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CARDIOVASCULAR SYSTEM

CARDIOVASCULAR SYSTEM . Juliet Ver-Bareng, M.D., FPSP. Outline. Physiologic properties of the heart Electrical properties < Excitability < Automaticity and Rhythmicity < Conductivity Mechanical properties < Contractility < Distensibility Regulation of cardiac activity

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CARDIOVASCULAR SYSTEM

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  1. CARDIOVASCULAR SYSTEM Juliet Ver-Bareng, M.D., FPSP

  2. Outline • Physiologic properties of the heart Electrical properties < Excitability < Automaticity and Rhythmicity < Conductivity Mechanical properties < Contractility < Distensibility • Regulation of cardiac activity Neural control Humoral control

  3. Circulation • Role of the blood vessels • Hemodynamics • Blood Pressure determination • Microcirculation – fluid exchange • Factors affecting venous return • Regulation of blood flow • Regulation of blood pressure

  4. Functions of the heart • Generating blood pressure - contraction of heart is responsible for movement of blood through the blood vessels • Routing blood to two circulation - pulmonary and systemic circulation 3. Ensuring one way blood flow - presence of valves (AV and semilunar valves) • Regulating blood flow - change in heart rate and force of contraction to match blood delivery to the changing metabolic needs of the tissues

  5. Physiologic Properties of the heart • Electrical Properties - Excitability = bathmotropy - Automaticity and Rhythmicity = chronotropy - Conductivity = dromotropy • Mechanical Properties - Contractility = inotropy - Distensibility = lucidotropy

  6. Types of ion channels in the heart

  7. Resting membrane potential • the difference in ionic charge across the membrane of the cell = -70 to -9o mV • resting membrane potential is permeable to K+, and is relatively impermeable to other ions • maintenance of this electrical gradient is due to the: Na+- K+ pump and the Na+- Ca++ exchange mechanism

  8. Electrical Properties A. Excitability – bathmotropy SA node, AV node Myocardia, Purkinje system Slow response AP Fast response AP

  9. Phases of fast response AP 4 = Resting Membrane Potential 0 = Rapid Depolarization 1 = Initial Repolarization 2 = Plateau 3 = Repolarization

  10. Phases of fast response AP Phase 0 - Rapid depolarization - due to opening of the fast Na+ channels and the subsequent rapid increase in the membrane conductance to Na+ (gNa) and a rapid influx of Na+ ions into the cell The fast Na+ channel made up of two gates at rest m gate closed h gate open Upon electrical stimulation of the cell, the m gate opens quickly while simultaneously the h gate closes slowly For a brief period of time, both gates are open and Na+ can enter the cell across the electrochemical gradient

  11. Phases of fast response AP Phase 1 – Initial repolarization - occurs with the inactivation of the fast Na+ channels - the transient net outward current causing the small downward deflection of the action potential is due to the movement of K+ and Cl- ions - Cl- ions movement across the cell membrane results from the change in membrane potential, from K+ efflux, and is not a contributory factor to the initial repolarization ("notch").

  12. Phases of fast response AP Phase 2- Plateauphase - sustained by a balance between inward movement of Ca2+ (ICa) through L-type calcium channels and outward movement of K+ through the slow delayed rectifier potassium channels, Iks.

  13. Phases of fast response AP Phase 3 - Rapid Repolarization phase - L-type Ca2+ channels close, while the slow delayed rectifier (IKs) K+ channels are still open - this ensures a net outward current, corresponding to negative change in membrane potential, thus allowing more types of K+ channels to open - this net outward, positive current (equal to loss of positive charge from the cell) causes the cell to repolarize - the delayed rectifier K+ channels close when the membrane potential is restored to about -80 to -85 mV

  14. Slow response AP Phases 4 - Spontaneous depolarization 0 - Triggered depolarization 3 - Repolarization

  15. Phases of slow response AP Phase 4 – Spontaneous Depolarization - Prepotential - Slow diastolic depolarization • depolarization by themselves • the resting potential of a pacemaker cell (-60mV to -70mV) is caused by; = a continuous outflow or "leak" of K+ through ion channel proteins in the membrane that surrounds the cells = a slow inward flow of Na+, called the funny current = an inward flow of calcium • This relatively slow depolarization continues until the threshold potential is reached • Threshold is between -40mV and -50mV

  16. Phases of slow response AP Phase 0 – Upstroke • Triggered depolarization • The SA and AV node do not have fast sodium channels like neurons, and the depolarization is mainly caused by a slow influx of calcium ions • The calcium is let into the cell by voltage-sensitive calcium channels that open when the threshold is reached.

  17. Phases of slow response AP Phase 3 - Repolarization • The Ca++channels are rapidly inactivated, soon after they open • Sodium permeability is also decreased • Potassium permeability is increased, and the efflux of potassium (loss of positive ions) slowly repolarizes the cell

  18. Ion channel inhibitor/blocker • Na+ channel = phase 0 (fast response - Tetrodotoxin • Ca++ channel = phase 0 (slow response AP) and phase 2 (fast response AP) - Verapamil - Nifidipine - Manganese • K+ channel = phase 3 - Amiodarone

  19. Refractory period • Absolute refractory period - duration when Na channel is closed • Relative refractory period - m gate closing and h gate opening • Super normal period - membrane potential close to the RMP

  20. effective refractory period (ERP) • absolute refractory period (ARP) of the cell • during the ERP, stimulation of the cell by an adjacent cell undergoing depolarization does not produce new, propagated AP → nontetanization of the heart • ERP acts as a protective mechanism in the heart by preventing multiple, compounded action potentials from occurring → limits the frequency of depolarization and therefore heart rate.

  21. Electrical Properties • Automaticity and Rhythmicity = Chronotropy - rate and rhythm prepotential = phase 4

  22. Heart Rate Normal range Bradycardia – vagal stimulation Tachycardia – sympathetic effect Vagal tone

  23. Mechanism of change in heart rate Prepotential: RMP TP Slope RMP TP Slope Parasympathetic ↓  ↓ Sympathetic  ↓ 

  24. Automaticity Pacemaker Discharge rate • SA node = 70 – 80 beats/min = primary pacemaker 2. AV node = 40 – 60 beats/min 3. Purkinje fibers = 30 – 40 beats/min Ectopic beat – successful impulses coming from other pacemaker cells and not from SA node

  25. Arrhythmia • when the heart rate is too fast or too slow or when the electrical impulses travel in abnormal pathways is the heartbeat considered abnormal An arrhythmia may occur for one of several reasons: • Instead of beginning in the sinus node, the heartbeat begins in another part of the heart • The sinus node develops an abnormal rate or rhythm • A patient has a heart block

  26. Abnormal Heart Rhythms

  27. Symptoms of Arrhythmia • Heartbeats are fast or slow, regular or irregular or short or long • Person feels dizzy, light-headed, faint or even loses consciousness • Person is experiencing chest pain, shortness of breath or other unusual sensations along with the palpitations • Palpitations happen when the patient is at rest or only during strenuous or unusual activity • Palpitations start and stop suddenly or gradually

  28. Electrical Properties • Conductivity = Dromotropy Conducting tissues: • SA node • AV node • Internodal tract • Interatrial tract or Bachmann’s bundle 5. Atrial muscles 6. Bundle of His 7. Bundle branches • Purkinje fibers • Ventricular muscles

  29. Conduction time

  30. Conduction of impulses • Physiologic delay – occurs at the AV node Mechanisms: • Size of the fibers - small a. interatrial tracts - enter the AV node b. His-nodal tract – leaves AV node • Contains fewer gap junctions Significance: allows time for ventricular filling

  31. Conduction of impulses Fastest conduction velocity - purkinje fibers Mechanism: fibers have the largest diameter Significance: ensures an almost simultaneous contraction of ventricles

  32. Characteristics of conduction Mechanism • One way direction ARP 2. Decremental sizes of fibers 3. Indefatigable ARP

  33. ECG P wave QRS T wave complex

  34. Basic Information derived from ECG tracings • Heart rate • Origin of excitation • Rhythm = regular or irregular 4. Conduction velocity = PR interval = normal, delayed or blocked • Mean Electrical Axis • Primary cardiac impairment = ST segment • Blood supply = large Q wave, ST segment and T wave

  35. EKG

  36. ECG Large boxes are used to estimate heart rate Measure from QRS to QRS1 large box = 300 bpm2 large boxes = 150 bpm3 large boxes = 100 bpm4 large boxes = 75 bpm5 large boxes = 60 bpm

  37. EKG Normal Sinus Rhythm (NSR) • originates in the SA node and follows the appropriate conduction pathways. • rate is normal, and the rhythm is regular • every beat has a P wave followed by QRS complex • EKG CriteriaRate: 60-100 bpm Rhythm: Regular P waves: look the same and originate from the same locus (SA node)PR interval: 0.12 - 0.20 secQRS: 0.08 -0.12 sec, narrow

  38. EKG: Heart Block First degree: regular rhythm PR interval > 0.12 sec Second degree: Mobitz I: Wenkebach: Rhythm:IrregularPR interval:Progressive lengthening followed by dropped beat QRS's appear to occur in groups. Mobitz II: PR interval:Constant on conducted complexes until a sudden block of AV conduction = P wave is abruptly not followed by a QRS Third degree: P wave: Independent P waves and QRS's (AV dissociation)QRS: wide (>0.12 sec) and slower (30-40 bpm) with ventricular escape rhythm.

  39. EKG Limb leads Precordial leads Mean Electrical Axis -30° to +110° limb leads

  40. Mean Electrical Axis Lead with the tallest QRS complex Perpendicular to the lead with equipotential QRS complex Complimentary Leads: I and aVF II and aVL III and aVR

  41. Mechanical Properties • Contractility – Inotropy Cardiac wall Sarcomere length = 2.2 – 2.6 μm

  42. Excitation-Contraction Coupling

  43. Contractility = Inotropy

  44. Systole = ejection of blood into the circulation

  45. Systole = contraction • Stroke volume = amount of blood ejected per contraction (beat) • Cardiac output = amount of blood ejected per minute

  46. Inotropism (+) = greater force of contraction → more blood ejected = results from an increased Ca++ concentration - sympathetic stimulation = via β2 receptors - epinephrine and norepinephrine - cardiac glycosides (digitalis) (-) = weaker force of contraction → less blood ejected - parasympathetic stimulation - hypoxia - acidosis

  47. Diastole = ventricular filling

  48. Diastole = relaxation = Lucidotropy • End Diastolic Volume (EDV) – amount of blood contained in the ventricle at the end of diastole • End Systolic Volume (ESV) – amount of blood left in the ventricle at the end of systole • SV = EDV - ESV

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