Download 6 Heart Physiology

Heart Physiology
Review of Heart Muscle
• Cardiocytes, myocardium
• Branched cells
• Intercalated discs- (desmosomes) and electrical junctions (gap junctions).
• Has actin and myosin filaments
• Has low resistance (1/400 the resistance of cell membrane)
• Atrial syncytium: Network of connecting cardiac cells
• Ventricular syncytium: Network of connecting cardiac cells
• Fibrous insulator exists (Bundle of His) between atrium and ventricle (what would
this do to any electrical activity trying to go through?)
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If the electrical signals from the atria were conducted directly into the ventricles
across the AV septum, the ventricles would start to contract at the top (base). Then
the blood would be squeezed downward and trapped at the bottom of the ventricle.
The apex to base contraction squeezes blood toward the arterial opening at the base of
the heart.
The AV node also delays the transmission of action potentials slightly, allowing the
atria to complete their contraction before the ventricles begin their contraction. This
AV nodal delay is accomplished by the naturally slow conduction through the AV
node cells. (Why are they slow conductors? Small diameter cells, fewer sodium
channels)
Fibers within the heart
• Specialized Fibers
– are the fibers that can spontaneously initiate an AP all by themselves!
– The AP will spread to all other fibers via gap junctions
– AKA “leading cells”
– But they are also muscle, so they do contract, albeit feebly!
– They are not nerves!!!!
• Contractile Fibers
– These maintain their RMP forever, unless brought to threshold by some other
cell
– They cannot generate an AP by themselves
– AKA “following cells”
– But they do have gap junctions, so once they’re triggered, they will help
spread the AP to neighbors.
Pathway of Heartbeat
• Begins in the sinoatrial (S-A) node
• Internodal pathway to atrioventricular (A-V) node
• Impulse delayed in A-V node (allows atria to contract before ventricles)
• A-V bundle (Bundle of His) takes impulse into ventricles
• Left and right bundles of Purkinje fibers take impulses to all parts of ventricles
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SPECIALIZED FIBERS: A-V Bundles and Purkinje fibers
A-V Bundles (Bundle of His)
• Only conducting path between atria and ventricles
• Divides into left and right bundles
• Time delay of 0.04sec
Purkinje System
• Fast conduction; many gap junctions at intercalated disks
How can these specialized fibers spontaneously “fire?”
• Can’t hold stable resting membrane potential
• Potentials drift (gradual depolarization)
• During this time, they have a gradually increasing perm to Na+ and less leaky to K+
(more “+” inside causes cell to depolarize, remember?)
Notice slow rise from rest to threshold.
This is called the “prepotential” or
“pacemaker potential”
Only specialized fibers of the heart can do
this.
This is what gives the heart it’s rhythm.
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These rhythms can ALSO be modified by the ANS
Neurotransmitters can cause faster or slower rise to threshold by altering ion
permeability.
Acetylcholine (ACh) slows the heart rate (parasympathetic division of ANS)
Norepinephrine (NE) speeds up the heart rate (sympathetic division of ANS)
Sympathetic and Parasympathetic
• Sympathetic – speeds heart rate by  Ca++ & Na+ channel influx and  K+
permeability/efflux (increases sodium and calcium permeability)
• Parasympathetic – slows rate by  K+ efflux &  Ca++ influx (decreases sodium and
calcium permeability)
• Which neurotransmitter will cause your heart to pound rapidly? Norepinephrine
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Additional Cardiac Physiology
 Cardiac Output (CO)
 Blood pressure
 Blood vessel resistance
 Baroreceptors
 Drugs affecting CO
Blood Flow (L/min)
• Blood flow is the quantity of blood that passes a given point in the circulation in a
given period of time.
• Overall flow in the circulation of an adult is 5 liters/min which is the cardiac output.
• HR = heart rate
• SV = stroke volume
• CO= HR X SV
• 70 b/min x 70 ml/beat =4900ml/min
Ventricular Ejection Volume = Stroke Volume
• Stroke Volume (SV)
– amount ejected from the left ventricle, ~ 70 ml
• End Diastolic Volume (EDV); ~120 ml; the amount that the left ventricle can hold
• End Systolic Volume (ESV): the amount left in the ventricle after the ventricle
contracts (40-50ml)
• SV/EDV= ejection fraction,
– at rest ~ 60%
– during vigorous exercise as high as 90%
– diseased heart < 50%
Cardiac Output (CO)
• Amount ejected by a ventricle in 1 minute
• CO = HR x SV
• Resting values, 4- 6 L/min
• Vigorous exercise, 21 L/min
• Cardiac reserve: difference between maximum and resting CO
• If resting CO = 6 L/min and after exercise increases to 21 L/min, what is the cardiac
reserve?
• CR = 21 – 6
• CR = 15 L/min
Volumes and Fraction
• End diastolic volume
= 120 ml
• End systolic volume
= 50 ml
• Ejection volume (stroke volume) = 70 ml
• Ejection fraction = 70ml/120ml = 58% (normally 60%)
• If heart rate (HR) is 70 beats/minute, what is cardiac output?
• Cardiac output = HR * stroke volume
CO = 70/min. * 70 ml
CO = 4900ml/min.
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Questions
• If EDV = 120 ml and ESV = 50 ml:
• What is the SV?
• 120-50 = 70 ml
• What is the EF?
• 70/120 = 58%
• What is the CO if HR is 70 bpm?
• 70/bpm * 70 ml = 4900ml/min.
Ohm’s Law
• Q=ΔP/R
• Flow (Q) through a blood vessel which is the same thing as saying Cardiac Output
(CO) through the heart, is determined by:
• 1) The pressure difference (DP) between the two ends of the circulatory tube (arteries
and veins)
– Directly related to flow
• 2) Resistance (R) of the vessel
– Inversely related to flow
Clinical Significance
• Normal blood pressure is 120/80 mm Hg.
• 120 represents systolic pressure, and 80 represents diastolic pressure. The average of
these two pressures is 100 mm Hg
120 + 80 = 200
200/2 = 100 (the average)
• Therefore, the average pressure in the first vessel leaving the heart (the aorta) is 100
mm Hg.
• “100 mm Hg” means the amount of pressure required to lift a column of mercury 100
mm in the air. This is how the original blood pressure cuffs work.
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In a normal person, the arterial pressure is 100 and the pressure in the veins is 0 (if
there were any pressure in the capillaries, they would blow out, so blood pressure
drops to zero by the time it gets there, and stays at zero in the veins.
• The pressure difference (ΔP) is normally
100 – 0 = 100
Remember, Cardiac Output (CO) is normally about 5 liters per minute.
Therefore, applying Ohm’s Law (Q=ΔP/R) to a normal person, we get this:
5 = 100/R
Solving for R:
R = 100/5
R = 20 PRU
• That means that the normal amount of resistance in the blood vessels is 20 PRU
(peripheral resistance units).
• Overall, the values for a normal person are:
5 = 100/20
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Clinical Significance:
Solve for Q (cardiac output)
• A person might have blood pressure higher than normal.
– They ate too much salt, so they are retaining water
• A patient has blood pressure of 140/100, yet their last BP reading a few weeks ago
was 120/80. When questioned, the patient said they ate a lot of salt and drank a lot of
water yesterday.
• Problem: What is their cardiac output right now? We can assume the resistance in
their blood vessels is normal since their BP was normal recently.
• Solution: First find the average arterial pressure
(140 + 100)/2 = 120
• Then apply Ohm’s Law (Q=ΔP/R)
x = 120/20
x = 6 (Cardiac output increases)
The heart is pumping with more force than normal. Since it takes more time to pump a
larger bolus, the heart rate is slower.
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A person might have blood pressure lower than normal.
– They are dehydrated
• A patient has blood pressure of 60/40, yet their last BP reading a few weeks ago was
120/80. When questioned, the patient said they just got back from a hike and they are
thirsty.
• Problem: What is their cardiac output right now? We can assume the resistance in
their blood vessels is normal since their BP was normal recently.
• Solution: First find the average arterial pressure
(60 + 40)/2 = 50
• Then apply Ohm’s Law (Q=ΔP/R)
x = 50/20
x = 2.5 (Cardiac output decreases)
The heart is pumping with less force than normal. Since it takes less time to pump a
smaller bolus, the heart rate is faster.
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What is CO if you change the resistance?
A patient might have higher vessel resistance if they have clogged arteries
(atherosclerosis) or calcium deposits in the arteries (arteriosclerosis).
• Problem: What is the cardiac output in a patient with BP of 120/80 and a higher than
normal resistance? Let’s say R = 30.
• Apply Ohm’s Law (Q=ΔP/R)
x = 100/30
x = 3.3 (Cardiac output decreases)
The heart is pumping with less force than normal. Since it takes less time to pump a
smaller bolus, the heart rate is faster.
Therefore, someone with a slow heart rate and large cardiac output might be suffering
from either a condition relating to high peripheral resistance or from low blood
pressure.
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Problem: What is the cardiac output in a patient with BP of 120/80 and a lower than
normal resistance? Let’s say R = 10.
• Apply Ohm’s Law (Q=ΔP/R)
x = 100/10
x = 10 (Cardiac output increases)
The heart is pumping with more force than normal. Since it takes more time to pump a
larger bolus, the heart rate is slower.
Therefore, someone with a slow heart rate and large cardiac output might be suffering
from either a condition relating to low peripheral resistance or from high blood
pressure.
Now let’s solve for ΔP (change in pressure) instead of Q (cardiac output)
• ΔP means subtracting the pressure in the veins (P2) from the average pressure in the
arteries (P1).
• Therefore, ΔP = P1 – P2
• Since P2 (blood pressure in the veins) is always 0, for our purposes, you could just
write P instead of ΔP.
• P symbolizes blood pressure. Since BP is written systolic/diastolic, you add up both
pressures and take the average.
• The average person’s blood pressure is 120/80, so the overall average pressure in the
aorta is about 100 mm Hg.
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What would you expect the blood pressure to be in a person who has increased
peripheral resistance (clogged arteries)? Let’s say R = 50
P = QR
P = (5)(50)
P = 250 (normal would be 100)
The person would have high blood pressure.
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What would you expect the blood pressure to be in a person who has decreased
peripheral resistance (athlete)? Let’s say R = 10
P = QR
P = (5)(10)
P = 50 (normal would be 100)
The person would have low blood pressure.
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What would you expect the blood pressure to be in a person who has increased
cardiac output (over-hydration)? Let’s say Q = 6
P = QR
P = (6)(20)
P = 120 (normal would be 100)
The person would have higher blood pressure.
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What would you expect the blood pressure to be in a person who has decreased
cardiac output (dehydration)? Let’s say Q = 4
P = QR
P = (4)(20)
P = 80 (normal would be 100)
The person would have lower blood pressure.
Now let’s solve for R
• What would you expect the peripheral resistance to be in a person who has decreased
cardiac output (congestive heart failure)? Let’s say Q = 4 (still 5 L of blood)
R = P/Q
R = 100/4
R = 25 (normal would be 20)
The person would have higher than normal resistance (there’s a traffic jam of the 5th liter of
blood trying to get through; the pressure pushes it out of the vessels and into the tissues,
resulting in edema)
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What would you expect the peripheral resistance to be in a person who has increased
cardiac output (exercising)? Let’s say Q = 6 (still has 5 liters of blood)
R = P/Q
R = 100/6
R = 16 (normal would be 20)
The person would have lower than normal resistance.
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What would you expect the peripheral resistance to be in a person who has decreased
blood pressure (aerobic athlete with more anastomoses, so they have more blood
vessels but same amount of blood)? Let’s say P = 80
R = P/Q
R = 80/5
R = 16 (normal would be 20)
The person would have low peripheral resistance.
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What would you expect the peripheral resistance to be in a person who has increased
blood pressure (over-hydration)? Let’s say P = 120
R = P/Q
R = 120/5
R = 24 (normal would be 20)
The person would have higher peripheral resistance.
Summary of Ohm’s Law
• Q=ΔP/R
• 1) As the cardiac output (Q) goes up, the pressure difference (DP) goes up. They are
directly related.
• 2) As Q goes up, Resistance (R) of the vessel goes down. They are inversely related.
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Remember, cardiac output is initially determined by this formula: CO= HR X SV
Don’t get that formula confused with Ohm’s Law, which just shows the
relationship between CO, blood pressure, and peripheral resistance.
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How does Ohm’s Law apply to patients?
• The patient presents with high blood pressure, normal CO: Is peripheral
resistance high or low?
• How to solve this type of problem:
• If the 1st component CO or PR or BP is high or low, then ask yourself if the next
component (CO or PR or BP) SHOULD be high or low. If the 2nd component is not
as it should be then the 3rd component is causing the difference.
How does Ohm’s Law apply to patients?
The patient presents with high blood pressure, normal CO:
Is peripheral resistance high or low?
– HOW TO SOLVE THIS PROBLEM: With high BP (the first component
given in this problem), you would expect high CO (the second component in
this problem), but instead, it is normal. That means that the peripheral
resistance (the third component in the problem) is causing the problem. So
does that mean R is high or low? Well, if the person has high BP caused by a
peripheral resistance problem, the R must be HIGH.
The patient presents with low blood pressure, normal CO:
Is peripheral resistance high or low?
The patient presents with high CO, normal blood pressure:
Is peripheral resistance high or low?
The patient presents with low CO, normal blood pressure:
Is peripheral resistance high or low?
The patient presents with high CO, normal peripheral resistance:
Is blood pressure high or low?
The patient presents with normal CO, low peripheral resistance:
Is blood pressure high or low?
The patient presents with normal CO, high peripheral resistance:
Is blood pressure high or low?
The patient presents with low CO, normal peripheral resistance:
Is blood pressure high or low?
The patient presents with high blood pressure, normal peripheral resistance:
Is cardiac output high or low?
The patient presents with normal blood pressure, low peripheral resistance:
Is cardiac output high or low?
The patient presents with normal blood pressure, high peripheral resistance:
Is cardiac output high or low?
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The patient presents with low blood pressure, normal peripheral resistance:
Is cardiac output high or low?
High BP or high vessel resistance causes edema
• Edema means excessive accumulation of tissue fluid.
• Edema may result from:
– High arterial blood pressure.
– Venous obstruction.
– Leakage of plasma proteins into interstitial fluid.
– Valve problems
– Cardiac failure
– Decreased plasma protein.
– Obstruction of lymphatic drainage.
– Elephantiasis
Other Factors Affecting CO
• Blood viscosity
• Total vessel length
• Vessel diameter
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Brain Centers involved in Short Term BP Control
 Vasomotor
 Adjusts peripheral resistance by adjusting sympathetic output to the arterioles
 Cardioinhibitory- transmits signals via vagus nerve to heart to decrease heart rate.
(parasympathetic)
 Cardioacceleratory/ contractility-sympathetic output
Vasomotor control: Sympathetic Innervation of Blood Vessels
 Sympathetic nerve fibers
innervate all vessels except
capillaries and precapillary
sphincters (precapillary sphincters follow local control)
 Innervation of small arteries and arterioles allow sympathetic nerves to increase
vascular resistance.
 Large veins and the heart are also sympathetically innervated.
Anatomy of the Baroreceptors
 Baroreceptors are nerve endings that respond to stretch in a blood vessel.
 They are located at the carotid bifurcation (between common carotid and
internal/external carotid arteries). This area is called the carotid sinus.
 There are also baroreceptors in the walls of the aortic arch.
 Signals from the carotid sinus are transmitted by the glossopharyngeal nerves .
 Signals from the arch of the aorta are transmitted by CNX (vagus nerve).
 Baroreceptors are important in short term regulation of arterial blood pressure.
Baroreceptors respond to changes in arterial pressure.
 As pressure increases the number of impulses from carotid sinus increases which
results in:
1) inhibition of vasoconstricton (so the blood vessels dilate, which lowers blood pressure)
2) activation of the vagal center (lowers blood pressure)
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Baroreceptors maintain relatively constant pressure despite changes in body posture.
Drugs Affecting Cardiac Output by affecting Blood Flow
Vasodilators
Bradykinin
Histamine
Elevated temperatures
Lactic acid
Carbon dioxide
Vasoconstrictors
Norepinephrine
Epinephrine
Angiotensin
Vasopressin (ADH)
Caffeine
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Drugs Affecting CO
• Atropine- parasympathetic blocking (blocks muscarinic AchR) agent, (+,+)
• Pilocarpine- drug that causes cholinergic neurons to release ACH. Since Ach
decreases heart rate, it causes (-, ) effect on heart.
• Propranalol- Reversible, competitive blocker of Beta1 receptor. So blocks
sympathetics effect of heart (-,-) Decrease heart rate and force of contraction, and
lowers blood pressure.
• Digoxin (shorter ½ life) or Digitoxin- come from group of drugs derived from
digitalis. Digitalis derived from foxglove plant. It has a (-,+) effect, neg chronotropic
and positive inotropic effect; slows heart rate but increases force of contraction. Is
only drug with this effect on heart.
• increases intracellular concentration of Ca.
• increase force of contraction by inhibiting Na+/K+ pump. So cells start to
accumulate Na.
• Disadvantage of using digitalis is that it’s extremely toxic. The optimal dose
is very close to lethal dose- stops heart
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