heart physiology
DESCRIPTION
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) - PowerPoint PPT PresentationTRANSCRIPT
Heart Physiology
1
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?)
Figure 9-1; Guyton & Hall 2
• 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 (instead of the 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, so they don’t depolarize as fast)
3
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.
4
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 bundle branches
• Purkinje fibers take impulses to all parts of ventricles
KEY Red = specialized cells;
all else = contractile cells
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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
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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?)
Na+
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Specialized fibers
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. 8
Specialized fibers of conductive system• These rhythms can
ALSO be modified by the ANS
• Neurotransmitters can cause faster or slower rise to threshold by altering ion permeability.
• Acetylcholine (ACh) from the Vagus nerve slows the heart rate (parasympathetic division of ANS)
• Norepinephrine (NE) speeds up the heart rate (sympathetic division of ANS)
K+ efflux
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• Sympathetic – speeds heart rate by Ca++ & Na+ channel influx and K+ permeability/efflux (increases sodium and calcium permeability)• Parasympathetic – slows rate by K+ efflux & Na+ and Ca++ influx (decreases sodium and
calcium permeability)
• Which neurotransmitter will cause your heart to pound rapidly?– Norepinephrine
Sympathetic and Parasympathetic
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Spread of Depolarization
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Direction of Depol
Resting Cell
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
Depolarizing Current!+ + +
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Direction of Depol
Stim microelectrode
Depolarizing Current!
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Direction of Depol
Stim microelectrode
Depolarizing Current!
++ +
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
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Direction of Depol
Stim microelectrode
Depol = spread of surface NEG charge
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Direction of Repolarization
Stim microelectrode
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Begin Repolarization
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Direction of Repolarization
Stim microelectrode
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Direction of Repolarization
Stim microelectrode
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Direction of Repolarization
Stim microelectrode
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Stim microelectrode
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Direction of Repolarization
Stim microelectrode
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Repolarization= spread of positive surface charge
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Stim microelectrode
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Direction of Repolarization
Stim microelectrode
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Repolarization= spread of POS surface charge
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Depolarization/Repolarization Cycle in the Atria
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=Resting cell
=Depol cell
Depolarization Begins
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=Resting cell
=Depol cell
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=Resting cell
=Depol cell
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=Resting cell
=Depol cell
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=Resting cell
=Depol cell
Depolarization Complete
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=Resting cell
=Depol cell
Repolarization Begins
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=Resting cell
=Depol cell
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=Resting cell
=Depol cell
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=Resting cell
=Depol cell
Repolarization Complete
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Depolarization/Repolarization Cycle in the Ventricles
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=Resting cell
=Depol cell
Depolarization Begins
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=Resting cell
=Depol cell
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=Resting cell
=Depol cell
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=Resting cell
=Depol cell
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=Resting cell
=Depol cell
Depolarization Complete
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=Resting cell
=Depol cell
Repolarization Begins
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=Resting cell
=Depol cell
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=Resting cell
=Depol cell
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=Resting cell
=Depol cell
Repolarization Complete
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Additional Cardiac Physiology
Cardiac Output (CO)Blood pressure Blood vessel resistanceBaroreceptorsDrugs affecting CO
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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 left
ventricle, ~ 70 ml• End Diastolic Volume (EDV)
~120 ml; the amount the left ventricle can hold.
• End Systolic Volume (ESV) the amount left in the ventricle after ventricle contracts (~50ml)
• SV/EDV= ejection fraction, – at rest ~ 60% – during vigorous exercise as
high as 90%– diseased heart < 50%
• 70/120 = 58% (normal)• 108/120 = 90% (exercise)• 60/120 = 50% (diseased) 57
Cardiac Output (CO)• Amount ejected by a ventricle in Amount ejected by a ventricle in 1 minute1 minute• CO = HR x SVCO = HR x SV• Resting values, 4- 6 L/minResting values, 4- 6 L/min• Vigorous exercise, 21 L/min Vigorous exercise, 21 L/min • Cardiac reserve: difference Cardiac reserve: difference
between maximum and resting CObetween maximum and resting COIf resting CO = 6 L/min and after exercise increases to 21 L/min, what is the cardiac reserve?
Cardiac reserve (CR) = Max CO – Resting COCR = 21 – 6CR = 15 L/min 58
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
= 70/min. * 70 ml = 4900ml/min. 59
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.
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Ohm’s Law• Q=P/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 (P) 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
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Like a CEO of a company is at the top
Like a BP cuff on your left arm
“R” stands for Right
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 Hg120 + 80 = 200200/2 = 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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Clinical Significance
• 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 (P) is normally100 – 0 = 100
Remember, Cardiac Output (CO) is normally about 5 liters per minute.
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Clinical Significance• Therefore, applying Ohm’s Law (Q=P/R) to a
normal person, we get this:5 = 100/RSolving for R:R = 100/5R = 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: Q=P/R
5 = 100/2065
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=P/R) x = 120/20x = 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. 66
Clinical Significance• 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=P/R) x = 50/20x = 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. 67
Clinical Significance• 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=P/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.
68
Clinical Significance• Problem: What is the cardiac output in a patient with BP
of 120/80 and a lower than normal resistance, perhaps they are athletes who have developed large arteries? Let’s say R = 10.
• Apply Ohm’s Law (Q=P/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 have a condition relating to low peripheral resistance, such as an aerobic athlete.
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Now let’s solve for P (change in pressure) instead of Q (cardiac output)
• P means subtracting the pressure in the veins (P2) from the average pressure in the arteries (P1).
• Therefore, P = P1 – P2• Since P2 (blood pressure in the veins) is always 0, for
our purposes, you could just write P instead of P.• 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.70
Solve for P
• 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.
71
Solve for P
• 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.
72
Solve for P
• 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.
73
Solve for P
• 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.
74
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) 75
Solve for R
• 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.
76
Solve for R• 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.
77
Solve for R
• What would you expect the peripheral resistance to be in a person who has increased blood pressure (obese person)? Let’s say P = 120
R = P/Q
R = 120/5
R = 24 (normal would be 20)
The person would have higher peripheral resistance.
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Summary of Ohm’s Law• Q=P/R• 1) As the cardiac output (Q) goes
up, the pressure difference (P) goes up. They are directly related.
• 2) As Resistance (R) of the vessel goes down (the vessel becomes larger; bigger freeway), Q goes up (more blood can go through; more cars can go through). They are inversely related.
• 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.
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.
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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 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?
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How does Ohm’s Law apply to patients?
• 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?
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How does Ohm’s Law apply to patients?
• 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?
• The patient presents with low blood pressure, normal peripheral resistance:
• Is cardiac output high or low?
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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.– Valve problems– Decreased plasma protein.– Leakage of plasma proteins
into interstitial fluid.– Cardiac failure– Obstruction of lymphatic
drainage. – Elephantiasis
Arterial Pressure = Cardiac Output x Total Peripheral Resistance
The kidneys provide Long Term BP control
The most important immediate regulator of BP is vessel resistance
Ways to ultimately change blood flow is to change Pressure and Resistance
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Other Factors Affecting CO• Blood viscosity (more viscosity decreases CO)• Total vessel length (longer vessel length decreases CO)• Vessel diameter (larger vessel diameter increases CO)
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Brain Centers involved in Short Term (immediate) BP Control
Vasomotor Adjusts peripheral
resistance by adjusting sympathetic output to the arterioles (sympathetic constricts blood vessels)
Cardioinhibitory- transmits signals via vagus nerve to heart to decrease heart rate. (parasympathetic)
Cardioacceleratory/ contractility-sympathetic output
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Vasomotor control: Sympathetic Innervationof 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.
Figure 18-2; Guyton and Hall
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Anatomy of the BaroreceptorsBaroreceptors 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. Figure 18-5; Guyton and Hall
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Baroreceptor Response to 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)
Constrict
Common Carotids
Constrictors
Pressure at
Carotid Sinuses
Arterial Pressure
Figure 18-5; Guyton and Hall
Baroreceptors respond to changes in arterial pressure.
Functions of the Baroreceptors• Maintains relatively constant pressure despite
changes in body posture.
DecreaseCardiac Output
Sensed ByBaroreceptors
Supine StandingDecreaseCentral
Blood Volume
VasomotorCenter
SympatheticNervous Activity
DecreaseArterial Pressure
Increase BP to normal
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Orthostatic HypotensionAlso known as postural hypotension, and
colloquially as head rush or dizzy spell.This is a form of hypotension in which a person's
blood pressure suddenly falls when standing up or stretching.
The symptom is caused by blood pooling in the lower extremities upon a change in body position.
It is quite common and can occur briefly in anyone, although it is particularly prevalent among the elderly, and those with low blood pressure.
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Drugs Affecting Cardiac Output
• VasodilatorsBradykininHistamineElevated temperaturesLactic acidCarbon dioxide
• VasoconstrictorsNorepinephrineEpinephrineAngiotensinVasopressin (synthetic ADH)Caffeine
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Drugs Affecting CO
• Atropine- blocks parasympathetic system (increase in sympathetic responses). Used for low blood pressure, especially emergencies like anaphylaxis and cardiac arrest. Also used sublingually for hospice patients with excess salivary secretions, and as a pre-op injection to decrease secretions that might get into the lungs during surgery.
• Pilocarpine- drug that causes skeletal muscle neurons to release ACH, which decreases heart rate. Used for tachycardia (beta blocker).
• Propranalol- blocks sympathetic effect of heart. This causes decreased heart rate and force of contraction, and lowers blood pressure. Used for someone with blood pressure that is too high.
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Drugs Affecting CO (2)• Digitoxin or Digoxin (shorter
½ life)- comes from group of drugs derived from digitalis. Digitalis is derived from the foxglove plant. Slows heart rate but increases force of contraction. This is the only drug with this effect on heart. – Disadvantage of using digitalis
is that it’s extremely toxic. The optimal dose is very close to lethal dose- stops heart. One of many drugs used for congestive heart failure, along with Lasix.
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Homework Packet• There is a packet of homework for heart
physiology posted on my website, under lecture unit 3.
• The answers are at the end of each group of questions in the packet.
• There are 28 of these questions with the exact same wording on the test.
• They are all fill in the blank, copied and pasted right from the HW packet.
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