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17 Cards in this Set
- Front
- Back
Thoracentesis
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Insertion site is 2nd intercostal space, midclavicular line on same side absent breath sounds, opposite of tracheal shift. Use 10-14g over the needle catheter 3-6 cm in length above 3rd rib into pleural space until air escapes. Remove needle, leave catheter in place until chest tube placed.
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Chest tube monitoring
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FOCA
F-fluctuation O-Output C-Color of drainage A-Air leaks (bubbles) |
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Ventilator monitoring
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DOPE
D-displaced tube O-Obstruction-secretions or pt biting tube P-Pneumothorax E-Equipment failure-detached or kink in tubing |
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4 types of shock
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Hypovolemic
Cardiogenic Obstructive Distributive |
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Hypovolemic Shock Etiology, underlying pathology
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1) Hemorrhage-whole blood loss
2) Burns-plasma loss |
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Cardiogenic Shock Etiology, underlying pathology
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1) Myocardial Infarction- loss of cardiac contractility
2) Dysrhythmias- reduced cardiac output 3) Blunt cardiac injury- loss of cardiac contractility |
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Obstructive Shock Etiology, underlying pathology
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1) Cardiac tamponade-compression of heart with obstruction to atrial filling
2) Tension pneumothorax- mediastinal sift with obstruction to atrial filling 3) Tension Hemothorax- combination of preceding |
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Distributive Shock Etiology, underlying pathology
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1) Neurogenic shock- loss of vasomotor tone due to decreases in sympathetic control
2) Anaphylactic shock- Vasodilation of vessels due to immune reaction to allergens e.g. release of histamine 3) Septic Shock- Mediated by systemic inflammatory response syndrome (SIRS) with hypotension and perfusion abnormalities |
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3 Stages of Shock
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1) Compensated
2) Progressive/uncompensated 3) Irreversible |
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Compensated shock stage
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Normal physiologic compensatory mechanisms, mediated by SNS are activated to restore adequate tissue perfusion and preserve vital organ function. Nonvital cells convert to anaerobic metabolism. Byproduct of this is lactic acid which causes cellular damage
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Progressive shock stage
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Compensatory mechanisms begin to fail and unable to maintain perfusion to vital organs. Further progression of lactic acidemia, activation of inflammatory response and deterioration of organ function.
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Irreversible Shock Stage
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Cellular destruction is so severe that death is inevitable
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Compensatory Mechanism of Shock- vascular response
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1) SNS inhibits baroreceptors causing vasoconstriction
2) Chemoreceptors and the bifurcation of the common carotid arteries and aortic bodies near the aorta are sensitive to low 02 and high C02. When arterial blood pressure is below 80 mm Hg they activate and cause vasoconstriction. |
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Compensatory Mechanism of Shock- Cerebral Response
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BP drops below 50 mm Hg, cerebral ischemia occurs. CO2 buildup on the brains vasomotor center will stimulate the CNS's ischemic response which further stimulates the SNS. LOC changes indicate cerebral ischemia
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Compensatory Mechanism of Shock- Renal Response
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Renal ischemia causes release of renin which causes angiotensin to release angiotensin 1, which converts to angiotensin 2 and causes:
-vasoconstriction of arterioles and some veins -stimulation of the SNS -retention of water by the kidneys -release of aldosterone from the adrenal cortex (sodium retention hormone) 10-60 min to activate fully |
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Compensatory Mechanism of Shock-Adrenal gland response
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Adrenals stimulated by SNS release catecholamines (epinephrine and norepinephrine)
Epi stimulates force of cardiac contraction (positive inotropy) and increase in heart rate (positive chronotorpy) and causes vasoconstriction. Norepi- vasoconstriction ACTH releases from pituitary causes adrenal release of cortisol. Cortisol elevates blood sugar and causes renal retention of water and sodium. |
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Compensatory Mechanism of Shock- Hepatic response
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glycogen stored in liver breaks down into glucose and heapatic vessels
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