By Dr.Tariq

1. Cardiovascular Physiology and Monitoring Tariq AlZahrani M.D Assistant professor College of medicine King Saud University

4. Cardiac Cell Types • Electrical cells Generate and conduct impulses rapidly • SA and AV nodes • Nodal pathways • No contractile properties • Muscle (myocardial) cells Main function is contraction • Atrial muscle • Ventricular muscle • Able to conduct electrical impulses • May generate its own impulses with certain types of stimuli

5. Atrio-ventricular (AV) node Sino-atrial (SA) node BUNDLE BRANCHES PURKINJE FIBERS

6. INTERCALATED DISC (TIGHT JUNCTION)

7. Nerve impulse Terminology • Resting state The relative electrical charges found on each side of the membrane at rest • Net positive charge on the outside • Net negative charge on the inside • Action Potential Change in the electrical charge caused by stimulation of a neuron

8. Action Potential Terms • Depolarization The sudden reversal of electrical charges across the neuron membrane, causing the transmission of an impulse • Minimum voltage must be met in order to do this • Repolarization Return of electrical charges to their original resting state

9. Automaticity (P Cells) Prepotential, Resting Potential, Diastolic Depolarization Action Potential Repolarization Distribution Of P Cells Factors That Affect Automaticity: Sympathetic and parasympathetic outflow will affect the prepotential phase Temperature RA and SAN stretch Hormones Drugs

10. Conduction Speed A-V nodal conduction: One way conduction A-V nodal Delay (0.1 sec) Factors Affecting Conductivity: Sympathetic and vagal infuince Temperature Hormons Ischemia Acidosis Drugs

11. PHASE Mechanical Response 0 = Rapid Depolarization (inward Na+ current) 1 = Overshoot (outward K+ current) 1 2 0 2 = Plateau (inward Ca++ current) 3 = Repolarization (outward K+ current) 0 MEMBRANE POTENTIAL (mV) 4 = Resting Potential 3 (outward K+ current) (inward Na+ current) 4 -90 TIME

12. ACTION POTENTIALS VENTRICULULAR CELL SAN 1 2 0 0 0 3 0 3 4 -50 -50 MEMBRANE POTENTIAL (mV) 4 -100 -100

14. Ca++ Release

16. THE ANATOMY OF BLOOD VESSELS Layers: Tunica interna (intima) Tunica media Tunica externa (adventitia)

17. Comparison of Veins and Arteries Arteries: Veins:

18. The Distribution of Blood

19. Cardiac Output CO = SV x HR • The amount of blood ejected from the ventricle in one minute • Stroke volume Amount of blood ejected from the ventricle in one contraction • Heart rate The # of cardiac cycles in one minute

20. Determination of Stroke Volume • Preload Amount of blood delivered to the chamber Depend upon venous return to the heart Also dependent upon the amount of blood delivered to the ventricle by the atrium • Contractility The efficiency and strength of contraction Frank Starling’s Law • Afterload Resistance to forward blood flow by the vessel walls

21. • End-diastolic volume (110-120 mL) • End-systolic volume (40-50 mL) • Stroke volume (70 mL) • Ejection fraction (60%)

22. Pressure-Volume Loops

23. Volume Load ► Pressure Load ►

24. Regulation of Cardiovascular System Neural Mechanisms Vasoconstriction Vaosdilation Baroreceptors Chemoreceptors

25. Nerve Supply of the Conduction System

27. HORMONAL REGULATION Epinephrine & Norepinephrine From the adrenal medulla Renin-angiotensin-aldosterone Renin from the kidney Angiotensin, a plasma protein Aldosterone from the adrenal cortex Vasopressin (Antidiuretic Hormone-ADH) _ ADH from the posterior pituitary ANP from RA

28. RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM Angiotensinogen (renin substrate) Angiotensin Aldosterone Kidney sodium & water retention  BP (Kidney) Renin Vasoconstriction Venoconstriction

29. VASOPRESSIN (ANTIDIURETIC HORMONE) Hypothalamic Osmoreceptors  BP via Posterior Pituitary  Vasopressin (ADH) Vasoconstriction  Water Venoconstriction Retention

33. How To interpret ECG? 1. Rate? 2. QRS Duration? 3. Stability?

34. ECG limb leads

36. Normal ECG

38. QRS complex corresponds to ventricular Depolarization

39. T wave corresponds to ventricular repolarization

41. Remember This 3, 3, 3 and 5 P duration = 3 small sqs = 0.12 sec. P height = 3 small sqs = 0.12 sec. QRS duration=3 small sq=0.12 sec. P-R interval = 5 small sq = 0.2 sec.

42. Right ventricular hypertrophy (precordial leads)

43. Left ventricular hypertrophy (precordial leads)

44. QRS voltage decrease • Myocardial infarction (decrease of excitable myocardium mass) • Fluids in the pericardium (short-circuits of currents within pericardium) • Pulmonary emphysema (excessive quantities of air in the lungs)

45. J-point: -Time point of completeddepolarization (zero reference) -The junction of the QRS and the ST segment ST-segment shift – sign of current of injury

46. Injury currents: constant source • Mechanical trauma • Infectious process • Ischemia

47. Ischemia=ST depression or T-wave inversion Represents lack of oxygen to myocardial tissue

48. Injury = ST elevation -- represents prolonged ischemia; significant when > 1 mm above the baseline of the segment in two or more leads

49. Infarct = Q wave— represented by first negative deflection after P wave; must be pathological to indicate MI

53. I, aVL, V5 + V6 = Lateral Wall = Circumflex Artery Blockage

54. Rate If regular: Divide 300/ number of large squares between 2 Rs = HR If irregular: count number of complexes in 6 sec. and multiply by 10 - Normal 60 -100 - Bradycardia < 60 - Tachycardia > 100 P = Sinus No P = Non sinus

55. Supraventricular Rhythm Rate > 100. QRS: Narrow. Stable or unstable. Rate < 60. QRS: Narrow. Stable or unstable. Sinus bradycardia. 1st degree HB. 2nd degree HB. Complete HB. Sinus tachycardia. PSVT. Atrialflutter. Atrial fibrillations.

56. Supraventricular Rhythm: Tachycardia Sinus Tachycardia

57. Supraventricular Rhythm: Tachycardia Paroxysmal SVT

58. Supraventricular Rhythm: Tachycardia Atrial Flutter

59. Supraventricular Rhythm: Tachycardia Atrial Fibrillations

60. Supraventricular Rhythm: Bradycardia Normal Sinus Rhythm Sinus Bradycardia

61. Supraventricular Rhythm: Bradycardia 1st Degree HB

62. Supraventricular Rhythm: Bradycardia 2nd Degree HB: Mobitz 1 Wenckebach. Progressive lengthening of the P-R interval with intermittent dropped beat.

63. Supraventricular Rhythm: Bradycardia 2nd Degree HB: Mobitz 2 Sudden drop of QRS without prior P-R changes

64. Supraventricular Rhythm: Bradycardia 3rd Degree HB

65. The right bundle brunch block (precordial leads)

66. Left bundle branch block (precordial leads)

67. Characteristics of PVCs • QRS prolongation due to slower conduction in the muscle fibers • QRS high amplitude due to lack of synchrony of excitation of RV and LV which causes partial neutralization of their contribution to the ECG • QRS and T-wave have opposite polarities, again due to slow conduction which causes repolarization to follow depolarization.

68. Ventricular Rhythm Idioventricular Rhythm.

69. Ventricular Rhythm Accelerated Idioventricular Rhythm.

70. Ventricular Rhythm

71. Ventricular Rhythm

72. Ventricular Rhythm Pacer Rhythm

73. Stability * Stable patient: think of drug therapy. * Unstable patient: think of electric therapy.

74. Treatment Supraventricular Rhythm: Stable = Drugs Adenosine. B blocker. Ca channel blocker. Digoxin. Unstable = Electric DC, Synchronized

75. Treatment Ventricular Rhythm: Stable = Drugs Amiodarone. Lidocaine. Procainamide. Unstable = Electric DC, Non Synchronized

77. Normal Venous Tracing a ► Atrial Contraction c ► Isometric (V) Contraction x ►Mid-Systole v ►Venous Filling (Atrial) y ►Rapid Filling (Ventricular)

80. THANK YOU