Ch 12 Heart and Circulatory System

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Ch 12 Heart and Circulatory System

• The Bodys Transport System

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• 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 hearts chambers and valves
  composed of simple squamous tissue

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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.

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• 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

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Characteristics of Heart Muscle Intercalated
discs allows heart to beat as one
unit Involuntary Striated One nuclei per cell
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Location of Heart
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Structure of the Heart
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• Main Veins into heart
• Coronary Sinus
• Superior Vena Cava
• Inferior Vena Cava
• Pulmonary Vein
• Main Arteries
• Coronary Artery
• Pulmonary Artery
• Aorta

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1
2
6
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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.

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Flow of blood through heart

• 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

B
C
A
9
1
6
5
7
3
8
4
2
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• Difference in myocardium thickness between R.
  ventricle and L. ventricle.
• Why?

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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

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Anatomy of AV valvesOne-way valves

• Atrioventricular valves
• Chordae tendineae
• Papillary muscles

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Semilunar Valves

• Located in Pulmonary Artery and Aortic Artery
• 3 flaps
• Prevents blood from flowing back into ventricles

Posterior
Anterior
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Valve position when ventricles relaxed
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Valve position when ventricles contract
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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

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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
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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 Ca2 enters
  sarcoplasm
• Ca2 also is released from SR
• Ca2 surge prolongs the depolarization phase and
  delays repolarization (excess ions in cell)
• Repolarization Ca2 begin to close K channels
  open and K leaves the cell.

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In Cardiac muscle, depolarization lasts longer.
Thus cardiac muscle cant increase tension with
another impulse tetanus doesnt occur. Why is
this important?
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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 hearts cardiac cells have this
  capability

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• 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
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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

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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

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• 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
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Sequence of Excitation

• Purkinje fibers
• Complete the pathway into the apex and
  ventricular walls

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Superior vena cava
Right atrium
1
The sinoatrial (SA) node (pacemaker) generat
es impulses.
Internodal pathway
Left atrium
2
The impulses pause (0.1 s) at
the atrioventricular (AV) node.
Purkinje fibers
The atrioventricular (AV) bundle connects
the atria to the ventricles.
3
4
The bundle branches conduct the impulses
through the interventricular septum.
Inter- ventricular septum
The Purkinje fibers depolarize the
contractile cells of both ventricles.
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(a) Anatomy of the intrinsic conduction system
showing the sequence of electrical excitation
Figure 18.14a
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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

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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.

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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

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• 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.

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QRS complex
Sinoatrial node
Ventricular depolarization
Ventricular repolarization
Atrial depolarization
Atrioventricular node
S-T Segment
P-Q Interval
Q-T Interval
Figure 18.16
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Depolarization
Repolarization
SA node
R
R
T
P
T
P
Q
S
1
Atrial depolarization, initiatedby the SA
node, causes theP wave.
Q
S
4
Ventricular depolarizationis complete.
R
AV node
R
T
P
T
P
Q
S
Q
2
With atrial depolarizationcomplete, the
impulse isdelayed at the AV node.
S
5
Ventricular repolarizationbegins at apex,
causing theT wave.
R
R
T
P
T
P
Q
S
Q
S
3
Ventricular depolarizationbegins at apex,
causing theQRS complex. Atrialrepolarization
occurs.
6
Ventricular repolarizationis complete.
Figure 18.17
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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

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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

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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 (4060 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

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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

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(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.
(d) Ventricular fibrillation. These
chaotic, grossly irregular ECG deflections
are seen in acute heart attack and
electrical shock.
(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 21.
Figure 18.18
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1.
2.
3.
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4.
5.
6.
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Pacemaker

• Used to correct nodes that are no longer are in
  rhythm.
• Becomes the new hearts pacemaker.

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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
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Stopping a Heart Attack

• Breaking apart the blockage is done with
• Medication
• Angioplasty
• Stents
• Coronary bypass surgery (CABG)

stent placement
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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

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Mechanical Events The Cardiac Cycle

• Cardiac cycle all events associated with blood
  flow through the heart during one complete
  heartbeat
• Systolecontraction
• Diastolerelaxation

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Phases of the Cardiac Cycle

• Ventricular fillingtakes 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

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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

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Phases of the Cardiac Cycle

• Ventricles relax
• Decrease in pressure causes blood to flow
  backward
• Backflow of blood in aorta and pulmonary trunk
  closes SL valves

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EKG and One Cardiac Cycle
Cardiac Cycle events during one heart beat
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Cardiac Cycle BPdescribes 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

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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

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• 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 bodys demands
• Change in HR or force of contraction
• Cardiac Reserve the hearts 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

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Factors that Influence Heart Rate

• Age
• Gender
• Exercise
• Body temperature

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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

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Factors that Control Cardiac Output

• Blood volume reflexes
• Autonomic Nervous System with assistance from
  neurotransmitters and hormones
• Norepinephrine
• Acethylcholine
• Thyroxine
• Ions
• Temperature

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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 dont need forceful contractions

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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-

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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
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• 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 TT moving out of way
• No/weak contractions

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• Temp gt 98.6F
• Increases HR and SV
• Increase CO

• Temperature lt 95 F
• Slows depolarization
• Slows contraction
• Decrease CO

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Exercise (by skeletal muscle and respiratory
pumps see Chapter 19)
Bloodborne epinephrine, thyroxine, excess Ca2
Exercise, fright, anxiety
Heart rate (allows more time for ventricular filli
ng)
Venous return
Sympathetic activity
Parasympathetic activity
Contractility
EDV (preload)
ESV
Stroke volume
Heart rate
Cardiac output
Initial stimulus
Physiological response
Result
Figure 18.22