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PSL 310 > Cardiac Physiology > Flashcards

Cardiac Physiology Flashcards

1
Q

What are the three layers of the heart?

A
  1. The myocardium-thick muscle layer
  2. Endocardium-flat cells that line the inner layer of the heart (continuous with endothelium of blood vessels)
  3. Epicardium-outer later of the heart, also called the visceral pericardium (layer on surface like the peel of an apple)

The heart is surrounded by pericardial fluid that is enclosed by the fibrous pericardium

The parietal pericardium lines the fibrous pericardium

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2
Q

What is the function of the pericardial fluid?

A

It is a lubricant so the heart can beat within the sac with no friction

The epicardium aka visceral pericardium and the parietal pericardium are membranes that secrete this fluid

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3
Q

What is the function of the 2 pumps in the heart?

A

The right side of the heart pumps blood to the lungs in the pulmonary circulation or circuit (from right atrium, right ventricle, pulmonary artery, lungs, pulmonary veins)

The left side pumps blood to the rest of the body in the systemic circulation or circuit (left atrium, left ventricle, to aorta, to diff muscles and organs, venae cavae back to right atrium, right ventricle)

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4
Q

Describe the flow of blood through the heart

A
  1. Deoxygenated blood enters the right atrium from the superior and inferior vena cava.
  2. The deoxygenated blood travels through the tricuspid valve (right atrioventricular valve) and enters the right ventricle. (The ventricle contracts)
  3. The deoxygenated blood then travels through the semilunar valve then into the pulmonary arteries where it goes to the lungs to exchange CO2 for O2. The blood is now oxygenated.
  4. The oxygenated blood returns to the heart via the pulmonary veins (normally 4) and enters the left atrium.
  5. The oxygenated blood then travels through the bicuspid valve (left AV) into the left ventricle. (Ventricle contracts)
  6. The blood then travels through the aortic semilunar valve into the aorta to all the body except the lungs and alveoli of lungs.

NOTE: The coronary arteries that supply the heart muscle branch off the aorta (just past semilunar valve). Blood returns to heart chamber via coronary sinus which drains into right atrium.

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5
Q

What causes myocardial infarction?

A

Myocardial infarction is death of cardiac cells.

This is due to the coronary arteries, which supply the heart muscle with nutrients and oxygen, becoming blocked.

The heart muscle is too thick to get nutrients through diffusion from blood inside the hearts chambers. It must rely on vessels.

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6
Q

What direction do the valves of the heart and veins flow?

A

They allow only 1 way flow of blood.

Valves close and prevent backward flow (unidirectional flow of blood)

How it works?

  • when pressure is greater behind the valve it opens
  • when pressure is greater in front of the valve it closes *doesn’t open in opposite direction because it’s one way
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7
Q

What is the purpose of the chordate tendineae?

A

Fibrous cords attached to the valve edges of cuspid (AV) valves

They restrain the valve edges (keeps the valve edges from going up into the atria when ventricles contract)

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8
Q

Right atrioventricular (AV) valve

A

3 cusps (tricuspid)

Valve leading from right atrium to the right ventricle

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9
Q

Left atrioventricular valve

A

2 cusps (bicuspid/mitral)

Located between left atrium and left ventricle

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10
Q

Aortic or pulmonary valve

A

Also known as the semilunar valve

The pulmonary valve is located in the right ventricle leading to the pulmonary arteries

The aortic valve is located in the left ventricle leading to the aortic artery

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11
Q

What are gap junctions?

A

Small connecting “tunnels” between cells

Allows the action potential to go from cell to cell-current (positive charge) flows into the next cell- causes an action potential in the next cell

*current carried by ions in the body

If action potential occurs in any part of the muscle, it passes throughout the muscle and the muscle contracts as a unit

Acts as functional syncytium = merging (connected) cells that act together (electrically and mechanically)

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12
Q

What are the two functional syncytia in the heart?

A

1 in the atria; 1 in the ventricles

They are separated by the heart’s fibrous skeleton which provide attachment for heart valves and for the hearts muscle fibers

*fibrous skeleton doesn’t conduct impulses

The 2 syncytia are separated except in one point (AV node)

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13
Q

How can the heart beat on its own?

A

Pacemaker potentials cause action potentials

Needs action potentials to cause contraction but does not require neural stimulation to contract

The action potential originates in the heart itself

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14
Q

Why does the inherent rate differ from the normal (or resting) rate?

A

The inherent rate equals 100 bpm with nothing affecting heart rate except the heart itself

The normal rate equals 70 bpm. This is because the parasympathetic nervous system is dominant at rest- acts as a brake on the heart.

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15
Q

How is heart rate changed?

A

By changing the slope of the pacemaker potential

Parasympathetic impulses decrease the slope of the pacemaker potential (flatter) . Takes longer to reach threshold-decreases heart rate

Sympathetic impulses increase slope of pacemaker potential (steeper). Quicker to reach threshold-increases heart rate.

How is the slope changed?

  • nerves (ANS)
  • hormone epineferen
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16
Q

What part of the heart sets the inherent rate and why?

A

The pacemaker or sinoatrial node (SA node)

The SA node is chosen because it gets to threshold the quickest/first

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17
Q

What happens if the SA node is damaged?

A

The normal pacemaker activity is 70 bpm (heart rate set by SA node, the fastest autorhythmic tissue).

If the SA node is damaged (nonfunctional), the AV node can take over and heart rate will decrease to 50 bpm.

If the AV node is nonfunctional the link to the ventricle will be lost (causes complete heart block) The purkinje fibers can take over but heart rate would be 30-40 bpm. (Person would be unconscious)

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18
Q

What is an ectopic focus?

A

pacemaker is taken over by ectopic focus. The whole heart will be driven more rapidly by an abnormal pacemaker

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19
Q

Why is the refractory period of cardiac muscle (of the membrane) long?

A
  • Prevents prolonged or tetanic contraction (tetanus) in the heart.
  • The heart needs a long enough refractory period to guarantee relaxation so blood can fill into heart.
  • a second contraction can be stimulated before the first is over, which means you can get summation, and if the stimulation is rapid enough, you get tetanus
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20
Q

What causes the plateau in cardiac action potential?

A

Depolarization first occurs due to opening of voltage gated Na+ channels

Then Na+ channels close

The plateau then occurs because K+ permeability decreases and Ca++ membrane permeability increases
Ca++ brings in positive charges from ECF and keeps membrane depolarized at plateau level (balances)

Depolarization then occurs when Ca++ and K+ change back to permeabilities before action potential.

Then K+ permeability increases positive change moves out which causes repolarization

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21
Q

How do Ca++ levels in the cytosol affect the strength of contraction of the heart?

A

Ca++ enters cell from ECF during action potential (during plateau) this can induce Ca++ release from SR.

A small amount of the Ca++ that entered the cell can directly activate contractile machinery (Ca++ binds to troponin)

The majority of the Ca++ that binds to troponin comes from SR

AN INCREASE OF CA++ IN CYTOSOL OF THE CRLL CAN INCREASE STRENGTH OF CONTRACTION

epinephrine and norepinephrine can increase strength of cardiac contraction by increasing Ca++ in cytosol

22
Q

What does the drug digitalis do?

A

Used to treat heart failure (heart fails as a pump) so digitalis increases the amount of Ca++ in the cytosol

23
Q

What occurs if all Ca++ channels on the heart muscle cells were blocked?

A

The heart would not be able to contract

24
Q

SA node

A

Sinoatrial node

Pacemaker of a normal heart

Near the superior vena cava

Mass of specialized cardiac muscle cells

Autorhythmic (100 bpm or 70)

Action potential generated from its pacemaker potential spreads from regular cell to cell through gap junctions.

Atria contract together

25
Q

AV node

A

Atrioventricular node (non conductive tissue surrounds atrial-ventricular junction=hearts fibrous skeleton)

AV node is the only link to the ventricles

AV node is specialized cardiac muscle cells in right atrium near ventricle

26
Q

AV bundle

A

Atrioventricular bundle =bundle of his

Is a bundle of conductive tissue in ventricular septum

Single bundle then it branches into right and left branches

27
Q

Purkinje fibers

A

These fibers carry the impulse to the thick myocardium (not to all cells, but to many cells, and then is regular cell to cell conduction)

Causes coordinated contraction of the ventricles together

28
Q

How does an electrocardiogram work?

A

An EKG is used to evaluate the electrical events of the heart

The depolarization and repolarization of the myocardium-action potential going through the heart-causes current in the body fluids outside of the heart

Tiny current flow can be detected on the surface of the body. Electrodes are places on skin to pick it up.

29
Q

A normal EKG

A

The SA node fires
P wave=atrial depolarization
PR segment =AV nodal delay
QRS complex=ventricular depolarization (atria repolarization the simultaneously)
ST segment=time during which ventricles are contracting and emptying
T wave=ventricular repolarization
Tp segment=time during which ventricles are relaxing and filling

30
Q

Tachycardia

A

Greater than 100 bpm occurs in normal hearts during exercises/ can occur in disease ( symptom of hyperthyroidism)

31
Q

Bradycardia

A

Less than 60 bpm

Athletes can have bradycardia (pump more blood per beat)

Bradycardia occurs in complete heart block

32
Q

Flutter

A

Very rapid over 200 bpm

regular

At these rapid rates filling times are compromised

Real problem if in the ventricles for greater than 30 sec

33
Q

Fibrillation

A

Cardiac chaos

Ventricle looks like squirming worms little areas of the ventricle are contracting and relaxing independently

Fibrillation chambers cannot pump blood; if ventricles are fibrillation you are in serious trouble because they are not pumping blood out of heart

34
Q

Atrial fibrillation vs ventricular fibrillation

A

Can survive with atrial fibrillation (you won’t have the atrium contracting tho to top off the ventricles so you will tire more easily)

Ventricular fibrillation is serious because you aren’t pumping blood out of the heart so defibrillation is necessary in order to reestablish normal rhythm

Expose myocardium to a strong current depolarize all cells at once

35
Q

Systole

A

Contraction

36
Q

Diastole

A

Relaxation

37
Q

How is stroke volume calculated?

A

Stroke volume is the difference between the diastole and systolic volume = 70 m/s normal resting SV

38
Q

Why are arteries elastic?

A

They need to expand with the volume of blood abs then recoil to maintain pressure to drive the blood through the tissues during diastole when the ventricles are relaxing

39
Q

How do we express blood pressure?

A

Systolic/diastolic pressure in mmHg

120/80 mmHg

40
Q

Cardiac cycle for the right side of the heart

A

The same as left but pressures are lower

Right heart wall is thinner

Right heart ejects same amount of blood as the left heart

41
Q

What is turbulent flow ?

A

Layers of blood breakup causes sound from vibrating structures nearby

The cause of heart murmurs is turbulent flow of blood

42
Q

Laminar flow

A

Layers slide over each other (is quiet)

Normal blood flow

43
Q

Why does turbulent flow occur?

A
  1. Stenosis- a narrowed valve does not open completely blood flows rapidly through narrowed valve
  2. Regurgitation or leaky valve does not close completely- blood flows backward against flow of blood
  3. Blood flowing through a hole in the septum
44
Q

What is cardiac output?

A

The amount of blood pumped by either ventricle per minute. (It is flow through systemic or pulmonary circulation)

Flow out of the two ventricles matches

Units: L/min

CO=HR X SV

SV= EDV-ESV

45
Q

Parasympathetic fibers

A

Travel in the Vagus to the SA NODE, Sv node, and atrial myocardium

Not much innervation of the ventricle

Secrete ACh

Acts as brake on the heart

Effect of parasympathetic fibers at AV node is increase in AV nodal delay

46
Q

Sympathetic nerves

A

Innervated the SA node, AV node, and the atrial and ventricular myocardium
(The entire myocardium)

Secrete

Cause less AV nodal delay

Affects force of contraction of the ventricles

47
Q

How does epinephrine and norepinephrine control HR?

A

Speeds up heart rate and increased contractility.

Acts on beta 1 receptors

Contractility is increased force of contraction not due to a change in EDV it is independent

48
Q

How do temperature and electrolytes affect heart rate?

A

Temp- hypothermia causes decreased HR (sometimes is induced in surgeries)

Electrolytes- ECF K+ concentration abnormalities can cause arrhythmias

Other hormones- thyroid hormones increase number of B1 receptors on the heart and increase HR

49
Q

Intrinsic control of stroke volume

A

When ventricle fills with more blood (increased EDV) more blood is ejected (increased stroke volume)

Increased EDV means increase cardiac fiber length

50
Q

What determines EDV (end diastolic volume)

A

Venous return

Increased venous return means increased EDV and SV

51
Q

Function of starling’s law

A

Keeps right and left cardiac outputs equal

This law makes sure blood will not accumulate on one side of the circulatory system

PSL 310 (8 decks)

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