Knowt
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
Clinical history of ischemic chest pain lasting > 20 minutes.
Changes in serial ECG tracings.
Rise in cardiac biomarkers (creatine kinase-MB, troponins, myoglobin).
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:
Increased heart rate
Increased contractility/stroke volume
Increased vasoconstriction of arterioles
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
Lipid-soluble: O2 and CO2
Small water-soluble: Water, glucose, amino acids pass via clefts.
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.
