1. Cardiovascular Physiology and Monitoring
Tariq Alzahrani M.D
Assistant Professor
College of Medicine
King Saud University

3. Coronary Circulation Blood Supply RCA LCA Conduction System SAN AVN
Coronary Perfusion Pressure
(50-120mmHg)
ADBP – LVEDP

4. Cardiac Cell Types • Electrical cells • Muscle (myocardial) 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. MEMBRANE POTENTIAL (mV)
PHASE
Mechanical Response
0 = Rapid Depolarization
(inward Na+ current)
1 = Overshoot
(outward K+ current) 1 2
2 = Plateau
(inward Ca++ current)
3 = Repolarization
(outward K+ current)
MEMBRANE POTENTIAL (mV)
4 = Resting Potential 3
(outward K+ current)
(inward Na+ current) 4
-90
TIME

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

13. Cardiac Myocyte
Structure
Ca++ Release
Excitation-Contraction Coupling

14. The Fibrous A-V Ring

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

16. Comparison of Veins and Arteries
Arteries: Veins:

17. The Distribution of Blood

18. 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

19. 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

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

21. Pressure-Volume Loops

22. Volume Load ►
Pressure Load ►

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

24. Nerve Supply of the Conduction System
Receives right vagal and right sympathetic supply
SAN
Receives left vagal and left sympathetic supply
AVN
The rest of the conduction system receive sympathetic supply (like ventricle)

26. 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

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

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

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

33. ECG limb leads

35. Normal ECG

36. P wave corresponds to depolarization of SA node
QRS complex corresponds to ventricular Depolarization
T wave corresponds to ventricular repolarization
Atrial repolarization record is masked by the larger QRS complex

37. Measurements Small square = 0.04 sec.
Large square = 5 small square = 0.2 sec.
One second = 5 large square.
One minute = 300 large square.

38. 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.

39. Right ventricular hypertrophy (precordial leads)

40. Left ventricular hypertrophy (precordial leads)

41. 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)

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

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

44. Ischemia= ST depression or T-wave inversion
Represents lack of oxygen to myocardial tissue
ST depression is where the ST segment drops below the baseline of the QRS segment; T wave inversion is where the T wave (following the QRS) is opposite the R wave (most often see flipped T’s)

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

46. Infarct = Q wave — represented by first negative deflection after P wave; must be pathological to indicate MI
Some patients can have normal Q waves; in order for it to be considered “pathologic”, or indicative of transmural MI, the Q wave must be > 0.04 sec wide and 1/3 or > the height of the R wave

47. What part of the heart is affected ?
II, III, aVF =
Inferior Wall I II
III
aVR
aVL
aVF V1 V2 V3 V4 V5 V6

48. Which part of the heart is affected ?
Leads V1, V2, V3, and V4 =
Anterior Wall MI I II
III
aVR
aVL
aVF V1 V2 V3 V4 V5 V6

49. What part of the heart is affected ?
I, aVL, V5 and V6
Lateral wall of left ventricle I II
III
aVR
aVL
aVF V1 V2 V3 V4 V5 V6

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

51. Rate - Normal 60 -100 - Bradycardia < 60 - Tachycardia > 100
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
- Bradycardia < 60
- Tachycardia > 100
P = Sinus
No P = Non sinus

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

53. Supraventricular Rhythm: Tachycardia
Sinus Tachycardia

54. Supraventricular Rhythm: Tachycardia
Paroxysmal SVT

55. Supraventricular Rhythm: Tachycardia
Atrial Flutter

56. Supraventricular Rhythm: Tachycardia
Atrial Fibrillations

57. Supraventricular Rhythm: Bradycardia
Normal Sinus Rhythm
Sinus Bradycardia

58. Supraventricular Rhythm: Bradycardia
1st Degree HB

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

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

61. Supraventricular Rhythm: Bradycardia
3rd Degree HB

62. The right bundle brunch block (precordial leads)

63. Left bundle branch block (precordial leads)

64. 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.

65. Ventricular Rhythm
Idioventricular Rhythm.

66. Accelerated Idioventricular Rhythm.

67. Ventricular Rhythm

68. Ventricular Rhythm

69. Ventricular Rhythm
Pacer Rhythm

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

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

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

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

77. THANK YOU