7 Coronary CirculationCoronary arteries are first branches of aorta at sinuses of Valsalva.Provides blood supply to heart during diastole (during resting phase or in between beats).Has left and right coronary branches
8 Left Coronary Artery 2 branches: Left circumflex—goes to left atrium, lateral and posterior ventriclesLeft anterior descending (“widow maker”)—goes to anterior and apex of LV, anterior septum, bundle of His, right and left bundle branches
9 Right Coronary Artery & Venous Drainage Goes to RA, RV, SA and AV nodes, posterior and septumVenous drainage is done by coronary sinus, cardiac veins, and thesbian veins
11 Blood Flow Realize that blood flow within the heart is bilateral Following one deoxygenated RBC:From body—IVC—RA—tricuspic valve—RV—pulmonic valve—pulmonary artery—lungs—pulmonary vein—LA—mitral valve—LV—aortic valve—aorta—to body
13 Cardiac CycleSystole—ventricular contraction—corresponds to “lub” sound which is closure of AV valves. This is the S1 part of cycle.Diastole—relaxation phase and atrial contraction-- corresponds to “dub” sound which is closure of semilunar valves. This is the S2 part of cycle.S3 is aortic valve closing just before pulmonic
14 So…to put it together….Blood from the vena cava and pulmonary artery flows into both atria when ventricles are relaxed and AV (tricuspid and mitral) valves are open.Atria have higher pressure than ventricles so blood pours into ventricles (passive filling).When 75% of blood is in ventricles, other 25% is pushed in by “atrial kick” (active filling).When ventricles are full, the stretch on the chordae tendinae cause the AV valves to snap shut causing the first heart sound (S1).
15 And then………Pressure in ventricles is greater than pressure in great vessels (pulmonary artery and aorta) so…Milliseconds later, the semilunar valves (pulmonic and aortic) open, and the ventricles contract.Blood is forced thru the great vessels.When pressure is low in ventricles, semilunar valves snap shut, causing the second heart sound (S2).
16 Preload & Afterload Preload—amount of stretch in ventricles at end of diastoleAfterload—resistance in great vessels against which ventricles must pump blood into circulation
17 Cardiac Output Cardiac output = Stroke Volume x Heart Rate Stroke volume 70 mL/beat; 4-7 L/min; exercise 20 mL/min. SV is determined by preload, afterload, and contractilityStarling’s Law—greater the stretch, the stronger the contractionHeart rate is controlled by ANS, CNS, and baroreceptors in heartEjection fraction is % of blood ejected by ventricles in one contraction
18 Chemical ConductionContraction depends on exchange of ions across the myocardial cell membrane—Na+, K+, Ca++Polarization—cell is ready to contract with ions in placeDepolarization—ventricular contractionRepolarization—resting phase during which ions are moving back to polarization state
25 Neck Vessels Carotid artery: Transports blood to brain 2nd branch of aortaPulsations are visiblePalpated between thyroid cartilage and SCMCoincides with apical pulse
26 Neck Vessels cont’d Jugular veins: Drain head and neck Return blood to heart via superior vena cava (SVC)Internal is visible in sternal notch in supine positionExternal may be visible superior to clavicle, but is difficult to see unless pt is in heart failure
27 Developmental Differences: Fetal Circulation Review 3 anatomical differences from adult :Foramen ovale—closes within 1 hr after birthDuctus arteriosus—closes within hrsDuctus venosusBlood flow differences:Returning blood enters RA—60% goes thru foramen ovale to LA to LV, then to aorta40% goes to RV into PA, but only 10% goes to lungs. 30% goes to aorta
28 Differences: Infants and Children PMI at 4th ICS, MCL until 7 yrs of ageSinus arrhythmia throughout childhoodSplit S2Faster pulse: 160 to 90Lower BP: 70/40 to 110/70
29 Differences: Older Adults SBP increases 40 mm d/t arterial wall changes causing slight enlargement of LV. No change in DBP.More likely to have arrhythmias, murmurs, extra sounds, bruits, activity intolerance, atypical MI sx, and orthostatic BP
30 Cultural DifferencesAll CV risk factors are higher among Blacks and Hispanics and lower in Asians and Pacific Islanders.Incidence of HD is higher in both male and female African Americans than in other groups and Latino women have higher incidence than white women.