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Cardiovascular Physiology

Cardiovascular Physiology. Electrophysiology of the Heart. Action Potentials Conduction Pathways EKG’s. Autorhythmic Cardiac AP. 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)

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Cardiovascular Physiology

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  1. Cardiovascular Physiology

  2. Electrophysiology of the Heart • Action Potentials • Conduction Pathways • EKG’s

  3. Autorhythmic Cardiac AP • 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 0 3 4

  4. Myocardial Action Potential • 0 – Na+ influx (voltage-gated) • 1 – Na+ inactivation and K+ (IK) outward • 2 – slow inward Ca2+ • 3 – Ca2+ inactivation and K+ outward (IK1) ARP RRP

  5. EKG Waves and Intervals QRS length R T P Q S 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 P-R interval Q-T interval

  6. EKG Reading 0.2 sec 0.04 sec 1.0 mV Test pulse HR = 1500/ small boxes between QRS complexes

  7. EKG Axis Determination Late Ventricular Depolarization Atrial Depolarization Septal Depolarization Apical Depolarization Repolarization Lead I:

  8. 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.

  9. Abnormalities • Rate: • Sinus bradycardia: <60 BPM at rest • Sinus tachycardia: >100 BPM at rest • A/V Heart Block: • 1st degree: P/R interval > 0.2 sec (slow AV node) • 2nd degree (Mobitz): • Type 1 (Wenckebach): slowly increasing PR interval until dropped QRS complex • Type 2: Sudden dropped QRS • 3rd degree (complete): no correlation between P and QRS waves

  10. 1st Degree AV Block- increased P-R interval 2nd Degree (Wenckebach)- increased P-R, then no QRS 2nd Degree (Mobitz II)- Isometric P-R, then no QRS 3rd Degree Preceded by Ventricular Escape no block

  11. Caridac Pump Dynamics • Cardiac Cycle • Pressure • Flow • Resistance • Elastance/Compliance

  12. 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.

  13. Length Tension Relationship Operating Range Tension % Max Active Tension Resting Tension 100 50 1.5 2.2 3.0 Sarcomere Length mm

  14. 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.

  15. 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 b1 agonists or cardiac glycosides (digoxin) Inhibit Na/K ATPase Decrease Ca export Increases inward Ca Causes PLB phosphorylation Activates SERCA

  16. Measuring Contractility

  17. 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.

  18. LV pressure/volume loops Normal Positive Inotropy When does the aortic valve open? When is the 2nd heart sound? Increased Afterload

  19. Electrical-Pump Coupling Diagram e d c • Atrial contraction causes increased atrial and ventricular pressure. • Mitral valve closes (1st heart sound), isovolumetric contraction begins. • Aortic valve opens, aortic pressure equals LV pressure. • Systolic pressure • Aortic valve closes (second heart sound), isovolumetric relaxation begins • Mitral valve opens b f a

  20. PV Loop and Cardiac Cycle

  21. Cardiac and vascular function Curves

  22. Questions

  23. Questions

  24. Pulse Pressure Pulse Pressure = SP-DP

  25. Normal Pressures • Right Atrium (Vena Cava)- 5 (systolic)/3 (diastolic) mmHg • Left Atrium (Pulmonary veins) 10/8 • Right Ventricle – 28/3 • Left Ventricle –125/8 • Aorta- 120/70

  26. Supine vs Standing

  27. 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 - pO2 detectors increase blood pressure in times of low pO2

  28. Central Chemoreceptors pO2 pCO2 H+ Central Chemoreceptors Sympathetic Outflow Contractility, VR, Respiration, Blood Pressure, etc

  29. 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(mL/min) =K[(Pc-Pi)-(pc-pi)] - Fick’s :CO = O2 Uptake / ([Arterial O2] - [Venous O2])

  30. Resistance • Parallel • Most vascular beds • Lower total Resistance • Independent control • Series • Sequential pressure drops • Portal circulations(Hepatic, Hypothalamic Hypophyseal, etc)

  31. Vasoactive Substances • Local • Metabolites (adenosine, K+, CO2) • Neurotransmitters (a1- constriction, b2-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

  32. 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

  33. 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

  34. 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 LaPlace- a dilated heart needs more tension to generate a given pressure • Symptoms: Pulmonary Congestion (edema), dyspnea, orthopnea

  35. Acute Blood Loss/Hemorrhagic Shock Blood Loss Decreased Ven. Return CO, MAP Decrease Compensation Decompensation 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 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

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