Broken-heart syndrome, also known as stress-induced cardiomyopathy, has been observed in patients experiencing acute emotional stress such as grief.
Initially noted in Japan in the early 2000s.
Predominantly affects elderly women presenting with symptoms resembling heart attacks.
ECGs reveal abnormal electrical activity and dilated left ventricles, but coronary arteries show no lesions commonly associated with heart attacks.
All symptoms revert to normal with supportive care within one month.
Blood from the myocardium is drained by cardiac veins into the coronary sinus, which empties into the right atrium.
Major cardiac veins include:
Great Cardiac Vein: Drains blood from regions supplied by the anterior interventricular artery.
Middle Cardiac Vein: Drains the area supplied by the posterior interventricular artery.
Small Cardiac Vein: Drains the posterior surfaces of the right atrium and ventricle.
Anterior Cardiac Veins: Drain the anterior surface of the right ventricle directly into the right atrium.
The heart functions through coordinated electrical impulses leading to contractions.
Cardiac muscle consists of:
Autorrhythmic Cells: Control and coordinate the heartbeat (pacemakers).
Contractile Cells: Execute the heart's pumping action.
The conducting system initiates contraction via action potentials that travel through the myocardium.
The heart's automatic contractions (autorhythmicity) are dictated by specialized cells within the conducting system.
SA Node: Primary pacemaker of the heart, located in the right atrium; generates 60-100 action potentials per minute.
AV Node: Backup pacemaker, slower than SA Node, generating 40-60 action potentials per minute.
Electrical impulses stimulate atrial contraction, followed by ventricular contraction through a timed process:
SA Node activity begins.
Stimulus spreads to the ventricles via the AV Node after a delay.
Ventricular contraction is coordinated to prevent backflow into the atria.
The contraction process is triggered by calcium influx, essential for the contractile process:
Pacemaker Cells have an unstable resting membrane potential that gradually depolarizes toward threshold.
Action potentials result in contraction lagging behind the depolarization.
The total duration of a heartbeat is approximately 370 milliseconds.
Atrial Systole: Atria contract, pushing blood into the ventricles.
Ventricular Systole: Ventricles contract, pushing blood out into arteries.
Diastole: Heart refills with blood; all chambers relax for efficient filling.
Cardiac action potentials display different phases:
Rapid Depolarization: Sudden influx of Na+ ions.
Plateau Phase: Prolonged phase due to Ca2+ influx, crucial for contraction.
Repolarization: K+ exits, returning the membrane potential to resting state.
The absolute refractory period is critical to avoid tetanic contractions, ensuring effective pumping.
The ECG records electrical activity of the heart.
Major components include:
P Wave: Atrial depolarization.
QRS Complex: Ventricular depolarization, associated with ventricular contractile action.
T Wave: Ventricular repolarization.
ECG helps in diagnosing arrhythmias and other heart conditions by evaluating wave patterns and timing.
The Cardiac Cycle is made up of:
Systole: Contraction of heart chambers.
Diastole: Relaxation and filling of heart chambers.
The contraction-relaxation phases must be well-timed:
Blood flows from higher pressure areas to lower.
Atrial systole occurs slightly before ventricular systole to optimize blood flow.
S₁ Lubb
: Closing of AV valves (beginning of ventricular contraction).
S₂ Dupp
: Closing of semilunar valves (beginning of ventricular filling).
S₃ and S₄ are softer sounds related to blood flow and rarely heard in healthy individuals.
Murmurs may indicate valve dysfunction or heart problems.