electrical properties of the heart

Electrical Properties of the Heart

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

• 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 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 takes impulse into ventricles

• Left and right bundles of Purkinje fibers take impulses to all parts of ventricles

KEY Red = specialized cells;

all else = contractile cells

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?)

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.

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) slows the heart rate (parasympathetic division of ANS)

• Norepinephrine (NE) speeds up the heart rate (sympathetic division of ANS) K+ efflux

• 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

Sympathetic and Parasympathetic

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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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

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Direction of Depol

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Direction of Depol

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Direction of Depol

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Direction of Depol

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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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Stim microelectrode

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Stim microelectrode

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Stim microelectrode

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Stim microelectrode

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Repolarization= spread of positive surface charge

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Stim microelectrode

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Repolarization= spread of POS surface charge

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Depolarization/Repolarization Cycle in the Atria

=Resting cell

=Depol cell

Depolarization Begins

=Resting cell

=Depol cell

=Resting cell

=Depol cell

=Resting cell

=Depol cell

=Resting cell

=Depol cell

Depolarization Complete

=Resting cell

=Depol cell

Repolarization Begins

=Resting cell

=Depol cell

=Resting cell

=Depol cell

=Resting cell

=Depol cell

Repolarization Complete

Depolarization/Repolarization Cycle in the Ventricles

=Resting cell

=Depol cell

Depolarization Begins

=Resting cell

=Depol cell

=Resting cell

=Depol cell

=Resting cell

=Depol cell

=Resting cell

=Depol cell

Depolarization Complete

=Resting cell

=Depol cell

Repolarization Begins

=Resting cell

=Depol cell

=Resting cell

=Depol cell

=Resting cell

=Depol cell

Repolarization Complete

Additional Cardiac Physiology

Cardiac Output (CO)Blood pressure and vessel resistance

BaroreceptorsDrugs 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, ~ 70 ml

• End Diastolic Volume (EDV)• SV/EDV= ejection fraction,

– at rest ~ 60% – during vigorous exercise as

high as 90%– diseased heart < 50%

• End-systolic volume: amount left in heart (50ml)

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 CO

If resting CO = 6 L/min and after exercise increases to 21 L/min, what is the cardiac reserve?

CR = 21 – 6CR = 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

= 70/min. * 70 ml = 4900ml/min.

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=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

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.

• 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.

• 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:5 = 100/20

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.

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.

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.

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.

Clinical Significance• 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=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 be suffering from either a condition relating to low peripheral resistance or from high blood pressure.

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

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.

Solve for P

• What would you expect the blood pressure to be in a person who has decreased peripheral resistance (dehydration)? Let’s say R = 10

P = QR

P = (5)(10)

The person would have low blood pressure.

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)

The person would have higher blood pressure.

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)

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 (dehydration)? Let’s say Q = 4

R = P/Q

R = 100/4

R = 25 (normal would be 20)

The person would have higher than normal resistance.

Solve for R

• What would you expect the peripheral resistance to be in a person who has increased cardiac output (over-hydration)? Let’s say Q = 6

R = P/Q

R = 100/6

The person would have lower than normal resistance.

Solve for R

• What would you expect the peripheral resistance to be in a person who has decreased blood pressure (dehydration)? Let’s say P = 80

R = P/Q

R = 80/5

The person would have low peripheral resistance.

Solve for R

• 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

The person would have higher peripheral resistance.

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 Q goes up, Resistance (R) of the vessel goes down. 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?

• The patient presents with low blood pressure, normal CO:

• The patient presents with high CO, normal blood pressure:

• The patient presents with low CO, normal blood pressure:

• The patient presents with high CO, normal peripheral resistance:

• Is blood pressure high or low?

• The patient presents with normal CO, low peripheral resistance:

• The patient presents with normal CO, high peripheral resistance:

• The patient presents with low CO, normal peripheral resistance:

• 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:

• The patient presents with normal blood pressure, high peripheral resistance:

• The patient presents with low blood pressure, normal peripheral resistance:

Arterial Pressure = Cardiac Output x Total Peripheral Resistance

Long Term BP control

According to Poiseuille’s law--Most important regulator is vessel resistance

Ways to ultimately change blood flow is to change Pressure and Resistance

Factors Affecting CO• Blood viscosity (decreases CO)• Total vessel length (longer decreases CO)• Vessel diameter (larger increases CO)

Poiseuille’s Law = Q =_Pr4

• Resistance (length)(viscosity)– (radius)4

Regulation of Blood Flow

• VasodilatorsBradykininHistamineNitric oxideElevated temperaturesPotassium/hydrogen ionsLactic acidCarbon dioxideAdenosine/ ADP

• VasoconstrictorsNorepinephrineEpinephrineAngiotensinVasopressin (ADH)Thromboxane

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 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

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

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

Drugs Affecting CO• Atropine- blocks parasympathetic

system (increase in sympathetic responses)

• Pilocarpine- drug that causes skeletal muscle neurons to release ACH, which decreases heart rate.

• Propranalol- blocks sympathetic effect of heart. This causes decreased heart rate and force of contraction, and lowers blood pressure.

Drugs Affecting CO (2)

• Digoxin (shorter ½ life) or Digitoxin- come from group of drugs derived from digitalis. Digitalis derived from foxglove plant. Slows heart rate but increases force of contraction. Is 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

Causes of Edema• 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

electrical properties of the heart

specialized cells

av node cells

heartspecialized fibers

slow conduction

ventricles divides

electrical signals

electrical properties

electrical activity

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