Cardiovascular Physiology Electrophysiology of the Heart Action Potentials
- Slides: 36
Cardiovascular Physiology
Electrophysiology of the Heart • Action Potentials • Conduction Pathways • EKG’s
Autorhythmic Cardiac AP 0 3 4 • Phase 4 Depolarization • only SA, AV, His/P • I(f) - “Funny” current, now thought to be inward Na+ • Phase 0 Depolarization • due to Ca++ influx • (L-type) • Officially, no phase 1 or 2 • Phase 3 Repolarization • Due to K+ permeability
Myocardial Action Potential ARP RRP • 0 – Na+ influx (voltage-gated) • 1 – Na+ inactivation and K+ (IK) outward • 2 – slow inward Ca 2+ • 3 – Ca 2+ inactivation and K+ outward (IK 1)
EKG Waves and Intervals QRS length R T P Q S P-R interval Q-T interval Normal: PR interval: 0. 12 -0. 2 sec QRS length: <0. 10 sec QT interval: 0. 3 -0. 4 sec Abnormalities in: QRS – ventricular depolarizaton problems P-R interval – A/V conduction problems
EKG Reading 0. 2 sec 0. 04 sec 1. 0 m. V Test pulse HR = 1500/ small boxes between QRS complexes
EKG Axis Determination Atrial Depolarization Lead I: Septal Depolarization Apical Depolarization Late Ventricular Depolarization Repolarization
Determining Mean Electrical Axis • Use 2 different leads • Measure the sum of the height and the negative depth of the QRS complex • Measure that vaule in mm onto the axis of the lead and draw perpendicular lines • The intersection is at the angle of the mean axis.
Abnormalities • Rate: – Sinus bradycardia: <60 BPM at rest – Sinus tachycardia: >100 BPM at rest • A/V Heart Block: – 1 st degree: P/R interval > 0. 2 sec (slow AV node) – 2 nd degree (Mobitz): • Type 1 (Wenckebach): slowly increasing PR interval until dropped QRS complex • Type 2: Sudden dropped QRS – 3 rd degree (complete): no correlation between P and QRS waves
1 st Degree AV Block- increased P-R interval 2 nd Degree (Wenckebach)- increased P-R, then no QRS 2 nd Degree (Mobitz II)- Isometric P-R, then no QRS 3 rd Degree Preceded by Ventricular Escape no block
Caridac Pump Dynamics • • • Cardiac Cycle Pressure Flow Resistance Elastance/Compliance
Starling’s Law of the Heart • The heart adjusts its pumping rate to the rate of blood return. How? – More blood returning stretches the atria and ventricles more. – Stretching heart SA node muscle causes faster rhythmicity. – Stretching heart muscle causes faster conduction. – Stretching heart muscle causes stronger, more complete contraction.
Tension % Max Length Tension Relationship Operating Range 100 Active Tension Resting Tension 50 1. 5 2. 2 3. 0 Sarcomere Length mm
Preload and Afterload • Preload: Wall tension at EDV (analogous to EDV or EDP – – As Preload increases, so does Stroke Volume. This is a regulatory mechanism. Factors that increase venous return, or preload: • • the muscular pump (muscular action during exercise compresses veins and returns blood to the heart), an increased venous tone, and increased total blood volume. Afterload: A sum of all forces opposing ventricular ejection. Roughly measured as Aortic Pressure. – As Afterload increases, stroke volume decreases.
Contractility • Increased by increasing myocardial Ca++ • Means greater shortening of fibers at a given fiber length. • Increased contractility = Increased CO (SV) – Positive Inotropy: • Increased HR (more Ca++ in the cell) • using b 1 agonists or cardiac glycosides (digoxin) Increases inward Ca Causes PLB phosphorylation Activates SERCA Inhibit Na/K ATPase Decrease Ca export
Measuring Contractility
Mechanisms of increased contractility= regulation of [Ca++] – – – The more crossbridges between actin and myosin are present, the higher the contractility. PK-A phosphorylates the Ca channels through which Ca leaves the SR and enters the myoplasm from the T-tubules. . This causes a greater amount of Ca flux through the channels and a greater net calcium influx into the cell. As sarcomeres shorten, they become less responsive to an increase in Ca++. So, positive inotropic effects work best on a heart that is working under stress. PK-A More Ca++ avail. for later.
LV pressure/volume loops Normal When does the aortic valve open? When is the 2 nd heart sound? Positive Inotropy Increased Afterload
c a b d Electrical-Pump Coupling Diagram e f a. Atrial contraction causes increased atrial and ventricular pressure. b. Mitral valve closes (1 st heart sound), isovolumetric contraction begins. c. Aortic valve opens, aortic pressure equals LV pressure. d. Systolic pressure e. Aortic valve closes (second heart sound), isovolumetric relaxation begins f. Mitral valve opens
PV Loop and Cardiac Cycle
Cardiac and vascular function Curves
Questions
Questions
Pulse Pressure = SP-DP
Normal Pressures – – – Right Atrium (Vena Cava)- 5 (systolic)/3 (diastolic) mm. Hg Left Atrium (Pulmonary veins) 10/8 Right Ventricle – 28/3 Left Ventricle – 125/8 Aorta- 120/70
Supine vs Standing
Controlling Arterial Pressure • • • Increasing TPR, SV, or HR increases Mean Art. Pressure. Increasing Arterial compliance reduces MAP. Baroreceptors – • Aortic Arch, Carotid Body – sense drastic changes in blood pressure, send impulse through CN IX and X to depressor centers and cardiac inhibitory centers Peripheral chemoreceptors – Also in aorta and carotid - p. O 2 detectors increase blood pressure in times of low p. O 2
Central Chemoreceptors p. O 2 p. CO 2 H+ Central Chemoreceptors Sympathetic Outflow Contractility, VR, Respiration, Blood Pressure, etc
Important Formulas - CO=HR x SV = VR in most pts. - Tension =(Pressure inside the chamber x radius) (2 x wall thickness) More generally, T ~ P x R - Mean Art. P. = (1/3 Pulse P. ) + Diast. P - Stroke Volume=EDV-ESV - Ejection Fraction= SV/EDV. Normal EF is 0. 5 -0. 75 - Starling: J(m. L/min) =K[(Pc-Pi)-(pc-pi)] - Fick’s : CO = O 2 Uptake / ([Arterial O 2] - [Venous O 2])
Resistance • Parallel – Most vascular beds – Lower total Resistance – Independent control • Series – Sequential pressure drops – Portal circulations(Hepatic, Hypothalamic Hypophyseal, etc)
Vasoactive Substances • Local – Metabolites (adenosine, K+, CO 2) – Neurotransmitters (a 1 - constriction, b 2 -dilation) – Hormones (Histamine, Bradykinin) • General – Renin-Angiotensin-Aldosterone System – conserves water and salt, constricts arterioles – ADH (Vasopressin) – vasoconstrictor and water conservation – ANP (Atrial Natriuretic Peptide) – arteriolar dilator and increased salt/water excretion
Hyperemia • Active Hyperemia: increased blood flow to meet metabolic demands – Exercising muscle – Active neurons • Reactive Hyperemia: Increased blood flow occurring after a period of inadequate blood flow – Heart after contraction – Transient Ischemic Attack
Special Circulations • Coronary: Mainly metabolic control. – vessels narrow during systole due to mechanical compression • Cerebral: Mainly metabolic. • Muscle: Metabolic and sympathetic during exercise, both symp and some para fibers – muscular activity moves venous blood back to heart • Skin: Sympathetic, Temperature regulated – Cold- vasoconstriction of arterioles, AV shunts take over – Warmth- vasodilation of arterioles • Fetal: Anatomical Shunts – Ductus Arteriosus, Foramen Ovale, Ductus Venosus
Congestive Heart Failure • Left Ventricle can’t pump blood properly • Causes: – HTN, CAD, Alcohol, others – Lead to dilation of the chamber and thinning of the ventricular walls • Law of La. Place- a dilated heart needs more tension to generate a given pressure • Symptoms: Pulmonary Congestion (edema), dyspnea, orthopnea
Acute Blood Loss/Hemorrhagic Shock Decreased Ven. Return Blood Loss tion Compensa Baroreceptor reflexes arteriolar vasoconstriction Chemoreceptor reflexes due to hypoxia Cerebral ischemic response causes further symp. response Increased capillary fluid reabsorption tissue fluid is re-absorbed Endogenous vasoconstrictors Epi, Ang II, Vasopressin RAAS Dec. renal perfusion activates renin, increases ang II, aldo CO, MAP Decrease Decompensa tion Cardiac Hypoperfusion/Failure Decreased CO due to LV ischemia Acidosis Due to lactate buildup Further depresses CO CNS Depression Medullary blood flow decrease leads to inhibition of CV centers Clotting Dysfunctions Pro-coag during early shock Anti-coag during late shock
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