The Heart
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Transcript of The Heart
Anatomy & PhysiologyBio 2402 Lecture
Dr shabeel pn
Review:
Cardiac Cycle Beginning of control system
Review of Cardiac Blood Flow
Be able to trace flow, from start to finish
Sequence of blood flow
Right atrium tricuspid valve right ventricle
Right ventricle pulmonary semilunar valve pulmonary arteries lungs
Lungs pulmonary veins left atrium Left atrium bicuspid valve left ventricle Left ventricle aortic semilunar valve
aorta Aorta systemic circulation
Two systems:
Pulmonary Systemic
Review of Cardiac Blood Flow
Function of chordae tendineae and papillary muscles?
What opens and closes the valves?
New section for today
Control system- Autorhythmic Fibers
See figure 18.14 on page 694 These fibers have an unstable resting
potential due to Na+ & Ca++ leakage in.
Control system- Autorhythmic Fibers
See figure 18.14 on page 694 These fibers have an unstable resting
potential due to Na+ & Ca++ leakage in.
Control system- role of instability of RMP
Sinoatrial node (SA) – Inherent rate of 100 BPM “Sinus Rhythm” – Heart’s pacemaker Location: Upper RA Fastest cells in system
Atrial (Bainbridge) Reflex
Atrial (Bainbridge) reflex – a sympathetic reflex initiated by increased blood in the atria Causes stimulation of the SA node Stimulates baroreceptors in the atria, causing
increased SNS (Sympathetic Nervous System) stimulation
Control system-
Atrioventricular Node (AV) –
Control system-
Atrioventricular Node (AV) – Impulse is delayed here 0.1 second (Why?)
Control system-
Atrioventricular bundle – (Bundle of His)
Control system-
Atrioventricular bundle – (Bundle of His) The only electrical connection between atria
and ventricles Rapidly conducts through Right Bundle
branch, (RBB), Left Bundle Branch (LBB) and Purkinje fibers
Control system-
Right Bundle branch, (RBB), - stimulates septal cells
Left Bundle Branch (LBB) – septal cells Purkinje fibers- most important, stimulates
most of the ventricular walls, and first stimulates the papillary muscles (why?)
Control system-
Time required: 220 ms from SA node to complete depolarization.
Longer time indicates conduction defect
Intrinsic Conduction System
Autorhythmic cells: Initiate action potentials Have unstable resting potentials called
pacemaker potentials Use calcium influx (rather than sodium) for rising
phase of the action potential
Pacemaker and Action Potentials of the Heart
Sequence of Excitation
Sinoatrial (SA) node generates impulses about 75 times/minute
Atrioventricular (AV) node delays the impulse approximately 0.1 second
Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His)
Sequence of Excitation
AV bundle splits into two pathways in the interventricular septum (bundle branches) Bundle branches carry the impulse toward the
apex of the heart Purkinje fibers carry the impulse to the heart apex
and ventricular walls
Cardiac Intrinsic Conduction
Heart Excitation Related to ECG
SA node generates impulse;atrial excitation begins
Impulse delayedat AV node
Impulse passes toheart apex; ventricular
excitation begins
Ventricular excitationcomplete
SA node AV node Purkinjefibers
Bundlebranches
Figure 18.17
Heart Excitation Related to ECG
SA node generates impulse;atrial excitation begins
SA node
Heart Excitation Related to ECG
Impulse delayedat AV node
AV node
Heart Excitation Related to ECG
Impulse passes toheart apex; ventricularexcitation begins
Bundlebranches
Heart Excitation Related to ECG
Ventricular excitationcomplete
Purkinjefibers
Extrinsic Innervation
Heart is stimulated by the sympathetic cardioacceleratory center
Heart is inhibited by the parasympathetic cardioinhibitory center
ECG – What it means
Electrical activity is recorded by electrocardiogram (ECG)
P wave corresponds to depolarization of SA node QRS complex corresponds to ventricular
depolarization T wave corresponds to ventricular repolarization Atrial repolarization record is masked by the larger
QRS complex SEE IP 9 Intrinsic Conduction System pages 3-6
ECG
Heart Sounds - valves
Heart sounds (lub-dup) are associated with closing of heart valves First sound occurs as AV (Tricuspid and Mitral)
valves close and signifies beginning of systole Second sound occurs when SL (Pulmonary &
Aortic) valves close at the beginning of ventricular diastole
Cardiac Cycle
Cardiac cycle refers to all events associated with blood flow through the heart Systole – contraction of heart muscle Diastole – relaxation of heart muscle
Phases of Cardiac Cycle
Ventricular filling – mid-to-late diastole Heart blood pressure is low as blood enters atria
and flows into ventricles AV valves are open, then atrial systole occurs
Phases of Cardiac Cycle
Ventricular systole Atria relax Rising ventricular pressure results in closing of
AV valves Isovolumetric contraction phase Ventricular ejection phase opens semilunar
valves
Phases of Cardiac Cycle
Isovolumetric relaxation – early diastole Ventricles relax Backflow of blood in aorta and pulmonary trunk
closes semilunar valves Dicrotic notch – brief rise in aortic pressure
caused by backflow of blood rebounding off semilunar valves
SEE IP9 Cardiac Cycle pages 3-19
Cardiac Output (CO) and Reserve
CO is the amount of blood pumped by each ventricle in one minute
CO is the product of heart rate (HR) and stroke volume (SV)
HR is the number of heart beats per minute SV is the amount of blood pumped out by a
ventricle with each beat Cardiac reserve is the difference between
resting and maximal CO
Cardiac Output (CO) - Example
CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)
CO = 5250 ml/min (5.25 L/min)
Stroke Volume
SV = end diastolic volume (EDV) minus end systolic volume (ESV)
EDV = amount of blood collected in a ventricle during diastole
ESV = amount of blood remaining in a ventricle after contraction
What affects Stroke Volume?
Preload – amount ventricles are stretched by contained blood
Contractility – cardiac cell contractile force due to factors other than EDV
Afterload – back pressure exerted by blood in the large arteries leaving the heart
Frank-Starling Law of the Heart
Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume
Slow heartbeat and exercise increase venous return to the heart, increasing SV
Blood loss and extremely rapid heartbeat decrease SV
Preload and Afterload
Chemical Regulation of Heart
The hormones epinephrine and thyroxine increase heart rate
Intra- and extracellular ion concentrations (Ca++, K+, Na+) must be maintained for normal heart function
SEE IP9 – Cardiac Output pages 3-9
Regulation of Heart Rate: Autonomic Nervous System
Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise
Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS
PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone
Heart Contractilityand Norepinephrine
Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system
GTP GDP
Inactive protein kinase A
Active protein kinase A
ATP cAMP
GTP
SR Ca2+
channel
Ca2+
Ca2+
bindsto
TroponinEnhancedactin-myosininteraction
Extracellular fluid
Cytoplasm
Adenylate cyclase
Ca2+
channel
Ca2+1-Adrenergicreceptor
Norepinephrine
Ca2+
uptakepump
Sarcoplasmicreticulum (SR)
Cardiac muscleforce and velocity
1
3
2
Figure 18.22
Extrinsic Factors Influencing Stroke Volume
Agents/factors that decrease contractility include: Acidosis Increased extracellular K+
Calcium channel blockers
Extrinsic Factors Influencing Stroke Volume
Contractility is the increase in contractile strength, independent of stretch and EDV (End Diastolic Volume)
Increase in contractility comes from: Increased sympathetic stimuli Certain hormones Ca2+ and some drugs
Cardiac Output
The big picture All factors: Key: Be able
to identify whether a factor influences SV or HR, and which direction
Control system- Clinical Applications
Arrhythmias Uncoordinated atrial and ventricular contractions
Control system- Clinical Applications
Ectopic Foci – Depolarization (beat) originates someplace other than SA node. May be triggered by high caffeine or nicotine Most common cause is low oxygen to a region of
the heart Premature Ventricular contractions (PVC’s) most
serious.
Control system- Clinical Applications
Ventricular Tachycardia – rapid rate stimulated by ventricular ectopic foci.
Control system- Clinical Applications
Ventricular Fibrillation – This is the quivering of muscle – uncoordinated No pumping is occurring Use of defibrillator is indicated here
Control system- Clinical Applications
Congestive Heart Failure Walls thinning, loss of strength May be on either side (r or l) If on left, fluid builds up in lungs (why?)
Treatment: Digitalis – (From poisonous Foxglove family of
plants) – slows the rate, but increases strength (contractility)
Clinical:What is a “Heart attack”?
(Page 692 Btm Left) Ishemia results in: anaerobic metabolism - lactic acid formation: Rising acidity hinders ATP & cannot pump out
Ca++, then: Gap junctions close - cells electrically isolated,
and: If ischemic area is large, pumping action
impaired.
Clinical Application – CHFCongestive Heart Failure
Congestive heart failure (CHF) is caused by: Coronary atherosclerosis Persistent high blood pressure Multiple myocardial infarcts Dilated cardiomyopathy (DCM)
Age-Related Changes Affecting the Heart
Sclerosis and thickening of valve flaps Decline in cardiac reserve – (max HR) Fibrosis of cardiac muscle – (normal) Atherosclerosis (You are as old as your
arteries)
Developmental Aspects of the Heart
Contraction detectable at 23 days
Developmental Aspects of the Heart
Contraction detectable at 23 days 4 chambers by day 25
Fetal Heart Development
Fetal heart structures that bypass pulmonary circulation Foramen ovale connects the two atria Ductus arteriosus connects pulmonary trunk and
the aorta
Congenital Heart Defects