Circulatory system. Terminology. Ventricles and resistance. Pressure gradients move blood through the heart and vessels.

Transcription

1 Circulatory system Pressure gradients move blood through the heart and vessels. Pulmonary circulation vs. systemic circulation (to pulmonary circuit) liver head and arms heart aorta diaphragm (from pulmonary circuit) other organs The heart is a dual pump pushing equal volumes of blood into systemic and pulmonary circuits Higher resistance through the systemic circuit intestines legs Terminology Pressure - force exerted by pumped blood on a vessel wall Resistance - opposition to blood flow from friction Systole heart chamber contraction Diastole heart chamber relaxation Ventricles and resistance Left ventricle Right ventricle Interventricular septum 1

2 Right pulmonary artery Left pulmonary artery vena cava Right atrium Tricuspid valve Right ventricle Right atrium Tricuspid valve Pulmonary semilunar valve Right ventricle vena cava Aorta Aorta Right pulmonary vein Left pulmonary vein Left atrium Bicuspid valve Right pulmonary vein Left pulmonary vein Aortic semilunar Left atrium valve Bicuspid valve Left ventricle Left ventricle 2

3 Valves ensure one-way flow When pressure is greater behind the valve, it opens. Shape of the AV valves is maintained by chordae tendineae Right atrium Tricuspid valve Leakproof seams semilunar valve When pressure is greater in front of the valve, it closes Papillary muscle contracts with ventricle Chordae tendineae Septum Right ventricle Ventricular Systole Ventricular Diastole Heart sounds 3

4 Blood pressure variation Heart myocardium Cardiac muscle fibers are interconnected by intercalated discs. Cardiac muscle Cardiac muscle cell Nucleus Intercalated discs Gap junctions Fasciae adherens Cardiac muscle cell Mitochondrion Nucleus Intercalated disc Sarcomeres with SR, AP causes Ca +2 release Branching, not linear like skeletal muscle Joined by intercalated discs, sarcolemma interlocks Gap junction Desmosome Cardiac muscle cells Mitochondrion T tubule Sarcoplasmic reticulum Z disc Nucleus Sarcolemma I band A band I band 4

5 APs at cardiac calls Contractile cardiac muscle cells aren t innervated, get APs from neighbors via gap jxns APs at cardiac calls Autorhythmic (Pacemaker) cardiac muscle cells are non-contractile and set the frequency of APs that contractile cells receive Impulses are intrinsic ANS influences the rhythm of pacemakers Pacemaker activity Slow depolarizations set off action potentials in a cycle Pacemaker cells only! These cells do not contract Cardiac muscle Spontaneous action potential Pacemaker cell Action potential spread to other cells Gap junctions Gap junctions 5

6 Conduction of contraction No gap junctions between atria and ventricles Fibrous insulating tissue prevents AP from directly spreading from atria to ventricles Pacemaker cell locations: SA node AV node Bundle of His Purkinje fibers Sinoatrial (SA) node Atrioventricular (AV) node Bundle of His Purkinje fibers ANS can influence: Sinus rhythm AV node delay Contractile strength determined by Ca 2+ release Arrhythmias Sinus sick syndrome sinus bradycardia or tachycardia Fibrillation conduction is disorganized and loops ventricles or atria quiver 6

7 Arrhythmias AV (heart) block transmission from AV node to ventricles is partially or completely blocked Conduction pathway has damage SA node (atria) and Purkinje fibers (ventricles) beat out of phase, P.fibers are very slow Problems with heart rhythm AV node rhythm is slower - bradycardia Problems with heart rhythm Ventricular fibrillation 7

8 Action potential in cardiac muscle Plateau phase These are contractile cells not pacemaker cells Long refractory period ensures no summation of twitches Threshold potential Relaxation of cardiac muscles is essential Electrocardiogram Currents from heart spread to body tissues and fluid Sum of all electrical activity spread to electrodes and recorded R P T P Q S PR ST TP interval 8

9 Cardiac cycle Ventricular and atrial diastole Cardiac cycle Atrial contraction Cardiac cycle Isovolumetric ventricular contraction Lub End diastolic volume is in the ventricles 9

10 Cardiac cycle Ventricular ejection Cardiac cycle Isovolumetric ventricular relaxation Dub End systolic volume is in ventricles Heart murmurs Lub-murmur-dub: a systolic murmur murmur-lub-dub: a diastolic murmur Valves can be stenotic (stiff) makes whistling sound when pushed open Valves can be insufficient (too loose) makes a swishing sound from backflow 10

11 Stroke volume (SV) (ml) Sympathetic signals increase stroke volume Extrinsically: conduction speed contraction strength Recall: muscle length and force Frank Starling law (intrinsic increase in stroke volume) Optimal length Increase in SV B1 A1 Normal resting length (Cardiac muscle does not normally operate within the descending limb of the length tension curve.) Increase in EDV End-diastolic volume (EDV) (ml) 11

12 Frank-Starling Law Cardiac muscle cells are typically at less than optimal length but become more optimal with stretch Would you expect type 1 or type 2 fibers in heart muscle? Adjustments to stroke volume Heart disease How do heart attacks occur, what leads to them? 12

13 Myocardial infarction Coronary artery disease Coronary arteries nourish cardiac cells Blockage due to plaques, embolisms, vascular spasm How cholesterol is 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 Development of atherosclerosis involves these factors: Inflammation along vessel, triggered by various factors (ox.ldls, signals from fat, other inflam., smoking, hypertension) Saturated fats and trans fats in diet raise LDLs and promote plaque formation 13

14 Development of atherosclerosis involves these factors: Inflammation promoted (LDL buildup, oxidation, WBCs are attracted and engulf LDLs) This area bulges into middle of vessel, can possibly rupture, snowball effect WBCs vessel wall Endothelium smooth muscle part of plaque Lipid center of plaque Development of atherosclerosis involves these factors: Inflammation along vessel, triggered by various factors (ox.ldls, signals from fat, other inflam., smoking, hypertension) Inflammation promoted (LDL buildup, oxidation, WBCs are attracted and engulf LDLs) This area bulges into middle of vessel, can possibly rupture, snowball effect Smooth muscle and fibroblasts (repair cells) may attempt to seal over the inflamed area, thickening it. Coronary bypass grafted arteries blockage 14

15 Often due to: Poor circulation to heart muscle (blockage) High blood pressure makes heart work harder Insufficient valve Heart disease Less blood leaving Continued sympathetic action can temporarily alleviate heart failure effects on output Kidney thus Heart disease fluid retention stroke volume Congestive heart failure 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. Congestive heart failure 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 now problematic. fluid retention is 15

16 What causes an enlarged heart? Can be due to thickening of heart muscle: To pump against high pressure Leaking or stiffness in heart valves What causes an enlarged heart? Can be due to thickening of heart muscle: To pump against high pressure Leaking or stiffness in heart valves Or due to over-dilation bc of heart failure (usually pulmonary edema) Stiffness in aortic valve Blood vessels are more than little tubes bringing blood to your body They are dynamic, changing flow, growing branches according to conditions Reconditioning of blood Intestines, kidneys, and skin receive blood flow in excess to their needs 16

17 Flow rate of blood pressure gradient F= or F= resistance P R Resistance is the opposition to blood flow through a vessel. It depends on: blood viscosity vessel length vessel radius Effect of radius on surface area Friction increases as surface area of contact increases more vessel wall in contact with blood less contact Effect of radius on resistance Arteries are a pressure reservoir Large radius of arteries, little resistance Elastic recoil from arteries drives flow of blood during diastole Arteries temporarily expand and hold pumped blood 17

18 Mean arterial pressure is the driving force for blood flow. mean arterial pressure = diastole pressure plus 1/3 the pulse pressure /3 (40) = 93 Arterioles give most resistance Arteriole radius changes to alter the distribution of blood and regulate blood pressure Vascular tone is a baseline of vascular resistance - changes in radius are possible Blood pressure drops sharply once in arterioles Local control of arteriolar resistance Mean blood pressure is identical to all organs Differences in arteriolar resistance determines the distribution of blood to different organs Mechanisms: endothelium cells release chemicals when O 2 and CO 2, acidity 18

19 Figure Page 354 Increased flow to skeletal muscles due to exercise Extrinsic (outside) controls on arterioles: Sympathetic signals cause general arteriole ion, increasing mean pressure Local controls dilate arterioles where blood is needed. Increased SNS Increased SNS dilate Local controls using signals from tissues dilate dilate 19

20 Capillaries O 2, CO 2 nutrients and wastes passively diffuse Thin vessels increase surface area of vessel wall contact Diffusion at capillaries Distance: Walls are one cell thick Area: small radius, high surface area of contact Speed: small radius causes slow flow Exchange at capillaries Direct diffusion blood gasses Between pores of endothelial cells small molecules can pass (not proteins) Pinocytosis larger molecules like proteins, lipids Some substances cross the capillary wall by bulk flow of fluids Ultrafiltration Reabsorption Bulk flow 20

21 Arteriole Bulk flow at capillaries outward ultrafiltration blood to venue inward reabsorption Bulk flow at capillaries Plasma proteins outward ultrafiltration blood to venue inward reabsorption blood tissue cells blood tissue cells Bulk flow occurs by the changing differences in hydrostatic and osmotic pressures between plasma (inside) and interstitial fluid (outside) When fluids leave capillaries, most plasma proteins remain Bulk flow at capillaries blood Plasma proteins outward ultrafiltration blood to venue inward reabsorption tissue cells Plasma has a higher concentration of proteins, producing osmotic pressure from interstitial fluid to plasma Plasma-colloid osmotic pressure Forces of bulk flow Plasma colloid pressure blood pressure (hydrostatic) Interstitial pressure 1 Plasma colloid pressure 25 Reabsorption Ultrafiltration 9 blood pressure (hydrostatic) Venule 21

22 Bulk flow Fluid is exchanged b/w plasma and interstitial fluid Site of short-term maintenance of fluid balance Interstitial fluid that is not absorbed by veins drains into lymphatic system Venule Arteriole lymphatic vessel Lymphatic System Lymph nodes Lymph formed from interstitial fluid Functions: Drainage channels Absorption of fats from intestine Deliver pathogens to nodes where there are many lymphocytes 22

23 Lymphatic vessels Fluid pressure fluid cannot push out from inside 23