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Cardiovascular > ACS and cardiopulmonary arrest > Flashcards

ACS and cardiopulmonary arrest Flashcards

1
Q

DDx of cardiopulmonary arrest during mechanical ventilation?

A

-misplaced ETT
-tPTX
-hypovolemia
-auto PEEP
-hypoxemia
-mucus plugging

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2
Q

DDx of cardiopulmonary arrest during CVC placement?

A

-tPTX
-tachyarrhythmia
-bradycardia/heart block

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3
Q

DDx of cardiopulmonary arrest during dialysis or plasmapheresis?

A

-hypovolemia
-transfusion rxn
-IgA deficiency/allergic rxn
-hyperkalemia

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4
Q

DDx of cardiopulmonary arrest after TBI?

A

-increased ICP (esp with bradycardia)
-DI induced hypovolemia (esp with tachycardia)

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5
Q

DDx of cardiopulmonary arrest with medication changes?

A

-anaphylaxis
-angioedema
-hypotension/vol depletion (ACE inhibitors)
-methemoglobinemia

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6
Q

DDx of cardiopulmonary arrest after MI?

A

-see tachyarrythmias VF and torsades
-tamponade
-cardiac rupture
-AV block

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7
Q

DDx of cardiopulmonary arrest after trauma?

A

-exsanguination
-TPTX
-tamponade
-abdominal compartment syndrome

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8
Q

DDx of cardiopulmonary arrest after burns?

A

-airway obstruction
-hypovolemia
-CO poisoning
-cyanide

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9
Q

What are appropriate interventions if cardiac arrest is thought to be due to auto-PEEP?

A

-reduce minute ventilation
-increase expiratory time
-bronchodilator
-suction airway

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10
Q

What is the treatment for methemoglobinemia?

A

Methylene blue

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11
Q

What is the treatment for cyclic antidepressant overdose?

A

-see seizures and tachycardia
-sodium bicarbonate

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12
Q

What is the treatment for organophosphate overdose?

A

-see severe bradycardia
-decontamination
-atropine
-pralidoxime

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13
Q

What is the treatment for CO poisoning?

A

100% O2

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14
Q

What is the treatment for cyanide overdose?

A

Hydroxocobalamin

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15
Q

What is the effect of hypoxemia on the cardiac system?

A

-initially it enhances the peripheral chemical drive to breath and increases heart rate
-profound hypoxemia depresses neural function leading to bradycardia refractory to autonomic influence

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16
Q

What is the rate that PaCO2 increases during respiratory arrest? What is the significance of this?

A

-during first apneic minute builds by 6-9mmHg
-after that increases by 3-6mmHg per minute
-this show rise in PaCO2 means life threatening hypoxemia occurs much more slowly compared to life threatening respiratory acidosis

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17
Q

What are causes of decreased LV preload sufficient enough to cause CV collapse?

A

-venodilation
-hemorrhage
-tamponade
-tension PTX

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18
Q

What are causes of increased RV afterload sufficient enough to cause CV collapse?

A

-air embolism
-PE
-RV doesn’t adjust to ejection impedance as well as LV does

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19
Q

What is the ACLS dose of epinephrine?

A

1mg q3-5min

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20
Q

What is the ACLS dose of amiodarone?

A

-first dose 300mg
-second 150mg

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21
Q

In ACLS what is the monophasic defibrillation dose?

A

360J

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22
Q

In ACLS what is the biphasic defibrillation dose?

A

120-200J

23
Q

What is the goal PetCO2 indicating high quality CPR? The goal DBP?

A
  • > 10mmHg
  • > 20mmHg
24
Q

What PetCO2 typically indicates ROSC?

A

40mmHg

25
Q

What fraction of the normal cardiac output is delivered during closed chest compressions?

A

⅓

26
Q

After how long of CPR do you predictably see tissue acidosis?

A

10 - 15 minutes

27
Q

What is the ideal CPR compression rate?

A

100 - 120 bpm

28
Q

By what account should the anterior chest be compressed during CPR?

A

2 inches

29
Q

Failure to fully release compressions during CPR is equivalent to what?

A

Pericardial tamponade or excessive PEEP

30
Q

What pressures regulate brain blood flow?

A

Difference between mean aortic pressure and right atrial pressure

31
Q

What pressures regulate coronary blood flow?

A

Difference between diastolic aortic pressure and right atrial pressure

32
Q

By how much should the dose of a medication be increased compared to IV if given intratracheal?

A

2 - 2.5x

33
Q

Which medications can be given intratracheal?

A

“NAVEL”
-naloxone
-atropine
-vasopressin
-epinephrine
-lidocaine

34
Q

For which medications is the intratracheal route contraindicated?

A

-norepinephrine (lung necrosis)
-CaCl2 (lung necrosis)
-NaHCO3 (inactivates surfactant)

35
Q

What are the reversible, precipitating factors for torsades?

A

-hypomagnesemia
-TCAs
-haloperidol
-type 1a antiarrhythmics
-quinolone antibiotics

36
Q

What are the “H’s” of reversible causes of VT/VF?

A

-hypovolemia
-hypoxia
-acidosis (H+)
-hypokalemia
-hyperkalemia
-hypothermia

37
Q

What are the “T’s” of reversible causes of VT/VF?

A

-tPTX
-tamponade
-toxins
-thrombosis (pulmonary)
-thrombosis (coronary)

38
Q

What voltage setting should be used in open chest defibrillation?

A

10 - 20J

39
Q

If cardioversion continues to produce bradyarrythmias that degenerate into VF what treatment should be attempted and what causes should be considered?

A

-increasing HR with atropine epinephrine or pacing
-overdose of digitalis CA channel blockers or beta-blockers

40
Q

How much MgSO4 should be given to a patient with refractory VT/VF?

A

1 - 2gm over several minutes

41
Q

If cardioversion continues to produce tachyarrythmias that degenerate into VF what treatment should be attempted and what causes should be considered?

A

-amiodarone 300mg, procainamide 20 - 50mg/min, lidocaine 1 - 1.5mg/kg
-excessive catecholamine stimulation

42
Q

Which EKG leads are best for detecting VF?

A

2 and 3

43
Q

For which conditions is NaHCO3 administration useful?

A

-severe acidosis
-hyperkalemia
-TCA overdose

44
Q

What is the origin of narrow QRS complex PEA?

A

Noncardiac

45
Q

What are some initial therapies that can be effective in regular, stable, wide-complex ventricular tachycardia?

A

adenosine and vagal maneuvers

46
Q

What is the initial treatment for irregular, stable, wide-complex ventricular tachycardia?

A

amiodarone 150mg IV
-if the pt is unstable they should not receive amiodarone but be cardioverted instead

47
Q

On the oxygen dissociation curve, what can cause a left shift?

A

left shift indicates increased Hgb affinity for oxygen and an increased reluctance to release oxygen
-CO poisoning
-hypothermia
-alkalosis
-decrease pCO2
-decreased 2,3-disphosphoglycerate
-Hgb-f

48
Q

On the oxygen dissociation curve, what can cause a right shift?

A

right shift indicates that Hgb has a decreased affinity for oxygen (so off loaded more easily)
-hyperthermia
-acidosis
-increased pCO2
-increased 2,3-disphosphoglycerate
-Hgb-SS

49
Q

What is the pathophysiology behind neurogenic shock?

A

sudden loss of sympathetic tone w/ preserved parasympathetic activity and autonomic instability
-systemic hypotension d/t decreased sympathetic fiber-mediated arterial and venous vascular resistance w/ venous pooling and loss of preload

50
Q

What level of spinal cord injury is most typically associated with neurogenic shock?

A

an injury to the cord above T6

51
Q

What are the contraindications to LVAD placement?

A

-ESRD (GFR < 30)
-severe bleeding
-chronic thrombocytopenia
-refusal of blood transfusion
-severe liver disease (bili > 2.5, INR > 2 w/ cirrhosis or portal HTN)
-ongoing smoking, EtOH, IVDU
-inability to adhere to medical regimen or poor social support

52
Q

What beta-blockers are useful in the setting of SVT w/ reactive airway disease?

A

cardioselective beta-blockers
-esmolol
-metoprolol
-atenolol

53
Q

What medication is preferred in SVT due to Wolfe-Parkinson White?

A

amiodarone

54
Q

If a patient develops new onset type II second degree block the lesion is likely where?

A

-occlusion of a septal branch off LAD
-can progress to 3rd degree block
-has a poorer prognosis than type I second degree block

Cardiovascular (6 decks)

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