11+D-Cardiovascular+Physiology

Page 1: Overview

  • Course Title: Cardiovascular Physiology-D

  • Lecturer: Dr. R. Ahangari

  • Institution: University of Central Florida, Orlando

  • References: Human Physiology by Linda S. Constanzo, Medline Plus

Page 2: ECG Electrodes

  • Standard Leads: Three standard leads designated as I, II, and III.

  • Lead I: Right arm (-) to left arm (+)

  • Lead II: Right arm (-) to left leg (+)

  • Lead III: Left arm (-) to left leg (+)

  • Function: These leads measure electrical potential changes in the frontal plane.

Page 3: ECG Leads - Views of the Heart

  • Chest Electrodes Placement:

    • V1: Fourth intercostal space, right of the sternum

    • V2: Fourth intercostal space, left of the sternum

    • V3: Between V2 and V4

    • V4: Fifth intercostal space at midclavicular line

    • V5: Level with V4 at left anterior axillary line

    • V6: Level with V5 at left midaxillary line (midpoint of armpit)

  • Views:

    • a. V1 & V2: Right Ventricle

    • b. V3 & V4: Septum/Lateral Left Ventricle

    • c. V5 & V6: Anterior/Lateral Left Ventricle

Page 4: Myocardial Infarction

  • Definition: Blood supply to myocardium is obstructed leading to muscle tissue death.

  • Causes:

    • Atherosclerosis: Plaque buildup in coronary arteries (cholesterol and cells)

    • Additional risk factors: Stress, male gender, diabetes, family history, high blood pressure, smoking, unhealthy cholesterol levels, chronic kidney disease.

Page 5: Symptoms of Myocardial Infarction

  • Chest Pain (Angina Pectoris): May move to other areas (arms, neck, jaw, back).

    • Descriptions include:

      • Tight band around chest

      • Severe indigestion

      • Pressure or heaviness

    • Duration: Typically > 20 minutes, not fully relieved by rest or medication.

  • Other Symptoms:

    • Sweating

    • Anxiety

    • Cough

    • Fainting

    • Dizziness

    • Nausea/Vomiting

    • Palpitations

    • Dyspnea

Page 6: Diagnostic Criteria

  1. Clinical history of ischemic chest pain lasting > 20 minutes.

  2. Changes in serial ECG tracings.

  3. Rise in cardiac biomarkers (creatine kinase-MB, troponins, myoglobin).

  4. High positive R wave, large negative Q waves, ST segment changes are indicative of MI.

  • Management: MI is a medical emergency; treatments include Oxygen, aspirin, nitroglycerin.

Page 7: Endocarditis

  • Definition: Inflammation of heart's inner lining (endocardium); often due to bloodstream infection.

  • Causes:

    • Bacteria from procedures (e.g., dental work) can affect damaged heart valves.

  • Risk Factors:

    • Artificial heart valves, congenital heart disease, valve problems, history of rheumatic heart disease.

Page 8: Symptoms of Endocarditis

  • Common Symptoms:

    • Abnormal urine color

    • Chills

    • Excessive sweating

    • Fatigue

    • Fever

    • Joint pain

    • Muscle aches

    • Night sweats

    • Nail abnormalities (splinter hemorrhages)

    • Paleness

Page 9: Diagnostic Tests for Endocarditis

  • Tests:

    • Blood culture/sensitivity (detects bacteria)

    • Chest x-ray

    • Complete blood count (may show anemia)

    • Echocardiogram

    • Erythrocyte sedimentation rate (ESR)

  • Treatment: Long-term, high-dose antibiotics for 4-6 weeks; surgery may be required for damaged heart valves.

Page 10: Mitral Stenosis

  • Definition: Valve disorder where mitral valve does not open fully, restricting blood flow.

  • Causes: Reduced valve area due to rheumatic fever or congenital conditions leading to pulmonary edema.

Page 11: Symptoms of Mitral Stenosis

  • Common Symptoms:

    • Atrial fibrillation

    • Chest discomfort (rare)

    • Difficulty breathing (especially during exercise or lying down)

    • Fatigue

    • Cough (possibly bloody)

  • Complications:

    • Atrial fibrillation, blood clots, heart failure, pulmonary edema, pulmonary hypertension.

Page 12: Mitral Stenosis (ECG Characteristics)

  • ECG Findings: Atrial fibrillation is present; no P waves visible, irregular rhythm.

  • Treatment Options:

    • Cardiac Glycosides, diuretics, β-blockers, Ca2+ channel blockers, anticoagulants, balloon valvotomy, surgical options.

Page 13: Mitral Regurgitation

  • Definition: Disorder where mitral valve does not close properly, causing backflow into the upper chamber.

  • Causes:

    • Mitral valve prolapse, congenital defects, atherosclerosis, endocarditis, heart tumors, hypertension, Marfan syndrome, untreated syphilis.

Page 14: Symptoms of Mitral Regurgitation

  • Common Symptoms:

    • Cough

    • Fatigue

    • Palpitations

    • Shortness of breath during activity or lying down

    • Nighttime urination

  • Treatment: Depends on symptoms and heart condition; may include antibiotics, antihypertensives, anticoagulants, digitalis, and diuretics.

Page 15: Cardiac Output Distribution

  • Distribution to various organs:

    • Cerebral: 15%

    • Coronary: 5%

    • Renal: 25%

    • Gastrointestinal: 25%

    • Skeletal Muscle: 25%

    • Skin: 5%

Page 16: Regulation of Arterial Pressure

  • Fast Mechanism: Neural regulation via baroreceptor reflex.

  • Slow Mechanism: Hormonal regulation (renin-angiotensin-aldosterone system).

  • Baroreceptors: Stretch receptors located in carotid sinuses, crucial for immediate blood pressure control.

Page 17: Baroreceptor Reflex Steps

  • Response to Decreased Arterial Pressure:

    • Reduced stretch decreases firing of carotid sinus nerve.

    • Initiates autonomic responses to increase blood pressure towards a set point (100 mm Hg).

    • Adjustments include decreased vagal activity and increased sympathetic output.

Page 18: Summary of Baroreceptor Reflex

  • Integration: Results in increased heart rate and blood pressure.

  • Pathway: Detection of low blood pressure -> Carotid baroreceptors -> Spinal cord -> Sympathetic chain -> Increased heart rate.

Page 19: Effects on Arterial Pressure

  • Physiological Responses:

    1. Increased heart rate

    2. Increased contractility/stroke volume

    3. Increased vasoconstriction of arterioles

    4. Increased vasoconstriction of veins.

Page 20: Renin-Angiotensin-Aldosterone System

  • Overview: Slow hormonal mechanism for blood volume regulation.

  • Components:

    • Renin: Enzyme

    • Angiotensin I: Inactive

    • Angiotensin II: Active, and subject to degradation.

Page 21: Regulation by Aldosterone

  • Effect on Kidneys: Modulates sodium (Na+) and water (H2O) absorption via nephron structures.

  • Pathway: Affects blood volume directly, influencing blood pressure.

Page 22: Other Regulations of Arterial Blood Pressure

  • Factors:

    • Cerebral ischemia

    • Chemoreceptors in carotid/aortic bodies

    • Vasopressin (ADH)

    • Atrial natriuretic peptide (ANP).

Page 23: Response to Cerebral Ischemia

  • Mechanism: a. Increased Pco2 triggers sympathetic outflow. b. Causes intense peripheral vasoconstriction, preserving blood flow to the brain. c. The Cushing reaction increases arterial pressure in response to intracranial pressure.

Page 24: Sensitivity of Carotid Bodies

  • Located in carotid arteries and aortic arch, sensitive to O2 levels.

  • Response to Low O2: Activates vasomotor centers, resulting in vasoconstriction and increased arterial pressure.

Page 25: Regulation by Antidiuretic Hormone (ADH)

  • Mechanism:

    • Detected by hypothalamus for blood water levels.

    • Adjusts ADH secretion affecting kidney function – less water absorption leads to higher urinary output and vice versa.

Page 26: Atrial Natriuretic Peptide (ANP)

  • Physiological Effects:

    • Binds to receptors, reducing blood volume and cardiac output.

    • Inhibits renin secretion; reduces aldosterone secretion and promotes vasodilation.

Page 27: Microcirculation and Lymph

  • Structure: Capillary beds regulated by precapillary sphincters; endothelial layer allows selective permeability.

Page 28: Substances Crossing Capillary Walls

  1. Lipid-soluble: O2 and CO2

  2. Small water-soluble: Water, glucose, amino acids pass via clefts.

  3. Large substances: Cross via pinocytosis; tight junctions in brain (blood-brain barrier).

Page 29: Lymph Function

  • Filtration: Excess fluid from capillaries returns to circulation via lymphatics.

  • Unidirectional Flow: Ensured by valves; maintained by muscle contractions.

  • Edema: Results when interstitial fluid accumulation exceeds transportation capacity.