The Heart

1. Chapter 20 The Heart

2. Heart Anatomy

3. Coverings of the Heart: Anatomy Pericardium – a double-walled sac around the heart composed of: A superficial fibrous pericardium A deep two-layer serous pericardium The parietal layer lines the internal surface of the fibrous pericardium The visceral layer or epicardium lines the surface of the heart They are separated by the fluid-filled pericardial cavity

4. Coverings of the Heart: Physiology The pericardium: Protects and anchors the heart Prevents overfilling of the heart with blood Allows for the heart to work in a relatively friction-free environment

5. Heart Wall Epicardium – visceral layer of the serous pericardium Myocardium – cardiac muscle layer forming the bulk of the heart Endocardium – endothelial layer of the inner myocardial surface

6. The Fibrous Skeleton 4 bands around heart valves and bases of pulmonary trunk and aorta that help stabilize valves & electrically insulate ventricular cells from atrial cells Distribute forces of contraction Add strength and prevent overexpansion of heart Elastic fibers return heart to original shape after contraction

8. Internal Anatomy

9. Left and Right Ventricles

10. Pathway of Blood Through the Heart and Lungs Right atrium ? tricuspid valve ? right ventricle? pulmonary semilunar valve ? pulmonary trunk/arteries ? lungs? pulmonary veins ? left atrium ? bicuspid (mitral) valve ? left ventricle ? aortic semilunar valve ? aorta ? systemic circulation ? superior & inferior vena cavae ?right atrium

11. Cardiac muscle Microscopic anatomy Striations (like skeletal mm) Typically uninucleate Fibers are short, branched and interconnected Plasma membranes of adjacent cardiac cells interlock at intercalated discs

12. Intercalated discs Contain desmosomes Anchor & prevent separation during contraction Contain gap junctions Allow ions to pass freely from cell to cell Transmits depolarizing current across entire heart Allows entire myocardium to behave like a functional syncytium

13. Cardiac Cells vs. Skeletal Fibers

14. Mechanism/events of contraction Automaticity or autorhythmicity Some cardiac muscle cells are self-excitable They can initiate their own depolarization (and therefore the rest of the heart) Remember…skeletal mm cells need to be independently stimulated by a nerve ending to contract

15. Organ vs motor unit contraction Gap junctions cause heart to contract as a whole or not at all via ion passage Remember…in skeletal muscle all cells of a given motor unit contract together but not necessarily all motor units of a given muscle

16. Length of absolute refractory period Cardiac mm refractory period is 30x longer to prevent tetany which would stop the hearts pumping action Cardiac cell contraction ~ 250 ms/refractory period~ 250 ms Skeletal mm contraction ~ 20-100 ms/ refractory period~ 1-2 ms

17. Electrical events of cardiac cntrx 1-influx of Na changes membrane potential from –90 mV to ~+30 mV 2-depol travels thru T-tubules to cause Ca release from SR 3-Ca causes cross-bridge activation Plateau results from Ca surge prolonging depol This allows for sustained contraction needed to eject blood from the heart

18. Energy requirements Cardiac muscle has many more mitochondria 25% of cardiac cell volume Compared to only 2% of volume in skeletal mm cell High resistance to fatigue! Relies almost exclusively on aerobic respiration Cardiac muscles store oxygen in myoglobin Cannot incur an O2 debt and still function normally

19. Electrical events of cardiac mm Intrinsic conduction Non-contractile cardiac cells both initiate & distribute impulses causing depolarization in a sequential pattern allowing the heart to beat as a coordinated unit (functional syncytium) Extrinsic conduction SNS & PsNS

20. Intrinsic conduction Autorhythmic cells have an unstable resting membrane potential continuously drifting towards threshold for firing (called pacemaker potentials or prepotentials) This mechanism is not fully understood but an influx of Ca instead of Na causes the rising phase of the action potential

21. Sequence of excitation of autorhythmic cells 1. Sinoatrial (SA) node…pacemaker In Rt atrial wall (inf to Sup. Vena cava) 2. Atrioventricular (AV) node Inf. Portion of interatrial septum above tricuspid valve 3. AV bundle (Bundle of His) The only electrical connection b/t atria & ventricles & moderator band 4. Rt & Lt bundle branches 5. Purkinje fibers (in ventricular walls)

22. Impulse Conduction through the Heart

23. Arrhythmias Irregular heart beats/rhythms Fibrillation – rapid, irregular, out-of-phase contractions Ectopic focus – defective SA node where another part of the heart must assume its role ie. AV node (junctional rhythm) SA node is called …sinus rhythm Extrasystole – premature contraction (b/f SA node initiates) Heart block – damage to the AV node which inhibits the ventricles from receiving pacing impulses from the SA node

24. Extrinsic innervation SNS – increases both rate and force of contraction PsNS – slows heart rate Brain stem nuclei (in medulla oblongata) Cardioacceleratory center Cardioinhibitory center

25. Autonomic Pacemaker Regulation Rate of spontaneous depolarization depends on: resting membrane potential rate of depolarization ACh (PsNS stimulation): slows the heart NE (SNS stimulation): speeds the heart

26. Cardioacceleratory center Sympathetic center Projects fibers to T1-T5 cord levels Synapse in C & upper T SNS chain ganglia Post-ganglionic fibers run thru the cardiac plexus to heart Parasympathetic center Sends impulses to the dorsal vagus nucleus in the medulla oblongata CN X sends (-) impulses to the heart

27. Electrocardiogram (ECG/EKG) 3 typical deflection waves P wave (atrial depol) – 0.08 s. QRS complex (vent. depol) – 0.08 s. T wave (vent. repol) – 0.16 s. Do not see atrial repol wave b/c it is hidden in the QRS complex

28. Typical EKG graph P-R interval – 0.16 s. From atrial excitation to beginning of ventr. excitation S-T segment Entire vent. myocardium is depolarized Q-T interval – 0.38 s. From vent. depol thru vent. repol.

29. Holter monitor

30. Cardiac cycle All events assoc. w/ the flow of blood thru the heart during one complete heartbeat Atrial systole (systole = contraction) Atrial diastole (diastole = relaxation) Ventricular systole Ventricular diastole Both sides pump same amount of blood with each beat Pressure changes on the left side of the heart are ~5x greater than in the right…why???

31. Cardiac cycle terminology End diastolic volume (EDV) Ventricles have max vol of blood in cycle 70% filling is passive/remaining 30% w/ atria contraction Isovolumetric contraction phase Vents begin to contract…AVs close/Semilunars not yet open (ventricles are ‘closed off completely’) End systolic volume (ESV) Remaining blood in vents after contraction Isovolumentric relaxation phase Chambers totally closed as remaining blood in great vessels flows backward to close semilunar valves Dicrotic notch – brief rise in aortic pressure caused by backflow of blood rebounding off semilunar valves

32. Pressure and Volume in the Cardiac Cycle

33. Cardiac cycle time Assume 75 bpm Cardiac cycle is ~0.8 s. Atrial systole ~0.1 s. Ventricular systole ~0.3 s. Remaining 0.4 s. heart is in total relaxation This is called the quiescent period When heart rate increases: all phases of cardiac cycle shorten, particularly diastole

34. Heart sounds Lub-dub, pause, lub-dub, pause…. Lub – closure of AV valves…vent cntrx Dub – closure of semilunar valves…vent relax Pause – quiescent period Murmurs: Incompetent valves – backflow of blood Normal vibration of thin heart walls Children/elderly

35. AV Valve Function – ‘lub’

36. Semilunar Valve Function – ‘dub’

37. Cardiac output (CO=HR x SV) CO = volume of blood pumped by each ventricle in 1 minute Stroke volume (SV) – amt of blood pumped with each beat Cardiac reserve is the difference between resting and maximal CO Ejection fraction is the percentage of EDV represented by the SV

38. Normal cardiac output HR ~ 75 bpm SV ~ 70 ml/beat CO = 75 x 70 CO = 5250 ml/min (5.25 L/min) Adult blood vol ~ 5L…entire volume of blood passes through each side of the heart once each minute

39. Regulation of stroke volume SV = EDV-ESV Normal SV ~ 70ml/beat…why? EDV ~ 120 ml (length of diast + venous pressure) ESV ~ 50 ml (arterial BP + force of vent cntrx) …each ventricle pumps out ~ 60% of its volume w/ each heartbeat

40. 3 important factors affecting SV 1. Preload – amt vents are stretched by retained blood Frank-Starling law of the heart Stretching of heart mm cause max cross bridging… bigger force of contraction 2. Contractility – increase in contractile strength independent of mm stretch and EDV…extrinsic factors Sympathetic stimulation Hormones (glucagon, thyroxine,epi all stimulate) Calcium and some drugs 3. Afterload – the pressure that blood must overcome for the ventricles to eject blood from the heart

41. Factors Affecting Stroke Volume

42. Vagal tone SNS & PsNS always maintain minimal stimulation to the heart with the PsNS being slightly more dominant a vagotomy causes an immediate increase in RHR by~25 bpm SA node has an inherent sinus rhythm of approx 80-100 bpm AV node generates 40-60 AP’s/min

43. Bainbridge (atrial) reflex Baroreceptors notice increased dilation of atria from increased venous return & result in 1-direct SA node stimulation and 2-baroreceptor triggered (+) adjustments to SNS leads to an increase in both HR and Force of contraction

44. Hormonal regulation of HR Epi/Norepi-(+) to rate & strength of contraction Thyroxine- normally enhances BMR and body heat production slower, more sustained increase in HR as compared to epi/norepi

45. Other factors w/ HR Age fetus 140-160 bpm & declines w/ age Sex females 72-80 bpm males 64-72 bpm Heat heat enhances metabolic rate of cardiac cells cold decreases heart rate Terms: tachycardia - >100 bpm bradycardia - <60 bpm

46. Coronary atherosclerosis

47. Coronary bypass

48. Congestive heart failure CO is so low that blood circulation cannot meet the needs of the tissues usually progressive w/ various causes coronary atherosclerosis increase in aortic bp…increase in ESV…LV hypertrophy MI’s lead to non-contractile scar tissue dilated cardiomyopathy (DCM) - vents become flabby & ineffective

49. Left sided heart failure Pulmonary congestion right side pumps to lungs but left side cannot accommodate returning blood…BV’s in lungs become engorged…pressure increases leaking fluid into tissues…pulmonary edema…person drowns (suffocates) Peripheral congestion Left side pumps to body but right side cannot accommodate returning blood…blood stagnates w/in organs & tissues… cannot effectively exchange O2/wastes edema is most noticeable in extremities (feet/ankles)

50. Developmental Aspects of the Heart By the end of the 3rd week: The embryo has a system of paired vessels The vessels forming the heart have fused

51. Development of Fetal Circulation Unique vascular modifications seen in prenatal development include umbilical arteries and veins, and three vascular shunts (occluded at birth) Ductus venosus – venous shunt that bypasses the liver Foramen ovale – opening in the interatrial septa to bypass pulmonary circulation Ductus arteriosus – transfers blood from the right ventricle to the aorta

52. Circulation in Fetus and Newborn

53. Occlusion of Fetal Blood Vessels Umbilical arteries and vein constrict and become fibrosed Fates of fetal vessels Proximal umbilical arteries become superior vesical arteries and distal parts become the medial umbilical ligaments The umbilical vein becomes the ligamentum teres The ductus venosus becomes the ligamentum venosum The foramen ovale becomes the fossa ovalis The ductus arteriosus becomes the ligamentum arteriosum