, or fungal
Pneumonia, bloodstream infection, IV, catheter, intra-abdominal, urosepsis, wounds
Will require vasopressor support, low systemic, vascular resistance, lactate, greater than two
Can start out as SIRS, progress to sepsis then septic shock, then multi organ dysfunction syndrome

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12
Q

Systemic inflammatory response syndrome

A

Reaction to anything that stimulates inflammatory response, infectious or non-infectious
Temperature less than 36 or greater than 38°C, heart rate greater than 90, respiratory rate greater than 20 or CO2 level less than 32, white blood cell count greater than 12,000 or less than 4000 or greater 10% bands seen with ECMO, if not treated progresses to sepsis

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13
Q

Sepsis

A

Life-threatening organ is function caused by disregulated host, response to infection, can affect respiratory hematology, cardiac renal, hepatic, and central nervous system
Cause hypotension less than 90 systolic and organ dysfunction
Test include SOFA sequential organ failure assessment or Q sofa
Sofa looks at PF ratio with or without mechanical ventilation, platelet counts, GCS, Bilirubin, Mapp, creatinine, if score increases by two points. Organ dysfunction due to hypo perfusion.
Q so far is clinic based and quick looks at respiratory rate greater than 22, GCS, systolic blood pressure, less than 100
2 of 3 equals organ dysfunction
Gram-positive or negative bacteria, activation of compliment, pro, inflammatory, cytokines, Kinan, regulation, cascade activated

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14
Q

Multi organ dysfunction syndrome

A

Progressive dysfunction of two or more organs do to uncontrolled inflammation. Can we do the Burns ,trauma, heat stroke
And organ failure and death with two organs, 54% mortality, five nearly 100% mortality
Two types primary and secondary

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15
Q

Primary mods

A

Specific ischemia, hypo perfusion
Decrease, perfusion, local tissue, general hypo, perfusion, set them up for a secondary mods

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16
Q

Secondary mods

A

Organ often distance from side of original injury
Three pathways
1 macrophages, trigger pro inflammatory cytokines, which damage endothelium, causing neutrophil adhesion, causing more tissue damage causing further inflammation, causing release of nitric oxide causing microvascular thrombi and DIC
2 heighten stress response causes increase and catecholamines cause hyper metabolism causes increase. Oxygen consumption causes catabolic state causes, decrease, systemic, vascular resistance.
3 neutrophil, activation, inflammatory response, causes reactive, oxygen species, which damages endothelium

17
Q

Timeline for mods

A

24 hours post injury. Patient will have fever increase heart rate, shortness of breath, altered mental status, hyper metabolic state.
24 hours is 72 hours ARDS
7 to 10 days hypermetabolic hyperdynamic state, bacteremia, hepatic, Renal, G.I. failure
14 to 21 days you have organ failure
21+ days linger, or improve slowly or die, slowly rare to see rapid improvement