Heart

  • SA Node → Beats at 70bpm per minute typically (sinus rhythm) and initiates electric impulses that spread throughout the atria, causing them to contract and pump blood into the ventricles.

Control of the Heart

  • Beta1-adrenergic receptors → these receptors, located primarily in the heart, play a crucial role in increasing heart rate and contractility by responding to catecholamines such as epinephrine and norepinephrine.

Cardiac function

  • Cardiac output → Volume of blood ejected by a ventricle in one minute and depends on heart rate and stroke volume.

    • CO = HR x SV

  • Stroke Volume → Amount of blood ejected from each ventricle with each contraction.

    • Varies with sympathetic stimulation and venous return

  • Heart Rate → Number of contractions of the ventricles each minute.

  • Cardiac Reserve → Ability of heart to increase output in response to increased demand.

  • Preload → mechanical state of heart at end of diastole with ventricles at their maximum volume.

  • Afterload → force required to eject blood from the ventricles and is determined by peripheral resistance to opening of semilunar valves.

  • Blood pressure → Force exerted by circulating blood against systemic arterial walls.

    • Blood pressure = Cardiac Output x Peripheral Resistance

    • SNS, epinephrine and or norepinephrine increase vasoconstriction by stimulating alpha1 receptors in arterioles of skin OR act on beta1-adrengeric receptors

    • Peripheral resistance → force opposing the flow of blood through the vessels, which is influenced by the diameter of the arterioles and the viscosity of the blood.

    • Pulse pressure → the difference between systolic and diastolic blood pressure, providing insight into the health of the arterial system and the overall cardiac function.

Heart Disorders

Diagnostic Tests

  • ECG → a test that measures the electrical activity of the heart, helping to identify irregular heartbeats, heart attacks, and other cardiac issues.

  • Auscultation / echocardiography / ultrasound → a procedure that uses sound waves to create images of the heart, allowing for the assessment of its structure and function, including valve issues and cardiac output.’

  • Exercise stress tests → a method used to evaluate the heart's performance under physical stress, typically involving monitored exercise, to detect potential coronary artery disease or other heart conditions.

  • Nuclear imaging → a technique that uses small amounts of radioactive material to visualize the heart's structure and blood flow, aiding in the diagnosis of coronary artery disease and assessing cardiac function.

    • Useful for identification of dead or damaged areas of the heart.

  • Single-photon emission computed tomography → Specialized computed tomography scan which measures cardiac ischemia at rest.

  • Cardiac catherization → passing of a catheter through a blood vessel into the ventricle to visualize inside of the heart and measure pressures, assess valve function, and evaluate coronary artery blockages.

    • Can help with fluroscopy and more.

  • Coronary angiography → A diagnostic procedure that uses X-rays to view the heart's blood vessels, providing detailed images of coronary arteries to identify any blockages or abnormalities.

  • Troponin blood test → Troponin is a type of protein found in cardiac muscle that is released into the bloodstream when there is damage to the heart muscle, making it an essential marker for diagnosing heart attacks and other cardiac conditions.

  • Doppler studies → A non-invasive ultrasound technique that evaluates blood flow through the heart and surrounding blood vessels, helping to assess heart valve function and detect any abnormalities in blood circulation.

  • Blood tests → serum triglyceride and cholesterol levels can be measure. Hemoglobin, hematocrit, blood cell counts, and differential count.

Drug Therapy

  • Vasodilators → reduce peripheral resistance by increasing lumen size of blood vessels systemically, causing an reduction in blood pressure and improving blood flow to the heart.

  • Beta blockers → Directly block beta1-androgenic receptors, preventing SNS increase of heart rate and contractility, resulting in decreased myocardial oxygen demand and improved cardiac efficiency.

  • Calcium channel blockers → Inhibit calcium ions into cardiac and smooth muscle fiber, causing reduced cardiac contractility and vasodilation, which lowers blood pressure and decreases myocardial oxygen consumption.

  • ACE inhibitors → block the conversion of angiotensin I to angiotensin II, leading to vasodilation, decreased blood pressure, and reduced strain on the heart.

    • Given to patients experiencing hypertension and CHF.

  • Diuretics → remove excess sodium and water from the body through the kidneys.

  • Anticoagulants → reduce risk of blood clot formation in coronary and systemic arteries by decreasing platelet adhesion through blocking of coagulation process.

    • Warfarin

Coronary Artery Disease

  • Arteriosclerosis → General term for all types of arterial changes.

    • Hardening changes in small arteries and arterioles.

    • Loss of elasticity and lumen narrows, causing obstruction.

    • Plaques of calcium, cholesterol and other substances accumulate in the arterial walls, leading to further narrowing and potentially resulting in ischemia or infarction.

  • Atherosclerosis → Presence of atheroma in large arteries

    • Plaques consisting of lipids, calcium, and possible inflammatory cells.

    • Related to diet, exercises and stress.

    • Risk Factors

      • Non-modifiable → Age (>40), Gender, genetic/familial.

      • Modifiable → Obesity, sedentary, smoking, diabetes, hypertension and contraceptives.

    • Diagnostic tests:

      • Usually no chest pain until 75% of the artery is occluded, which can lead to significant risk for myocardial infarction.

      • Varicose circulation can also indicate underlying cardiovascular issues, as they may be caused by weakened valves and veins in the legs.

      • Lipid levels, exercise stress tests and nuclear medicine studies.

    • Treatment

      • Weight loss, increased exercise, lowering of total serum cholesterol and LDL.

      • Reduce sodium intake, controlling hypertension and smoking.

Angina Petoris

  • Deficit of oxygen to heart muscle even after autoregulation.

  • Chest pain present with certain patterns clear:

    • classic → it presents as a tight, squeezing sensation in the chest, often radiating to the left arm or jaw.

    • exertional → it occurs during physical activity or emotional stress, often subsiding with rest.

    • unstable → it can happen at rest or with minimal exertion, may last longer, and can signal a more severe condition.

  • Signs include: substernal chest pain, emotional stress, pallor, diaphoresis and nausea.

  • Treatments include coronary vasodilators first then beta-blockers, which help to reduce heart workload and improve oxygen supply.

    • Anti-anxiety and stress-reduction.

Myocardial Infarction

  • Also known as a heart attack, it is the death of myocardial tissue because of ischemia.

  • Type 1 Myocardial Infarction occurs when a coronary artery is totally obstructed, leading to myocardial death.

    • Thrombus may form in coronary artery.

    • Vasospasm may occurs with a partial occlusion by an atheroma, which then leads to a total obstruction.

    • Part of thrombus breaks away which forms another lodging in a smaller vessel, blocking that one.

    • Transmural in nature— this type of infarction involves the full thickness of the myocardial wall, resulting in significant tissue damage and complications.

  • Type 2 Myocardial infarction occurs by a mismatch in myocardial oxygen supply and demand, often related to conditions such as severe anemia, coronary artery spasm, or hypotension.

  • Type 3 myocardial infarctions are fatal by nature, while type 4 and 5 are resultant from medical procedures.

Pathophysiology

  • At point of obstruction, heart tissue becomes necrotic, and area of injury, inflammation, and ischemia develops around necrotic zone.

  • Cell destruction leads to leaking of intracelluar enzymes like creatine kinase (CK) and troponins into the bloodstream, which are important biomarkers for diagnosing myocardial infarctions.

  • Blood supply interruption after 20-30 minutes leads to irreversible damage to the myocardial tissue, causing scar damage.

    • Collateral circulation can help although dependent on location.

Signs and Symptoms

  • Pain in substernal chest which radiates to arm, shoulder, jaw, or neck is an hallmark of MI.

  • Pallor, nausea, diaphoresis, dizziness and weakness, dysnpea, anxiety and fear, hypotension, and a low-grade fever are signs.

Diagnostic Tests

  1. Changes in ECG will become present during an MI.

  2. Serum enzymes and isoenzymes released from necrotic cells follow a pattern with lactic dehydrogenase, aspartate aminotransferase, and creatine phosphokinase being elevated.

  3. Serum levels of myosin and cardiac troponin are elevated a few hours after MI with troponin being the significant marker.

  4. Electrolyte levels may be abnormal.

  5. Leukocytosis and an elevated

Cardiac Cycle

  1. Diastole 1 → Ventricles relaxed and empty; aortic and pulmonary valves closed.

  2. Diastole 2 → Atria fill and valves remain closed.

  3. Diastole 3 → Increased atrial pressure opens AV valves and ventricles fill.

  4. Systole 1 → Atria contract and empty; ventricles are full.

  5. Systole 2 → Ventricles start contracting, increasing pressure and AV valves close while atria relax.

  6. Systole 3 → Ventricles contract, ventricular pressure forces aortic and pulmonary valves open and blood gets ejected.

Congestive Heart Failure

  • Condition where heart is unable to pump enough blood to meet metabolic needs of the body.

  • Reduced blood flow into systemic circulation occurs, causing kidneys to release more renin and aldosterone. This causes increased afterload due to increased vasoconstriction and increased blood volume to heart.

  • SNS response acts to increase heart ate and peripheral resistance.

  • Chambers of the heart dilate (enlarge) and cardiac muscle hypertrophies (cardiomegaly) causing increased oxygen demand.

Effects of heart not maintaining pumping capability:

  1. Cardiac Output or Stroke volume decreases → various organs suffer a “forward” effect. This causes dysfunction, lethargy, acidosis and build up on opposing heart chamber.

  2. “Backup” congestion → blood flow gets diverted, leading to pulmonary or systemic congestion, potentially resulting in symptoms such as edema, shortness of breath, and elevated blood pressure.

Congenital Heart Defects

Pathophysiology

  • Normal Valve → Blood flows freely forward with no backflow.

  • Stenosis → Less blood flows through narrowed opening w/ no backflow.

  • Incompetence → Blood flows freely forward with regurgitated backward flow.

Compensation and Signs

  • Through sympathetic response, heart increases rate and force of contraction to increase cardiac output; this increases oxygen demand on heart, dilating it and causing hypertrophy.

    • Respiratory rate may also increase if oxygen deficit occurs and acidosis is present.

  • Pallor and cynaosis, tachycardia, dsnpea

Symptoms List

  • Pallor → pale skin or a noticeable lack of color, often resulting from decreased blood flow or anemia.