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Cardiology Exam > Cardiac Arrest > Flashcards

Cardiac Arrest Flashcards

1
Q

cardiac arrest - defined

A

*lack of perfusion (blood flow) to the body as a result of no cardiac pump function or collapse of blood pressure
*current annual incidence is 180-250,000 per year; less than 5% of out-of-hospital arrests survive
*the BRAIN is the organ most susceptible to decreased blood flow & suffers irreversible damage within 5 minutes of absent perfusion

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2
Q

myocardial infarction - defined

A

*death of cardiac muscle tissue, usually related to obstruction of a coronary artery
*MI can cause cardiac arrest through ventricular tachycardia/fibrillation, but is not SCA in and of itself

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3
Q

cardiac arrest (contrasted to MI)

A

*result of ELECTRICAL MALFUNCTION of the heart
*commonly caused by abnormal heart rhythms like ventricular fibrillation
*fatal about 90% of the time
*heart stops beating
*victim is unconscious with no pulse
*condition usually comes on suddenly, with no warning
*treatment requires CPR and defibrillation with an AED to restore heart rhythm

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4
Q

myocardial infarction (contrast to cardiac arrest)

A

*result of coronary artery blockage
*commonly caused by lifestyle factors like diet, obesity, smoking, and alcohol
*fatal about 14% of the time
*heart continues beating
*victim is conscious with a pulse
*warning symptoms include chest pain, dizziness, shortness of breath, sweating
*treatment requires medication and/or surgery to restore normal blood flow

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5
Q

causes of cardiac arrest/sudden cardiac death

A

*arrhythmias
*hypertrophic cardiomyopathy
*coronary heart disease
*coronary anomalies
*valvular heart disease
*ruptured aorta

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6
Q

risk factors for sudden cardiac death

A

*prior coronary events
*EF < 30% or heart failure
*arrhythmia risk markers
*post-MI

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7
Q

categories of cardiac arrest

A
  1. shockable heart rhythms:
    -ventricular tachycardia
    -ventricular fibrillation
  2. non-shockable heart rhythms:
    -pulseless electrical activity
    -asystole
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8
Q

relationship between electrical and mechanical activity of the heart

A

*electrical activity always precedes mechanical activity
*mechanical activity cannot occur without electrical activity
*however, electrical activity CAN occur without mechanical activity

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9
Q

non-shockable rhythm: pulseless electrical activity (PEA)

A

*also known as electromechanical dissociation
*refers to cardiac arrest in which the ECG shows a heart rhythm that should produce a pulse, but does not
*PEA activity is found initially in about 55% of people in cardiac arrest
*image shows the EKG (green) with the associated mechanical activity (red)

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10
Q

common causes of pulseless electrical activity (PEA)

A

5 H’s and 5 T’s:
*hypovolemia
*hypoxia
*hydrogen ion (acidosis)
*hyperkalemia
*hypokalemia
*hypothermia

*toxins
*tamponade
*tension pneumothorax
*thrombosis (coronary)
*thrombosis (pulmonary)
*trauma

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11
Q

non-shockable rhythm: asystole

A

*no electrical activity
*no mechanical activity

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12
Q

causes of asystole

A

*hypovolemia
*hypoxia
*hydrogen ions (acidosis)
*hypothermia
*hyperkalemia
*hypoglycemia

*tablets (drug OD)
*tamponade
*tension pneumothorax
*thrombosis (coronary)
*thrombosis (pulmonary)
*trauma

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13
Q

shockable rhythm: ventricular tachycardia

A

*typical regular rhythm, rate > 100 bpm
*wide QRS complex 120 msec+
*slow ventricular activation outside normal ventricular conduction system
*tachycardia originates below the AV node
*high risk of sudden cardiac death

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14
Q

shockable rhythm: ventricular fibrillation

A

*disorganized rhythm with no identifiable waves
*abnormally fast and chaotic heart rate; ventricles quiver rather than beat
*electricity generated within the ventricle itself
*high risk of sudden cardiac death

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15
Q

causes of ventricular tachycardia & ventricular fibrillation

A

*myocardial ischemia/MI
*coronary artery disease
*valvular heart disease
*heart failure
*cardiomyopathy
*electrolyte imbalances (hypokalemia, hyperkalemia, hypercalcemia)
*drug intoxications
*acid-base imbalance

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16
Q

goal of treating cardiac arrest

A

goal = “return of spontaneous circulation” (ROSC)

17
Q

algorithm for treating cardiac arrest

A
  1. unresponsive? → open airway & look for signs of life
  2. CPR until defibrillator/monitor attached
  3. assess rhythm (shockable vs. nonshockable)
    4a. if shockable, shock, then continue CPR
    4b. if non-shockable, resume CPR
18
Q

assessing the pulse in an unresponsive patient

A

*the carotid pulse is significant because the absence suggests there is NO CEREBRAL PERFUSION
*once you have identified that there is not enough blood flow to the brain (no pulse), then you need to start restoring circulation

19
Q

assessing need for defibrillation

A

*torsades de pointes, ventricular tachycardia, and ventricular fibrillation are not compatible with life
*these rhythms prevent the heart from pumping normally
*by defibrillating (electrical shock) the heart, you are putting all the cells into the absolute refractory period and allowing the sinus node to take over the rhythm

*the defibrillator/IED assesses whether the patient has a shockable rhythm or not

20
Q

chest compressions - uses

A

*chest compressions are used in both patients with non-shockable rhythms or in patients with shockable rhythms that have been shocked and fall back out of rhythm

21
Q

chest compressions - overveiw

A

*critical aspect of resuscitation (timely/rapidity of initiation, rate, and depth are important)
*place patient on a firm surface (backboard, deflation of air mattress)
*hand in the middle of the chest, 5cm of depression, allow complete recoil

22
Q

timeliness in cardiac resuscitation

A

*early defibrillation is important for ROSC (chances of survival reduce by 7-10% for each minute that defibrillation is delayed, if in a shockable rhythm)
*early initiation of CPR leads to greater change of ROSC and survival
*early, deep chest compressions actually help make defibrillation more successful

23
Q

chest compressions: rate

A

*a faster rate of compressions is associated with better achievement of ROSC
*rate 100-120 compressions per minute
*deliver > 80 per minute (that means minimal interruptions - don’t keep stopping to check rhythm)

*duty cycle:
-time between the start of one compression and the start of the next
-target is 50% (as much time relaxing as compressing)

24
Q

chest compressions: depth

A

*deeper chest compression depth leads to better outcomes and survival
*should be 5cm deep
*allowing recoil further enhances the effect of deeper compressions

25
Q

physiology of chest compressions - overview

A

2 components of how chest compressions work:
1. external cardiac massage
2. thoracic chest pump

26
Q

physiology of chest compressions: external cardiac massage

A

*chest compressions directly compress the heart between the depressed sternum and the thoracic spine
*this ejects blood into the systemic and pulmonary circulations while backward flow during decompression is limited by the cardiac valves

27
Q

physiology of chest compressions: thoracic pump

A

*suggests that chest compressions intermittently increase global intra-thoracic pressure, with equivalent pressures exerted on vena cava, heart, and aorta
*blood flow maintained in and out of thoracic cavity by chest compressions
*compressions (and recoil) create pressure differences between the thoracic cavity with the abdomen and head that drive blood flow

28
Q

medication treatment for cardiac arrest

A

*during CPR:
-ensure patent airway, oxygenation, intubation, obtain IV access
*give EPINEPHRINE (1 amp) every 3 minutes
*address reversible causes; consider:
-lignocaine, amiodarone, atropine, buffers, etc)

29
Q

therapeutic hypothermia in cardiac arrest - recommendation

A

*targeted temperature management (32-36 degree Celsius) is recommended for ALL COMATOSE survivors of cardiac arrest (both shockable and non-shockable) [if they are comatose FOLLOWING RESUSCITAITON]
*hypothermia improves survival and neurological outcomes after cardiac arrest

30
Q

how does therapeutic hypothermia improve outcomes following cardiac arrest ?

A

the basic mechanisms through which hypothermia protects the brain are clearly multifactorial and include at least the following:
*reduction in brain metabolic rate
*effects of cerebral blood flow
*reduction of critical threshold for oxygen delivery
*blockade of excitotoxic mechanisms
*calcium antagonism
*preservation of protein synthesis
*reduction of brain thermopooling
*a decrease in edema formation
*modulation of the inflammatory response
*neuroprotection of the white matter
*modulation of apoptotic cell death

31
Q

therapeutic hypothermia in cardiac arrest - protocol

A
  1. initiating:
    -start cooling immediately
    -analgesia/sedation (to prevent shivering)
    -recognize/treat shivering
  2. maintenance:
    -close attention to BP, O2 sat, volume, glucose, K+, seizures
  3. rewarming:
    -begin 24 hours after induction
    -warm by 0.25 degrees C per hour
    -watch BP, glucose, K+
  4. normothermia:
    -avoid fevers
32
Q

who benefits the most from therapeutic hypothermia in cardiac arrest?

A

*those who arrest with ventricular tachycardia/ventricular fibrillation do better than those who do not
*earlier cooling leads to better outcomes

Cardiology Exam (52 decks)

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