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Circulatory system Pressure gradients move blood through the heart and vessels. Pulmonary circulation vs. systemic circulation.

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Presentation on theme: "Circulatory system Pressure gradients move blood through the heart and vessels. Pulmonary circulation vs. systemic circulation."— Presentation transcript:


2 Circulatory system Pressure gradients move blood through the heart and vessels. Pulmonary circulation vs. systemic circulation

3 head and arms (to pulmonary circuit) aorta (from pulmonary circuit) heart other organs diaphragm liver intestines legs “Double pump” both ventricles pump an equal volume of blood into systemic and pulmonary circuits Higher resistance through the systemic circuit

4 Pressure - force exerted by pumped blood on a vessel wall Resistance - opposition to blood flow from friction

5 vena cava Right atrium Tricuspidvalve vena cava Right ventricle

6 Pulmonarysemilunarvalve Left pulmonary artery Right pulmonary artery Right atrium Tricuspidvalve Right ventricle

7 Aorta Left atrium Right pulmonary vein Left pulmonary vein Bicuspidvalve Left ventricle

8 Aorta Left pulmonary vein Right pulmonary vein Aorticsemilunarvalve Left atrium Left ventricle

9 When pressure is greater behind the valve, it opens. When pressure is greater in front of the valve, it closes Valves ensure one-way flow Leakproof “seams” semilunar valve

10 Right atrium Tricuspid valve Right ventricle Papillary muscle contracts with ventricle Chordae tendineae Septum Shape of the AV valves is maintained by chordae tendineae

11 Ventricular Systole Diastole

12 Blood pressure variation

13 Heart myocardium Cardiac muscle fibers are interconnected by intercalated discs.

14 Desmosome Gap junction Intercalated disc Action potential Junctions between cardiac muscle cells

15 Pacemaker activity Slow depolarizations set off action potentials in a cycle

16 Pacemaker cell Spontaneous action potential Action potential spread to other cells Gap junctions Cardiac muscle Self-excitable muscles - action potential gradually depolarizes, then repolarizes Gap junctions

17 No gap junctions between atria and ventricles Fibrous insulating tissue prevents AP from directly spreading from atria to ventricles

18 Sinoatrial (SA) node Purkinje fibers Atrioventricular (AV) node Pacemaker locations: SA node AV node Bundle of His Purkinje fibers Conduction of contraction Bundle of His

19 Problems with heart rate AV node rhythm is slower - bradycardia

20 Heart block – a type of bradycardia. Ventricles pump slowly and out of rhythm of atria Problems with heart rate

21 Ventricular fibrillation Atrial fibrillation

22 Plateau phase Threshold potential Action potential in cardiac muscle

23 Action potential Contraction Refractory period Long refractory period ensures no summation of twitches Relaxation of cardiac muscles is required

24 Electrocardiogram (ECG or EKG) Currents from electrical activity of heart spread to body tissues and fluid This electrical activity is detected by electrodes and transformed to waveforms P R Q S T P PRSTTP interval

25 time (seconds) bradycardia tachycardia ventricular fibrillation

26 Ventricular and atrial diastole Cardiac cycle

27 Atrial contraction Cardiac cycle

28 Isovolumetric ventricular contraction Cardiac cycle “Lub” End diastolic volume is in the ventricles

29 Ventricular ejection Cardiac cycle

30 Isovolumetric ventricular relaxation Cardiac cycle “Dub” End systolic volume is in ventricles



33 Systolic or diastolic murmurs Often due to stenosis or regurgitation at a valve (“whistle” vs. “swish”) Normal heart “lub-dup” Diastolic mitral stenosis “lub-dup-whistle” Diastolic aortic regurgitation “lub-dup-swish” Systolic aortic stenosis “lub-whistle-dup” Systolic tricuspid regurgitation “lub-swish-dup” Diastolic patent ductus arteriosus What are heart murmurs?


35 Extrinsically: conduction speed contraction strength Sympathetic signals increase stroke volume

36 Optimal length End-diastolic volume (EDV) (ml) Normal resting length Increase in SV Stroke volume (SV) (ml) B1 A1 Increase in EDV Frank Starling law (intrinsic increase in stroke volume)

37 Would you expect type 1 or type 2 fibers in heart muscle? Cardiac muscle cells are highly resistant to fatigue – Many mitochondria, larger mitochondria, myoglobin, high vascularization. – Mitochondria convert lactate pyruvate glucose Mitochondria

38 How does the heart regulate its contration?

39 Heart disease What is a heart attack, what causes it? Why some heart attacks worse than others?

40 Heart failure Due to: Poor circulation to heart muscle (blockage) High blood pressure makes heart work harder Insufficient valve Less blood leaving

41 Heart failure Continued sympathetic action can temporarily alleviate heart failure effects on output Kidney fluid retention thus stroke volume

42 Stroke volume is so low that blood backs up in blood vessels leading to heart Failure on left side - blood collects in pulmonary circuit and causes pulmonary edema. Oxygenation decreases. Response of kidneys to fluid retention is now problematic. Congestive heart failure

43 Due to thickening of heart muscle: – To pump against high pressure – Leaking or stiffness in heart valves Due to over-dilation due bc of heart failure (usually pulmonary edema) What causes an enlarged heart?

44 Heart attacks, strokes Blockage due to plaques, embolisms Arteriosclerosis

45 smooth muscle part of plaque vessel wall Endothelium Lipid center of plaque Plaques in blood vessels LDLs, inflammation contribute to plaque formation

46 Cholesterol carried in the blood: – High-density lipoprotein - helps move cholesterol back to liver for removal – Low-density lipoprotein - used by cells, excess LDL infiltrates artery walls

47 Saturated fats and trans fats raise LDLs and are atherogenic Free radicals oxidize LDLs and make them more likely to attach to plaques

48 blockage grafted arteries Coronary bypass

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