Human Anatomy and Physiology

Human Anatomy and Physiology
Cardiovascular System: The Heart: Part B

Heart B Objectives Describe the components of heart’s intrinsic conduction system Draw and label a normal electrocardiogram tracing Name some abnormalities detected on ECG tracing Describe normal heart sounds Name and explain the effects of common factors that regulate stroke volume and heart rate

What do you Remember about Physiological roles of Calcium?
Bones: Structure of bone matrix Osteoblasts/ osteoclasts PTH/ to some extent calcitonin Muscle contraction Excitation-contraction coupling Role in blood clotting Role in cell stimulation as second messenger Nerve impulse Neurotransmitter release via gated Ca+2 channels For depolarization in some special senses

1 2 3 Action Depolarization is potential due to Na+ influx through
fast voltage-gated Na+ channels. A positive feedback cycle rapidly opens many Na+ channels, reversing the membrane potential. Channel inactivation ends this phase. 1 Plateau 2 Tension development (contraction) Membrane potential (mV) 1 3 Tension (g) Plateau phase is due to Ca2+ influx through slow Ca2+ channels. This keeps the cell depolarized because few K+ channels are open. 2 Absolute refractory period Depolarization: Na influx through fast voltage gated Na channels/ A positive feedback cycle rapidly opens many Na channels, reversing the membrane potential quickly Plateau phase: calcium influx through slow calcium channels/ very diff from skeletal muscle/ those fast Na channels opened slow Ca channels so extracellular Ca surges into membrane…so instead of depolarization, the polarization lingers…also more Ca entering cell so cells are continuing to contract. There are a few K channels open now so some movement towards depolarization Repolarization: Ca channels finally inactivated, K channels opened. During repolarization, Ca is pumped back into SR and the extracellular space Notice the action potential and contractile phase last longer in cardiac than skeletal muscle Repolarization is due to Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its resting voltage. 3 Time (ms) Figure 17.12

Energy Requirements of Cardiac Muscle
More mitochondria Aerobic respiration Means it must get oxygen Any energy source glucose lipids/ fatty acids proteins lactic acid ISCHEMIC

Action potential Threshold Pacemaker potential 2 2 3 1 1 1 2 3
Different from other cells as they DO NOT have a stable resting potential Sometimes called the cardiac pacemaker cells Note the unstable resting potential…always continuously depolarizing…drifting slowly to threshold These spontaneously changing membrane potentials are called pacemaker potentials or prepotentials…and they trigger the action potential that spreads throughout heart 3 steps: pacemaker potential: special prperties of ion channels of the sarcolemma. end of action potential closes K channels and opens slow Na channels…Na influx alters balance between K loss and membrane becomes less negative Depolarization: @ threshold (-40mV), Ca channels open and this (not really Na) produces rising phase of action potential and reverses membrane potential Repolarizaiton: as in other excitable cells, the falling pahse of the action potential and repolarization reflect opening of K channels and K eflux from cell Pacemaker potential This slow depolarization is due to both opening of Na+ channels and closing of K+ channels. Notice that the membrane potential is never a flat line. 1 Depolarization The action potential begins when the pacemaker potential reaches threshold. Depolarization is due to Ca2+ influx through Ca2+ channels. 2 Repolarization is due to Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its most negative voltage. 3 Figure 17.13

Autorhythmic Cells Review
Have unstable resting potentials (pacemaker potentials or prepotentials) due to open slow Na+ channels At threshold, Ca2+ channels open Explosive Ca2+ influx produces the rising phase of the action potential Repolarization results from inactivation of Ca2+ channels and opening of voltage-gated K+ channels Remember our neurons and skeletal muscles can stay at a resting membrane potential

Heart Physiology: Electrical Events
The cardiac muscle does not depend on the nervous system to contract Setting the basic heart contraction rhythm depends on: Presence of gap junctions Intrinsic cardiac conduction system: A network of noncontractile (autorhythmic) cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart Intrinsic cardiac conduction system: NON contractile cells…their job is to initiate and distribute an impulse (depolarization) in an orderly and sequential fashion They need gap junctions to then spread the ions quickly Cells of this intrinsic cardiac conduction system are autorhythmic cells

Autorhythmic cardiac cells
Not all cardiac muscle cells are autorhythmic…only a small percentage Located throughout heart to set up a stimulation sequence Sinatrial node → atrioventricular node → atrioventricular bundle → right and left bundle branches → Purkinje fibers in ventricular walls Autorhythmic cells are found only in the following areas and

(a) Anatomy of the intrinsic conduction system showing the
Superior vena cava Right atrium The sinoatrial (SA) node (pacemaker) generates impulses. 1 Internodal pathway The impulses pause (0.1 s) at the atrioventricular (AV) node. 2 Left atrium The atrioventricular (AV) bundle connects the atria to the ventricles. 3 Purkinje fibers The bundle branches conduct the impulses through the interventricular septum. 4 Sinoatrial node (SA node): crescent shaped located in right atrial wall, just inferior to entrance of the superior vena cava 75 beats per minute Pace setter for heart…no other region of conduction system has faster depolarization rate Pacemaker and its rhythm is called the sinus rhythm Atrioventricular node (AV node) Gets depolarization ions through gap junctions from SA node and via internodal pathway Located in inferior portion of interatrial septum, immediately above tricuspid valve Impulse is delayed here for about .1sec allowing entire atria to respond and complete their contraction before ventricles contract The AV node is the slowest portion of the conduction system Atrioventricular bundle (AV bundle/ bundle of His) Superior part of interventricular septum NOT connected by gap junctions…only electrical connection between AV node and AV bundle Fibrous cardiac skeleton is nonconducting and insulates the rest of AV junction Right and left bundle branches …basically AV bundle split into two branches Head to apex Subendocardial conducting network (Purkinje fibers): essentially long strands of barrel shaped cells Bulk of depolarization is based on gap junctions between the ventricular muscle cells Inter- ventricular septum The Purkinje fibers depolarize the contractile cells of both ventricles. 5 (a) Anatomy of the intrinsic conduction system showing the sequence of electrical excitation Figure 17.14a

Heart Physiology: Sequence of Excitation
Sinoatrial (SA) node Known as the Heart Pacemaker Located in right atrial wall just inferior to entrance of superior vena cava Generates impulses about 75 times/minute Depolarizes faster than any other part of the myocardium SA node characteristic rhythm is called the sinus rhythm and determines the heart rate

Atrioventricular (AV) node Located on inferior portion of interatrial septum, immediately above tricuspid valve Smaller diameter fibers; fewer gap junctions Delays impulses approximately 0.1 second This allows the atria to respond and complete their contraction before the ventricles contract Would naturally depolarizes 50 times per minute in absence of SA node input

Atrioventricular (AV) bundle This is also called the bundle of His In the superior part of the interventricular septum The atria and ventricles are not connected by gap junctions so…this is the Only electrical connection between the atria and ventricles

Right and left bundle branches Two pathways in the interventricular septum that carry the impulses toward the apex of the heart

Purkinje fibers Complete the pathway into the apex and turn superiorly up the ventricular walls Bulk of depolarization along Purkinje fibers or cell to cell transmission via gap junctions Because left ventricle is so much larger than right, Purkinje network more elaborate on left AV bundle and Purkinje fibers naturally depolarize only 30 times per minute in absence of AV node input

(a) Anatomy of the intrinsic conduction system showing the
Superior vena cava Right atrium The sinoatrial (SA) node (pacemaker) generates impulses. 1 Internodal pathway The impulses pause (0.1 s) at the atrioventricular (AV) node. 2 Left atrium The atrioventricular (AV) bundle connects the atria to the ventricles. 3 Purkinje fibers The bundle branches conduct the impulses through the interventricular septum. 4 Inter- ventricular septum The Purkinje fibers depolarize the contractile cells of both ventricles. 5 (a) Anatomy of the intrinsic conduction system showing the sequence of electrical excitation Figure 17.14a

Summary of Intrinsic Conduction System
Total time between initiation of impulse by SA node and depolarization of last ventricular muscle cell .22 seconds in a healthy heart Ventricular contraction almost immediately follows ventricular depolarization wave a “wringing” motion from apex toward atria. Ejects blood in ventricles into large arteries Timing is everything Cardiac conduction system coordinates and synchronizes heart activity Without it impulses would travel much more slowly…. .3 to .5 m/s too slow as some fibers contract long before others

Homeostatic Imbalances
Defects in the intrinsic conduction system Arrhythmias: irregular heart rhythms Uncoordinated atrial and ventricular contractions Fibrillation rapid, irregular contractions; useless for pumping blood Heart must be defibrillated quickly to prevent death Ectopic focus Abnormal pacemaker or AV node takes over (40-60 bpm) Extrasystole Small region of heart becomes overexcited (caffeine, nicotine) and adds extra contraction Heart block Any damage to AV node so ventricles don’t get pacing impulse Arrhythmias…irregular heart rhythms Fibrillation is a condition of rapid, irregular or out of phase contractions in which control of heart rhythm is taken away from SA node must correct via defibrillating by electric shock/ inplantable cardioverter defibirllators (ICDs) or pacemakers Ectopic focus: an abdnormal pacemaker that takes place of SA node/ usually the AV node so the heart rate is bpm Extrasystole: A premature contraction. here the SA node is working fine…but there is a small area that starts beating faster than SA…usually result of too much caffeine (many cups), nicotine (excessive smoking). The problem is that the contraction that is started by these temporary stimulated areas is excessively long , so the heart fills a long time…then the next normal contraction is felt like a thud. Really bad if it is premature ventricular contractions Heart block: no impulses get through to ventricles…the only route for impulse transmission is from atria to ventricles through the AV node…so damage to AV node interferes with ventricles ability to receive pacing impulses…in total heart block, no impulses arrive to ventricles so they beat at their own autoarrhythmic cells pace…too slow to maintain adequate circulation. Partial block some impulses get through but not enough for adequate pacing…in both instances artificial pacemakers inserted

Extrinsic Innervation of the Heart
Heartbeat is modified by the ANS Cardiac centers are located in the medulla oblongata Cardioacceleratory center innervates SA and AV nodes, heart muscle, and coronary arteries through sympathetic neurons Increases both rate and force of heartbeat Cardioinhibitory center inhibits SA and AV nodes through parasympathetic fibers in the vagus nerves Slows heart beat Although it’s the intrinsic conduction system that sets the basic heart rate the ANS modifies the march sympathetic is accelerator increasing both rate and force of heartbeat parasympathetic is brakes Cardiac centers in medulla oblongata cardioacceleratory center to sympathetic neurons in T1-T5 level cardioinhibitory center sends impulses to the parasympathetic dorsal vagus nucleus in medulla…more stimulation on SA and AV nodes

Dorsal motor nucleus of vagus The vagus nerve (parasympathetic)
decreases heart rate. Cardioinhibitory center Medulla oblongata Cardio- acceleratory center Sympathetic trunk ganglion Thoracic spinal cord Sympathetic trunk Sympathetic cardiac nerves increase heart rate and force of contraction. Although it’s the intrinsic conduction system that sets the basic heart rate the ANS modifies the march sympathetic is accelerator increasing both rate and force of heartbeat parasympathetic is brakes Cardiac centers in medulla oblongata cardioacceleratory center to sympathetic neurons in T1-T5 level/ note where it stimulates the heart: SA and AV nodes, heart muscle, coronary arteries cardioinhibitory center sends impulses to the parasympathetic dorsal vagus nucleus in medulla…more stimulation on SA and AV nodes AV node SA node Parasympathetic fibers Sympathetic fibers Interneurons Figure 17.15

Parasympathetic Sympathetic Eye Eye Brain stem Salivary glands Skin*
Cranial Salivary glands Sympathetic ganglia Heart Cervical Lungs Lungs T1 Heart Stomach Thoracic Stomach Pancreas Liver and gall- bladder Pancreas L1 Liver and gall- bladder Adrenal gland Lumbar Bladder Bladder Genitals Genitals Sacral Figure 14.3

Electrocardiogram (ECG) Electrokardiogram (EKG)
QRS complex Sinoatrial node Ventricular depolarization Ventricular repolarization Atrial depolarization Atrioventricular node Electrical currents generated and transmitted through the heart spread throughout the body and can be detected with a machine called an electrocardiograph. An electrocardiogram ECG or EKG is the graphic record of heart activity measured by this machine. The reason we use EKG is that the original electrocardiograph was made by a Dutch scientist and in Dutch/German it is Kardio with a K Important to note this is a composite of all action potentials generated by nodal and contractile cells at a given time…it is NOT a tracing of a single action potential To record an ECG, recording electrodes (typically 12 leads) are placed at various sites on the body surface S-T Segment P-Q Interval Q-T Interval Figure 17.16

EKG leads Remember: An EKG/ ECG is a COMPOSITE
of all action potentials generated at a given time Important to note this is a composite of all action potentials generated by nodal and contractile cells at a given time…it is NOT a tracing of a single action potential To record an ECG, recording electrodes (typically 12 leads) are placed at various sites on the body surface. Three are bipolar leads that measure the voltage difference either between the arms or between an arm and a leg, nine others are unipolar leads. For our lab you will just be using 3..two wrist and an ankle.

QRS complex Ventricular depolarization Ventricular Atrial
Sinoatrial node Ventricular depolarization Ventricular repolarization Atrial depolarization Atrioventricular node Typical ECG has three almost immediatedly distinguishable waves or deflections: P wave: small/ lasts about .08 seconds/ results from the movement of depolarization wave from SA node through atria/ about .1 sec after P wave begins, the atria contract (think of your heart…not much of contraction relatively speaking) QRS complex: results from ventricular depolarization/ complicated shape because the paths of depolarization wave travels through the ventricular walls produces lots of changes in current direction/ time for each ventricle to depolarize depends on its size relative to the other ventricle/ average duration .08 seconds T wave: caused by ventricular repolarization/ lasts .16 seconds/ repolarization is slower than depolarization so T wave is more spread out and has a lower amplitude (height on image) than QRS complex/ atrial repolarization not really visible because it takes place during ventricular excitation so it usually obscured by the QRS complex S-T Segment P-Q Interval Q-T Interval Figure 17.16

Electrocardiography Electrocardiogram (ECG or EKG): a composite of all the action potentials generated by nodal and contractile cells at a given time Three waves P wave: depolarization of SA node Atria contracts .1second after P wave starts QRS complex: ventricular depolarization Ventricles contract after QRS starts T wave: ventricular repolarization Atrial reopolarization is masked by large QRS

Atrial depolarization, initiated by the SA node, causes the P wave. Q
Repolarization R R P T T Q P S 1 Atrial depolarization, initiated by the SA node, causes the P wave. Q S 4 Ventricular depolarization is complete. AV node R R P T P T Q S With atrial depolarization complete, the impulse is delayed at the AV node. 2 Q S 5 Ventricular repolarization begins at apex, causing the T wave. AV valves open/ SL valves closed AV valves open/ atrial contraction/ SL valves closed AV valves would start to close here (lub) as ventricles depolarize and begin to contract/ SL valves closed AV valves stay closed/ SL valves open/ ventricles contract SL valves close (dub) / ventricles repolarize and stop contraction…relax/ AV valves still closed AV valves open again/ can start filling ventricle again R R P T P T Q S Q 3 S Ventricular depolarization begins at apex, causing the QRS complex. Atrial repolarization occurs. 6 Ventricular repolarization is complete. Figure 17.17

QRS complex Ventricular depolarization Ventricular Atrial
Sinoatrial node Ventricular depolarization Ventricular repolarization Atrial depolarization Atrioventricular node P-R or P-Q interval: time from the beginning of atrial excitation to the beginning of ventricular excitation/ about .16 seconds Most accurately called the P-Q interval since Q marks the beginning of ventricular excitation, but the Q wave is not always visible P-R interval marks: atrial depolarization/ atrial contraction/ passage of depolarization wave through the rest of the conduction system and beginning of ventricular excitation P-R is good estimate of atrial function…if too long may indicate first degree heart block or electrolyte disturbances S-T segment: When action potentials of the ventricular myocytes are in their plateau phases…the entire ventricular myocardium is depolarized and ventricular contraction is occurring. If this segment is elevated or depressed, indicates cardiac ischemia Q-T interval lasts about .38 seconds and is the period from the beginning of ventricular depolarization through repolarization/ if prolonged reveals abnormal repolarization that increases risk of ventricular arrhythmias/ some medications can cause Q-T interval to be longer S-T Segment P-Q Interval Q-T Interval Figure 17.16

(a) Normal sinus rhythm. (b) Junctional rhythm. The SA
node is nonfunctional, P waves are absent, and heart is paced by the AV node at beats/min. Normal heart rate is 60 to 100 beats per minute Less than 60: bradycardia More than 100: tachycardia (c) Second-degree heart block. Some P waves are not conducted through the AV node; hence more P than QRS waves are seen. In this tracing, the ratio of P waves to QRS waves is mostly 2:1. (d) Ventricular fibrillation. These chaotic, grossly irregular ECG deflections are seen in acute heart attack and electrical shock. Figure 17.18

Reading Heart Rate from EKG
Each little square is 25mm/sec Multiply by 60 sec/min Divide by the number of squares from R to R peak Alternative method: Count number of QRS complexes in 6 sec Multiply by x10 Can count any peak…just want to know how many squares in entire cardiac cycle, or one heart beat Many machines will mark the 3 second intervals for counting purposes…three seconds is 15 large squares Better to count for 6 seconds than just three EKG paper is a grid where time is measured along the horizontal axis. Each small square is 1 mm in length and represents 0.04 seconds. Each larger square is 5 mm in length and represents 0.2 seconds. Voltage is measured along the vertical axis. 10 mm is equal to 1mV in voltage.

One more method Use the sequence Count from the first QRS complex, the first thick line is 300, the next thick line 150 etc. Stop the sequence at the next QRS complex. When the second QRS complex is between two lines, take the mean of the two numbers from the sequence

Entire strip is 6 seconds: This heart rate is __ beats/ min?
Normal heart rate is 60 to 100 beats per minute Less than 60: bradycardia More than 100: tachycardia

Heart Sounds Two sounds (lub-dub) associated with closing of heart valves First sound occurs as AV valves close and signifies beginning of systole Second sound occurs when SL valves close at the beginning of ventricular diastole Heart murmurs: abnormal heart sounds most often indicative of valve problems Because mitral (left AV) valve closes slightly before tricuspid valve (rt AV), the aortic SL generally snaps shut just before the pulmonary valve…so technically can auscultate 4 sounds 

Aortic valve sounds heard in 2nd intercostal space at
right sternal margin Pulmonary valve sounds heard in 2nd intercostal space at left sternal margin Mitral valve sounds heard over heart apex (in 5th intercostal space) in line with middle of clavicle Tricuspid valve sounds typically heard in right sternal margin of 5th intercostal space Figure 17.19

Mechanical Events: The Cardiac Cycle
Cardiac cycle: all events associated with blood flow through the heart during one complete heartbeat Systole—contraction Diastole—relaxation Always follow the electrical events seen in the ECG Marked by a succession of pressure and blood volume changes Note: the “cardiac cycle” is really the mechanical part that FOLLOWS the electrical impulse (the EKG) Look at specifically changes in pressure and volume Systole: squeeze…contraction Diastole: relax, open up, dialate

(mid-to-late diastole)
Left heart QRS P T P Electrocardiogram Heart sounds 1st 2nd Dicrotic notch Aorta Pressure (mm Hg) Left ventricle Atrial systole Left atrium EDV Ventricular volume (ml) SV ESV Atrioventricular valves Open Closed Open Start with heart in total relaxation…atria and ventricles quiet/ mid to late diastole Ventricular filling: Pressure in heart is low Blood returning from body is flowing passively into ventricles through open AV valves/ SL valves are closed More than 80% of ventricular filling occurs in this relaxed state…as fills AV valves slowly drift towards closed position Last 20% of ventricular blood is delivered in atrial contration (systole) after P wave…note slight bump in atrial and ventricular pressure This is the EDV: end diastolic volume where ventricles have the maximum volume of blood as they move to systole Now the atria relax and the ventricles depolarize (QRS complex) Ventricular systole: as ventricles begin to contract…pressure greater than in atria and AV valves close (lub) there is a brief period where both AV and SL valves are closed…and ventricles contracting…this is isovolumetric contraction phase…blood volume in chambers remain constant as ventricle contract (kindof like isometric exercises? ) as ventricular pressure rises, finally exceeds pressure in large arteries pushing on ventricles, this pushes SL valves open, blood rushes from ventricles into arteries (aorta and pulmonary trunk)…during this period the blood pressure in aorta normall reaches 120mm Hg (the pulmonary artery would be only about 24 mm Hg as it doesn’t need to push so far) Atria are relaxed but see a short rise in pressure because of ventricular systole or push 3. Isovolumetric relaxation: during brief phase following the T wave, the ventricles relax…there is still some blood left in their chambers, this is the ESV (end systolic volume)…ventricles no longer compressed so pressure drops quickly and blood in aorta and pulmonary trunk falls back toward heart…this is caught in SL “cups” and slams these doors shut (dub)…the blood fills up and splashes back into arteries, called the dicrotic notch on pressure graph…again, so change in volume of chambers as both valves are closed here Aortic and pulmonary valves Closed Open Closed Phase 1 2a 2b 3 1 Left atrium Right atrium Left ventricle Right ventricle Ventricular filling Atrial contraction Isovolumetric contraction phase Ventricular ejection phase Isovolumetric relaxation Ventricular filling 1 2a 2b 3 Ventricular filling (mid-to-late diastole) Ventricular systole (atria in diastole) Early diastole Figure 17.20

Phases of the Cardiac Cycle
Ventricular filling—takes place in mid-to- late diastole AV valves are open 80% of blood passively flows into ventricles Atrial systole occurs, delivering the remaining 20% Follows depolarization of P wave Sudden slight rise in atrial pressure End diastolic volume (EDV): volume of blood in each ventricle at the end of ventricular diastole

Ventricular systole Atria relax and ventricles begin to contract Rising ventricular pressure results in closing of AV valves Isovolumetric contraction phase (all valves are closed) In ejection phase, ventricular pressure exceeds pressure in the large arteries, forcing the SL valves open At this point blood pressure in aorta reaches 120 mm Hg End systolic volume (ESV): volume of blood remaining in each ventricle

Isovolumetric relaxation occurs in early diastole Follows T wave Ventricles relax because blood in their chambers (called end systolic volume or ESV) is no longer compressed Backflow of blood in aorta and pulmonary trunk closes SL valves and causes dicrotic notch (brief rise in aortic pressure) Here ventricles are totally closed chambers again

(mid-to-late diastole)
Left heart QRS P T P Electrocardiogram Heart sounds 1st 2nd Dicrotic notch Aorta Pressure (mm Hg) Left ventricle Atrial systole Left atrium EDV Ventricular volume (ml) SV ESV Atrioventricular valves Open Closed Open Start with heart in total relaxation…atria and ventricles quiet/ mid to late diastole Ventricular filling: Pressure in heart is low Blood returning from body is flowing passively into ventricles through open AV valves/ SL valves are closed More than 80% of ventricular filling occurs in this relaxed state…as fills AV valves slowly drift towards closed position Last 20% of ventricular blood is delivered in atrial contration (systole) after P wave…note slight bump in atrial and ventricular pressure This is the EDV: end diastolic volume where ventricles have the maximum volume of blood as they move to systole Now the atria relax and the ventricles depolarize (QRS complex) Ventricular systole: as ventricles begin to contract…pressure greater than in atria and AV valves close (lub) there is a brief period where both AV and SL valves are closed…and ventricles contracting…this is isovolumetric contraction phase…blood volume in chambers remain constant as ventricle contract (kindof like isometric exercises? ) as ventricular pressure rises, finally exceeds pressure in large arteries pushing on ventricles, this pushes SL valves open, blood rushes from ventricles into arteries (aorta and pulmonary trunk)…during this period the blood pressure in aorta normall reaches 120mm Hg (the pulmonary artery would be only about 24 mm Hg as it doesn’t need to push so far) Atria are relaxed but see a short rise in pressure because of ventricular systole or push 3. Isovolumetric relaxation: Aortic and pulmonary valves Closed Open Closed Phase 1 2a 2b 3 1 Left atrium Right atrium Left ventricle Right ventricle Ventricular filling Atrial contraction Isovolumetric contraction phase Ventricular ejection phase Isovolumetric relaxation Ventricular filling 1 2a 2b 3 Ventricular filling (mid-to-late diastole) Ventricular systole (atria in diastole) Early diastole Figure 17.20

Summary of Cardiac Cycle
Blood flow through the heart is controlled by pressure changes Blood flows down a pressure gradient through any available opening Right and left side essentially same except for the actual pressure Pulmonary circulation is low-pressure typical systolic and diastolic pressures for pulmonary artery: 24 and 8 mm Hg respectively Systemic circulation must be high pressure Systolic/ diastolic aortic pressure: 120 and 80 mg Hg Assuming the average heart beats 75 times each minute, the cardiac cycle lasts about .8 seconds with the atrial systole counting for .1 sec and the ventricular systole counting for .3 sec…the remaining .4 sec is total heart relaxation or quiescent period

Cardiac Output (CO) Volume of blood pumped by each ventricle in one minute CO = heart rate (HR) x stroke volume (SV) HR = number of beats per minute SV = volume of blood pumped out by a ventricle with each beat 75bpm x 70mL/beat = 5.25 L/ min Average adult blood volume: 5 L In general, the SV correlates with the force of the ventricular contraction EDV – ESV The HR would be how many times this volume was pushed out So CO would be measured in volume/ minute Normal adult cardiac output would be : 75 bpm x 70 ml/beat so 5250 mL per minute or 5.25 L per minute The normal adult blood volume is 5L (a little more than a gallon) so that means the entire blood supply passes through each side of the heart at least once per minute!

Cardiac Output (CO) CO at rest (ml/min) =
HR (75 beats/min)  SV (70 ml/beat) = 5.25 L/min Cardiac reserve: difference between resting and maximal CO In nonathletic people, the cardiac reserve is typically 4-5 times the resting cardiac output which is about L/ min Maximal CO may reach 35 L/min in trained athletes, which is 7 times the resting CO As HR increases, CO would increase Can increase SV with exercise pump more blood with each pump when exercise Cardiac Reserve: Difference between resting and maximal CO

Exercise (by skeletal muscle and respiratory pumps; see Chapter 19)
Heart rate (allows more time for ventricular filling) Bloodborne epinephrine, thyroxine, excess Ca2+ Exercise, fright, anxiety Venous return Sympathetic activity Parasympathetic activity Contractility EDV (preload) ESV Look at factors that affect cardiac output overall, stroke volume and heart rate specifically Stroke volume: EDV-ESV EDV: normally about 120mL/ affected by how long ventricular diastole lasts and venous pressure ESV: normally 50 mL/ determined by arterial blood pressure and force of ventricular contraction Each ventricle pumps 70 mL which is about 60% of blood in its chamber We are going to look at this in more detail by describing preload (EDV)/ contractility and afterload (affect ESV) Stroke volume Heart rate Cardiac output Initial stimulus Physiological response Result Figure 17.22

Regulation of Stroke Volume
SV = EDV (end diastolic volume) – ESV EDV= end diastolic volume ESV= Volume of blood in ventricles and end of filling Sometimes called afterload Three main factors affect SV Preload Contractility Afterload In this slide on D2L, there was a typo…the preload is EDV and afterload is ESV

Preload: degree of stretch of cardiac muscle cells before they contract (Frank-Starling law of the heart) Cardiac muscle exhibits a length-tension relationship At rest, cardiac muscle cells are shorter than optimal length Slow heartbeat and exercise increase venous return Increased venous return distends (stretches) the ventricles and increases contraction force In a normal heart, the higher the preload, the higher the stroke volume The relationship between preload and stroke volume is called the Frank Starling Law of the Heart Most important factor in preload is venous return…anything that changes that ultimately affects stroke volume and CO Exercise…increases EDV (increases venous pressure so fills more/ faster) during vigorous exercise, SV may double Slowing heart rate…increases EDV (allows more time to fill) The more stretch you get as fill, the more contraction force during systole Conversely, low venous return would result from extremely rapid heart rate or sever blood loss Remember that both systemic and pulmonary circulations are in series…that means if one side of heart suddenly pumps more blood than the other, the increased venous return to the opposite ventricle will increase cardiac muscle stretch and thus increase cardiac output so no backup or accumulation of blood can occur in heart

actin-myosin interaction
Extracellular fluid Norepinephrine Adenylate cyclase Ca2+ b1-Adrenergic receptor Ca2+ channel G protein (Gs) ATP is converted to cAMP Cytoplasm a Phosphorylates plasma membrane Ca2+ channels, increasing extracellular Ca2+ entry GDP Inactive protein kinase A Active protein kinase A Phosphorylates SR Ca2+ channels, increasing intracellular Ca2+ release Phosphorylates SR Ca2+ pumps, speeding Ca2+ removal and relaxation b c Contractility of cardiac muscle is defined as the strength of contraction at a given muscle length Contractility is independent of muscle stretch and EDV Rises when more calcium ions enter the cytoplasm from extracellular fluid and the SR Enhanced contractility means more blood is ejected from the heart (increased SV and lower ESV) Increased sympathetic stimulation increases contractility epinephrine or norepinephrine binding intitiate cyclic AMP to open Ca gated channels/ release Ca from SR more Ca binding to troponin/ increase cross bridges binding in muscle/ increase contraction strength Other chemicals can influence Ca and contractility positive inotropic agents (ino= muscle) are epinephrine, thyroxine, glucagon, drug digitalis, and high levels of extracellular calcium ions negative inotropic agents (decrease or impair contractility) are: acidosis (excessive H ions), rising extracellular K ions, drugs called calcium channel blockers Enhanced actin-myosin interaction binds to Ca2+ Troponin Ca2+ Ca2+ uptake pump SR Ca2+ channel Cardiac muscle force and velocity Sarcoplasmic reticulum (SR) Figure 17.21

Contractility: contractile strength at a given muscle length, independent of muscle stretch and EDV increase contractility Increased Ca2+ influx into cytoplasm due to sympathetic stimulation Hormones (thyroxine, glucagon, and epinephrine) Factors that increase contractility are called positive inotropic agents (ino= muscle, fiber) Negative inotropic agents decrease contractility Acidosis Increased extracellular K+ Calcium channel blockers

Afterload: pressure that must be overcome for ventricles to eject blood In most people, afterload is not a major determinant of stroke volume because afterload is relatively constant Hypertension increases afterload, reducing the ability of ventricles to eject blood, resulting in increased ESV and reduced SV Afterload is the back pressure exerted by arterial blood …basically the pressure the ventricles must overcome to eject blood Usually 80 mm Hg in aorta and 10 mm Hg in pulmonary trunk (diastole blood pressure) In healthy individuals, the afterload is not usually a major determinant of stroke volume because it is relatively constant However hypertension (high blood pressure) increases the level the ventricles must overcome…increases the afterload Ventricles have to work harder and result is more blood remains in heart after systole, increases ESV, reduces SV

Regulation of Heart Rate
A healthy cardiovascular system results in relatively constant stroke volume. Weakened heart or temporary stressors can affect stoke volume and cardiac output Positive chronotropic factors increase heart rate Negative chronotropic factors decrease heart rate Positive chronotropic factors chrono = time increase heart rate Negative chronotropic factors decrease heart rate

Exercise (by skeletal muscle and respiratory pumps; see Chapter 19)
Heart rate (allows more time for ventricular filling) Bloodborne epinephrine, thyroxine, excess Ca2+ Exercise, fright, anxiety Venous return Sympathetic activity Parasympathetic activity Contractility EDV (preload) ESV ANS exerts the most important extrinsic controls affecting heart rate emotional stressors: fright, anxiety physical stressors (exercise) activate the sympathetic nervous system: norepinephrine released at synapses: binds to B1(beta 1) adrenergic receptors in heart, causing threshold to be reached more quickly, as a result, SA node fires more rapidly and heart responds by beating faster Enhances Ca2+ movements in contractile cells which lowers ESV so SV doesn’t decline here as it would if only heart rate were increased Parasympathetic stimulation reduces heart rate when a stressful situation is over…mediated by actetylcholine neurotransmitter which opens K+channels and hyperpolarizes membranes…takes some time because vagal innervation of ventricles is sparse Under resting conditions, both ANS divisions continue to send impulses to SA node of heart, but dominant influence is inhibitory, called vagal tone. Our heart rate is generally slower than it would be if vagal nerve was not innervating it…so cutting a vagal nerve results in immediate increase in heart rate of about 25 bpm. Sensory input that activates either division of ANS is usually generated by baroreceptors which respond to changes in systemic blood pressure…add that to mix next chapter Stroke volume Heart rate Cardiac output Initial stimulus Physiological response Result Figure 17.22

Autonomic Nervous System Regulation
Sympathetic nervous system is activated by emotional or physical stressors Norepinephrine causes the pacemaker to fire more rapidly (and at the same time increases contractility) Enhances Ca2+ movements in contractile cells

Parasympathetic nervous system opposes sympathetic effects Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels The heart at rest exhibits vagal tone (parasympathetic) as the dominant influence on SA node Because vagal innervation of the ventricles is sparse, parasympathetic activity has little or no effect on cardiac contractility

Atrial (Bainbridge) reflex: a sympathetic reflex initiated by increased venous return Stretch of the atrial walls stimulates the SA node Also stimulates atrial stretch receptors activating sympathetic reflexes

Chemical Regulation of Heart Rate
Hormones Epinephrine from adrenal medulla enhances heart rate and contractility Thyroxine increases heart rate and enhances the effects of norepinephrine and epinephrine Intra- and extracellular ion concentrations (e.g., Ca2+ and K+) must be maintained for normal heart function Hormones: Epinephrine: same cardiac effects as norepinephrine Thyroxine: increases body metabolism and heat generation also increases heart rate and enhances effect of epinephrine and norepinephrine Ions: important to have normal plasma electrolyte balances reduced Ca2+ blood levels (hypocalcemia) depressed the heart hypercalcemia increase heart rate and contractility…up to a point…arrhythmias hypokalemia (low blood K+ levels) is life threatening…heart beats feebly and arrhythmically hyperkalemia alters electrical activity of heart by depolarizing the resting potential and may lead to heart block and cardiac arrest

Other Factors that Influence Heart Rate
Age Resting heart rate fastest in fetus, gradually declines throughout life Gender Faster in females (72-80 bpm) than males (64- 72bpm) Exercise Increases heart rate while exercising, but resting heart rate is lower in physically fit Body temperature Heat increases heart rate by enhancing metabolic rate of cardiac cells/ cold decreases Less important than neural factors Resting heart rate in fetus: bpm Resting heart rate in trained athletes can be as low as 40 bpm Heat increases heart rate…so why you feel heart beating with fever

Homeostatic Imbalances
Tachycardia: abnormally fast heart rate (>100 bpm) May result from elevated body temperature, stress, certain drugs, or heart disease If persistent, may lead to fibrillation Bradycardia: heart rate slower than 60 bpm May result from low body temperature, certain drugs, or heart disease May be desirable result of endurance training May result in grossly inadequate blood circulation particularly in poorly conditioned people Bradycardia of athletes: with physical and cardiovascular training: heart hypertrophies and SV increases so lower resting heart rate but still provides the same Cardiac output

Congestive Heart Failure (CHF)
Progressive condition where the CO is so low that blood circulation is inadequate to meet tissue needs Caused by Coronary atherosclerosis Clogging of coronary vessels with fatty buildup Persistent high blood pressure Aortic diastolic pressure over 90 mm Hg Multiple myocardial infarcts Depresses pumping efficiency because of dead heart cells Dilated cardiomyopathy (DCM) Ventricles stretch and become flabby Normal aortic diastolic pressure is 80 mm Hg and the left ventricle needs to exert only a little above that to eject blood…but when 90 mm Hg or more…really puts strain on left ventricle…eventually the stress takes its toll and myocardium becomes weaker Multiple MI s depress pumping ability because fibrous (non contractile) tissue replaces the dead heart cells DCM: cause often unknown/ drug toxicity (alcohol, cocaine, excess catecholamines, chemotherapeutic agents and inflammation of heart following an infection are implicated in some instances) The heart tries to work harder as result in increasing calcium levels in cardiac cells…results in hypertrophy and weakness Because heart is a double pump, each side can initially fail independent of the other…pulmonary congestion occurs if left side fails, essentially suffocating someone Peripheral congestion occurs is right side fails…edema and inability to get nutrients / oxygen Failure of one side eventually leads to whole heart failure prevention: removing excess fluid with diruetics/ reducing afterload with drugs that drive down blood pressure/ increase contractility with digitalis

Human Anatomy and Physiology

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Human Anatomy and Physiology

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