Anatomy

1
Anatomy PhysiologyBio 2402 Lecture

• Instructor Daryl Beatty
• Day 5 Class 5
• The Heart Circulation, Part 3

2
Review

• Cardiac Cycle
• Beginning of control system

3
Review of Cardiac Blood Flow

• Be able to trace flow, from start to finish

4
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

5
Two systems

• Pulmonary
• Systemic

6
Review of Cardiac Blood Flow

• Function of chordae tendineae and papillary
  muscles?
• What opens and closes the valves?

7
New section for today
8
Control system - Autorhythmic Fibers

• See figure 18.14 on page 694
• These fibers have an unstable resting potential
  due to Na Ca leakage in.

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Control system - Autorhythmic Fibers

• See figure 18.14 on page 694
• These fibers have an unstable resting potential
  due to Na Ca leakage in.

10
Control system - role of instability of RMP

• Sinoatrial node (SA)
• Inherent rate of 100 BPM
• Sinus Rhythm Hearts pacemaker
• Location Upper RA
• Fastest cells in system

11
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

12
Control system -

• Atrioventricular Node (AV)

13
Control system -

• Atrioventricular Node (AV)
• Impulse is delayed here 0.1 second (Why?)

14
Control system -

• Atrioventricular bundle (Bundle of His)

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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

16
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?)

17
Control system -

• Time required 220 ms from SA node to complete
  depolarization.
• Longer time indicates conduction defect

18
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

19
Pacemaker and Action Potentials of the Heart
20
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)

21
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

22
Cardiac Intrinsic Conduction
23
Heart Excitation Related to ECG

SA node generates impulse atrial excitation
begins
Impulse delayed at AV node
Impulse passes to heart apex ventricular excitati
on begins
Ventricular excitation complete
SA node
AV node
Purkinje fibers
Bundle branches
Figure 18.17
24
Heart Excitation Related to ECG
SA node generates impulse atrial excitation
begins
SA node
25
Heart Excitation Related to ECG
Impulse delayed at AV node
AV node
26
Heart Excitation Related to ECG
Bundle branches
Impulse passes to heart apex ventricular excitati
on begins
27
Heart Excitation Related to ECG
Ventricular excitation complete
Purkinje fibers
28
Extrinsic Innervation

• Heart is stimulated by the sympathetic
  cardioacceleratory center
• Heart is inhibited by the parasympathetic
  cardioinhibitory center

29
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

30
ECG

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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

32
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

33
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

34
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

35
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

36
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

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Cardiac Output (CO) - Example

• CO (ml/min) HR (75 beats/min) x SV (70 ml/beat)
• CO 5250 ml/min (5.25 L/min)

38
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

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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

40
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

41
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

42
Extrinsic Factors Influencing Stroke Volume

• Agents/factors that decrease contractility
  include
• Acidosis
• Increased extracellular K
• Calcium channel blockers

43
Preload and Afterload
44
STOP HERE

• Lesson 5 starts

45
Chemical Nervous Regulation of the Heart

• Autonomic Regulation
• Hormonal regulation

46
Regulation of Heart Rate Autonomic Nervous System

• Two cardioregulatory centers in the
  MedullaCardioinhibitory
• Cardioacceleratory
• (Remember how fast would the SA node like to
  control it?)

47
Regulation of Heart Rate Autonomic Nervous System

• Sympathetic nervous system (SNS) stimulation is
  activated by stress, anxiety, excitement, or
  exercise
• Works by increasing rate and contractility
• Rate at SA and AV node
• Contractility by Norepinephrine at the myocardium
• This also affects blood pressure!

48
Regulation of Heart Rate Autonomic Nervous System

• 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
• Acetylcholine increases permeability to K

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Chemical Regulation of Heart

• The hormones epinephrine and thyroxine increase
  heart rate
• Extracellular ion concentrations (Ca, K, Na)
  must be maintained for normal heart function
• SEE IP9 Cardiac Output pages 3-9

50
Heart Rate control

• Earliest trigger for increased respiration
  receptors in joints sense motion.
• J
• Increased body temperature triggers heart rate
  blood is heat transfer fluid for body.
• Hypothermia depresses heart rate- conserves core
  temperature.

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Heart Contractilityand Norepinephrine
Extracellular fluid
Norepinephrine
b1-Adrenergic receptor
Ca2
Adenylate cyclase
Ca2 channel

• Sympathetic stimulation releases norepinephrine

Cytoplasm
GTP
1
GDP
GTP
ATP
cAMP
Active protein kinase A
Inactive protein kinase A
Ca2
3
Ca2 uptake pump
2
Enhanced actin-myosin interaction
binds
Troponin
to
Ca2
SR Ca2 channel
Cardiac muscle force and velocity
Sarcoplasmic reticulum (SR)
Figure 18.22
52
Cardiac Output

• The big picture
• All factors
• Key Be able to identify whether a factor
  influences SV or HR, and which direction

53
Control system - Clinical Applications

• Arrhythmias
• Uncoordinated atrial and ventricular contractions

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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 (PVCs) most
  serious.

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Control system - Clinical Applications

• Ventricular Tachycardia rapid rate stimulated
  by ventricular ectopic foci.

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Control system - Clinical Applications

• Ventricular Fibrillation
• This is the quivering of muscle uncoordinated
• No pumping is occurring
• Use of defibrillator is indicated here

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ClinicalWhat 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.

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Clinical Application CHFCongestive Heart
Failure

• Congestive heart failure (CHF) is caused by
• Coronary atherosclerosis (Coronary Artery
  Disease)
• Persistent high blood pressure
• Multiple myocardial infarcts
• Valve Problems
• Dilated cardiomyopathy (DCM)

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Clinical Application CHFCongestive Heart
Failure

• Congestive heart failure
• Sign Sometimes walls hypertrophy appearance
  might be very robust.
• Symptom Tachycardia when untreated
• Cardiac Output insufficient to meet need
• Very little Cardiac reserve ability to work
• May occur with either right or left ventricle
• Result if right? Result if left?
• Edema in lower extremities or fluid retention in
  lungs.

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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)

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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)

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Developmental Aspects of the Heart

• Contraction detectable at 23 days

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Developmental Aspects of the Heart

• Contraction detectable at 23 days
• 4 chambers by day 25

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Fetal Heart Development

• Fetal heart structures that bypass pulmonary
  circulation
• Foramen ovale connects the two atria
• Ductus arteriosus connects pulmonary trunk and
  the aorta

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Congenital Heart Defects
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Circulation Blood Flow

• What determines how much blood flow a given organ
  or tissue needs?

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Circulation Blood Flow

• What determines how much blood flow a given organ
  or tissue needs?
• Rate of metabolism or oxygen demand
• Brain has a high rate of demand
• Skeletal muscle is highly variable

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Key terms

• Blood Pressure expressed in mmHg (Why?)
• Usually arterial
• Blood flow - result of a pressure gradient

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Key terms

• PR Peripheral Resistance (total is the
  difference in Diastolic Systolic pressures
• Most is found in the capillaries
• Affected by the viscosity
• Long term Hematocrit affects it
• Short term hydration level affects it
• Restrictions (diameter) of vessels affects it.
  (how?)

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Which Blood Pressure?

• Systolic Pressure (short pulse)
• Diastolic Pressure (longer time)
• Pulse Pressure (subtract SP-DP)
• Mean Arterial Pressure Diastolic 1/3 pulse
  pressure. (Long term control by the kidneys)
• Primary control is Vaso motor control via
  Sympathetic NS.

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Blood Pressure Homeostasis

• Rapid Mechanisms
• Vasoconstriction (vessel contraction) Medulla
  O. controls (Vasomotor tone)
• Response to Positional hypotension
• Long Term Mechanisms
• Renin-Angiotensin Mechanism
• Renin secreted by kidneys
• Aldosterone (Adrenal cortex)