Cardio Mod 3

Question 1

Cardiac Layers (6)

Answer 1

A. Endocardium
1. Similar to the endothelial cells that line blood vessels – smooth “frictionless” surface

B. Myocardium
1. cardiac muscle cells (contractile tissue)

C. Epicardium (visceral pericardium)
1. connective tissue layer (aka visceral pericardium)

D. Parietal space (pericardial cavity)

1. pericardial fluid to reduce friction during heart movement
2. Clinical: pericardial effusion (cardiac tamponade)

E. Parietal pericardium
1. connective tissue layer insulating the heart

F. Fibrous pericardium
1. fibrous sac that “contains” the heart

Question 2

Muscle fibers - Myocardial Cells (Contractile Cells)

Answer 2

a. Composed of many myofibrils, single nucleus, mitochondria, sarcoplasma reticulum and cytoplasm
b. These components are “wrapped” up by the plasma membrane called the sarcolemma

Question 3

Sarcolemma– Myocardial Cells (Contractile Cells)

Answer 3

a. Cell/plasma membrane of the muscle fiber
b. “Surrounds” the myofibrils and also penetrates into the myofibrils with invaginations called T-tubules
c. Spreads the action potential throughout muscle fiber
• Lengthwise along the sarcolemma and penetrates deep into myofibrils via T-tubules
d. This arrangement allows for a rapid transmission of action potential

Question 4

Myofibrils–Myocardial Cells (Contractile Cells)

Answer 4

a. Composed of myofilaments
• Protein filaments that provide mechanical shortening/lengthening of the muscle fiber
• Myofilaments are arranged in units called sarcomeres

b. Subunits of myofibrils are called: sarcomeres
• Sarcomeres are repeating units arranged in series (end to end) along the length of the myofibril
• Each sarcomere contains the myofilaments

Question 5

Myosin (thick) microfilament

Answer 5

• Chains of myosin molecules wrapped together each with protruding globular heads form myosin microfilament
• Globular heads bind to actin and swivel causing mechanical shortening of sarcomere
• Head contains:
(i) Binding site for actin
(ii) receptor for ATPase

Question 6

Myofilaments

Answer 6

a. Composed of protein chains known as actin and myosin microfilaments

Question 7

Actin (thin) microfilament

Answer 7

• Two chains of actin molecules wrapped together form actin microfilament

(i) Tropomyosin is a protein “wrapped” around the length of the actin microfilament
(ii) Troponin is a protein attached (associated) intermittently along the length of the tropomysion

Question 8

Function of troponin and tropomyosin

Answer 8

(i) Allows exposing/covering of the binding site on actin for the myosin globular heads
1. If binding site is covered – sarcomere/muscle fiber can’t contract
2. If binding site exposed - myosin head can bind to actin which allow the mechanical contraction of the sarcomere/muscle fiber

Question 9

Tropnin has sub-components

Answer 9

1. Troponin T – binds the troponin to the tropomyosin and actin
2. Troponin C – contains binding site for calcium
   a. Calcium is the “on/off” switch for contraction
3. Troponin I – inhibits ATPase
   a. ATP is needed fuel for contraction

Question 10

The bands and zones of an individual sarcomere

Answer 10

• Z lines (Z line to Z line = sarcomere)
• A band
• H zone
• M band
• I band

Question 11

M Band

Answer 11

(i) Central portion of the H zone
(ii) Area where the myosin filaments thickens
(iii) Connects the myosin filaments together

Question 12

I Band

Answer 12

(i) Area of sarcomere that contains only actin

Question 13

H Zone

Answer 13

(i) Lighter central portion of the A band that contains only myosin (thick filament)

Question 14

A Band

Answer 14

(i) Dark band that extends over the full length of the myosin filament and small portion of the actin filament

Question 15

Z lines

Answer 15

(i) Anchors/connect the thin filaments

Question 16

Myocardial contraction and relaxation

Answer 16

A. Muscle contraction is result of muscle fiber shortening
B. The cross-bridge theory describes the molecular events that cause the muscle fiber to shorten
1. Calcium binds to troponin – C which exposes binding site on actin
2. Myosin head is attached to actin
3. Myosin head binds to actin which releases the ADP and P and causes the myosin head to swivel
4. ATP binds to myosin head
5. ATP “breaks down” to ADP and P which causes the release myosin head from actin to relaxed position

Question 17

Excitation-contraction coupling

Answer 17

1. Action potential travels across sarcolemma and down the T-tubules
2. Action potential reaches the sarcoplasma reticulum (which stores calcium) and signals the release of calcium to diffuse into the microfilaments and bind to Troponin-C.
3. If calcium binds to Troponin-c then actin binding site is exposed for the myosin head to bind

Question 18

Summary of cardiac muscle fiber characteristics

Answer 18

A. single nucleus
B. extremely large number of mitochondria
1. supply ATP for cardiac muscle
C. extensive T-tubule system
1. facilitate rapid action potential-calcium release in muscle cell for contraction
D. interclated disc
1. between muscle fibers to allow action potential to travel from cell to cell (syncytium)
2. desmosomes – attach each muscle fiber to the next
3. gap junction – allows electrical action potential to spread through the intercalated disc from one muscle fiber to the next

Question 19

Frank Starling’s Law of the Heart

Answer 19

1. Length-tension relationship between length of myocardial muscle and force generation

Question 20

In healthy cardiac muscle–Frank Starling’s Law of the Heart

Answer 20

Length of cardiac muscle fiber (sarcomere) is directly related to force generated by the muscle fiber
a. Function application:
• End-diastolic volume (filling of ventricles) determines the amount of “stretch” on the cardiac muscle fibers, therefore:
(i) Increased end-diastolic volume = increased contractility
(ii) Increased contractility = increased stroke volume/cardiac output

Question 21

Frank Starling’s Law of the Heart—“Un-healthy” cardiac muscle = heart failure

Answer 21

a. cardiac muscle has been dilated/damaged

b. sarcomeres are lengthened “too far” and Frank Starling Law no longer applies

Question 22

LaPlace’s Law

Answer 22

1. Wall tension (contraction force) is directly related to the product of intraventricular pressure x internal radius (ventricular volume) and inversely related to wall thickness
2. What does it mean?
   a. A dilated, thin walled ventricle full of blood requires even more time to generate a contraction force (wall tension) strong enough to generate the intraventricular pressures needed to eject blood from the heart.
   b. This makes form poor cardiac output and performance
3. Clinical:
   a. Heart failure (dilated thinned wall heart) or aneurysm

Question 23

Preload

Answer 23

1. Left ventricular preload is the pressure generated in the left ventricle at the end of diastole (ventricular filling).
2. Preload = left end-diastolic pressure

Question 24

What determines preload in healthy heart?

Answer 24

a. Left end-diastolic volume (Starling’s Law of Heart)

b. ↑ Left end-diastolic volume = ↑ preload = ↑ stroke volume/cardiac output

Question 25

Healthy diastolic function

Answer 25

a. increased preload with increased stroke volume | b. “For all input there is corresponding output”

Question 26

Diastolic dysfunction

Answer 26

a. Reduced ventricular wall compliance b. Ventricular hypertrophy results in less ventricular filling (decreased end diastolic volume) but an increased preload c. Output (stroke volume) is reduced despite the increased preload d. However - EF remains the same e. Excessive left end-diastolic filling pressures will cause “congestive back-up” in pulmonary circulation

Question 27

Afterload

Answer 27

1. The force the left ventricle must generate during systole to overcome aortic pressure to open the aortic valve. 2. Increased afterload means ventricle has to work harder to eject blood a. Physically takes “longer contraction time” for ventricle to generate necessary force to eject blood. b. Increased afterload with insufficient contraction time = reduced stroke volume

Question 28

Clinical- Afterload

Answer 28

a. elevated systemic blood pressure, aortic stenosis and dilated ventricle represents elevated afterload b. if afterload increases then there is decreased stroke volume (and increased end systolic volume) c. hypertrophy is form of compensation to increased afterload

Question 29

Cardiovascular Control Centers (3)

Answer 29

1. located in medulla (lower region of brainstem) 2. synapse with sympathetic and parasympathetic pathways to the heart 3. autonomic response at rest and during exercise

Question 30

Autonomic response at rest and during exercise

Answer 30

a. Rest • Parasympathetic dominate at the SA node b. Easy exercise • Removal of parasympathetic influence on SA node c. Intensive exercise • Increased sympathetic influence on SA node

Question 31

Synapse with sympathetic and parasympathetic pathways to the heart

Answer 31

a. Sympathetic – increase HR and contractility | b. Parasympathetic – decrease HR and contractility

Question 32

Arterial Baroreceptors

Answer 32

a. Located in aortic arch and carotid sinus (“systemic” stretch receptors) b. Stimulation of these receptors will decrease HR c. Pressure changes stimulate baroreceptors to change HR which also lead to change BP • ↑ pressure will cause barorecptors to ↑ parasympathetics and ↓ sympathetics (i) Net result: ↓ HR, ↑ vasodilation which ↓ BP • ↓ pressure will cause the opposite

Question 33

Atrial Receptors

Answer 33

a. Stretch (volume) receptors located in both R/L atria as described above b. These receptors will stimulate control of blood volume control • ↑ atria volume will release ANP from atria • ANP will stimulate kidneys to excrete both urine (diuretic) and sodium • End result is reduced blood volume c. Stimulation (stretch) of these receptors will increase HR (opposite of baroreceptors described above) • The arterial baroreceptors have dominant role in maintaining HR compared to the atrial receptors

Question 34

Bainbridge reflex (stretch receptors in atria)

Answer 34

* ↑ HR after IV infusion (increase blood volume) * ↑ IV fluid will ↑ stimulation of stretch (volume) receptors in the atria which will stimulate sympathetic influence to heart

Question 35

Myocardial Contractility

Answer 35

1. Ability of ventricular walls to contract (force production) 2. Two factors determine contractility a. Sympathetic nervous input b. Increased stretch of ventricle (in healthy cardiac muscle)

Question 36

Starling’s Law of the Heart

Answer 36

(i) Increase preload = increase contractility of healthy cardiac muscle (i.e. ventricle)

Question 37

2 Factors Determining Cardiac Output

Answer 37

A. CO = HR x SV B. Examples: 1. Increased HR a. increased sympathetics and decreased parasympathetics 2. Increase stroke volume a. ↑ venous return • ↑ blood volume • ↑ sympathetic activity to veins b. ↑ end-diastolic volume c. ↑ preload