CHA Cardiac 1

What is cardiac output (CO)?

The amount of blood the heart pumps per minute.

What is the formula for cardiac output?

CO = stroke volume × heart rate (CO = SV × HR).

What can low cardiac output indicate?

Heart failure, shock, or other cardiovascular problems.

What is systole?

Contraction of the chambers; atria contract first, then ventricles.

What is diastole?

Relaxation of the chambers and refilling with blood.

What is preload?

The volume of blood in the ventricles at the end of diastole.

What increases afterload?

Hypertension and vasoconstriction.

What does increased afterload do to the heart?

Makes the ventricle work harder and increases cardiac workload.

What is the SA node?

The heart's pacemaker; it generates the electrical impulse.

What happens at the AV node?

The impulse is briefly delayed before traveling to the ventricles.

What is the purpose of the coronary arteries?

Supply oxygenated blood and nutrients to the myocardium.

What is the LAD?

Left anterior descending artery; called the 'widowmaker' in the lecture.

What is the LCX?

Left circumflex coronary artery.

What are two major branches associated with the RCA?

The posterior descending artery and acute marginal artery.

What is ischemia?

Lack of oxygen to tissue.

What is infarction?

Obstruction causing tissue death.

What is coronary artery disease (CAD)?

Impaired blood flow to the myocardium.

What is atherosclerosis?

Plaque accumulation in arterial walls that narrows or can block blood flow.

What are modifiable cardiac risk factors?

Smoking, high cholesterol, sedentary lifestyle, obesity, diabetes, and hypertension.

What are nonmodifiable cardiac risk factors listed in lecture?

Older age, male sex, African American race, congenital disease, and genetics.

What is primary cardiac prevention?

Exercise, heart-healthy diet, and avoiding smoking.

What is secondary cardiac prevention?

Blood pressure and cholesterol screening.

What does LDL do?

Contributes to plaque buildup; it is the 'bad' cholesterol.

What does HDL do?

Helps carry LDL away; it is the 'good' cholesterol.

What are triglycerides?

A type of fat in the blood.

What does troponin indicate?

Myocardial injury; it is highly specific for the heart.

What is CK?

An enzyme found in cardiac, skeletal muscle, and brain tissue that rises with damage.

What is CK-MB?

A creatine kinase fraction associated more specifically with cardiac muscle.

What is myoglobin after MI?

The first detectable marker after an MI, according to the course materials.

What does C-reactive protein indicate?

Inflammation and increased cardiovascular risk.

What does homocysteine indicate?

It is an amino acid associated with coronary artery disease risk.

What are natriuretic peptides associated with?

Increased cardiac pressure and heart failure.

What does an ECG measure?

The heart's electrical activity.

What does an echocardiogram evaluate?

Heart wall motion, thickness, chamber size, blood-flow velocity, and ejection fraction.

What is normal ejection fraction in the lecture?

About 50–70%.

What does low ejection fraction indicate?

Reduced cardiac output and decreased tissue perfusion.

What can a cardiac stress test assess?

Cardiac response to exertion or medication-induced stress, including chest pain and ECG changes.

What is a pharmacologic stress test used for?

Patients who cannot exercise adequately on a treadmill.

What is an arteriogram?

Imaging of arteries after contrast is injected to identify occlusions.

What is a cardiac catheterization used for?

Direct visualization of coronary arteries and possible treatment of an occlusion.

What are major cardiac medication classes in the lecture?

Vasodilators, vasopressors, diuretics, antidysrhythmics, cardioglycosides, anticoagulants, antiplatelets, thrombolytics, and lipid-lowering agents.

What do vasodilators do?

Increase blood-vessel diameter and can decrease blood pressure.

What do vasopressors do?

Cause vasoconstriction to increase vascular resistance and support blood pressure.

What do diuretics do?

Increase urine output by reducing sodium reabsorption and blood volume.

What do antidysrhythmics do?

Help correct abnormal electrical impulses and cardiac rhythms.

What does digoxin do?

Slows heart rate and has a positive inotropic effect that can improve cardiac output.

What should be assessed before giving digoxin?

Apical pulse for one full minute and signs of toxicity.

What do anticoagulants do?

Prevent clot formation through the coagulation cascade.

What do antiplatelets do?

Prevent platelets from aggregating and forming clots.

What do thrombolytics do?

Break down fibrin in blood clots.

What is a major danger of thrombolytics?

Serious bleeding, including intracranial bleeding.

What do statins do?

Lower LDL cholesterol.

What should be monitored with statins?

Liver enzymes.

What happens to myocardial cells after about 10 seconds of coronary occlusion?

They become hypoxic and anaerobic metabolism begins.

Why does angina cause pain?

Lactic acid accumulates and irritates myocardial nerve fibers during ischemia.

What are common manifestations of angina?

Chest pain/pressure, cool clammy pale skin, elevated HR/BP, and possibly S3 or S4.

What is stable angina?

Predictable pain with exertion/stress that is relieved by rest or nitroglycerin.

How long does stable angina typically last in the course?

Less than 5 minutes.

What is Prinzmetal (variant) angina?

Angina caused by coronary artery spasm, often occurring at night or early morning.

How is Prinzmetal angina treated?

Calcium channel blockers and nitrates.

What is unstable angina?

Sudden or severe ischemic chest pain at rest/minimal exertion that is not relieved by rest or usual medications.

Why is unstable angina an emergency?

It indicates acute coronary ischemia and carries a risk of MI.

What is acute coronary syndrome (ACS)?

Prolonged myocardial ischemia that is not immediately reversed; includes unstable angina, NSTEMI, and STEMI.

What symptoms can occur with ACS?

Substernal/epigastric chest pain, radiation to neck/left shoulder/arm, dyspnea, diaphoresis, pallor, cool skin, tachycardia, or hypotension.

What ECG changes can occur with ACS?

ST depression and T-wave inversion.

What is a STEMI?

An MI associated with ST-segment elevation, usually from severe/complete coronary occlusion.

What does ST-segment elevation indicate?

Serious myocardial injury and a STEMI requiring immediate intervention.

What does ST-segment depression suggest?

Myocardial ischemia, often involving the subendocardium.

What is an NSTEMI?

Myocardial infarction with cardiac biomarker elevation but without ST elevation on the ECG.

How do you distinguish unstable angina from NSTEMI?

Both may have ischemia/ECG changes; NSTEMI has elevated cardiac biomarkers, while unstable angina does not.

What is a myocardial infarction (MI)?

Persistent coronary occlusion causing irreversible myocardial cell death.

What are classic MI symptoms?

Severe crushing pain unrelieved by rest/nitro, radiation to arm/neck/jaw, dyspnea, diaphoresis, tachycardia, anxiety/doom, and decreased LOC.

What ECG change is classically associated with STEMI?

ST-segment elevation.

What happens to troponin after myocardial necrosis?

It rises; the course notes it can remain elevated for about a week.

What is the earliest detectable MI marker in the course?

Myoglobin.

What are major complications of MI?

Dysrhythmias, pump failure, cardiogenic shock, infarct extension, structural defects, and pericarditis.

Why do PVCs matter after an MI?

They can progress to ventricular tachycardia or ventricular fibrillation.

When is ventricular fibrillation especially likely after MI?

The course notes the first hour is a high-risk period.

What is cardiogenic shock after MI?

Severe pump failure causing low cardiac output and inadequate tissue perfusion.

What is the 'time is muscle' concept?

Earlier reperfusion limits myocardial damage; best outcomes occur with rapid treatment.

What are the goals of MI care?

Relieve pain, reduce damage, maintain cardiovascular stability, decrease workload, and prevent complications.

What does MONA stand for in this course?

Morphine, oxygen, nitroglycerin, aspirin.

What is the course's first action in MONA?

Oxygen.

When is morphine used in ACS/MI?

For severe pain/anxiety and to decrease myocardial oxygen demand.

What should be assessed before giving morphine?

Level of consciousness, respiratory rate, and blood pressure.

When should morphine be avoided per the course?

Low respiratory rate, altered mental status, or low blood pressure.

When is nitroglycerin used?

Stable/unstable angina, MI, and prophylactically before exertion when prescribed.

What should be assessed before nitroglycerin?

Blood pressure and heart rate.

What is a major nitroglycerin contraindication?

Concurrent PDE5 inhibitor use, such as sildenafil.

What are common nitroglycerin effects/teaching points?

Headache; sit or lie down; it causes vasodilation and should be kept available/protected from light.

What does nitroglycerin decrease?

Preload, afterload, cardiac workload, and myocardial oxygen demand.

What is an important nitroglycerin safety issue?

Do not combine it with PDE5 inhibitors because severe hypotension can occur.

What does aspirin do in ACS/MI?

Inhibits platelet aggregation and helps prevent further clot formation.

What aspirin dose is taught for suspected MI/ACS?

324 mg chewable aspirin (four 81-mg tablets).

What aspirin dose is used for daily prevention in the case study?

81 mg daily.

What is a major aspirin contraindication discussed?

GI bleeding; weigh benefit versus risk.

When are thrombolytics used in MI?

When appropriate reperfusion by PCI/cath is not available in time.

What should be assessed before thrombolytics?

Active bleeding, recent trauma, recent surgery, prior thrombolytic use, and anticoagulant use.

What trauma example did the course emphasize before thrombolytics?

CPR counts as trauma.

What is a major thrombolytic contraindication?

Recent hemorrhagic stroke.