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
AV node
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
AV bundle
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
Purkinje fibers
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
How does an electrocardiogram work?
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
A normal EKG
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
Tachycardia
Greater than 100 bpm occurs in normal hearts during exercises/ can occur in disease ( symptom of hyperthyroidism)
31
Bradycardia
Less than 60 bpm Athletes can have bradycardia (pump more blood per beat) Bradycardia occurs in complete heart block
32
Flutter
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
Fibrillation
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
Atrial fibrillation vs ventricular fibrillation
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
Systole
Contraction
36
Diastole
Relaxation
37
How is stroke volume calculated?
Stroke volume is the difference between the diastole and systolic volume = 70 m/s normal resting SV
38
Why are arteries elastic?
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
How do we express blood pressure?
Systolic/diastolic pressure in mmHg 120/80 mmHg
40
Cardiac cycle for the right side of the heart
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
What is turbulent flow ?
Layers of blood breakup causes sound from vibrating structures nearby The cause of heart murmurs is turbulent flow of blood
42
Laminar flow
Layers slide over each other (is quiet) | Normal blood flow
43
Why does turbulent flow occur?
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
What is cardiac output?
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
Parasympathetic fibers
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
Sympathetic nerves
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
How does epinephrine and norepinephrine control HR?
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
How do temperature and electrolytes affect heart rate?
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
Intrinsic control of stroke volume
When ventricle fills with more blood (increased EDV) more blood is ejected (increased stroke volume) Increased EDV means increase cardiac fiber length
50
What determines EDV (end diastolic volume)
Venous return | Increased venous return means increased EDV and SV
51
Function of starling’s law
Keeps right and left cardiac outputs equal This law makes sure blood will not accumulate on one side of the circulatory system