Cardiac Anatomy and Physiology II

1. Cardiac Anatomy and Physiology II Vincent Conte, MD Clinical Assistant Professor FIU College of Nursing Nurse Anesthesia Program

2. Coronary Artery Anatomy • The Heart is an aerobic organ that depends on a constant supply of oxygen to meet its high metabolic demands • It requires an elaborate arterial and venous network to ensure that myocardial cells are adequately supplied with oxygen • The arterial system consists of epicardial and subendocardial vessels

3. Coronary Circulation • The epicardial vessels are located superficially and most commonly become obstructed at areas of bifurcation where blood flow is turbulent rather than laminar • Significant obstruction (>50%) can result in myocardial ischemia or infarction as a result of increased resistance to flow across the stenotic areas

6. ECG and Coronary Anatomy

7. Coronary Circulation • The RIGHT coronary artery (RCA) normally supplies the right atrium, most of the RIGHT ventricle and a variable portion of the LEFT ventricle (the Inferior wall) • In 85% of persons, the RCA gives rise to the POSTERIOR DESCENDING ARTERY (PDA) which supplies the septum and inferior wall • This is referred to as a “RIGHT Dominant Circulation”

8. Coronary Circulation • In the remaining 15% of people, the PDA is a branch of the LEFT coronary artery • This is called a “LEFT Dominant Circulation” • The LEFT coronary artery normally supplies the LEFT atrium, most of the interventricular septum and the LEFT ventricle

9. Coronary Circulation • After a short course, the LEFT MAIN coronary artery bifurcates into the LEFT ANTERIOR DESCENDING (LAD) and the CIRCUMFLEX Artery (CX) • The LAD supplies the septum and anterior wall and the CX supplies the lateral wall • The arterial supply to the SA node is derived from the RCA in 60% of people, and from the LAD in the remaining 40%

12. Coronary Perfusion • Coronary perfusion is unique in that it is INTERMITTENT rather than continuous • During contraction, intramyocardial pressures approach that of systemic pressures completely occluding the intramyocardial portions of the coronary arteries

13. Coronary Perfusion • Thus, Coronary perfusion pressure is usually determined by the difference between aortic pressure and ventricular pressure and the left ventricle is almost totally perfused entirely during DIASTOLE • As a determinant of myocardial blood flow, arterial diastolic pressure is MORE important than Mean Arterial Pressure (MAP)

15. Coronary Perfusion • Decreases in Aortic pressure or increases in ventricular end-diastolic pressures can reduce coronary perfusion • Increases in heart rate also decrease coronary perfusion because the faster the heart beats, the less time there is for diastole for perfusion to take place

17. Coronary Perfusion • Coronary blood flow normally parallels myocardial metabolic demand • Under normal conditions, changes in myocardial blood flow are entirely due to variations in coronary arterial tone in response to metabolic demand • Hypoxia causes coronary vasodilation through the release of Adenosine

18. Coronary Perfusion • Autonomic innervation is primarily Sympathetic in nature • B2 receptors are stimulated during sympathetic Activity and cause coronary vasodilation • Parasympathetic activity on the coronary vasculature is generally minor and weakly vasodilatory

19. Coronary Perfusion • Myocardial oxygen demand is usually the most important determinant of myocardial blood flow • The myocardium extracts 65% of the oxygen in the arterial blood, compared to 25% in other tissues • Therefore the myocardium cannot compensate for reductions in blood flow by extracting more oxygen from the blood

20. Coronary Perfusion • Any increases in myocardial oxygen demand must be met by an increase in coronary blood flow • Heart rate and to a lesser extent, ventricular end-diastolic pressure are important determinants of both supply and demand

22. Ventricular Pressure-Volume Diagrams

23. Pressure/Volume Loop • Analysis of pump function can be simplified by simultaneous measurements of chamber size and pressure obtained during the entire cardiac cycle • This relationship can be plotted as ventricular volume versus ventricular pressure or as a PRESSURE/VOLUME LOOP

25. Pressure/Volume Loop • The Loop can be divided up into 4 distinct phases • Phase 1: D to A During early and mid-ventricular diastole, filling of the ventricle is passive. In late diastole the atrium contracts (“a” wave) which results in the final end-diastolic volume (LVEDV) and pressure (LVEDP)

27. Pressure/Volume Loop 2) Phase II: A to B Isovolumetric (isometric) contraction results in progressive rise in pressure with little change in volume. This corresponds to isometric contraction of the isolated muscle preparation

29. Pressure/Volume Loop 3) Phase III: B to C When intraventricular pressure exceeds aortic pressure the aortic valve opens (B) and ejection begins. At point (C) the aortic valve closes when ventricular pressure drops below diastolic pressure

31. Pressure/Volume Loop 4) Phase IV (C to D): This is the period of isovolumetric relaxation. No change in volume occurs until left ventricular pressure falls below left atrial pressure and the mitral valve opens

33. Pressure/Volume Loop • Several important points are derived from these diagrams regarding the diastolic pressure/volume relationship • Large changes in ventricular volume can occur with only small changes in ventricular diastolic pressure • Large changes in ventricular pressure can occur with only small changes in ventricular volume

34. Pressure/Volume Loop 3) The left ventricular diastolic volume (LVDV) and the left ventricular diastolic pressure (LVDP) DO NOT have a predictable relationship 4) The atrium is an important “Booster Pump” which completes filling. Normal synchronous atrial contraction contributes 15-20% of the end-diastolic volume

36. Pressure/Volume Loops in various Pathological States

38. Aortic Stenosis • Note the pressure rise during diastole is slightly steeper than in the normal curve • This reflects the decreased ventricular compliance and the diastolic pressures are correspondingly elevated for a given diastolic volume • The extremely high systolic pressure rise is the most distinguishing characteristic of this pressure/volume loop

40. Mitral Stenosis • The pressure/volume loop of MS is similar to the normal curve since Left ventricular function is usually normal • Reduced left ventricular preload causes a decrease in LVEDP and stroke volume • Often peak systolic pressure is lower than normal

42. Aortic Insufficiency • The loop demonstrates two different scenarios; Acute Aortic Insufficiency and Chronic Aortic Insufficiency • The loop for CHRONIC AI (#2) shows minimally elevated LVEDP despite the enormous increase in diastolic volume, a reflection of the highly compliant left ventricle

43. Aortic Insufficiency • With the chronic AI since the aortic pressure is low, isovolumetric contraction is brief and ejection begins early • The loop for acute aortic insufficiency demonstrates the more rapid rise in diastolic filling pressure because the ventricle is operating on the steep portion of its normal pressure/volume curve • Stroke volume, EF and peak systolic pressure are all reduced

45. Mitral Insufficiency • Note that there is very little increase in LVEDP until very large end-diastolic volumes are reached • This is a reflection of the highly compliant left ventricle • Since regurgitant ejection into the left atrium begins almost immediately, the isovolumetric phase of ventricular systole is virtually eliminated

46. Break Time!!!

47. Cardiovascular Monitoring

48. Monitoring • Basically the monitors that you will be using for cardiac patients are: • A-Line (radial, femoral) • CVP (Triple lumen most common) • Introducer • Swan Ganz Catheter

49. Invasive Arterial Pressure Monitoring • The indications for invasive arterial blood pressure monitoring are: • Induced Hypotension • Anticipation of wide blood pressure swings • End-organ disease requiring beat-to-beat blood pressure regulation • The need for frequent ABG analysis

50. A-Lines • CONTRAINDICATIONS to A-line placement are: • Catheterization should be avoided in arteries w/o documented collateral blood flow • Catheterization should be avoided in extremities where there is pre-existing vascular insufficiency (Raynaud’s disease)