Ischemic Heart Disease and Conduction Disorders

Flashcards covering the foundational concepts of ischemic heart disease, heart anatomy, conduction, and complications as presented in Chapter 16.

Acute coronary syndrome (ACS)

A condition resulting from ischemia, comprising unstable angina and myocardial infarction.

What are the four chambers of the heart?

Right and left atrium, right and left ventricle

What does the right atrium do?

Receives blood from superior and inferior vena cava and coronary sinus

What does the right ventricle do?

Pumps blood to the lungs

What does the left atrium do?

Receives blood from pulmonary veins

What does the left ventricle do?

Pumps blood to the body

Myocardial infarction (MI)

Prolonged ischemia leading to myocardial cell death.

Epicardium

The outer tissue layer of the heart.

Myocardium

The muscle layer of the heart.

Endocardium

The tissue layer that lines the interior of the heart.

LAD

Left anterior descending artery.

Pulmonary circuit

A low pressure system where blood travels from the right ventricle to the left atrium to pick up oxygen at the lungs.

Systemic circuit

A high pressure system where blood travels from the left ventricle to the right atrium to deliver oxygen to body tissues.

Systolic

The phase of heart contraction.

Diastolic

The phase of heart relaxation.

Sinoatrial node (SA node)

The pacemaker of the heart's conduction system.

Phase 0 (Cardiac Action Potential)

Phase where fast sodium channels open and increase the potential from $-90\,mV$ to $+20\,mV$.

Phase 1 (cardiac muscle action potential)

Peak, abrupt, closure fast sodium channels

Phase 2 (cardiac muscle action potential)

Plateau, slow sodium-calcium channels

Phase 3 (cardiac muscle action potential)

Repolarization, K+ channels open

Phase 4 (cardiac muscle action potential)

Resting potential, Na+/K+ pump

Absolute refractory period

Occurring during phases 0, 1, 2, and part of 3, this period ensures cells cannot be re-stimulated, allowing the heart to relax and fill with blood. Protects against fatal arrhythmias.

What is a dysrhythmia (arrhythmias)?

A disruption in electrical signal. Can be supraventricular (SA node, AV node), or ventricular (Bundle of His, bundles branches, Purkinje fibers, and ventricle muscle).

Where can a block most commonly be found?

The AV node

Ectopic pacemaker

An electrical signal source outside the normal conduction pathway, such as a premature ventricular contraction (PVC).

STEMI

ST segment elevation myocardial infarction, indicating an infarction through the cell wall.

NSTEMI

Non-ST segment elevation myocardial infarction, indicating an infarction that is not through the cell wall.

What is angina pectoris?

Chest pain

What can cause myocardial ischemia?

Blood clot, atherosclerotic plaque, coronary artery vasospasm (Prinzmetal’s or variant angina)

What does angina cause?

ADP and lactic acid accumulation resulting in pain

Stable angina

Consistent, chronic chest pain that is often self-medicated with nitroglycerin.

Unstable angina

A medical emergency involving a new chest pain episode or increased severity, indicating new regions of ischemia.

Anginal Equivalents

Signs of MI that differ from classic angina, such as dyspnea, extreme fatigue, or epigastric pain, more commonly seen in women.

What are some risk factors, signs, and symptoms of angina and CAD?

Risk: cigarette smoking, diabetes mellitus, hypercholesterolemia, metabolic syndrome.

Signs: chest pain brought on my exertion, crushing sensation on left side of chest, pain radiating to shoulder, jaw, and down arm. Levine’s sign. Pain does not change with alteration in position, respiration or cough.

How can angina and CAD be diagnosed?

Blood lipids, blood pressure, ECG (non-confirmatory test of ST elevation), hs-CRP, cardiac enzymes, chest x-ray, calcium computed tomography, cardiac angiogram, cardiac catheterization, cardiac troponin

Prinzmetal’s angina

A variant angina caused by coronary artery vasospasm.

Levine’s sign

A clenched fist over the sternum used by patients to describe chest pain.

Cardiac troponin (cTn)

The confirmatory blood test for myocardial infarction.

Intravascular coronary angiography

The gold standard for diagnosing CAD, though it carries a risk of rupturing atherosclerotic plaques.

What can be used as a treatment for CAD what is non-invasive and decreases risk of plaque rupture?

Non-invasive coronary computed tomographic angiography (CCTA)

What is a graded exercise stress test?

Echocardiogram or thallium injection (scintigraphy) to look at the heart under stress and determine areas of injury

What is the goal/treatment for CAD?

Goal: relieve symptoms and prevent MI

Treatment: oxygen, nitrates (vasodilators), aspirin (decrease platelet adherence), beta blockers (decrease myocardial oxygen demand), calcium antagonists (ateriole dilation), ACE inhibitors (decrease BP and resistance)

Percutaneous transluminal coronary angioplasty (PCTA)

A procedure using a balloon-tipped catheter to push plaque against the arterial wall. A catheter with a blade reduces the plaque, and a stent is placed to maintain an open vessel.

What are the classifications of MI?

Type 1: spontaneous due to plaque or thrombus

Type 2: lack of oxygen to meet demands

Type 3: MI resulting in death with no biomarkers

Type 4: MI due to stent insertion

Type 5: MI due to CABG

Coronary artery bypass graft (CABG)

A surgical option that creates new routes around occlusions, often using the saphenous vein of the leg. Traditionally a heart pump is used, but there can be off pump procedures.

What dictates MI damage?

Location, length of time (greater than 30 minutes=0.5 hours irreversible damage), available collateral circulation.

What is the zone of ischemia?

The area of infarct surrounded by area of injury, some cells in this area will recover.

What are necrotic cells?

Altered electrical activity (ECG changes), release cellular contents (cardiac markers such as troponin)

What are some signs and symptoms of MI?

Crushing chest pain, Levine’s sign, pain radiating to shoulder, jaw, down left arm, sweating, nausea, anxiety, angina equivalents.

CPK-MB

A cardiac enzyme that rises within 4 hours of an MI and subsides over 3 to 4 days.

What is cTnI?

A blood test. Rise 4-8 hours after chest pain onset, baseline with 5-9 days.

How is an MI diagnosed?

ECG (cannot confirm MI), blood tests, echocardiogram, radionuclide myocardial perfusion

How in an MI treated?

Anti-platelet, oxygen, nitrates, morphine, anticoagulants

CABG

Tissue plasminogen activator (tPA)

Percutaneous coronary intervention

Beta blockers to reduce heart rate and myocardial oxygen demand

Calcium channel antagonists to decrease coronary arteriole constriction

What are some complications of an MI?

Post myocardial infarction dysrhythmias, reentry

Reentry

A post-MI complication where ischemic areas do not conduct impulses as expected, causing impulses to re-activate already depolarized areas. Disrupt normal rhythm and destabilize the heart electrically.

What is an atrioventricular block?

An anterior and inferior wall MI, where the SA atrial impulse fails to be conducted to the ventricles causing a prolonged PR interval.

What is premature ventricular contraction?

Ventricle beats independently (shows a widened QRS complex), that may occur singularly or in patterns, sporadic and infrequent PVCs do not require treatment, but 2 sequential PVCs (couplets) may produce dangerous ventricular rhythm. Sporadic PVCs are the most common arrhythmia post-MI.

Atrial Fibrillation

An arrhythmia characterized by the absence of coordinated atrial contractions and multiple irregular fibrillatory P waves. May or may not stimulate a rapid ventricular response, and increase risk of clot formation and stroke.

Ventricular Tachycardia

A rapid rhythm with a rate greater than $100\,\text{bpm}$ characterized by a series of widened QRS waves without P or T waves. Does not allow for effective pumping. Signs include dyspnea, palpitations, and lightheadedness.

Ventricular Fibrillation

An uncoordinated quivering of the ventricle with no effective pumping, potentially leading to death. May be precipitated by PVC falling on the T wave, interrupting refractory period.

Papillary muscle rupture

An MI complication that can cause mitral insufficiency and back up blood into the left atrium. Dyspnea and crackles may develop.

Thromboembolism

Poorly contracting heart chambers cause stagnant blood, increase risk of clot formation.

What is a ventricular aneurysm?

A potential complication of an MI, it is a weakened, bulging area of heart wall that may rupture. Surgical intervention needed.

What is pericarditis?

Pericardial friction rub that causes stabbing pain with inspiration, occurs 2-3 days post MI. May occur as component of Dressler’s syndrome.

Dressler’s syndrome

A hypersensitivity reaction to tissue necrosis in MI that can include pericarditis.

What is heart failure?

Ability of the heart to generate sufficient pressure becoming compromised

What does LV heart failure cause?

Hypotension, fluid backs up into pulmonary circuit.

What does RV heart failure cause?

Fluid back up into the systemic circulation leading to jugular vein distension and peripheral edema.

Infectious Endocarditis (IE)

Normally caused by a bacterial infection, usually Staphylococcus aureus, that causes vegetations to develop on heart valves. The vegetation’s can break off and enter the blood stream (septic embolism).

What are some risk factors for infectious endocarditis?

Prosthetic valves, pacemakers, intravascular devices, IV drug use, dental procedures, pneumonia, pyelonephritis. Overall different potential causes account for different categories.

What causes native valve endocarditis?

Group A beta hemolytic streptococcus (GABHS)

Septic emboli

Fragments of vegetations that break off during infectious endocarditis and enter the bloodstream.

Duke Criteria

The standard diagnostic criteria for infectious endocarditis based on labs and echocardiographic findings.

What is the treatment of infectious endocarditis?

IV antibiotics for 6 weeks or longer?

Is infectious endocarditis acute or subacute?

Both