Cardiac disorders DETAILED

What is myocardial ischemia?

Heart muscle gets too little oxygen. It happens when oxygen supply cannot meet the heart's metabolic needs.

What causes myocardial ischemia?

Oxygen demand exceeds oxygen supply. Reduced coronary flow or increased workload can create this imbalance.

What is myocardial infarction (MI)?

Irreversible death of heart muscle. It develops when ischemia lasts long enough to permanently damage cells.

How can prolonged ischemia cause MI?

Long-term oxygen loss kills heart cells. Without oxygen, heart cells cannot maintain normal energy production.

Why does lactic acid build up during ischemia?

Cells switch to anaerobic metabolism. Oxygen shortage forces cells to produce energy without enough oxygen.

How does atherosclerosis cause ischemia?

Plaque narrows coronary arteries. Less blood can pass through the narrowed artery to the myocardium.

What is coronary thrombosis?

A clot blocks coronary blood flow. The clot may partly or completely obstruct the artery.

What is coronary vasospasm?

Sudden narrowing of a coronary artery. The narrowed vessel temporarily delivers less oxygen to heart muscle.

Which angina is linked to vasospasm?

Prinzmetal's angina. Its underlying mechanism is temporary coronary artery constriction.

How can anemia cause ischemia?

Blood carries less oxygen. Low hemoglobin reduces oxygen delivery even if blood flow is normal.

What is microvascular ischemia?

Small coronary vessels cannot supply enough blood. Large coronary arteries may appear relatively unobstructed.

What is angina pectoris?

Chest discomfort caused by myocardial ischemia. It is a symptom of ischemia, not necessarily tissue death.

What is stable angina?

Predictable chest pain, often with exertion. It usually improves when oxygen demand falls.

What usually relieves stable angina?

Rest or nitroglycerin. Both reduce the oxygen supply-demand mismatch.

What is unstable angina?

New, worsening, or unpredictable chest pain. It may occur at rest and is not reliably relieved by rest.

Why is unstable angina an emergency?

It may progress to MI. It signals a potentially dangerous reduction in coronary blood flow.

What is microvascular angina?

Angina from small coronary vessel dysfunction. It involves dysfunction of small coronary vessels.

Does angina alone cause myocardial necrosis?

No. MI causes irreversible cell death. Necrosis distinguishes MI from angina without infarction.

What does high-sensitivity troponin detect?

Myocardial injury. It is released when cardiac muscle cells are damaged.

What does hs-CRP indicate?

Inflammation. It is not specific enough to diagnose a heart attack.

What does an ECG measure?

Heart electrical activity. It helps detect ischemic changes and abnormal rhythms.

What can coronary angiography show?

Narrowed or blocked coronary arteries. The images show where coronary blood flow is restricted.

What are four goals of angina treatment?

Relieve pain; improve oxygen supply; reduce demand; prevent MI. Treatment aims to correct the oxygen supply-demand imbalance.

What do nitrates do?

Dilate blood vessels and reduce heart workload. Vasodilation can improve symptoms and decrease oxygen demand.

What does aspirin do?

Reduces platelet aggregation. This helps prevent growth of platelet-rich clots.

When may oxygen be given for angina?

When oxygen saturation is low. Supplemental oxygen is not automatically needed for every patient.

What is CABG?

Surgery that bypasses blocked coronary arteries. A graft carries blood around an obstructed coronary segment.

Is ischemia always irreversible?

No. It may improve if blood flow returns. Restoring flow early may prevent permanent cell death.

What are the three steps of hemostasis?

Vasoconstriction; platelet plug; coagulation. Fibrin strengthens the platelet plug into a stable clot.

What does von Willebrand factor do?

Helps platelets attach at vessel injury. It connects circulating platelets to exposed vessel collagen.

What does glycoprotein IIb/IIIa bind?

Fibrinogen, helping platelets clump. Fibrinogen forms bridges between neighboring platelets.

What does thromboxane A2 promote?

Platelet aggregation. This helps platelets gather at a damaged vessel.

What do intrinsic and extrinsic pathways activate?

Factor X. Factor X activation helps generate thrombin.

What does thrombin make from fibrinogen?

Fibrin. Fibrin forms the mesh that stabilizes a clot.

What two nutrients are needed for coagulation?

Calcium and vitamin K. Both are important for normal clot formation.

What determines the severity of an MI?

Location, ischemia duration, collateral circulation. Longer ischemia and fewer collateral vessels generally mean worse injury.

What is collateral circulation?

Alternative vessels supplying blood to tissue. These vessels can reduce damage when a main artery is blocked.

What is the zone of necrosis?

Irreversibly dead myocardial tissue. Dead cells cannot regain normal contractile function.

What is the zone of ischemia?

Oxygen-deprived tissue that may recover. Early restoration of blood flow may save this tissue.

What is the zone of injury?

Damaged tissue that may still recover. It is damaged but may not yet be permanently dead.

What is a classic MI symptom?

Crushing chest pressure or pain. Chest pressure may be accompanied by sweating or nausea.

Where can MI pain radiate?

Shoulder, jaw, or left arm. Pain can spread beyond the chest.

What is diaphoresis?

Excessive sweating. It can accompany sympathetic activation during MI.

What is Levine's sign?

A clenched fist held over the chest. It is a classic gesture associated with pressure-like chest pain.

What are anginal equivalents?

Dyspnea, dizziness, faintness, or epigastric discomfort. These can occur instead of typical chest pain.

Can MI occur without chest pain?

Yes. This may be a silent MI. Absence of chest pain does not exclude myocardial injury.

What is STEMI?

MI with characteristic ST-segment elevation. ST elevation is a characteristic ECG pattern.

What is NSTEMI?

MI without characteristic ST elevation. Troponin is still elevated because myocardial cells die.

Do STEMI and NSTEMI both cause necrosis?

Yes. Both involve myocardial cell death. The ECG pattern differs, but both are true infarctions.

What coronary blockage is often linked to STEMI?

Acute complete coronary occlusion. A sudden blockage severely reduces oxygen delivery.

What damage pattern is often linked to NSTEMI?

Subendocardial myocardial injury. This affects the inner portion of the ventricular wall.

What can ST depression suggest?

Myocardial ischemia. It is an ECG clue, not a diagnosis by itself.

What can abnormal T waves suggest?

Myocardial ischemia. T waves reflect ventricular electrical recovery.

Can an ECG alone rule out every MI?

No. Consider symptoms and biomarkers. Serial biomarkers and clinical findings are also necessary.

What is the main MI blood biomarker?

Cardiac troponin. A rise and fall helps identify an acute injury.

What troponin pattern suggests acute MI injury?

A rise and/or fall in elevated troponin. The change over time is as important as a single result.

What is CK-MB?

An enzyme released with myocardial injury. It is less specific than cardiac troponin.

When does CK-MB begin rising per the slides?

About four hours after MI. The slide gives an approximate timing, not an exact clock.

When does CK-MB return toward baseline?

About three to four days. The level falls as the enzyme clears from blood.

What does echocardiography assess?

Heart structure, wall motion, and pumping. It can reveal abnormal wall motion after MI.

What are four major MI complications?

Dysrhythmias, heart failure, shock, thromboembolism. Each complication follows from damaged heart muscle or poor pumping.

Why can MI cause dysrhythmias?

Damaged tissue disrupts electrical conduction. Injured cells can create abnormal conduction pathways.

What is cardiogenic shock?

Severe pump failure with poor tissue perfusion. Low output can deprive vital organs of oxygen.

How can MI cause thromboembolism?

Weak pumping causes blood stasis and clots. A clot can break loose and block a distant vessel.

What does papillary muscle rupture cause?

Mitral regurgitation and pulmonary congestion. The mitral valve may leak blood back into the left atrium.

What finding may signal papillary muscle rupture?

New murmur, dyspnea, or crackles. Valve leakage raises pressure toward the lungs.

What is a ventricular aneurysm?

A weakened ventricular wall bulges outward. The damaged wall bulges rather than contracting normally.

What is post-MI pericarditis?

Inflammation of the heart's outer sac. The pericardium is the sac surrounding the heart.

What symptoms suggest pericarditis?

Sharp inspiratory pain and a friction rub. Inflamed pericardial layers rub against each other.

What is Dressler's syndrome?

Immune-mediated inflammation after myocardial injury. It is a post-injury inflammatory response.

What are four goals of MI treatment?

Restore flow; limit damage; reduce demand; prevent complications. Early restoration of blood flow limits damage.

What is PCI? (Percutaneous Coronary Intervention)

Procedure to reopen a blocked coronary artery. It restores perfusion to threatened heart muscle.

What is reperfusion injury?

Extra tissue injury after blood flow returns. Oxygen return can trigger inflammation and oxidative stress.

What is myocardial stunning?

Temporary weak contraction after reperfusion. The dysfunction is temporary even after blood flow returns.

What do beta blockers do after MI?

Lower heart rate and oxygen demand. Slower heart rate lowers myocardial oxygen requirements.

What do calcium channel blockers do?

Reduce coronary artery constriction. Some reduce coronary vasospasm and vascular resistance.

What do thrombolytics do?

Break down clots in selected patients. They are used only in suitable clinical situations.

What do anticoagulants do?

Reduce further clot formation. They help stop clots from extending or forming.

What is the heart's normal conduction pathway?

SA → AV → His → branches → Purkinje. The impulse must reach the ventricles to produce coordinated beats.

What is the SA node?

The heart's natural pacemaker. It normally sets the pace for the heart.

What does the AV node do?

Delays the signal so ventricles can fill. This delay allows ventricular filling before contraction.

What does the P wave represent?

Atrial depolarization. It represents atrial electrical activation.

What does the QRS complex represent?

Ventricular depolarization. It represents ventricular electrical activation.

What does the T wave represent?

Ventricular repolarization. It reflects ventricular recovery after contraction.

What is tachycardia?

An abnormally fast heart rate. Rapid rhythms can reduce filling and cardiac output.

What is bradycardia?

An abnormally slow heart rate. Severe slow rhythms may decrease cardiac output.

What is atrial fibrillation (AFib)?

Disorganized atrial electrical activity. Atria quiver rather than contracting effectively.

What does AFib look like on ECG?

Irregularly irregular rhythm; no distinct P waves. Atrial activity is disorganized, so distinct P waves disappear.

Why does AFib increase stroke risk?

Blood pools, clots form, and may travel to brain. Stagnant atrial blood is more likely to clot.

Where do AFib clots often form?

Left atrial appendage. This pouch is a frequent site of clot formation.

What does a Watchman device address?

Clot risk from the left atrial appendage. It blocks off the appendage in selected patients.

What is a PVC?

An early ventricular beat. It occurs before the expected next normal beat.

What does a PVC look like on ECG?

Premature, wide QRS complex. Ventricular activation spreads abnormally, widening the QRS.

What is ventricular bigeminy?

Every second beat is a PVC. The pattern repeats as normal beat, PVC.

What is ventricular trigeminy?

Every third beat is a PVC. The pattern repeats every three beats.

What is ventricular quadrigeminy?

Every fourth beat is a PVC. The pattern repeats every four beats.

Why is an R-on-T PVC dangerous?

It may trigger ventricular fibrillation. It falls during a vulnerable period of repolarization.

What is ventricular tachycardia (VT)?

Rapid ventricular rhythm with ineffective pumping. The fast rate can prevent adequate ventricular filling.

What does VT look like on ECG?

Fast rhythm with repeated wide QRS complexes. A wide QRS suggests ventricular-origin electrical activation.

Why does VT lower cardiac output?

Less filling time reduces stroke volume. Short filling time reduces blood ejected each beat.