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.