Cardiac Arrest Flashcards
cardiac arrest - defined
*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
myocardial infarction - defined
*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
cardiac arrest (contrasted to MI)
*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
myocardial infarction (contrast to cardiac arrest)
*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
causes of cardiac arrest/sudden cardiac death
*arrhythmias
*hypertrophic cardiomyopathy
*coronary heart disease
*coronary anomalies
*valvular heart disease
*ruptured aorta
risk factors for sudden cardiac death
*prior coronary events
*EF < 30% or heart failure
*arrhythmia risk markers
*post-MI
categories of cardiac arrest
- shockable heart rhythms:
-ventricular tachycardia
-ventricular fibrillation - non-shockable heart rhythms:
-pulseless electrical activity
-asystole
relationship between electrical and mechanical activity of the heart
*electrical activity always precedes mechanical activity
*mechanical activity cannot occur without electrical activity
*however, electrical activity CAN occur without mechanical activity
non-shockable rhythm: pulseless electrical activity (PEA)
*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)
common causes of pulseless electrical activity (PEA)
5 H’s and 5 T’s:
*hypovolemia
*hypoxia
*hydrogen ion (acidosis)
*hyperkalemia
*hypokalemia
*hypothermia
*toxins
*tamponade
*tension pneumothorax
*thrombosis (coronary)
*thrombosis (pulmonary)
*trauma
non-shockable rhythm: asystole
*no electrical activity
*no mechanical activity
causes of asystole
*hypovolemia
*hypoxia
*hydrogen ions (acidosis)
*hypothermia
*hyperkalemia
*hypoglycemia
*tablets (drug OD)
*tamponade
*tension pneumothorax
*thrombosis (coronary)
*thrombosis (pulmonary)
*trauma
shockable rhythm: ventricular tachycardia
*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
shockable rhythm: ventricular fibrillation
*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
causes of ventricular tachycardia & ventricular fibrillation
*myocardial ischemia/MI
*coronary artery disease
*valvular heart disease
*heart failure
*cardiomyopathy
*electrolyte imbalances (hypokalemia, hyperkalemia, hypercalcemia)
*drug intoxications
*acid-base imbalance
goal of treating cardiac arrest
goal = “return of spontaneous circulation” (ROSC)
algorithm for treating cardiac arrest
- unresponsive? → open airway & look for signs of life
- CPR until defibrillator/monitor attached
- assess rhythm (shockable vs. nonshockable)
4a. if shockable, shock, then continue CPR
4b. if non-shockable, resume CPR
assessing the pulse in an unresponsive patient
*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
assessing need for defibrillation
*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
chest compressions - uses
*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
chest compressions - overveiw
*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
timeliness in cardiac resuscitation
*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
chest compressions: rate
*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)
chest compressions: depth
*deeper chest compression depth leads to better outcomes and survival
*should be 5cm deep
*allowing recoil further enhances the effect of deeper compressions
physiology of chest compressions - overview
2 components of how chest compressions work:
1. external cardiac massage
2. thoracic chest pump
physiology of chest compressions: external cardiac massage
*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
physiology of chest compressions: thoracic pump
*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
medication treatment for cardiac arrest
*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)
therapeutic hypothermia in cardiac arrest - recommendation
*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
how does therapeutic hypothermia improve outcomes following cardiac arrest ?
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
therapeutic hypothermia in cardiac arrest - protocol
- initiating:
-start cooling immediately
-analgesia/sedation (to prevent shivering)
-recognize/treat shivering - maintenance:
-close attention to BP, O2 sat, volume, glucose, K+, seizures - rewarming:
-begin 24 hours after induction
-warm by 0.25 degrees C per hour
-watch BP, glucose, K+ - normothermia:
-avoid fevers
who benefits the most from therapeutic hypothermia in cardiac arrest?
*those who arrest with ventricular tachycardia/ventricular fibrillation do better than those who do not
*earlier cooling leads to better outcomes