TOPIC 2 Circulatory System – The Heart

1. Biology 221 Anatomy & Physiology II TOPIC 2 Circulatory System – The Heart Chapter 18 pp. 675-710 E. Lathrop-Davis / E. Gorski / S. Kabrhel Interactive Physiology: Cardiovascular System

2. N Function & Size • Function: provide pressure for movement of blood through blood vessels by alternately contracting (systole) and relaxing (diastole) • Size • 250 – 350 grams • extends from 2nd rib to 5th intercostal space

3. Location • within the pericardial cavity in mediastinum of the thoracic cavity • directly posterior to the sternum, ~2/3 lies left of midline Fig. 18.1, p. 677

4. N Pericardium & Pericardial Cavity • Fibrous pericardium – outer layer of pericardial sac • stabilizes heart in mediastinum • Serous pericardium • parietal layer • visceral layer = epicardium http://www.cyber-nurse.com/veetac/horrorctam.htm

5. N Pericardium & Pericardial Cavity • Pericardial cavity • pericardial fluid • Pericarditis – inflammation of the pericardium • normally hinders production of serous fluid • cardiac tamponade –fluid in pericardial cavity increases http://www.cyber-nurse.com/veetac/horrorctam.htm http://www.cyber-nurse.com/veetac/horrorctam.htm

6. N Chambers of the Heart • 2 Atria – receive blood from veins • auricles – fill with blood from venae cavae • coronary sulcus = atrioventricular groove • interatrial septum • fossa ovalis – remnant of foramen ovale • pectinate muscles • Base Fig. 18.4b p. 679

7. N Chambers of the Heart • 2 Ventricles pump blood into arteries • anterior interventricular groove • posterior interventricular groove • interventricular septum • papillary muscles attach to chordae tendineae • trabeculae carneae • Apex Fig. 18.4b p. 679

8. Structure of the Heart Wall Composed of 3 layers: • Epicardium = visceral pericardium • Myocardium • Endocardium Fig. 18.2, p. 677 http://www.cyber-nurse.com/veetac/horrorctam.htm

9. N Structure of the Heart Wall • Epicardium = visceral pericardium • serous membrane • mesothelium • areolar connective tissue • adipose accumulates in grooves • Myocardium • cardiac muscle, blood vessels and nerves • fibrous skeleton • Endocardium – endothelium Fig. 18.2, p. 677

10. N Great Vessels of Heart Arteries – carry blood away from heart • pulmonary artery (trunk) – pulmonary circ. • aorta – systemic circulation Fig. 18.4, p. 679-680

11. N Great Vessels of Heart Veins – return blood to heart • pulmonary veins – pulmonary circulation • superior & inferior venae cavae – systemic circulation • coronary sinus and other coronary veins - coronary circulation Fig. 18.4, p. 679-680

12. N Atrioventricular (AV) Valves • allow blood to flow from atria to ventricles when latter are relaxing • prevent flow from ventricles to atria when ventricles are contracting* • mitral (bicuspid) • tricuspid Fig. 18.8, p. 685 Return to cardiac cycle

13. N Semilunar (SL) Valves • allow blood to flow from ventricles to arteries when ventricles are contracting • prevent back flow from arteries to ventricles when ventricles relax* Fig. 18.8, p. 685 Fig. 18.4, p. 681 Return to cardiac cycle

14. N Heart Sounds • Normal sounds - closure of valves • “lub” – closure of AV valves • “dup” –closure of semilunar valves Fig. 18.19, p. 695

15. N Valve Disorders • Rheumatic heart disease (RHD) – strep (Streptococcus pyogenes) infection leads to inflammation of heart and valves; heart valves become stiffened into partially closed position • Murmur – abnormal heart sound associated with bad valves • incompetance – damaged valve allows backflow of blood • stenosis – narrowing of passageway through valve

16. Fibrous Skeleton • Internal connective tissue framework • Functions include: • stabilizes positions of muscle cells and valves • supports muscle cells, blood vessels, nerves • helps spread force of contraction through heart • prevents over-distention • helps maintain shape of heart • physically and electrically separates atrial and ventricular musculatures

17. Cardiac Anatomy Review, pp. 8-9 N Microanatomy of the Myocardium • Cardiac muscle • short, branching, uninucleate cells • striated – sliding filament movement • Connected by intercalated discs • gap junctions • functional syncytium • desmosomes • Numerous large mitochondria • aerobic respiration • high O2 demand • myoglobin http://www.usc.edu/hsc/dental/ghisto/musc/c_20.html Fig. 18.11, p. 688

18. Cardiac Anatomy Review, pp. 6-7 N Blood Flow Through the Heart • Pulmonary – to and from capillary beds associated with alveoli of lungs • brings deoxygenated blood to lungs; returns oxygenated blood to heart • Systemic – to and from capillary beds of the tissues of the body • brings oxygenated blood to tissues; returns deoxygenated blood to heart Fig. 18.5 p. 682

19. N Coronary Blood Supply • Anastomoses – provide collateral circulation • Blood enters coronary vessels during diastole, empties during systole • Autoregulation – coronary arteries dilate when demand for nutrients and oxygen increases • Capillaries present in endomysium (endo = within; mysium = muscle) • areolar CT within intracellular space between muscle cells • endomysium connected to fibrous skeleton

20. Coronary Blood Supply: Arteries • Branches of aorta • Supply oxygen-rich blood to myocardium • Right coronary artery • branches serve right atrium and right ventricle, SA and AV nodes, and posterior walls of both ventricles Fig. 18.7, p. 683

21. Coronary Blood Supply: Arteries • Left coronary artery • branches serve interventricular septum and anterior walls of both ventricles, left atrium and posterior wall of left ventricle • branches into anterior interventricular artery and circumflex artery Fig. 18.7, p. 683

22. N Coronary Circulation: Veins • Coronary Sinus • great cardiac vein - drains area supplied by anterior interventricular artery • other left and posterior coronary veins - drain left side and posterior of heart • Anterior cardiac veins – drain anterior surface of right ventricle Fig. 18.7, p. 683 Fig. 18.4, p. 679

23. Coronary Circulation: Disorders • Occlusion – blockage; in a vessel, tissue downstream will be deprived of oxygen and nutrients • Ischemia – transient state of oxygen deficit leading to reversible changes in cell structure and function • Infarction – localized area of cell death (necrosis) resulting from anoxia; causes include • disruption of arterial circulation serving the area • disruption of venous drainage

24. N Comparison with Skeletal Muscle • All-or-none law - either an event occurs completely (e.g., contraction) or it does not (no partial contraction) • in skeletal muscle, applies to motor units • in cardiac muscle, applies to entire organ • Length of absolute refractory period • skeletal muscle – 1-2 ms  allows tetanus • cardiac muscle ~ 250 ms  prevents tetanus Fig. 18.12, p. 689

25. N Comparison with Skeletal Muscle Means of stimulation • skeletal muscle – only contracts in response to stimulation by somatic motor neuron • cardiac muscle • certain cells are self-excitatory = autorhythmicity • autonomic innervation changes rate of depolarization • sympathetic innervation increases rate • parasympathetic innervation decreases rate • also responds to epinephrine

26. Cardiac Action Potential, p. 3 Types of Cardiac Muscle Cells Autorhythmic cardiac muscle cells • capable of spontaneously depolarizing to produce pacemaker potentials • conduct action potentials through myocardium • not contractile • form intrinsic conduction system

27. Cardiac Action Potential, p. 4 Types of Cardiac Muscle Cells Contractile cardiac muscle cells • depolarization spreads from autorhythmic cells via gap junctions • action potential leads to contraction as myofilaments slide past each other • responsible for alternating contraction (systole) and relaxation (diastole) that creates pressure on blood

28. Cardiac Action Potential, p. 5 Conduction Through the Heart • Action potential spreads rapidly through conduction system and contractile cells via gap junctions • Atria and ventricles functionally separated by fibrous skeleton • Time to total depolarization ~ 220 ms (~0.22s) in a healthy heart

29. Cardiac Action Potential, p. 6-10 N AP: Autorhythmic Cells - Overview • Ion channels allow ion movements • Na+ ( Na+/K+) leakage channels • Voltage-gated K+ channels • Voltage-gated Ca2+ channels • Ion movements affect membrane potential • Resting membrane potential is negative Fig. 18.13, p. 697

30. Cardiac Action Potential, p. 6-10 AP: Autorhythmic Cells - Steps • Pacemaker potential • Action potential depolarization • Action potential repolarization Fig. 18.13, p. 697

31. Cardiac Action Potential, p. 6-10 N Autorhythmic AP:Pacemaker Potential • gradual change in membrane potential from resting (- 60 to -70 mV) toward threshold • Na+ channels open  net gain of + charge  slow depolarization = pacemaker potential • closure of voltage-gated K+ channels contributes to slow depolarization Fig. 18.13, p. 697

32. Cardiac Action Potential, p. 6-10 Autorhythmic AP: Depolarization • at threshold (~ -40 mV), voltage-gated Ca2+ channels open  Ca2+ enters from extracellular fluid  rapid depolarization of action potential Fig. 18.13, p. 697

33. Cardiac Action Potential, p. 6-10 N Autorhythmic AP: Repolarization • depolarization causes voltage-gated K+ channels to open  K+ leaves  cell repolarizes • decrease in voltage causes Ca2+ channels to close, aids repolarization • after a while, K+ channels start to close, Na+ channels open; cycle starts over • Na+/K+ pump Fig. 18.13, p. 697

34. Cardiac Action Potential, p. 11 AP: Contractile Cells • Connected to autorhythmic cells by gap junctions • Ion channels allow ion movements • Voltage-gated Na+ channels • Voltage-gated K+ channels • Voltage-gated Ca2+ channels • Resting membrane potential is negative Fig. 18.12, p. 689

35. Cardiac Action Potential, p. 12-17 AP: Contractile Cells - Steps • Depolarization • Plateau • Repolarization Fig. 18.12, p. 689

36. Cardiac Action Potential, p. 12-17 N Contractile AP: Depolarization • Sodium (and calcium) ions pass from autorhythmic cells via gap junctions • Contractile cell depolarizes from resting to threshold • At threshold, fast voltage-gated sodium channels open  Na+ rushes in  depolarization to ~ +30 mV Fig. 18.12, p. 689

37. Cardiac Action Potential, p. 12-17 N Contractile AP: Plateau • After a short time, Na+ channels close and voltage-gated K+ channels open  membrane potential begins to fall • Voltage-gated Ca2+ channels also open and allow Ca2+ influx • Ca2+ influx balances K+ efflux (channels close temporarily) resulting in plateau Fig. 18.12, p. 689

38. Cardiac Action Potential, p. 12-17 N Contractile AP: Plateau • combination of Ca2+ influx and inactivation of K+ channels results in plateau, coupled with slow return of Na+ channels to ready position results in long absolute refractory period • Why would this be important to heart function? • Ca2+ influx causes contraction Fig. 18.12, p. 689

39. Cardiac Action Potential, p. 12-17 Contractile AP: Repolarization • rapid repolarization occurs as Ca2+ channels close and K+ channels reopen • K+ influx returns membrane to resting potential • Ca2+ actively transported out of cell and into sarcoplasmic reticulum • Na+/K+ pump restores ion levels to resting Fig. 18.12, p. 689

40. Intrinsic Conduction System, pp. 3-4 Electrical Conduction - Overview sinoatrial (SA) node  internodal pathway to atrioventricular (AV) node & atria  atrioventricular (AV) bundle (bundle of His)  right and left bundle branches  Purkinje fibers  ventricles (starting at apex) Fig. 18.14, p. 691

41. Intrinsic Conduction System, pp. 3-4 Conduction Pathway: SA Node • Sinoatrial (SA) Node • located in right atrial wall, inferior to opening of superior vena cava • acts as normal pacemaker  sinus rhythm • intrinsic rate ~ 100 APs/min • ~ 75 APs / min at rest under normal hormonal and neural control • resting HR varies; more fit, slower heart rate • AP spreads to atria and to AV node via internodal pathway Fig. 18.14, p. 691

42. Intrinsic Conduction System, pp. 3-4 Conduction Pathway: AV Node • Atrioventricular (AV) Node • located in inferior interatrial septum above tricuspid valve • connects atria and ventricles • short delay (~ 0.1 s) -- Why is this delay important?

43. Intrinsic Conduction System, pp. 3-4 Conduction Pathway: AV Bundle • Atrioventricular (AV) Bundle (bundle of His) • Right and Left Bundle Branches • run through interventricular septum toward apex of heart Fig. 18.14, p. 691 Fig. 18.17, p. 694

44. Intrinsic Conduction System, pp. 3-4 N Conduction Pathway: Purkinje Fibers • run through interventricular septum to apex of heart where they turn and run superiorly through outer wall of ventricles • supply papillary muscles before rest of ventricular wall • Why would this be important? Fig. 18.14, p. 691 Fig. 18.17, p. 694

45. Electrocardiograph (ECG) • Measures electrical changes in heart • Electrocardiograph – instrument used to measure changes • Leads • combinations of electrodes used to detect changes • 12 standard leads • I – right arm (-) -> left arm (+) • II – right arm (-) -> left leg (+) • III – left arm (-) -> left leg (+) • Chest leads http://www.cardioliving.com/consumer/Heart/Electrocardiogram.shtm

46. Electrocardiogram (ECG) • Electrocardiogram – recording of the changes in membrane potential • Series of deflections from baseline – correspond to spread of action potential through myocardium • Analysis – ECG shows: • overall heart rate • wave shape, height and duration • deviations from normal

47. Intrinsic Conduction System, pp. 5-6 ECG Waves - Overview • P Wave • PR Interval • QRS complex • QT segment • T wave Fig. 18.16, p. 694

48. Intrinsic Conduction System, pp. 5-6 ECG : P wave, PR Interval • P wave - depolarization of SA node followed by atrial depolarization • P-R (P-Q) interval • time from beginning of atrial depolarization to onset of ventricular depolarization; • includes spread of AP through atria and conducting system Fig. 18.16, p. 694

49. ECG Analysis: QRS and T • QRS complex – spread of depolarization through system and both ventricles • Q-T segment – time from onset of ventricular depolarization to end of repolarization • T wave – repolarization of ventricles Fig. 18.16, p. 694 http://www.emergency-nurse.com/resource/clipart/clipart9.htm

50. Common Cardiac Arrhythmias • Sinus bradycardia – impulses arise at SA node at slower than normal rate (<60 per minute) • Sinus tachycardia – impulses arise at SA node at faster than normal rate (>100 per minute at rest) http://www.rnceus.com/ekg/ekgsb.html http://home.earthlink.net/~avdoc/infocntr/htrhythm/hrstachy.htm