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35 Cards in this Set
- Front
- Back
What clinically feasible interventions have actually been shown to consistently improve survival from cardiac arrest?
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- Early CPR
- Early defibrillation - CPR before defibrillation after prolonged arrest - Prolonged hypothermia induced after return of spontaneous circulation********* |
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Define sudden unexpected death.
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- Death within 24 hours of symptom onset in a previously functional individual
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What is the basic pathophysiologic cascade of cardiac arrest (focus at the cellular level)?
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- Tissue hypoxia
- Cessation of aerobic metabolism - Transition to anaerobic metabolism - Depletion of ATP - Failure of maintenance of cellular ionic gradients - Intracellular Ca overload - Generation of free radicals - Mitochondrial dysfunction - Altered gene expression - Activation of catabolic enzymes (phospholipases, endonucleases, proteases) - Activation of inflammation |
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What percent of baseline cardiac output can be generated by standard chest compressions?
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- 30% *Decreases with time to initiation and duration
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How do chest compression result in circulation of blood?
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- “Cardiac compression model”
o Heart is squeezed between sternum and thoracic spine o Generating a pressure gradient between the ventricle and great vessels o Heart valves prevent retrograde flow • Likely minor role - “Thoracic pump model” o Chest compression causes an increase in intrathoracic pressure which creates a pressure gradient between intrathoracic vascular bed and extrathoracic arterial bed • Likely major role |
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Define postresuscitation syndrome.
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- Multiorgan injury and failure occurring after severe global ischemia
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What is the term for reversible postarrest myocardial dysfunction?
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cardiac stunning
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Provide a DDx for nontraumatic cardiac arrest (table 7.1).
**THINK Hs and Ts and derive DDx from that |
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How does electrocution cause cardiac arrest?
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- Primary dysrhythmia or apnea
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List indicators of inadequate blood flow during cardiopulmonary resuscitation (table 7.3).
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What is a minimum coronary perfusion pressure that must be generated in order to achieve ROSC in initial attempts at defibrillation have failed?
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- Coronary perfusion pressure>15mmHg
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How is coronary perfusion pressure measured (and calculated)?
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How is coronary perfusion pressure measured (and calculated)?
- Arterial diastolic pressure (measured by intraarterial catheter) – central venous pressure (measures by central line at the right atrium) - EDP - LVEDP |
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Is there an arterial pressure measure that also predicts ROSC?
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- Arterial diastolic pressure >40mmHg predicts ROSC
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What are the benefits of PetCO2 in a patient in cardiac arrest?
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What are the benefits of PetCO2 in a patient in cardiac arrest?
- Reliable indicator of cardiac output during CPR o Target PetCO2>10mmHg (prior to vasopressor administration) - Determining pseudo-EMD (higher PetCO2) vs. true EMD (Lower PetCO2 - Detecting success of resuscitation measures - Confirm intubation of the trachea EMD - electromyocardial dissociation - pseudo is when still have some contraction but no pulse |
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What is the differential diagnosis of undetectable PetCO2 in an arrest patient?
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- Failure to intubate the trachea
- Massive PE - Inadequate chest compressions |
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What ScVO2 should be target during arrest to determine adequacy of chest compressions?
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>40%
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Provide an algorithm for treatment of cardiac arrest. (fig 7.4)
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When should CPR be considered prior to defibrillation (even if immediately available)?
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- Duration of untreated cardiac arrest is prolonged >4-5 minutes a brief period of CPR (90-180 seconds) before defibrillation has been shown to improve likelihood of ROSC and survival
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Discuss the evidence for chest compression before defibrillation
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Cobb 1998 JAMA - retrospective +
Wik 2003 JAMA - only vfib >5min + Jacobs 2005 Emerg med Oz - 2005 ILCOR guidelines - bystander defib, EMS >5min 2 min before/multiple people 1 cpm 1 get defib ready |
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Who should receive immediate angioplasty post ROSC?
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- Evidence of acute myocardial ischemia and
o Thrombolytic exclusion criteria o Drug resistant hypertension o Cardiogenic shock - +/- Patients with high risk for occult critical coronary stenosis |
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In what patients post ROSC should transcutaneous pads be placed and transvenous pacing be considered?
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- New LBBB
- RBBB with LAFB or LPFB - Second degree type II block - Third-degree block |
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Explain the significance of the oxygen delivery (DO2)/Oxygen consumption (VO2) curve post ROSC.
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- Oxygen extraction ratio increases and mixed venous oxygen saturation decreases in response to decreased oxygen delivery
- Below the critical DO2, VO2 become delivery dependent - Anaerobic metabolism and lactate production result (dysoxia) |
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Provide a goal-directed guide to the post resuscitation care of the cardiac arrest patient.
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What are complications of standard CPR?
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- Aspiration (hypoxia, pneumonia, ARDS)
- Hepatic trauma (exsanguinations) - Gastroespohageal trauma (fatal mediastinitis or hemorrhage) - Cardiac trauma (cardiac contusion, hemopericardium, pericardial effusions) - Bone trauma (sternal and rib fractures, hemothrorax, and bone marrow emboli) |
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What are alternative methods of chest compression?
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- Interposed abdominal compressions
- Active comporession-decompression - Vest (circumferential) compressions - Open-chest cardiac massage - Cardiopulmonary bypass - Cough cardiopulmonary resusciatation |
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.What medications can be delivered via the ETT?
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- Epinephrine
- Atropine - Lidocaine |
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Generally how are meds given via by the ETT?
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- 2.5 times standard IV dose
- Diluted to 10cc in NS or sterile water - Via catheter placed through ETT - Followed by 4-5 rapid PPVs - NAVEL |
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What is the mechanism of epinephrine in arrest?
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- Alpha stimulation
- Increased PVR - Shunting of blood to cerebral and coronary circulations - Improved coronary perfusion pressure and cerebral perfusion pressure - +/- B1 agonism increasing myocardial contractility |
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What is vassopressin?
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- Vasoactive peptide hormone
- Normally released form pituitary gland in response to hypovolemia or hypotension - Potent vasoconstrictor (via G-protien mediated second messenger increases in ctytosolic CA and increased smooth muscle contraction) |
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What is the evidence for vasopressin?
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lindner 97 Lancet - >epi
Stiel 2001- inp - no diff Wenzel 2004 - faso better but screwy analysis |
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What is the evidence for amiodarone?
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- Improved survival to hospital, but not discharge in persistent VF
Kudenchuk 1999 NEJM -impr to hosp Dorian 2002 NEJM - amio>lido surv hosp adm |
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What Vaughab-Williams class is amiodarone?
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3
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What is the dose of amiodarone for persistent VF?
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- 300mg IV bolus (may give additional 150mg at 30min)
- Post resuscitation o 1mg/min for 6 hours (360mg) o 0.5mg/min over 18 hours (540mg) - Breakthrough VF or VT o Bolus 150mg |
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What is the dose of MGSO4?
List indications for MGSO4. |
- 2 g in 100 cc 5%dextrose over 1-2 minutes
- Torsades de points - Hypomagnasemia |
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List indications for NAHCO3.
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- Hyperkalemia (known or suspected)
- TCAs - Preexisting metabolic academia |