Ch 12 Heart and Circulatory System The Body’s Transport System

4 Chambered Heart – size of clenched fist 2 Atria 2 Ventricles Arteries (efferent vessels) Veins (afferent vessels) Layers of the Heart Epicardium – outmost layer; covers surface of heart Myocardium – muscle layer; contains cardiac muscle, blood vessels and nerves Endocardium – lines heart’s chambers and valves; composed of simple squamous tissue

Two Circuits for Blood Pulmonary Circuit: right side of heart; receives blood and transports de-oxygenated blood to lungs. Systemic Circuit: left side of heart; supplies body with oxygenated blood.

Pericardium is the shiny covering around the heart. Function: To reduce friction between surrounding surfaces as heart beats Protect the heart Anchor the surrounding structures

Characteristics of Heart Muscle. Intercalated discs. Involuntary Characteristics of Heart Muscle Intercalated discs Involuntary Striated One nuclei per cell Intercalated disks - allows heart to beat as one unit

Location of Heart

Structure of the Heart

Main Veins into heart Main Arteries Coronary Sinus Superior Vena Cava Inferior Vena Cava Pulmonary Vein Main Arteries Coronary Artery Pulmonary Artery Aorta 5 1 2 6

Blood flow through the Heart De-oxygenated blood from the body enters the R atrium and is pumped to the R ventricle. From the R ventricle deO2 blood is sent to the lungs where gas exchange occurs. Oxygenated blood enters the L atria and is sent to the L ventricle where it is sent to the body via the aorta.

Flow of blood through heart C Superior Vena Cava Inferior Vena Cava R. atrium R. ventricle Pulmonary trunk (artery) Pulmonary vein L. atrium L. ventricle Aorta A. Brachiocephalic B. L. Common Carotid C. L. Subclavian A 9 1 6 5 7 3 8 4 2

Coronary Arteries

Vein

Difference in myocardium thickness between R. ventricle and L Difference in myocardium thickness between R. ventricle and L. ventricle. Why?

Valves of the Heart Atrioventricular Valves - one way valves; prevent back flow of blood -chordae tendineae - papillary muscles Tricuspid – 3 flaps Found between R atrium and R. ventricle Bicuspid (mitral) – 2 flaps Found between L atrium and L. ventricle

Anatomy of AV valves One-way valves Atrioventricular valves Chordae tendineae Papillary muscles

Semilunar Valves Located in Pulmonary Artery and Aortic Artery 3 flaps Prevents blood from flowing back into ventricles Posterior Anterior

Valve position when ventricles relaxed

Valve position when ventricles contract

Heart Sounds Two sounds (lubb-dupp) 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

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 18.19

Blood Flow and Valve Function

Cardiac Muscle Contraction Rapid Depolarization: Threshold is reached along the membrane. Causes Na+ channels in the sarcolemma to open Na+ enters cell reversing membrane potential from –90 mV to +30 mV (Na+ gates close) Plateau: Calcium channels open and Ca+2 enters sarcoplasm Ca+2 also is released from SR Ca+2 surge prolongs the depolarization phase and delays repolarization (excess + ions in cell) Repolarization: Ca+2 begin to close; K+ channels open and K+ leaves the cell.

In Cardiac muscle, depolarization lasts longer In Cardiac muscle, depolarization lasts longer. Thus cardiac muscle can’t increase tension with another impulse; tetanus doesn’t occur. Why is this important?

Heart Physiology: Electrical Events Intrinsic cardiac conduction system A network of noncontractile (autorhythmic) cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart Nodes – cells that are responsible for starting the impulse Conducting cells – distribute the impulse to the myocardium 1 % of the heart’s cardiac cells have this capability

Internal Conduction System 1. Sinoatrial node 2. AV node 3. AV bundle or Bundle of HIS 4. R and L bundle branches 5. Purkinge fibers Nodes – cluster of nervous tissue that begins an impulse. 5

Sequence of Excitation Sinoatrial (SA) node (pacemaker) Generates impulses about 70-80 times/minute (sinus rhythm) Depolarizes faster than any other part of the myocardium

Sequence of Excitation Atrioventricular (AV) node Delays impulses approximately 0.1 second Allows for Atria to contract Depolarizes 40-60 times per minute in absence of SA node input

Sequence of Excitation Conducting Cells Atrioventricular (AV) bundle (bundle of His) Right and left bundle branches Two pathways in the interventricular septum that carry the impulses toward the apex of the heart Sequence of Excitation

Sequence of Excitation Purkinje fibers Complete the pathway into the apex and ventricular walls

(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 18.14a

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 QRS complex: ventricular depolarization (AV node) T wave: ventricular repolarization

Normal EKG has 3 distinct waves. 1st wave (P) - SA node fires - Natural Pacemaker - fires around 70-80 times/minute The atria depolarize Impulse is being generated across R and L atria via diffusion. .1s after P wave, atria contract.

AV Node fires; depolarization of ventricles. AV node – back up pacemaker - Beats 40-60 times/minute - Impulse is delayed at bundle of HIS until Atria contract. 2nd wave (QRS) AV Node fires; depolarization of ventricles. Q-R interval represents beginning of atrial repolarization and AV node firing; ventricles depolarize R-S interval represents beginning of ventricle contractions S-T End of Ventricular depolarization

3rd Wave (T) T wave repolarization of ventricles Ventricles return to normal relaxed state. In a healthy heart, size, duration and timing of waves is consistent. Changes reveal a damage or diseased heart.

QRS complex Ventricular depolarization Ventricular Atrial Sinoatrial node Ventricular depolarization Ventricular repolarization Atrial depolarization Atrioventricular node S-T Segment P-Q Interval Q-T Interval Figure 18.16

Atrial depolarization, initiated by the SA node, causes the P wave. Repolarization P T Q S Atrial depolarization, initiated by the SA node, causes the P wave. 1 Figure 18.17, step 1

Atrial depolarization, initiated by the SA node, causes the P wave. Repolarization P T Q S Atrial depolarization, initiated by the SA node, causes the P wave. 1 R AV node P T Q S 2 With atrial depolarization complete, the impulse is delayed at the AV node. Figure 18.17, step 2

Atrial depolarization, initiated by the SA node, causes the P wave. Repolarization P T Q S Atrial depolarization, initiated by the SA node, causes the P wave. 1 R AV node P T Q S 2 With atrial depolarization complete, the impulse is delayed at the AV node. R P T Q S 3 AV node depolarizes; Ventricular depolarization begins at apex, causing the QRS complex. Atrial repolarization occurs. Figure 18.17, step 3

Ventricular depolarization is complete. Repolarization P T Q S Ventricular depolarization is complete. 4 Figure 18.17, step 4

Ventricular depolarization is complete. Repolarization P T Q S 4 Ventricular depolarization is complete. R P T Q S Ventricular repolarization begins at apex, causing the T wave. 5 Figure 18.17, step 5

Ventricular depolarization is complete. Repolarization P T Q S Ventricular depolarization is complete. 4 R P T Q S Ventricular repolarization begins at apex, causing the T wave. 5 R P T Q S Ventricular repolarization is complete. 6 Figure 18.17, step 6

Atrial depolarization, initiated by the SA node, causes the P wave. Q Repolarization R R P T Q P T S 1 Atrial depolarization, initiated by the SA node, causes the P wave. Q S Ventricular depolarization is complete. 4 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 Ventricular repolarization begins at apex, causing the T wave. 5 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 18.17

Homeostatic Imbalances Defects in the intrinsic conduction system may result in: Arrhythmias: irregular heart rhythms Uncoordinated atrial and ventricular contractions Fibrillation: rapid, irregular contractions; useless for pumping blood

Problems with Sinus Rhythms Tachycardia: Heart rate in excess of 100 bpm when at rest If persistent, may lead to fibrillation Bradycardia: Heart rate less than 60 bpm when at rest May result in grossly inadequate blood circulation May be desirable result of endurance training

Homeostatic Imbalances Defective SA node may result Ectopic focus: abnormal pacemaker takes over No P waves; If AV node takes over, there will be a slower rhythm (40–60 bpm) Defective AV node may result in Partial or total heart block Longer delay at AV node than normal No all impulses from SA node reach the ventricles Ventricular fibrillation: cardiac muscle cells are overly sensitive to stimulation; no normal rhythm is established

Problems with Sinus Rhythms 2nd degree heart block; Missed QRS complex SA node is sending impulses, but the AV node is not sending the impulses along the bundle branches 1st degree is represented by a longer delay between P & QRS

(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 40 - 60 beats/min. (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 18.18

1. 2. Normal Rhythm Bradycardia tachycardia 3.

4. 5. Delayed AV Node (1st degree heart block) and missed QRS (2nd degree heart block) Atrial fibulation No P wave; Sa node not firing 6.

Pacemaker Used to correct nodes that are no longer are in rhythm. Becomes the new heart’s pacemaker.

Myocardial Infarction A Heart Attack is caused by oxygen not getting to the heart muscle usually by blockages in the coronary arteries site of blockage

Stopping a Heart Attack Breaking apart the blockage is done with: Medication Angioplasty Stents Coronary bypass surgery (CABG) stent placement

Normal and Restricted Blood Circulation

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 Persistent high blood pressure Multiple myocardial infarcts

Mechanical Events: The Cardiac Cycle Cardiac cycle: all events associated with blood flow through the heart during one complete heartbeat Systole—contraction Diastole—relaxation

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% End diastolic volume (EDV): volume of blood in each ventricle at the end of ventricular diastole

Phases of the Cardiac Cycle Ventricular systole Atria relax and ventricles begin to contract Rising ventricular pressure results in closing of AV valves In ejection phase, ventricular pressure exceeds pressure in the large arteries, forcing the Semilunar valves open End systolic volume (ESV): volume of blood remaining in each ventricle

Phases of the Cardiac Cycle Ventricles relax (diastole) Decrease in pressure causes blood to flow backward Backflow of blood in aorta and pulmonary trunk closes SL valves

Cardiac Cycle

EKG and One Cardiac Cycle

Cardiac Cycle & BP describes the contracting and relaxing stages of the heart. Includes all events that occur in the heart during one complete heart beat. Blood Pressure Systolic pressure: (top number) measurement of the force on the arterial walls when the L ventricle contracts. Diastolic pressure: (bottom number) measurement of the force on the arterial walls when the L ventricle is relaxed. Normal BP = 120/80 Hypertension Hypotension

Cardiac Output Volume of blood pumped by each ventricle in 1 minute. CO = Heart rate (HR) x Stroke volume (SV) Heart Rate (beats/minute) Stroke Volume – volume of blood pumped out of the L. ventricle with each beat. Why Left ventricle? SV = EDV(end diastolic volume) – ESV (end systolic volume) Stroke volume can be determined by subtracting systolic BP volume from diastolic BP volume Stroke volume/pulse pressure = SBP – DBP

Cardiac Output in a normal adult is 4.5 – 5 Liters of blood per minute At rest: CO (ml/min) = HR (75 beats/min)  SV (70 ml/beat) = 5.25 L/min Varies with body’s demands Change in HR or force of contraction Cardiac Reserve – the heart’s ability to push cardiac output above normal limits difference between resting and maximal CO Healthier hearts can have a large increase in C.R. Athlete 7X C.O. = 35L/minute Nonathlete 4X C.O. = 20L/minute

Factors that Influence Heart Rate Age Gender Exercise Body temperature

Regulation of Stroke Volume Contractility: contractile strength at a given muscle length, independent of muscle stretch and EDV Factors which increase contractility Increased Ca2+ influx due to sympathetic stimulation Hormones (thyroxine and epinephrine) Factors which decrease contractility Increased extracellular K+ Calcium channel blockers

Factors that Control Cardiac Output Blood volume reflexes Autonomic Nervous System with assistance from neurotransmitters and hormones Norepinephrine Acethylcholine Thyroxine Ions Temperature

Blood Volume Reflexes Frank Starling Law of the Heart Stroke volume is controlled by Preload - the degree to which cardiac muscles are stretched just before they contract. “More blood in = More blood out” Increase in stretch is caused by an Increase in the venous return to the right atrium which causes the walls of the right atrium to stretch. Increase in stretch causes SA node to depolarize faster; increasing HR Increase in stretch also increases force of contraction; Stroke volume At rest heart walls are not overstretched; ventricles don’t need forceful contractions

Autonomic Nervous System Controlled by Medulla oblongata Parasympathetic (Resting and Digesting) Stimulates Vagus nerve (CN X) – decreases SV and HR; decreasing CO Acetylcholine – decreases HR and SV; opposite action on cardiac muscle then on skeletal muscle (stimulates) Sympathetic (Fight or Flight) – prepares the body for stress Secretes Norephinephrine and epinephrine – increases HR and SV; increasing CO Increasing HR causes overstretch (Frank S. law) Beta blockers-

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. AV node SA node Parasympathetic fibers Sympathetic fibers Interneurons Figure 18.15

Hypercalcemia Excess Ca ions in muscle cell Extended state of contraction; fatal Hypocalcemia Low Ca levels; results in no/weak contractions Hyperkalemia High levels of K Interferes with depolarization of SA and AV nodes Results in heart block Increase in Na Blocks Ca No Ca; no T&T moving out of way No/weak contractions

Temp > 98.6°F Increases HR and SV Increase CO Temperature < 95° F Slows depolarization Slows contraction Decrease 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 Stroke volume Heart rate Cardiac output Initial stimulus Physiological response Result Figure 18.22