Transcript 11 Heart - bloodhounds Incorporated

Physiology
Cardiovascular System
Cardiac Muscle and the Heart

Myocardium

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
Heart muscle
Sits in the media stinum of the thoracic cavity
Left Axis Deviation


May have a right axis deviation with obesity and/or
pregnancy
May hang in the middle of the thoracic cavity if the individual
is very tall
The Heart
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The heart has four chambers
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Right and left atrium
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
Atria is plural
Right and left ventricle
Blood Flow Through the Heart

Deoxygenated blood enters the right atrium of
the heart through the superior and inferior vena
cava

Deoxygenated blood

Has less than 50% oxygen saturation on hemoglobin
Hemoglobin

Quaternary Structure

Four Globin proteins


Four Heme attach to each Globin


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Globin carries CO2, H+, PO4
Heme binds O2 and CO
Heme contains an Iron ion
About 1 million hemoglobin molecules per red blood cell
Oxygen carrying capacity of approximately 5 minutes
Heart Valves Ensure One-Way Flow
of Blood in the Heart

Atrioventricular Valves
Located between the atria and the ventricle
 Labeled Right and Left

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Right Valve is also called Tricuspid
Left Valve is also called Bicuspid or Mitral
Heart Valves
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Papillary muscles are attached to the chordae tendinae
Chordae tendinae are also connected to the AV valves
Just prior to ventricular contraction the papillary
muscles contract and pull downward on the chordae
tendinae
The chordae tendinae pull downward on the AV valves

This prevents the valves from prolapsing and blood
regurgitating back into the atria.
Follow Path of Blood through Heart
Blood Flow


Due to gravity deoxygenated blood enters the right/left atrium
(by way of the pulmonary veins) and flows through the open AV
valve directly into the ventricles
The filling of the ventricles with blood pushes the AV valve
upward


They are held in place by the chordae tendinae
Right before the valves shuts completely the atria contract from
the base towards the apex of the heart in order to squeeze more
blood into the ventricle

The AV valves snapping shut creates the “Lub” sound of the heart beat
Blood Flow

When the AV valves are shut the Pulmonary and
Aortic semi-lunar valves are also shut
Diastole
 Quiescence of the heart

Myocardial Contraction (Systole)



After Diastole occurs the ventricles begin to contract from the
apex towards the base of the heart
The deoxygenated blood on the right side of the heart is pushed
through the pulmonary trunk after opening the semi-lunar valve
to the pulmonary arteries into the lungs to become oxygenated.
The oxygenated blood on the left side of the heart is pushed
through the aorta after opening the semi-lunar valve into the
systemic circulation
Blood Flow

The Ventricles do not have enough pressure to
push all of the blood out of the pulmonary trunk
and aorta
The blood falls back down due to gravity
 The semi-lunar valves snap shut


The “Dup” sound of the heart beat
Blood Flow

Blood is always flowing from a region of higher
pressure to a region of lower pressure
Atrial and Ventricular Diastole
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The heart at rest
The atria are filling with blood from the veins
The ventricles have just completed contraction
AV valves are open
Blood flow due to gravity
Atrial Systole: Completion of
Ventricular Filling

The last 20% of the blood fills the ventricles due
to atrial contraction
Early Ventricular Contraction

As the atria are contracting
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Depolarization wave moves through the conducting
cells of the AV node down to the Purkinje fibers to
the apex of the heart
Ventricular systole begins
AV Valves close due to Ventricular pressure

First Heart Sound
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S1 = Lub of Lub-Dup
Isovolumic Ventricular Contraction
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AV and Semilunar Valves closed
Ventricles continue to contract
Atrial muscles are repolarizing and relaxing
 Blood flows into the atria again
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Ventricular Ejection
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The pressure in the ventricles pushes the blood
through the pulmonary trunk and aorta
Semi-lunar valves open
 Blood is ejected from the heart
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Ventricular Relaxation and Second
Heart Sound

At the end of ventricular ejection
Ventricles begin to repolarize and relax
 Ventricular pressure decreases
 Blood falls backward into the heart
 Blood is caught in cusps of the semi-lunar valve

Valves snap shut
 S2 – Dup of lub-dup

Isovolumetric Ventricular Relaxation

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Semilunar valves close
AV valves closed
The volume of blood in the ventricles is not
changing
When ventricular pressure is less than atrial
pressure the AV valves open again

The Cardiac Cycle begins again
Cardiac Circulation


Blood flowing through the heart has a high fat
content
Curvature as well as diameter of the arteries is
important to blood flow through the heart

Vasoconstriction due to sympathetic nervous system
input

Norepinephrine/Epinephrine

Alpha Receptors not Beta
Myocardial Infarction
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Heart Attack

Due to plaque build up in the arteries

Decrease in blood flow to myocardium
Depolarization of muscle cannot occur due to
myocardial death
 Myocardium doesn’t work as a syncytium any
longer
 Destruction of gap junction or “connexons”
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Atherosclerosis
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Plaque in the arteries
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Elevated Cholesterol in the blood
Cholesterol is cleared by the liver
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HDL – High Density Lipoprotein
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LDL – Low Density Lipoprotein
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H for healthy
L for Lethal
Omega 3 fatty acids
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“Rotorooter” for the arteries
If a Patient Has a Left Atrial
Infarction Then

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
What happens to heart contraction and blood flow
through the heart?
What type of symptoms might your patient have?
What recommendations might you give the patient to
live a better life?

There are some things they better not do or they will die.
What are these things (in general)?
Angioplasty/Open Heart Surgery
Cardiac Muscle & Heart

Heart muscle cells:
 99% contractile
 1% autorrhythmic
Cardiac Muscle Cells Contract Without
Nervous Stimulation
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Autorhythmic Cells
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Pacemaker Cells set the rate of the heartbeat
Sinoatrial Node
 Atriventricular Node
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Distinct from contractile myocardial cells
Smaller
 Contain few contractile proteins
 http://www.youtube.com/watch?v=7K2icszdxQc

Excitation-Contraction (EC) Coupling
in Cardiac Muscle

Contraction occurs by same sliding filament activity as in
skeletal muscle
some differences:
 AP is from pacemaker (SA node)
 AP opens voltage-gated Ca2+ channels in cell membrane
 Ca2+ induces Ca2+ release from SR stores
 Relaxation similar to skeletal muscle
Ca2+ removal requires Ca2 -ATPase (into SR) & Na+/Ca2+ antiport
(into ECF)
[Na+] restored via?
http://www.youtube.com/watch?v=rIVCuC-Etc0
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Cardiac Contraction

Action Potentials originate in Autorhythmic Cells
 AP spreads through gap junction
 Protein tunnels that connect myocardial cells
 AP moves across the sarcolemma and into the t-tubules
 Voltage-gated Ca +2 channels in the cell membrane
open
 Ca +2 enters the cell which then opens ryanodine
receptor-channels
 Ryanodine receptor channels are located on the
sarcoplasmic reticulum and Ca +2 diffuses into
the cells to “spark” muscle contraction
 Cross bridge formation and contraction occurs
Myocardial Contractile Cells
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In the myocardial cells there is a lengthening of
the action potential due to Ca +2 entry
http://www.youtube.com/watch?v=OQpFFiLdE0E
AP’s in Contractile Myocardial Cells
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Phase 4: Resting Membrane Potential is -90mV
Phase 0: Depolarization moves through gap junctions
 Membrane potential reaches +20mV
Phase 1: Initial Repolarization
 Na+ channels close; K + channels open
Phase 2: Plateau
 Repolarization flattens into a plateau due to
 A decrease in K + permeability and an increase in Ca +2
permeability
 Voltage regulated Ca +2 channels activated by
depolarization have been slowly opening during
phases 0 and 1
 When they finally open, Ca +2 enter the cell
 At the same time K + channels close
 This lengthens contraction of the cells
 AP = 200mSec or more
Phase 3: Rapid Repolarization
 Plateau ends when Ca +2 gates close and K + permeability
increases again
Myocardial Autorhythmic Cells
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Anatomically distinct from contractile
cells – Also called pacemaker cells
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Membrane Potential = – 60 mV
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Spontaneous AP generation as gradual
depolarization reaches threshold
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Unstable resting membrane
potential (= pacemaker potential)
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The cell membranes are “leaky”
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Unique membrane channels that
are permeable to both Na+ and K+
Myocardial Autorhythmic Cells, cont’d.
If-channel Causes Mem. Pot. Instability
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Autorhythmic cells have different membrane
channel: If - channel
allow
current
(= I ) to flow
f = “funny”:
researchers didn’t
understand initially
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If channels let K+ & Na+ through at -60mV
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Na+ influx > K+ efflux
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Slow depolarization to threshold
Myocardial Autorhythmic Cells, cont’d.
“Pacemaker potential” starts at ~ -60mV, slowly drifts
to threshold
AP
Myocardial Autorhythmic Cells, cont’d.
Channels involved in APs of Cardiac
Autorhythmic Cells
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Slow depolarization due to If channels
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As cell slowly depolarizes: If -channels close &
Ca2+ channels start opening
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At threshold: lots of Ca2+ channels open  AP
to + 20mV
Repolarization due to efflux of K+
Autorhythmic Cells
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No nervous system input needed
Unstable membrane potential
 -60mV Ca +2 channels open
 Calcium influx creates the steep depolarization phase of the
action potential
 At the peak of the action potential Ca +2 channels close and slow
K+ channels open
 Repolarization of the autorhythmic action potential is due to the
efflux of K +
 Pacemaker potential not called resting membrane potential
At -60mV If (funny) channels permeable to K + and Na + open
Na + influx exceed K + efflux
 The net influx of positive charge slowly depolarizes the
autorhythmic cells
 As the membrane becomes more positive the If channels gradually
close and some Ca +2 channels open
 The influx of Ca +2 continues the depolarization until the membrane
reaches threshold
http://www.youtube.com/watch?v=3HvIKsQb6es
Autonomic Neurotransmitters
Modulate Heart Rate
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The speed at which pacemaker cells depolarize
determines the rate at which the heart contracts
The interval between action potentials can be
altered by changing the permeability of the
autorhythmic cells to different ions
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Increase Na + and Ca +2 permeability speeds up
depolarization and heart rate
Decrease Ca +2 permeability or increase K + permeability
slow depolarization and slows heart rate
http://www.youtube.com/watch?v=OQpFFiLdE0E
http://www.youtube.com/watch?v=j2iY1cT2gEE
Autonomic Neurotransmitters
Modulate Heart Rate
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The Catecholamines: norepi and epi increases
ion flow through If and Ca+2 channels
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More rapid cation entry speeds up the rate of the
pacemaker depolarization
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Β1-adrenergic receptors are on autorhythmic cells
cAMP second messenger system causes If channels to
remain open longer
http://www.youtube.com/watch?v=3HvIKsQb6es
Autonomic Neurotransmitters
Modulate Heart Rate
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Parasympathetic neurotransmitter
(Acetylcholine) slows heart rate
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Ach activates muscarinic cholinergic receptors that
Increase K+ permeability and
 Decrease Ca+2 permeability
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Electrical Conduction in the Heart
Coordinates Contraction
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Action potential in an autorhythmic cell
Depolarization spread rapidly to adjacent cells through gap
junctions
Depolarization wave is followed by a wave of contraction
across the atria from the sinoatrial node on the right side of
the heart across to the left side of the heart and then from
the base to the apex
From AV nodes to the atrioventricular bundle in the
septum (Bundle of His)
Left and right bundle branches to the apex
Purkinje Fibers through the ventricles branches from apex
to base and stopping at the atrioventricular septum
Pacemakers Set the Heart Rate
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SA Node is the fastest pacemaker
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Approximately 72 bpm
AV node approximately 50 bpm
Bundle Branch Block
 Complete Heart Block
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Electrocardiogram
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Einthoven’s triangle
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Electrodes are attached to both arms and left leg to form a
triangle
Lead I- negative electrode attached to right arm
Lead II – positive electrode attached to left arm
Lead III – Ground attached to the left leg
Electrocardiogram ECG (EKG)
•
Surface electrodes record electrical activity deep within
body - How possible?
•
•
Reflects electrical activity of whole heart not of single cell!
EC fluid = “salt solution” (NaCl)  good conductor of
electricity to skin surface
Signal very weak by time it gets to skin
•
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ventricular AP = ? mV
ECG signal amplitude = 1mV
EKG tracing =  of all electrical potentials generated by all
cells of heart at any given moment
ECG
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P wave
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Depolarization of the atria
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QRS complex
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Ventricular depolarization
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Atrial contraction begins almost at the end of the P wave
Ventricular contraction begins just after the Q wave and continues
through the T wave
T wave
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Ventricular repolarization
ECG
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PQ or PR segment
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Q wave
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Conduction through bundle branches
R wave
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Conduction through AV node and AV bundle
Conduction beginning up the Purkinje Fibers
S wave Conduction continue up half way
ST segment
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Conduction up the second half of Ventricles
ECG
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When an electrical wave moving through the
heart is directed toward the positive electrode,
the ECG waves goes up from the baseline
If net charge movement through the heart is
toward the negative electrode, the wave points
downward
Einthoven’s Triangle and the 3 Limb Leads:
+
I
RA –
–
II
III
+
+
LA
–
Why neg. tracing for
depolarization ??
Net electrical current
in heart moves towards
+ electrode
Net electrical current in
heart moves towards
- electrode
EKG tracing goes
up from baseline
EKG tracing goes
Down from baseline
Info provided by EKG:
1.
2.
3.
HR
Rhythm
Relationships of EKG components


each P wave followed by QRS complex?
PR segment constant in length? etc. etc.
For the Expert:
Find subtle changes in shape or duration of
various waves or segments.
Indicates for example:
 Change in conduction velocity
 Enlargement of heart
 Tissue damage due to ischemia (infarct!)
Prolonged QRS complex
Injury to AV bundle can increase duration of QRS complex
(takes longer for impulse to spread throughout ventricular
walls).
Heart Sounds (HS)

1st HS: during early ventricular contraction  AV valves close

2nd HS: during early ventricular relaxation  semilunar valves close
Gallops, Clicks and Murmurs
Turbulent blood flow produces heart
murmurs upon auscultation
Plumbing 101:
Resistance Opposes Flow
3 parameters determine resistance (R):
Tube length (L)
1.
1.
Constant in body
Tube radius (r)
2.
1.
Can radius change?
Poiseuille’s law
8L 
R=
r4
Fluid viscosity ( (eta))
3.
1.
Can blood viscosity change??
Blood Flow Rate  P/ R

R  1 / r4
Velocity (v) of Flow
Depends on Flow Rate and Cross-Sectional Area:

Flow rate (Q) = volume of blood passing
one point in the system per unit of time
(e.g., ml/min)


If flow rate   velocity 
Cross-Sectional area (A) (or tube diameter)

If cross sectional area   velocity 
v = Q /A
Blood Flow

Mechanistic: Because the contractions of the heart
produce a hydrostatic pressure gradient and the
blood wants to flow to the region of lesser
pressure. Therefore, the Pressure gradient (P)
is main driving force for flow through the
vessels
Blood Flow Rate  P/ R
Pressure

Hydrostatic pressure is in all directions

Measured in mmHg: The pressure to
raise a 1 cm column of Hg 1 mm

Sphygmomanometer

Flow is produce by Driving Pressure

Pressure of fluid in motion decreases over
distance because of energy loss due to
friction
Blood Flow Rate  P/ R
Unique Microanatomy of Cardiac
Muscle Cells

1% of cardiac cells are autorhythmic
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Intercalated discs with gap junctions and
desmosomes
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Electrical link and strength
SR smaller than in skeletal muscle
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Signal to contract is myogenic
Extracelllar Ca2+ initiates contraction (like
smooth muscle)
Abundant mitochondria extract about 80% of
O2
Cardiac Muscle Cell Contraction is
Graded

Skeletal muscle cell: all-or-none contraction in
any single fiber for a given fiber length. Graded contraction in skeletal
muscle occurs through?

Cardiac muscle:


force  to sarcomere length (up to a maximum)
force  to # of Ca2+ activated crossbridges
(Function of intracellular Ca2+: if [Ca2+]in low  not
all crossbridges activated)
http://www.youtube.com/watch?v=OQpFFiLdE0E
http://www.youtube.com/watch?v=j2iY1cT2gEE
http://www.youtube.com/watch?v=j2iY1cT2gEE
Length Tension Relationship
In order to increase heart rate at
the SA node
A.
B.
C.
D.
Potassium permeability across the membrane must
increase
Sodium permeability across the membrane must
increase
Potassium impermeability across the membrane
must increase
Sodium impermeability across the membrane must
increase
The neurotransmitter responsible for
increasing potassium permeability at the
SA node is
A.
B.
C.
D.
Norepinephrine
Epinephrine
Acetylcholine
Serotonin
The initiation of the heartbeat
normally originates from the
A.
B.
C.
D.
Atrio-ventricular (A-V) node of the heart
Sino-atrial (SA) node of the heart
Central nervous system
Thyroid
The systemic circulation
A.
B.
C.
D.
E.
Receives more blood than the pulmonary
circulation does
Receives blood from the left ventricle
Is a high pressure system compared to the
pulmonary circulation
Both (b) and (c) above are correct
All of the above are correct
The chordae tendinae
A.
B.
C.
D.
E.
Keep the AV valves from opening in the
opposite direction during ventricular
contraction
Hold the AV valves during diastole
Hold the right and left ventricles together
Transmit the electrical impulse form the atria to
the ventricles
Contract when the ventricles contract
The aortic valve prevents backflow of blood
from the aorta into the left ventricle during
ventricular diastole
A. True
B. False
A mammalian heart has
__________ chamber(s)
A.
B.
C.
D.
One
Two
Three
Four
Ectopic focus is the place where
A.
B.
C.
D.
E.
An abnormally excitable area of the heart
initiates a premature action potential
All of the electrical impulses of the heart
normally terminate
An ECG lead is attached on the outside of the
chest
A heart valve is attached
The chordae tendineae attach to a valve
During isovolumetric ventricular
contraction
A.
B.
C.
D.
E.
Rapid filling of the ventricles occurs
No blood enters or leaves the ventricles
The maximum volume of blood is ejected
The maximum rate of ejection occurs
None of the above is correct
The type of intercellular junction that connects
cardiac muscle fibers and allows for direct,
electrical synapsing is known as a
A. Tight junction
B. Desmosome
C. Plasmodesmata
D. Gap junction
Cardiac muscle
A.
B.
C.
D.
E.
Has a shortening velocity that is greater than that
of glycolytic (white) skeletal muscle fibers
Has a more extensive sarcoplasmic reticulum than
skeletal muscle
Is an electrical syncytium
Has a resting potential that depends mainly on
sodium distribution
All of the above are correct
Spontaneous depolarization of
the sinoatrial node is produced by
A.
B.
C.
D.
E.
An inward leak of sodium and an increase in the
outward leak of potassium
An inward leak of sodium and a decrease in the
outward leak of potassium
Opening of fast sodium channels and a decrease in
the outward leak of potassium
Opening of fast sodium channels and an increase
in the outward leak of potassium
Neural impulses from the sympathetic nerves
A heart murmur is characterized
by
A.
B.
C.
D.
Rapid heart contraction
Irregular heart contraction
Mitral valve prolapse
Semilunar valve dysfunction
The P wave of a normal
electrocardiogram indicates
A.
B.
C.
D.
Atrial depolarization
Ventricular depolarization
Atrial repolarization
Ventricular repolarization
Damage to the _______ is
referred to as heart block
A.
B.
C.
D.
SA node
AV node
AV bundle
AV valve
Stenosis of the mitral valve may initially cause
a pressure increase in the
A.
B.
C.
D.
Vena cava
Pulmonary circulation
Left ventricle
Coronary circulation
The tricuspid valve is closed
A.
B.
C.
D.
E.
While the ventricle is in diastole
By the movement of blood from the
atrium to ventricle
By the movement of blood from atrium
to ventricle
While the atrium is contracting
When the ventricle is in systole