This document discusses the anatomy and physiology of the cardiovascular system. It begins by describing the conduction system of the heart, including the sinoatrial node, atrioventricular node, bundle of His, and Purkinje fibers. It then discusses the membrane potential of ventricular cardiac muscle cells and its relationship to electrocardiograms. Several major cardiovascular reflexes are also outlined, including the arterial baroreceptor reflex. The document provides detailed descriptions of coronary artery anatomy and blood flow regulation to the myocardium. Pathophysiology of ventricular septal defects and their management are summarized.

1. CARDIOVASCULAR
PHYSIOLOGY PART 2
DR IBRAHIM HASSAAN ,MBCHB,MSC,EDAIC
29/04/2023

2. THE CONDUCTION SYSTEM OF HEART
• THE SAN LIES IN THE POSTEROLATERAL WALL OF THE R ATRIUM. 3 INTERNODAL
TRACTS CONNECT THE SAN TO THE AVN WHICH LIES IN THE R ATRIUM BEHIND
THE TRICUSPID VALVE. (P-WAVE)
• THE ATRIA AND VENTRICLES ARE OTHERWISE ELECTRICALLY INSULATED FROM
EACH OTHER BY FIBROUS TISSUE.
• THE DELAY IN CONTRACTION BETWEEN THE ATRIA AND VENTRICLES IS
ESSENTIAL TO ALLOW ADEQUATE TIME FOR VENTRICULAR FILLING FROM ATRIAL
CONTRACTION AND IS ACHIEVED BY THE AVN. THIS IS ACHIEVED BY A
REDUCTION IN THE NUMBER OF GAP JUNCTIONS BETWEEN THE ADJACENT CELLS
AND TRANSMISSION IN A UNIDIRECTIONAL MANNER. (PR INTERVAL)

3. • THE NEXT TRACTS ARE AVN BUNDLE OF HIS L AND R BUNDLE BRANCHES
PURKINJE FIBRES. THE LBB DIVIDES INTO ANTERIOR AND POSTERIOR FASCICLES.
• THE PURKINJE FIBRES EXIST THROUGHOUT THE VENTRICULAR SYNCYTIUM AND
ARE LARGE ALLOWING VERY FAST TRANSMISSION OF APS. (QRS COMPLEX)

5. THE MEMBRANE POTENTIAL OF VENTRICULAR CARDIAC MS
,ECG RELATION , IONIC RULES AND THE DIFFERENCES
BETWEEN CARDIAC AND NERVE POTENTIAL

6. MAJOR CARDIOVASCULAR REFLEXES
• ARTERIAL BARORECEPTOR
• BEZOLD-JARISCH
• BAINBRIDGE

7. ARTERIAL BARORECEPTOR
HIGH-PRESSURE ARTERIAL BARORECEPTORS:
LOCATED WITHIN THE WALLS OF THE AORTIC ARCH AND CAROTID SINUS
TO CONTROL PERFUSION PRESSURES TO THE CORONARY AND CEREBRAL CIRCULATIONS.
THEY ARE INVOLVED IN THE RAPID SHORT-TERM CONTROL OF BLOOD PRESSURE.
LOW-PRESSURE BARORECEPTORS:
LOCATED IN THE CHAMBERS OF THE HEART, LARGE SYSTEMIC VEINS AND THE PULMONARY
VASCULATURE.
THESE RECEPTORS BRING ABOUT CHANGES IN BLOOD VOLUME AND ARE INVOLVED IN THE
SLOWER AND SUSTAINED CONTROL OF BLOOD PRESSURE

8. THE HIGH-PRESSURE
BARORECEPTORS WORK
• THE AORTIC ARCH AND CAROTID SINUS BARORECEPTORS DISCHARGE IMPULSES ALONG
THE VAGUS AND GLOSSOPHARYNGEAL NERVES, RESPECTIVELY, TO THE NUCLEUS
TRACTUS SOLITARIUS IN THE MEDULLA. HERE,
• THE VASOMOTOR AND CARDIO INHIBITORY CENTERS MODULATE SYMPATHETIC AND
PARASYMPATHETIC OUTFLOW, IN TURN RESTORING BLOOD PRESSURE TOWARDS
NORMAL.
• AS BLOOD PRESSURE RISES, THE RATE OF DISCHARGE ALONG THESE NERVES INCREASES,
LEADING TO A REDUCTION IN SYMPATHETIC OUTFLOW AND INCREASE IN
PARASYMPATHETIC TRANSMISSION.
• AS THIS SYSTEM RELIES ON NEURAL TRANSMISSION, IT IS EXTREMELY FAST AND IS
RESPONSIBLE FOR THE BEAT-TO-BEAT CONTROL OF BLOOD PRESSURE.
• ALTHOUGH HIGH-PRESSURE BARORECEPTORS RESPOND TO BOTH A RISE AND A FALL IN

9. MAJOR CARDIOVASCULAR REFLEXES

10. THE CORONARY CIRCULATION
• THE TOTAL CORONARY BLOOD FLOW IS ABOUT 250 ML/MIN, WHICH EQUATES
TO 5% OF THE CARDIAC OUTPUT.
• MAY INCREASE UP TO FIVEFOLD DURING STRENUOUS EXERCISE
• MYOCARDIAL O2 EXTRACTION IS GREATER IN THE HEART (AROUND 70% AT
REST) THAN IN ANY OTHER ORGAN; IN CONTRAST, RESTING SKELETAL MUSCLE
O2 EXTRACTION IS ONLY 25%.

11. THE CORONARY CIRCULATION
RIGHT CORONARY ARTERY:
• ARISES FROM THE ANT AORTIC SINUS,
• THE RCA SUPPLIES THE RA, RV, SA NODE(65% ) AND AV NODE (80%) & REST OF THE
CONDUCTING SYSTEM IN 80%
• IT TRAVELS ALONG THE RIGHT AV GROOVE, BEFORE DIVIDING INTO:
*THE SA BRANCH
*THE RIGHT MARGINAL ARTERY, TOWARDS THE APEX AND SUPPLIES THE RV
*THE RIGHT CORONARY ARTERY CONTINUES IN THE AV GROOVE UNTIL IT REACHES
THE POSTERIOR INTERVENTRICULAR GROOVE WHICH SUPPLIES THE POSTERIOR PART
OF THE SEPTUM AND THE AV NODE.
‘LEFT DOMINANCE’. IN AROUND 15% OF THE POPULATION, THE POSTERIOR
INTERVENTRICULAR ARTERY IS NOT A BRANCH OF THE RIGHT CORONARY ARTERY,
BUT IS INSTEAD A BRANCH OF THE LEFT CIRCUMFLEX ARTERY

12. THE LEFT CORONARY ARTERY
• ARISES FROM THE LEFT POSTERIOR AORTIC SINUS.
• SUPPLIES THE LA, AVAND MOST OF THE AV SEPTUM
• THE LEFT CORONARY ARTERY TRAVELS A SHORT DISTANCE IN THE LEFT ATRIOVENTRICULAR
(AV) GROOVE (LESS THAN 2.5 CM) BEFORE BIFURCATING INTO
• THE LEFT ANTERIOR DESCENDING (LAD) ARTERY (LEFT INTERVENTRICULAR ARTERY).
• THE LEFT CIRCUMFLEX ARTERY.

13. THE VENOUS DRAINAGE OF THE HEART
THE CORONARY SINUS LIES IN THE RIGHT ATRIUM BETWEEN THE SUPERIOR AND INFERIOR VENA
CAVAL OPENINGS.
• THE MAIN VEINS DRAINING INTO THE CORONARY SINUS ARE
*GREAT CARDIAC VEIN, WHICH ACCOMPANIES THE AIVA
*MIDDLE CARDIAC VEIN, WHICH LIES IN THE INFERIOR INTERVENTRICULAR GROOVE
* SMALL CARDIAC VEIN, WHICH ACCOMPANIES THE MARGINAL BRANCH OF THE RIGHT CORONARY
ARTERY
*OBLIQUE VEIN, WHICH DRAINS THE POSTERIOR HALF OF LEFT ATRIUM
THE ANTERIOR CARDIAC VEINS ARE SMALL VEINS THAT ARISE ON THE ANTERIOR SURFACE OF THE
RV AND DRAIN INTO THE RA.
THE THEBESIAN VEINS, THE SMALLEST OF THE CARDIAC VEINS, DRAIN DIRECTLY INTO THE FOUR
CHAMBERS OF THE HEART. THE THEBESIAN VEINS ARE PREDOMINANTLY FOUND IN THE RA AND RV.
NOTE: THE FEW THEBESIAN VEINS THAT DRAIN INTO THE LEFT SIDE OF THE HEART (CONTRIBUTE TO
ANATOMICAL SHUNT)

14. BLOOD FLOW TO THE MYOCARDIUM
• THE CORONARY ARTERIES RUN ALONG THE EPICARDIAL SURFACE, AND THEIR ARTERIOLES
PENETRATE INTO THE MYOCARDIUM AT AN APPROXIMATE RIGHT ANGLE.
THE LV
DURING SYSTOLE, THE PRESSURE WITHIN THE CONTRACTING MUSCLE OF THE LV EXCEEDS CORONARY
ARTERIAL PRESSURE; THE INTRAMUSCULAR ARTERIOLES ARE COMPRESSED, PREVENTING BLOOD FLOW
TO THE MYOCARDIUM.
DURING DIASTOLE, THE HEART RELAXES AND ITS PRESSURE FALLS; BLOOD FLOW TO THE MYOCARDIUM
RESUMES BLOOD FLOW TO THE LV IS THEREFORE INTERMITTENT.
THE RV
THE PRESSURE GENERATED WITHIN THE RV IS MUCH LESS THAN THAT OF THE LV; THE RIGHT
VENTRICULAR MYOCARDIUM IS THEREFORE PERFUSED THROUGHOUT THE CARDIAC CYCLE

15. BLOOD FLOW TO THE MYOCARDIUM

16. HOW IS CORONARY BLOOD FLOW
AUTOREGULATED
• METABOLIC: INCREASED MYOCARDIAL ACTIVITY, LOCAL TISSUE HYPOXIA AND INCREASED
METABOLIC WASTE PRODUCTS SUCH AS H+, K+, ADENOSINE AND CO2 CAUSE VASODILATATION OF
THE CORONARY VESSELS, THEREBY INCREASING CORONARY BLOOD FLOW
• MYOGENIC: WHEN THE PRESSURE WITHIN A SMALL ARTERY OR ARTERIOLE IS INCREASED, THE
SMOOTH MUSCLE WITHIN THESE VESSELS AUTOMATICALLY CONSTRICTS,.
• ENDOTHELIAL: VARIOUS VASOACTIVE SUBSTANCES INCLUDING (NO), ENDOTHELIUM-DERIVED
RELAXING FACTOR (EDRF) AND (PGI2), ALL OF WHICH PRODUCE VASODILATATION; CONVERSELY
ENDOTHELIN AND THROMBOXANE A2 PRODUCE VASOCONSTRICTION.
• AUTONOMIC:
• HORMONAL: ATRIAL NATRIURETIC PEPTIDE CAUSES VASODILATATION WHILE VASOPRESSIN AND
ANGIOTENSIN II CAUSE VASOCONSTRICTION.

17. WHAT IS THE PATHOPHYSIOLOGY OF VSD
LESION CONSISTS OF AN OPENING BETWEEN THE LEFT VENTRICLE (LV) AND THE
RIGHT VENTRICLE (RV), CAUSED BY A DEFECT IN THE WALL THAT SEPARATES
THESE TWO CHAMBERS, THE INTERVENTRICULAR SEPTUM (IVS).

18. VSDS MAY RESULT IN:
• SHUNTING – BLOOD FLOW ACROSS THE DEFECT;
• PULMONARY HYPERTENSION;
• CONGESTIVE HEART FAILURE (CHF).
THE MAJOR DETERMINANTS OF THE HAEMODYNAMIC STATE OF A PATIENT WITH VSD ARE:
• VSD SIZE;
• SYSTEMIC VASCULAR RESISTANCE (SVR);
• PULMONARY VASCULAR RESISTANCE (PVR);
• ASSOCIATED ANOMALIES (AORTIC INSUFFICIENCY, OBSTRUCTION TO LV OR RV OUTFLOW
TRACTS).
IF THE VSD IS SMALL ENOUGH TO LIMIT SHUNTING BY CREATING RESISTANCE TO BLOOD FLOW,
IT IS CALLED RESTRICTIVE. WHEN THERE IS NO RESISTANCE TO BLOOD FLOW ACROSS THE VSD, IT

19. THERE ARE FOUR TYPES OF VSDS
PERIMEMBRANOUS THE MOST FREQUENT TYPE; THEY INVOLVE THE MEMBRANOUS SEPTUM,
BORDERED BY THE AV VALVE, THE TRICUSPID VALVE IS OFTEN ABNORMAL
MUSCULAR (CAN BE SUBDIVIDED ACCORDING TO LOCATION, SUCH AS APICAL, CENTRAL,
MARGINAL)
5 TO 20% OF DEFECTS, THE SECOND MOST COMMON FORM OF VSDS
INLET (ALSO CALLED AV CANAL, AV SEPTUM)
5 TO 10% OF VSDS
LOCATED ON THE AREA OF THE SEPTUM ,IMMEDIATELY INFERIOR TO THE TRICUSPID
VALVE;
SUBARTERIAL 5 TO 7% OF DEFECTS; LOCATED BELOW THE PULMONARY VALVE
(SUBPULMONARY)

20. CLASSIFICATION BY SIZE
BASED ON MAXIMUM DIAMETER OF VSD WHEN COMPARED TO NORMAL SIZE OF AORTIC
VALVE ANNULUS
• SMALL – LESS THAN 1/3 OF NORMAL AORTIC VALVE ANNULUS DIAMETER;
• MODERATE – 1/3 TO 2/3 OF THE DIAMETER OF THE AORTIC VALVE ANNULUS;
• LARGE – MORE THAN 2/3 OF NORMAL AORTIC VALVE ANNULUS SIZE.
BASED ON AMOUNT OF PULMONARY BLOOD FLOW RELATIVE TO SYSTEMIC BLOOD FLOW
(QS) – QP:QS RATIO
• SMALL – QP:QS RATIO LOWER THAN 1.5;
• MODERATE – QP:QS RATIO OF 1.5 TO 2.0;
• LARGE – QP:QS RATIO HIGHER THAN 2.0.

21. MANAGEMENT
CHILDREN WITH SMALL (RESTRICTIVE) VSDS USUALLY DO NOT REQUIRE ANY MEDICAL
OR SURGICAL THERAPY, SINCE THEY ARE USUALLY ASYMPTOMATIC AND RATE OF
SPONTANEOUS CLOSURE IS HIGH.
SPONTANEOUS CLOSURE OF VSDS OCCURS IN
• MUSCULAR DEFECTS UP TO 80%
• PERIMEMBRANOUS DEFECTS WILL OFTEN CLOSE SPONTANEOUSLY
• SUBARTERIAL VSDS SPONTANEOUS CLOSURE OF MAY OCCUR
• INLETIT IS RARE.
• BABIES WITH MODERATE OR LARGE DEFECTS WILL FREQUENTLY NEED MEDICAL
THERAPY (DIURETICS)
AND SURGERY, AS THEY WILL LIKELY DEVELOP CONGESTIVE HEART FAILURE.

22. SURGICAL MANAGEMENT
INDICATIONS FOR SURGERY
• CONGESTIVE HEART FAILURE AND / OR FAILURE TO THRIVE (REFRACTORY TO
MEDICAL THERAPY);
• MODERATE OR LARGE DEFECTS, UNLIKELY TO CLOSE SPONTANEOUSLY (WITH OR
WITHOUT SYMPTOMS);
• DEVELOPMENT (OR PROGRESSION) OF AORTIC VALVE LEAFLET PROLAPSE AND /
OR AORTIC INSUFFICIENCY;
• ASYMPTOMATIC (OLDER) CHILDREN WITH QP:QS RATIO HIGHER THAN 2.0