CARDIOVASCULAR SYSTEM

Transcription

1 CARDIOVASCULAR SYSTEM HEART Heart: general comments Pumps blood through 60K miles of vessels C.O. = 5 liters/minute at rest 1

2 Cardiovascular System double pump systemic circuit pulmonary circuit Both circuits arteries capillaries veins red? blue? Section 20-1: lab topics pp

3 Pericardium: 3 layers fibrous pericardium fibrous CT prevents overstretch anchors heart in the mediastinum pericardium lines pericardial cavity secretes pericardial fluid 2 layers parietal pericardium visceral pericardium (epicardium) epicardium myocardium Cardiac muscle tissue endocardium smooth endothelial lining confluent with lining of vessels Heart wall 3

4 Chambers, Valves In lab handout Atria Ventricles Atrioventricular (AV) valves, L and R Semilunar valves Aortic valve Pulmonary valve cardiac skeleton (fibrous skeleton) stabilizes heart valves isolates ventricular cells from atrial cells Nature of the isolation is 4

5 Valves at work (1st of 2 slides) Valves at work (2nd of 2 slides) 5

6 coronary circulation coronary arteries cardiac veins coronary sinus thebesian veins many anastomoses Overview of Cardiac Physiology 6

7 Cardiac Physiology Two types of heart cells 1. conducting cells control & coordinate heartbeat 2. contractile cells generate pressure to propel blood Bundle branches Purkinje fibers 7

8 Cardiac Conduction system specialized cells that Initiate/distribute impulses components: SA node internodal pathways To atrial muscle cells AV node AV bundle bundle branches Purkinje fibers To ventricular muscle cells conducting cells exhibit prepotentials cation leak SA node (natural pacemaker) located in wall of R atrium spontaneously depolarizes X/minute AV node 40-60X/minute Purkinje fibers 20-40X/minute 8

9 AV node Conducts impulses from to maximal conductance rate of AV node 230 impulses per minute determines maximal heart rate 230 beats per min 9

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12 ECG/EKG P wave QRS complex T wave Useful for assessing heart detection of arrhythmias Where is the wave for atrial repolarization? 12

13 Cardiac Arrhythmias Abnormal patterns of electrical activity Reduce pumping efficiency Indicate damage to myocardium pacemakers or conduction system Some causes exposure to drugs electrolyte imbalances in ECF Contractile cells bulk of heart: myocardium action potentials are due to increased [Ca ++ ] sarcoplasm calcium-troponin interactions result in contraction- just like skeletal muscle gap junctions allow cytoplasm to be confluent in adjacent cells ions flow through depolarize neighboring cell 13

14 action potential in contractile cells voltage-gated fast Na + channels open at threshold due to cation flow from adjacent cell rapidly depolarize the membrane plateau, voltage-gated slow Ca ++ channels open allow depolarization to persist voltage gated slow K + channels allow repolarization long refractory period lack of membrane response absolute refractory period Na channels closed and inactivated contraction cannot reoccur relative refractory period channels can open requires stronger than usual stimulus 14

15 Calcium ions & Cardiac Contraction sources of calcium: ECF and SR roles of ECF Ca +2 ions bind to troponin for contraction: accounts for 20% of calcium used during contraction stimulate release of Ca +2 from SR (this is the other 80% of Ca +2 ions binding to troponin for contraction) FYI heart is highly sensitive to [Ca +2 ] pla hypercalcemia cardiac arrhythmias hypocalcemia weak heartbeat, arrhythmias Action Potentials and contraction Skeletal muscle Refractory period brief, precedes contraction so multiple rapid stimuli cause tetany. Cardiac muscle Refractory period extends into relaxation phase so no tetany is possible 15

16 Pattern of activity of the heart Contraction Relaxation Contraction Relaxation etc. Cardiac cycle Phases of the cycle: systole and diastole Used to refer to chamber activity Systole -- contraction Blood ejected Diastole -- relaxation Chamber fills with blood Blood flows due to differences in pressure 16

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18 Atrial systole Atria contract blood forced into ventricles Atrial contribution to ventricular volume Only 30% of ventricular volume End-diastolic volume (EDV) At this point each ventricle holds the maximal amount of blood for this cycle Ventricular systole 2 phases First phase: isovolumetric contraction Pressure rises AV Valves are pushed closed no blood moves 18

19 Ventricular systole 2 phases Second phase: ventricular ejection Ventricular pressure is enough to open aortic and pulmonary valves L ventricular pressure exceeds aortic pressure of ~ 80 mmhg FYI: R ventricular pressure exceeds pulmonary trunk pressure of ~ 10 mm Hg Ventricular systole Blood is ejected ml blood stroke volume Stroke volume at rest: ~60% of end diastolic volume (EDV) (called ejection fraction) End-systolic volume at rest: Amount of blood remaining 50 ml 19

20 ventricular diastole isovolumetric relaxation All valves are closed until. ventricular pressure drops below atrial pressure then AV valves open, blood flows in. cardiodynamics Movements and forces generated by the heart Cardiac output (CO) CO = HR X SV Given: HR is 80 beats/min and SV is 70 ml/beat CO = 80 beats/min X 70 ml/beat = 5600 ml/min = 5.6 L/min 20

21 Factors affecting Cardiac Output Factors affecting HR autonomic innervation reflexes hormones others 21

22 Factors affecting Heart Rate Autonomic innervation vagus nerves sympathetic cardiac nerves Control emanates from cardiac centers in the medulla oblongata cardioacceleratory center cardioinhibitory center Autonomic innervation Both ANS divisions innervate SA node AV node Atria Sympathetic division ventricles 22

23 Autonomic reflexes cardiac reflexes: baro- and chemoreceptor monitoring Monitor BP and blood gases Aorta and carotid arteries Autonomic tone determines heart rate Finely adjusted up or down depending on stimuli Parasympathetic effects dominate Autorhythmic cells & HR How can we change heart rate? 23

24 Autonomic Innervation Effects on SA node ANS alters permeability of SA node parasympathetic division Ach opens K+ channels sympathetic division NE opens Na-Ca channels Factors affecting HR: the atrial reflex Atrial reflex Responds to increased venous return Stretch of right atrial walls causes an increase in HR Receptors stretch receptors in the right atrium 24

25 Factors affecting Heart Rate Hormones that increase the HR EPI NE Thyroid hormone Venous Return Increased venous return initiates atrial reflex Also stretched SA nodal cells depolarize more rapidly Factors affecting Cardiac Output 25

26 Factors affecting Stroke Volume Recall SV = EDV - ESV SV is effected by changes in EDV or ESV EDV depends on 1. Filling time 2. Venous return Affected by many factors Changes in CO, BP, circulation patterns Skeletal muscle activity 26

27 Preload determines ESV Preload: Degree of stretch of heart prior to contraction If EDV is large, so is preload...implications: Striated muscle when slightly stretched can form more cross bridges, and contract more forcefully More blood in = more blood out Frank-Starling principle or Starling s law of the heart As EDV increases, so does SV ESV determined by 1 preload: determines ESV 2 contractility: forcefulness of contraction determined by Humoral agents (+ or - inotropic agents) Hormones, ECF [ion] s ANS 3 afterload: pressure that must be exceeded for blood to be ejected from heart Increased afterload = increased ESV = decreased CO 27

28 Factors affecting Stroke Volume Summary: Factors affecting Cardiac Output 28

29 Congestive Heart Failure Heart fails as a pump various causes: myocardial infarcts, chronic high blood pressure, congenital defects, coronary artery disease, etc. Left heart failure = pulmonary edema Pulmonary congestion Right heart failure = peripheral edema especially noticeable in feet & ankles 29