Cardiovascular Anatomy and Physiology REVIEW

1. Cardiovascular Anatomy and Physiology REVIEW Reading: Brubaker 2:37-56

2. Myocardial Infarct (LAD) Normal Heart Photos: Klatt, Edward C. MD, WebPath.edu

3. Primary Cardiac Function = Tissue Perfusion • Morbidity and Mortality of Cardiovascular Disease: • Inadequate Cardiac Output • Reduced Perfusion (O2) to the “BIG THREE” vital organs: • Brain, Heart, Lungs • Other Organ Failure: • Kidneys, Liver, GI, Skeletal Muscle

4. Cardiac Anatomy: • Pericardium: Visceral / Parietal connective tissue “wrapping” • Epicardium: next to the heart • Pericardial space: fluid filled • Fibrous/serous pericardium: Prevents overdistension of the heart and produces fluid Cardiac Tamponade: Life threatening Accumulation of fluid in p. space

5. Layers of Heart Tissue: • Pericardium: Double Layered • Outer, Fibrous: Tough connective fibrous tissue - Parietal • Inner, Serous:Epithelial and thin connective tissue layer -Visceral,epicardium

6. Heart Layers: • Myocardium: Cardiac muscle layer • Endocardium: Connective + Epithelial Tissue • Structural “Scaffolding • Valves • Chordae Tendinae

7. Endothelial “Scaffolding” • Endocardium • The fibrous network forms • chambers of the Ventricles

8. Myocardium: • You end up with a very strong muscle • in the shape of a multi-chambered pump

9. Coronary Arteries: • Left Coronary Artery: • Origin: Left side of AORTA • Supplies: Anterior/Left Heart • Right Coronary Artery: • Origin: Rt. Side of AORTA • Supplies: Right Heart

11. Rt. Marginal Branch

12. Coronary Artery Bloodflow Regulation: • Aortic Pressure is primary regulator • Sympathetic: Net Increase in Bloodflow • Parasympathetic: Maintain Bloodflow • Metabolic: Bloodflow = VO2

13. Cardiac Cycle and Coronary Artery Flow: • Systole: The aortic valve opens, and “covers” the Coronary arteries • Blood flow is prevented • Diastole: The aortic valve closes, “opens” the coronaries • Blood Flow is restored What would be the effect of increased HR on Coronary blood flow (perfusion)?

14. Coronary Artery Disease: CAD • When critical bloodflow to the heart muscle is compromised, The Heart Cannot “Rest” from its work! • DEMAND > SUPPLY (Ouch!) • Arteriosclerosis: “Hardening of the arteries” (could be just aging) • ATHEROsclerosis: The hardening and progressive narrowing is caused by lipid deposits provoking fibrosis and calcification Progressively PATHOLOGICAL!

15. Fatty Arteries: Normal Coronary Artery Atherosclerotic Artery Photos: Klatt, Edward C., WebPath.com

16. Cardiovascular Function: PUMP: Heart contractions propel Blood throughout the circulation!

17. Cardiac Cycle: • Ventricular Systole: • Ventricles Contract – eject blood • Tri/Bicuspid valves close • First Heart Sound: “Lubb” • Ventricular Diastole: • Ventricles relax, fill • Pulmonary/Aortic Valves close • Second Heart Sound: “Dupp”

18. The Atria: • “Collection” of blood from either: • Right: The systemic circulation (low PO2) • Left: The pulmonary circulation (high PO2) • Atrial Contraction: • Empties the final 30% of the End Diastolic Volume (EDV) What is the impact of Atrial Fibrillation On Cardiac Output?

19. Right Ventricle pumps blood to the lungs • Right Ventricle contracts • Increased pressure causes tricuspid valve closure • Blood leaves heart via Pulmonary Artery • Only artery with O2

20. Left Ventricle Pumps Blood to the Body Aorta • The Left Ventricle contracts • Mitral Valve: Closes • Aortic Valve: Opens • Blood is pumped out via the Aorta

21. Terms: • Preload: The pressure in the left ventricle immediately before contraction: • Mostly related to volume EDV • Afterload: The pressure in the left ventricle immediately after contraction: • Mostly related to Vascular resistance • Ejection Fraction:The amount of blood ejected by the LV – expressed as a % of the EDV

22. Systemic Arterial Blood Pressure • Systolic: Systole causes increased pressure in the arterial vessels: • Systolic pressures indicate the strength of cardiac contraction • Diastolic: During diastole, arterial pressure is at it’s lowest • Diastolic Pressures indicatethe total resistance to blood flow

23. Cardiac Output: HR X SV • CO = HR X SV • “Emergencies” • SNS Autonomic NS • Increase HR/SV = Increase CO • “Relaxing” – Status Quo: • PSNS Autonomic NS • Decrease HR = Decrease CO

24. Electrophysiology of the Heart: ECG P: Atrial Depolarization/contraction QRS: Ventricular Depol/Contraction T: Ventricular Repolarization

25. Cardiac Muscle Cells: • Striated, Branched, Intercalated Discs • Slower Action Potential than nerve or skeletal muscle cells • Voltage Gated Ca++ Channels!

26. Electrical Activity: Excitation - Contraction • To contract, cardiac muscle cells must depolarize and propagate an Action Potential • The Conduction of Action Potentials and Contractions must be well coordinated to efficiently pump blood.

27. Depolarization Na+ and Ca++ Channels open Plateau: All but Ca++ channels close Repolarization K+ open and Ca++channels close Depolarization: Na+ channels open Repolarization: Voltage Gated K+ channels open / Na+ channels close Action Potentials:Cardiac vs. Skeletal

28. Myocardial Action Potential 2 +40 1 AP 0 3 0 mV 4 4 -100 ECG

29. Why the Plateau Phase and Calcium? • Plateau Phase: LongerRelative Refractory period: • Cannot be re-stimulated – permitting coordinated contraction of entire heart muscle. • Calcium: Important in the automaticity of cardiac myocytes • Links excitation to contraction • Increases contraction force

30. Coordinating the Beats… • Contractions of the ventricles and atria must alternate • The excitation of the heart muscle follows a predictable path

31. Conduction System: • SA Node: 90-100 bpm • AV Node: Slows the message down • AV Bundles: (also His): • L./R. Bundle Branches: • Purkinje Fibers:

32. SA Heart Conduction System • The Sino-Atrial node(SA) serves as the pacemaker for the heart. • When the SA node fires, it causes both atria to contract • The excitation-contraction signal is then “conducted” to the ventricles via the AV Node

33. Heart Rate Control • Each heart cell can contract independently and automatically • The entire heart must not contract at the same time. • Excitation-Contraction of the heart is coordinated from “top to bottom” • The excitation-contraction pathway is called “The Conduction System”

34. Extrinsic Control of Heart Rate • The SA node has an Intrinsic Rate of 90-100 bpm – “Default Rate” • External controls modify the heart rate: both at rest and during exercise • Controls: Parasympathic Nervous System, Sympathetic Nervous System, Endocrine System

35. Parasympathetic Nervous System • “Maintenance” control • Vagus nerve innervates heart at the SA Node with some control of the AV Node • Causes reduced HR • Neurotransmitter: Acetylcholine (“cholinergic”) • Atropine blocks blocks PSNS and increases HR

36. Sympathetic Nervous System • “Rescues” in homeostatic emergencies (like exercise) • Increases HR • Increases Systolic contractility (Increased BP) • Increases Mental acuity (you are prepared for battle!) • Neurotransmitter: Norepinepherine (Adrenaline = “adrenergic”) • Propranolol (SNS Beta-receptor blocker) reduces HR

37. Endocrine System • The adrenal medulla (above kidney) secretes Catecholamines: • Epinephrine • Norepinephrine • Stimulated by and mimics the Sympathetic Nervous System • Slower/Longer acting

38. Regulation of Cardiac Output: • Cardiac Output: Changes in CO are responses to “Homeostatic Emergencies”: • Pressure Emergencies • Chemical Emergencies

39. Baroreceptors: Sensing Pressure Emergencies • Increase CO = Increase Systolic BP • Emergency 1: Decreased Pressure • Increase SNS: Increased HR X SV = Increased CO • Problem 2: Increased Pressure • Decrease SNS: Decrease HR = Decreased CO

40. Chemoreceptors: Sensing Metabolism Emergencies • Emergency 1: Increased Metabolic Rate: • Increased CO2, H+ (decreased pH) • Increased SNS …CO • Problem 2: Decreased Metabolic Rate: What’s the Problem? • Decreased CO2/ H+ (increased pH) • Decreased SNS …CO • Conserver the rescue efforts

41. Intrinsic Regulation of Cardiac Output: Starling’s Law • Increased Venous Return • Increased cardiac muscle stretch • Increase contraction force • Increased SV = Increased CO • Occurs without SNS/PSNS involvement • Exercise….

42. Final Question: • In a Heart Transplant, the heart is “denervated” • How does someone with a heart transplant respond to exercise?

43. Hints: • Remember – Starling’s Law of the Heart • Remember that though the nerves are no longer signaling, there is another (though slower and longer acting) source of control…

44. Blood Vessels And Circulation

45. Peripheral Circulation: • Systemic Circulation: • Blood vessels directing blood to the body tissues • Left Heart to Right Heart • Pulmonary Circulation: • Blood vessels directing blood to the lungs for gas exchange • Right Heart to Left Heart What do we call the circulation to The heart?

46. Perfusion Homeostasis: • Internal Environment: Depends on appropriate perfusion (Blood flow) • Homeostasis: A constant balance of choices in maintaining central blood pressure (to maintain the “Big 3”) and distribution to demanding tissues

47. Three Vessel “Tunics”: • Tunica Adventitia (Externa): Fibrous connective tissue • Tunica Media: Smooth Muscle and elastic connective tissue • Tunica Intima: Endothelium (forms the valves in veins)

48. Arteries: • Vessels taking blood Away From The Heart • Usually O2 and nutrient rich…”Supply” to tissues

49. Arteries: Structure/Function • High Pressure Conduits: • Elastic Connective Tissue: Expands with systole, and recoils with diastole • Smooth Muscle: Assist in “pumping” and “directing” blood flow • Endothelium: Smooth inner surface

50. Veins: • Vessels returning blood Back To The Heart • Usually low in O2 – carrying wastes for removal