| What is sudden cardiac death? | Unexpected natural death from a cardiac cause within short period of time.
Death occurs <1 hour from onset of symptoms
Death often contributed to arrhythmia, 40% unwitnessed (ECG only can provide definitive info)
Prodromal nonspecific symptoms (ischemia (chest pain), tachyarrhythmia (palpitation) and congestive heart failure (dyspnea) |
| What is cardiovascular collapse? | Sudden loss of effective blood flow due to cardiac or vascular issue that resolves on its own (neurocardio syncope/vasovagal) or requires intervention (arrest)
Occurs in same mechanism of cardiac arrest + vasodepression and transient loss of blood flow. |
| What is cardiac arrest? | Abrupt cessation of cardiac mechanical function, may be reversible by prompt intervention, mechanism include V.Fib, V.Tach, asystole, bradycardia, pulseless electrical activity, non cardiac mechanical factors (pulmonary embolism) |
| What is sudden cardiac death? | Sudden irreversible cessation of all biological functions. |
| How is epidemiology of cardiac death causes? | Asystole is most common mechanism recorded at initial contact (45% of cases), pulseless electrical activity (20%), VF (25%)
Acute low CO state can present clinically as cardiac arrest (massive acute pulmonary embolus, internal blood loss due to aneurysm rupture, intense anaphylaxis, cardiac rupture with tamponade
Most common cause of sudden natural death are cardiac disorders
In young people, SCD occurs 1 in 100,000, peak age 45-75: 1-2 in 1000 |
| What are etiologies causing cardiac death? | These include CAD, hypertrophic cardiomyopathy, valvular heart disease, Mechanical factor (MVP) for elderly
idiopathic LVH, coronary anomalies, ruptured aorta (for young people)
Most imp for old : CAD, for young: hypertrophic cardiomyopathy |
| What is coronary artery disease causing SCD? | 80% of people with SCD have CAD due to atherosclerotic coronary arteries.
Non atherosclerotic coronary artery disease are found in little number of SCDs include coronary arteritis, embolism, dissection, congenital malformation (left coronary artery from pulmonary artery/ from right coronary artery/...)
No specific pattern of CAD causing CSD, acute occlusion of minimally stenosed coronary artery can result in disasterous outcome more than severely stenosed coronary artery with jeopardized myocardium protected by collaterals. |
| What are cardiomyopathies causing CSD? | Second largest group of pt experiencing CSD, hypertrophic CM occurs in 2 in 1000 young adults, causes death to 4-6% / year for children (2-4% for adults) |
| What is hypertrophic cardiomyopathy? | Hx of sustained V.Tach, SCD, familty hx of cardiac death, diverse genotype, recurrent syncope, episodes of non-sustained V.Tach, massive LVH (risk factors for SCD) |
| What is idiopathic dilated cardiomyopathy? | 10% of SCD in adults, mortality ranges from 10-50% annually depending on severity
Syncope is important variable identifying pt with risk of SCD.
Arrhythmogenic RV dysplasia is a kind of CM on chromosome 1 and 14q23-q24
Exercise can precipitate V.Tach annual incidence 2%. two pathological patterns: fatty and fibrofatty myocardial infiltration.
We can see epsilon wave in sinus rhythm due to intraventricular conduction |
| What is LVH? | Multiple diseases can cause it, valvular heart disease, obstructive and non-obstructive hypertrophic CM, primary pulmonary HTN with RVH and congenital disorders.
We could see V.Tach due to MI, interstitial fibrosis, electrolyte disturbance (although QT interval is prolonged due to HTN) |
| What are valvular disease causing CSD? | Low risk of CSD(if asymptomatic)
after prosthetic aortic valve replacement, still there is a risk for CSD due to arrhythmias, prosthetic valve dysfunction or coexisting CAD.
It is the second most common cause of death after valve replacement surgery (CSD) 2-4% after 7 years (20% of postop deaths)
We don't know if mitral valve prolapse caused CSD, although its prevalence is high, but risk increases in case we have it with mitral regurg, LV dysfunction, myxomatous degeneration (risk to get infective endocarditis, cerebroembolus, SCD) |
| What are congenital heart diseases causing CSD? | Tetralogy of fallot, transposition of great arteries, aortic stenosis, and pulmonary vascular obstruction
Also it was a late complication after surgical repair of tetralogy of fallot/ transposition/ pulmonary HTN.
In tetralogy of fallot, QRS prolonged according to RV size predicting the death time. |
| What are primary electrophysiological abnormalities causing CSD? | Congenital prolonged QT, WPW syndrome, idiopathic V.Fib (Brugada's), catecholaminergic polymorphic V. Tach, congenital AV block.
some acquired diseases (prolonged QT, node diseases (lenegre, lev disease), BBB) |
| What is WPW syndrome causing CSD? | WPW pt have risk of SCD <1 per 1000 pt years of followup.
mechanism of CSD is atrial fib, with rapid conduction to ventricles over accessory pathways making ventricular fib |
| What are triggers for expression of cardiac arrest? | Alteration of coronary blood flow (ischemia, reperfusion after ischemia)
Low CO (heart failure (chronic or acute decomp), shock)
Systemic metabolic abnormality (electrolyte imbalace hypokalemia, hypoxemia, acidosis)
Neurodisturbance (fluctuations (central/ humoral), receptor function)
Toxic response (proarrhythmic drugs, cardiac toxins like cocaine, drug interactions) |
| How is prediction and prevention of cardiac arrest? | Primary prevention is identifying risks, secondary prevention are measures taken to prevent recurrent arrest after one has already occurred.
Only practical strategy is risk control (age, smoking, cholesterol, DM, BP, LVH, CRP)
After major CV event (MI) risk of death is highest in 6-18 months after the event, and platues baseline of underlying disease.
Rate of resusication depends on mechanism of event, pulseless VT has best outcome, then comes VF.
asystole and PEA have dismal outcome stats |
| What is tx of CSD? | Five stages: BLS and evaluation
Public access defibrilation, ACLS (maintain organ perfusion and ventilation includes intubation, IV insertion and defibrillation), post-resusication care, long term management |
