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129 Cards in this Set

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Why must the heart maintain adequate blood flow?
To meet the constant metabolic demands of all tissues of the body under all conditions. The heart must maintain an adequate CO to meet this demand.
The perfusion of tissue is regulated by what?
Cardiac output and the modification of systemic vascular resistance.
Cardiac output is a measure of what?
A measure of cardiac performance.
Cardiac Output (CO) is what volume of blood?
It is the VOLUME of blood pumped by each ventricle/min


It is NOT the total amount of blood pumped by the heart. (only the amt/min)
Cardiac output is normally ? on the right and left side of the heart.
Normally equivalent on both sides.
Normally the volume of blood flowing through the ? circulation and ? circulation is equivalent.
Normally the volume of blood flowing through the pulmonary circulation and systemic circulation is equivalent.
CO is the amount of blood ? by the heart.
Ejected by the heart
What are the two direct contributors to CO? Which is the largest contributor?
Heart Rate (beats/min) and Stroke volume (L/beat) are the direct contributors. (these are effected by a number of factors...see p. 7; slide 2)

Heart rate is by far the largest contributor to CO.
Heart rate is determined primarily by what influences?
Determined PRIMARILY by autonomic influences on the SA node. So the heart is innervated by both the parasympathetic and sympathetic divisions of the ANS.
The SA node is the ? of the heart.
The pacemaker of the heart.
The threshold for AP is reached approximately how many times per minute due to ANS innervation of the heart?
~70 times/min

The average heart rate is 70 beats/min.
What effect does the paraympathetic ns have on heart rate?
Decreases the firing rate of the SA node when stimulated by the pns. This is because it causes an increase in [K+] permeability of pacemaker potential.

So there is a decreased Heart rate and decreased CO.
What effect does the sympathetic ns have on heart rate?
Increases the firing rate of the SA node because of a decrease in [K+] permeability.

So increased HR and increased CO.
Parasympathetic innervation of the heart is via what?
Vagus nerve.
The parasympathetic innervation of the heart stimulates what components?
1. Atria

2. SA nodes

3. AV nodes
Sympathetic innervation of the heart is via what?
Several nerves
Sympathetic innervation of the heart stimulates what components? What is the important difference from pns innervation?
1. Atria (increases contraction)

2. SA nodes

3. AV nodes (increases elec. pulse)

4. Ventricles

The ventricles are only stimulated by the sympathetic. This is key to strong contractions.
If you cut the nerves responsible for parasympathetic stimulation of the heart what happens to a person's HR?
It would increase to about 90 beats/min. (because parasympathetic innervation is the 'brake')
What is the overall effect of parasympathetic stimulation of the heart?
Decreased HR via influence on SA node.
Parasympathetic stim. has an ? influence at the SA node. What does this cause?
Has Ach influence at SA node.

This causes increased permeability to K+ by slowing the closure of K+ channels.

This results in a decrease in the rate of spontaneous APs.
Describe parasympathetic stimulation at the AV node?
Increased K+ permeability hyperpolarizes the membrane, retarding initiation of excitationn at the node.

This results in a decrease in the node's excitability, prolonging impulse transmission to ventricles.
What is the overall effect of sympathetic stimulation on HR?
Speeds up HR in emergency or exercise situations.
Sympathetic stimulation relies on ? influence on the SA node. What is the result?
Norepinephrine influence on SA node.

Decreased K+ permeabilty by accelerating inactivation of K+ channels. This results in a 'less' negative inside of cells (DEPOLARIZED).

This results in an increased rate of depolarization, reaching threshold more rapidly and more frequent APs.
Describe sympathetic influence at the AV node?
Increased conduction velocity, presumed via enhancement of slow, inward Ca2+ current.

This results in a reduced AV nodal delay via increased conduction velocity.
PNS on SA node =

? SA node firing rate=

? HR =

? CO =

? slope of pacemaker potential =

? K+ permeability.
PNS on SA node =

Decreased SA node firing rate=

Decreased HR =

Decreased CO =

Decreased slope of pacemaker potential =

Increased K+ permeability.
SNS stimulation tends toward ? faster b/c of ? K+ permeability.
SNS stimulation tends toward repolarization faster b/c of decreased K+ permeability.
Sympathetic and parasympathetic effects on heart rate are what?
Antagonistic (coordinated and controlled)
Heart rate is determined by a balance between what?
A balance between inhibitory effects of the vagus nerve (PNS) and stimulatory effects of cardiac sympathetic nerves.
At rest what dominate in controlling heart rate?
At rest, parasympathetic tone dominates.
With no nervous stimulation from the PNS what would heart rate be at? What is this based upon?
With no pns stimulation, heart would beat at 70-100 beats/min. This is based on SA node spontaneous discharge.
The coordination of pns and sns stimulation of heart rate is achieved by what?
By the cardiovascular control center in the brain stem.
Remember; the right side of the heart has ? pressure and the left side of the heart has ? pressure relative to each other.
Right side = lower pressure

Left side = higher pressure
How are stroke volume (SV) and CO related?

If stroke volume increase then CO increases.

If stroke vol. decreases then CO decreases.
List the 3 mxms that control SV.
1. Contractile properties of the heart (increase SV)

2. Preload

3. Afterload
What is preload?
In cardiac physiology, preload is the volume of blood present in a ventricle of the heart, after passive filling and atrial contraction. If the chamber is not mentioned, it is usually assumed to be the left ventricle.

Related to the term EDV. The max amt of blood in the ventricles. Causes tension.
A higher end-diastolic volume implies a ? preload.
A higher end-diastolic volume implies a higher preload.
Preload ? with exercise, thus increasing what?
Preload increases with exercise (slightly), increasing blood volume (overtransfusion) and excitement (sympathetics).
Increased preload =

? SV =

? CO
Increased preload =

Increased SV =

Increased CO
What is afterload?
In cardiac physiology, afterload is used to mean the tension produced by a chamber of the heart in order to contract. If the chamber is not mentioned, it is usually assumed to be the left ventricle.

The term end-systolic pressure is related.
Everything else held equal, as afterload increases, cardiac output ?.
Everything else held equal, as afterload increases, cardiac output decreases.
In the case of the left ventricle, the afterload is a consequence of what? Explain.
In the case of the left ventricle, the afterload is a consequence of the blood pressure, since the pressure in the ventricle must be greater than the blood pressure in order to open the aortic valve.
Afterload is the resistance the ventricles will meet as they do what?
Eject blood into the arteries.
Increased After load =

? SV =

? CO
Increased afterload =

decreased SV =

decreased CO

(because takes more effort to open up valves)
Preload is pretty much equivalent to what?
End diastolic volume.
Preload is controlled by what?
Venous return through the right atria.
Increased venous return =

? preload =

? SV
Increased venous return =

Increased preload =

Increased SV
What things might increase venous return?
1. Increased respiratory pump activity

2. Increased skeletal muscle pump activity

3. Increased kidney activity

4. Increased contraction of veins
How is kidney activity related to venous return?
Because it controls H2O and extracellular fluid volume. So it controls vascular volume.
How are veins related to venous return and stroke volume?
Increased contraction = increased venous return = increased preload = increased SV.

Veins have the ability to stretch ('floppy'). There is a contraction and relaxation of the small amt of muscle found in veins. Arteries do not have this characteristic. Because of this ability veins can hold a large volume. (relaxed = more blood; contract = less blood)
Increased EDV results in ? SV.
Increased SV
The Frank-starling law of the heart refers to the intrinsic relationship between what two things?
Intrinsic rel. b/n EDV and SV.
The Frank-Starling law of the heart states what?
That the more the ventricle is filled with blood during diastole (end-diastolic volume), the greater the volume of ejected blood will be during the resulting systolic contraction (stroke volume).
The Frank-Starling law implies that the more you stretch the heart muscle the more you do what?
The more you activate the cross-bridges and increase stroke volume.
The heart has the ? ability to vary stroke volume.
Inherent ability (intrinsic control)
The hearts intrinsic control of stroke volume is dependent upon what relationship of cardiac muscle?
Dependent upon the length-tension relationship of cardiac muscle (similar to skeletal muscle)
Unlike skeletal muscle, the ? ? of cardiac muscle is less than optimal for max. tension.
The 'resting length' is less than optimal for max. tension.
Doing what to cardiac muscle fiber length brings the length closer to optimal for max. tension?
Increasing cardiac muscle fiber length.
What is the main determinant of fiber length?
The degree of diastolic filling.
Stroke volume is determined by the extent of ? and ? activity.
Venous and sympathetic activity.
Concerning control of SV:

Venous return = ? control

Sympathetic activity = ? control

What do both do?
Venous return = intrinsic control

Sympathetic activity = extrinsic control

Both increase SV by increasing the strength of contraction of the heart.
According to the Frank-Starling Law the heart normally pumps what?
Normally pumps all the blood returned to it.
According to the Frank-Starling Law increased venous return results in what?
Increased SV
The extent to which the heart is filled with blood is known as what?
Preload (the workload imposed on the heart before contraction)
What are 2 advantages associated with the Frank-Starling law?
1. Equalizes output between left and right sides (pulmonary and systemic circulation)

2. When larger CO needed, venous return increases (sympathetic stim.), resulting increase in EDV automatically increases SV.
As you increase EDV (preload) what do you do to SV?
Increase SV (Frank-starling law)
As you increase afterload what do you do to SV?
Decrease SV (because you decrease ESV)
The mxm of cardiac length-tension relationship depends on the extent of what to a degree?
Depends of the extent of overlap of thick and thin filaments, to a degree (just like skeletal).
What is the major factor related to the mxm of the cardiac length-tension relationship? Explain.
The major factor is the length dependence of myofilament Ca2+ sensitivity.

As cardiac muscle fiber is stretched due to greater ventricular filling, myofilaments are pulled closer together.

Thick and thin filament distance is reduced.

This allows more interaction b/n actin and myosin when Ca2+ pulls troponin-tropomysin complex away from actin's cross bridge sites = increased Ca2+ sensitivity.
The extrinsic control of SV involves what?
Cardiac sympathetic nerves and epinephrine.
During extrinsic control of SV cardiac sympathetic nerves and epinephrine have what effect on heart contractility?
Enhance heart contractility. This refers to the strength of contraction at any EDV.

The heart contracts more forcefully, squeezing out more blood.
During extrinsic control of SV the heart contracts more forcefully, squeezing out more blood. What is this caused by?
Caused by increased Ca2+ influx triggered by norepinephrine and epinephrine.

Increased Ca2+ allows more force via great cross-bridge recycling.

The max increase in contractile strength is ~100% greater than normal.
How does extrinsic control of SV also effect venous return?
The sympathetic nerves and epinephrine stimulate constriction of veins and ENHANCE venous return. This squeezes more blood forward to increase EDV.
Cardiac output is the product of ? ? and ? ?.
Product of SV and Heart rate.
Stroke volume via varying muscle fiber length is dependent upon what?
Dependent upon ventricular filling before contraction (ie, venous return (preload) = intrinsic control)

And sympathetic stimulation (extrinsic control)
Heart rate occurs via ? and ? stimulation.
Via sympathetic and parasympathetic stimulation.
Heart failure is primariliy a disease of what?
Heart failure is essentially the inability of the heart to maintain what?
Inability to maintain an adequate Cardiac Output (CO) to meet the constant metabolic demand of all tissues.
List the two basic types of cardiac dysfunction that lead to CHF.
1. Systolic dysfunction

2. Diastolic dysfunction
Describe systolic dysfunction?
Decreased ejection of blood from heart during systole (contraction).

Decreased contractility and decreased ejection fraction.

Decreased volume (decreased mL/min)
What is an ejection fraction?
The amount of blood pumped out of a ventricle with each heart beat.
List 4 possible causes of systolic dysfunction.
1. Cardiomyopathy

2. Ischemic heart disease

3. Fluid overload

4. HTN (heart chronically works against increased afterload of elevated aortic pressure)

(there are more causes than just these)
Describe diastolic dysfunction?
Impaired filling of ventricles during diastole.

Related to :
Poor ventricular filling,
Small ventricle size,
Ventricular hypertrophy,
Poor compliance,
Congestion of tissues.
What are some possible causes of diastolic dysfunction?
1. Mitral stenosis

2. LV hypertrophy

3. Cardiomyopathy

4. Transient ischemic heart disease
The output of both sides of the heart should be what?
Equal (but one or both sides could be impaired)
The left side of the heart is the '?'.
'Powerhouse'...propels blood into system
List some sx of Right sided Heart failure?
1. Congestion of peripheral tissue (edema, 'pitting' of feet and ankles)

2. GI congestion (affect eating, anorexia, wt. loss)

3. Liver congestion (b/c inferior vena cava branch, portal system backed up)
List some sx of Left sided HF?
1. Decreased Cardiac Output
(increased fatigue b/c decreased oxygen in tissues b/c decreased blood to tissues)

2. Pulmonary congestion (fluid in lungs, impairs gas exchange, develops cyanosis which is observable in lips b/c low oxygen)

3. Pulmonary edema (difficulty breathing, paroxysmal nocturnal dyspnea)
What is PND?
Paroxysmal nocturnal dyspnea.

Related to pulmonary edema (left sided HF).

PND is caused by increasing amounts of fluid entering the lung during sleep and filling the small, air-filled sacs (alveoli) in the lung responsible for absorbing oxygen from the atmosphere. This fluid typically rests in the legs during the day when the individual is walking around and redistributes throughout the body (including the lungs) when recumbent.

PND is a sign of severe heart failure.
List some generalized CHF sx?
1. Fluid retention/edema

2. Respiratory (dyspnea, othopnea)

3. Fatigue and weakness

4. Cachexia and malnutrition

5. Cyanosis
Sx of Right or Left HF?:

Fluid retention/edema
Sx of Right or Left HF?:

Respiratory (dyspnea, orthopnea)
Sx of Right or Left HF?:

Fatigue and weakness
Sx of Right or Left HF?:

Cachexia and malnutrition
Sx of Right or Left HF?:

Concerning Left sided heart failure, what happens to the following three characteristics:

1. Right ventricular output

2. Pressure

3. Pulmonary tissue
1. Right ventricular output exceeds left ventricular output

2. Pressure backs up

3. Fluid accumulates in pulmonary tissues
In Left sided HF when the Right ventricular output exceeds the left ventricular output what happens?
The left side pools blood. This creates increased pressure in the left ventricle. This back pressure goes back through the atrium to the pulmonary circulation and causes fluid accumulation in the lungs/congestion.
Concerning Right sided HF, what happens to each of the following three characteristics:

1. Left ventricular output

2. Pressure

3. Systemic tissue
1. Left ventricular output exceeds right ventricular output

2. Pressure backs up

3. Fluid accumulates in systemic tissue
During Right sided HF where does pressure back up to?
Mostly to the inferior vena cava to systemic circulation to veins in legs where fluid will start to accumulate (in ankles, etc)
The prime defect in heart failure is what?
A decrease in cardiac contractility.
During HF the intrinsic ability of the heart to do what is reduced?
Reduced ability to develop pressure and eject SV.
When there is a decrease in cardiac contractility the heart operates on a ? ? ? curve. So the Frank-Starling curve is shifted ?.
Operates on a lower length-tension curve.

So the Frank-Starling curve is shifted downward.
Decreased contractility = ? SV
Decreased stroke volume. (even if there is the same volume of blood in the heart...there is less contractility)
List the 2 major compensatory measures in heart failure.
1. Sympathetic activity to heart increased, increasing contractility

2. Kidneys retain salt and water to increaes blood volume
During HF the body still tries to maintain what?
Homeostasis (tries to increase CO during HF)
Circulating ? is elevated when the sympathetic activity of the heart is increased during HF.
Circulating catecholamines (Epi and NE) are elevated. (helps stim. heart to improve contractility)
During HF the kidneys may retain salt and H2O to increase blood vol. Increased circulating blood volume does what to EDV? Preload? SV? CO?
Increases end-diastolic volume = Increased preload = increases stroke volume = increased CO.
When the kidneys retain salt and water to increase blood volume what effect does it have on the heart muscle fibers? What does this allow the heart to do?
Results in a stretching of heart muscle fibers allows heart to pump out normal SV.
When kidney's retain salt and water to increase blood volume what happens to the volume of cells?
Cell volume is increased (this is how blood volume is increased)
When kidney's retain salt and water to increase blood volume the heart is operating at ? cardiac muscle fiber length.
Compensatory HF (sympthetic and kidney effects) are what kind of changes?
What is the Renin-Angiotensin-Aldosterone Mxm and how does it relate to compensatory HF?
Mxm is activated during HF.

Releases Angiotensin.

Angiotensin then release aldosterone.
What does angiotensin cause to occur?
Increased Vascular tone =

Increased vasc. resistance =

Increased BP in blood vessels =

Increased afterload.
What does aldosterone cause to occur?
Increased salt and water retention during HF.
Do compensatory HF pts have tachycardia?
What does increased sympathetic stimulation do to the Frank-Starling curve? Why is this important.
Shifts the Frank-Starling curve of failing heart to the left. This represents an increase in contractility towards normal. This is important because you don't have to increase your EDV as much as you do in uncompensated HF so you don't have to retain as much fluid to maintain SV.
What does decompensated HF result from?
Eventually, the heart can no longer pump out normal SV, despite compensatory you enter decompensated HF.
What happens to cardiac muscle fibers during decompensated HF?
Cardiac muscle fibers stretched to point at which they operate in descending limb of length-tension curve.
What are two reasons for decompensated HF?
1. Too much neurotransmitter stim. from sympathetic compensation...leads to apoptosis

2. Kidneys retain more and more water during compensation...leads to a stretch in the sarcomeres.
In decompensated HF, ? and ? failure occur.
Backward and forward failure occur.
What is backward failure during decompensated HF?
Blood cannot enter and be pumped out by heart, so backs up in venous system.

Congestion in veins : "congestive heart failure"
What is forward failure during decompensated HF?
Heart fails to pump adequate blood volume forward to tissues due to smaller and smaller SV.
Decompensated heart failure illustrates the importance of what?
High blood pressure increases what?
Workload...caused by an increase in afterload
When ventricles contract, forcing out blood, they must overcome what?
They must exceed pressure in major arteries (the afterload).
Increased BP in arteries means what for the ventricles?
The ventricles must contract more forcefully to exceed this BP.
The heart may compensate for chronic high BP by doing what?
Increasing in size.

A diseased heart or one weakened by age may not be able to do what in response to BP? What does this lead to?
May not be able to compensate. Leads to heart failure
Even if the heart can initially compensate for chronic elevated BP, what can extra workload eventually do?
Can eventually cause pathology.
Hypertrophy in the long term can eventually cause what?
Heart failure