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41 Cards in this Set
- Front
- Back
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Which stage of shock?
compensatory mechanisms - baroreceptor reflex stimulation - alpha/beta receptor stimulation - RAA system stimulation - pre- and post- capillary constriction |
non-progressive stage
- baroreceptor reflex stimulation: sympathetic NS, catecholamines released. - alpha/beta receptor stimulation: vasoconstriction (alpha1) pronounced in large vascular beds (skin, GI), increase HR and contractility (beta-1). - RAA system stimulation: increase preload, vasoconstriction. - pre- and post- capillary constriction: transcapillary refill. |
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Which stage of shock?
effects of compensation - increase CO (preload, HR, contractility increased) - maintain MAP (CO and afterload increase) |
non-progressive stage
- baroreceptor reflex stimulation: sympathetic NS, catecholamines released. - alpha/beta receptor stimulation: vasoconstriction (alpha1) pronounced in large vascular beds (skin, GI), increase HR and contractility (beta-1). - RAA system stimulation: increase preload, vasoconstriction. - pre- and post- capillary constriction: transcapillary refill. |
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Which stage of shock?
compensatory mechanisms - aoerobic to anaerobic metabolism, lactic acid production - humoral/vasoactive agents released |
progressive stage
- reduced CO and BP - aoerobic to anaerobic metabolism: glycolysis, lactic acid production, ATP depletion, organ failure - humoral/vasoactive agents released: vasodilation (adenosine, NO, serotonin) - reversal of transcapillary refill: precapillary arteriolar vasodilation, post-capillary venular vasoconstriction |
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Which stage of shock?
effects of compensation - decreased CO and BP - organ failure - reversal of transcapillary refill |
progressive stage
- reduced CO and BP - aoerobic to anaerobic metabolism: glycolysis, lactic acid production, ATP depletion, organ failure - humoral/vasoactive agents released: vasodilation (adenosine, NO, serotonin) - reversal of transcapillary refill: precapillary arteriolar vasodilation, post-capillary venular vasoconstriction |
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Which stage of shock?
- vascular collapse - toxic free-oxygen radicals - resistant to therapy |
irreversible stage
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Is this shock?
- sBP 85mmHg - urine output 0.4 cc/kg/hr - anion gap acidosis - skin pallor, cyanosis |
Yes.
- sBP <90mmHg or 30% reduction - urine output < 0.5 cc/kg/hr - metabolic acidemia - tissue hypoperfusion |
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Is this shock?
- sBP 80mmHg - urine output 0.4 cc/kg/hr - anion gap acidosis - skin mottling on knees |
Yes.
- sBP < 90mmHg, or 30% reduction - urine output <0.5 cc/kg/hr - anion gap acidosis - tissue hypoperfusion (skin) |
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Is this shock?
- sBP 70mmHg - urine output 0.4 cc/kg/hr - anion gap acidosis - restlessness, confusion |
Yes.
- sBP < 90mmHg, or 30% reduction - urine output <0.5 cc/kg/hr - anion gap acidosis - tissue hypoperfusion (brain): coma also possible |
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Is this shock?
- sBP 40mmHg - urine output 0.1 cc/kg/hr - anion gap acidosis - arrythmias, tachycardia, MI |
Yes.
- sBP < 90mmHg, or 30% reduction - urine output <0.5 cc/kg/hr - anion gap acidosis - tissue hypoperfusion (cardiovascular) |
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Is this shock?
- sBP 50mmHg - urine output 0.2 cc/kg/hr - anion gap acidosis - renal failure |
Yes.
- sBP < 90mmHg, or 30% reduction - urine output <0.5 cc/kg/hr - anion gap acidosis - tissue hypoperfusion (kidney) |
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Is this shock?
- sBP 65mmHg - urine output 0.4 cc/kg/hr - anion gap acidosis - tachypnea, altered V/Q matching |
Yes.
- sBP < 90mmHg, or 30% reduction - urine output <0.5 cc/kg/hr - anion gap acidosis - tissue hypoperfusion (lung) |
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Is this shock?
- sBP 95mmHg - urine output 0.3 cc/kg/hr - tachycardia, tachypnea, diaphoresis, renal failure |
Yes.
- sBP < 90mmHg, or 30% reduction - urine output <0.5 cc/kg/hr - anion gap acidosis - tissue hypoperfusion (cardiovascular, lung, skin, kidney) * although sBP is > 90mmHg, this person might be uncontrolled HTN before, so it is possible to have 30% reduction in sBP. |
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Is this shock?
- sBP 95mmHg - urine output 0.5 cc/kg/hr - skin pallor |
No.
- sBP < 90mmHg, or 30% reduction - urine output <0.5 cc/kg/hr - anion gap acidosis - tissue hypoperfusion (skin) |
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What is the most common cause of death for patients in shock?
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respiratory failure
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Which type of shock is this?
- BP: 105/78 - HR: 92 - RR: 24 - skin: palor, cool - blood in the stool |
hypovolumic shock (whole blood loss)
- HR: increase - contractility: increased - preload (major): low - afterload: increased - SVR: increased |
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Which type of shock?
- HR: increase - contractility: increased - preload: low - afterload: increased - SVR: increased |
hypovolumic
- decreased CO from reduced preload |
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What is the most common type of shock?
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hypovolumic
- whole blood loss: hemorrhagic - plasma loss: water, electrolyte, protein. eg thermal burn - protein-free fluid loss: water, electrolyte. eg dehydration |
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Which type of shock can this cause? be specific.
- thermal burn |
hypovolumic: plasma loss
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Which type of shock can this cause? be specific.
- dehydration |
hypovolumic: protein-free fluid loss
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Which type of shock can this cause? be specific.
- whole blood loss (internal bleeding) |
hypovolumic: hemorrhagic
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Which stage of shock is this patient in?
- blood loss: 1000ml or 20% - HR: >100 - BP: 110/80 - RR: 20-30 |
progressive stage (class II hypovolumic shock)
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How to treat hypovolumic shock?
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- rapid IV infusion (2 catheters): isotonic crystalloid (normal saline)
- adequate oxygenation: PaO2 >60mmHg, SaO2 >90% - adequate ventilation - maintain MAP>60mmHg, urine output >0.5cc/kg/hr - hemodynamic monitoring |
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Which type of shock is this?
- BP: 85/60mmHg - HR: 50 - skin: cool - cardiac: s4, JVD - ECG: ST elevation in leads V1-V4 - lung: rales in bases |
cardiogenic shock (AMI: anterior)
- HR: increase or decrease - contractility (major): decrease - preload: increase/no change - afterload: increase - SVR: increase |
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Which type of shock is this?
classic signs: - JVD - S3/S4 - inspiratory rales |
cardiogenic shock
- HR: increase or decrease - contractility (major): decrease - preload: increase/no change - afterload: increase - SVR: increase |
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Which type of shock is this?
- HR: increase or decrease - contractility: decrease - preload: increase/no change - afterload: increase - SVR: increase |
cardiogenic shock
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What are the primary and seconday treatment for cardiogenic shock?
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1) primary: correct cardiac dysfunction (thrombolytics for AMI)
2) secondary: improve CO - increase contractility by inotropes (dobutamine) - decrease preload using loop diuretics (furosemide), or vasodilator (nitroglycerin) - decrease afterload using vasodilators (nitroglycerin, sodium nitroprusside) if sBP>100, or vasoconstrictor if sBP< 90. 3) reduce demands: analgesics/sedatives, antpyretics, correct hypoxemia, correct acid-base disorders) |
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How to reduce O2 demands in cardiogenic patients?
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- analgesics/sedatives
- antipyretics - correct hypoxemia - correct acid-base disorders |
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Name the commonly used inotrope used in cardiogenic shock.
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dobutamine
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Which type of shock causes the highest mortality?
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cardiogenic shock
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What is the most likely cause of cardiogenic shock?
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AMI
others: - RVI - acute mitral regurgitation - ventricular septal rupture |
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Pathophysiology of cardiogenic shock.
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- loss of LV myocardium (AMI)
- stunned myocardium (injured but not necrotic tissue) |
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Which type of shock is this?
- BP: 80/50mmHg - HR: 130 - RR: 34 - temp: 103F - skin: warm - lung: wheezing, rales |
distributive shock (septic)
- HR: increase - contractility: decrease - preload: decrease - afterload (major): decrease |
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Which type of shock is this?
- HR: increase - contractility: decrease - preload: decrease - afterload: decrease - SVR: decrease |
distributive shock
- septic - analphylactic - spinal - drug/toxin ingestion |
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What is the common cause of septic shock? organism?
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- hospital acquired
- gram - rods: endo- / exo-toxins, primary mediators of inflammation (TNF, interleukins) - pneumonia |
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What is the primary treatment for septic shock?
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treat infection
- two broad spectrum antibiotics - surgery if peritonitis (i.e. spaces where drugs can't reach) |
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What is the secondary treatment for septic shock?
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- increase preload: fluid resusitation
- increase contractility: inotropic agent - increase afterload: vasopressive agents (NE, high dose DA, phenylephrine) |
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Name this drug.
- recumbanent protein C (anti-inflammatory, anti-thrombotic) - helpful in certain patients under septic shock |
Drotrecogen (Xigris)
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Which type of shock is this?
- HR: increase - contractility: increase - preload: increase/no change/decrease - afterload: increase |
obstructive shock
- effect on preload depends on the location of the obstruction |
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Which type of shock is this?
- HR: 95 - BP: 130/90 - RR: 25 - cardiac: markedly dilated jular vein |
obstructive shock
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Possible causes of obstructive shock.
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- cardiac temponade
- tension pneumothorax - massive pulmonary embolus - thoracic aortic dissection |
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What is the primary and secondary treatment for obstructive shock?
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- primary: reverse obstruction
- secondary: increase preload (fluid resusitation), inotropes (DA, dobutamine) |
