Cardio Mod 3 Flashcards
Cardiac Layers (6)
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)
- pericardial fluid to reduce friction during heart movement
- 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
Muscle fibers - Myocardial Cells (Contractile Cells)
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
Sarcolemma– Myocardial Cells (Contractile Cells)
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
Myofibrils–Myocardial Cells (Contractile Cells)
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
Myosin (thick) microfilament
• 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
Myofilaments
a. Composed of protein chains known as actin and myosin microfilaments
Actin (thin) microfilament
• 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
Function of troponin and tropomyosin
(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
Tropnin has sub-components
- Troponin T – binds the troponin to the tropomyosin and actin
- Troponin C – contains binding site for calcium
a. Calcium is the “on/off” switch for contraction - Troponin I – inhibits ATPase
a. ATP is needed fuel for contraction
The bands and zones of an individual sarcomere
- Z lines (Z line to Z line = sarcomere)
- A band
- H zone
- M band
- I band
M Band
(i) Central portion of the H zone
(ii) Area where the myosin filaments thickens
(iii) Connects the myosin filaments together
I Band
(i) Area of sarcomere that contains only actin
H Zone
(i) Lighter central portion of the A band that contains only myosin (thick filament)
A Band
(i) Dark band that extends over the full length of the myosin filament and small portion of the actin filament
Z lines
(i) Anchors/connect the thin filaments
Myocardial contraction and relaxation
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
Excitation-contraction coupling
- Action potential travels across sarcolemma and down the T-tubules
- 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.
- If calcium binds to Troponin-c then actin binding site is exposed for the myosin head to bind
Summary of cardiac muscle fiber characteristics
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
Frank Starling’s Law of the Heart
- Length-tension relationship between length of myocardial muscle and force generation
In healthy cardiac muscle–Frank Starling’s Law of the Heart
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
Frank Starling’s Law of the Heart—“Un-healthy” cardiac muscle = heart failure
a. cardiac muscle has been dilated/damaged
b. sarcomeres are lengthened “too far” and Frank Starling Law no longer applies
LaPlace’s Law
- Wall tension (contraction force) is directly related to the product of intraventricular pressure x internal radius (ventricular volume) and inversely related to wall thickness
- 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 - Clinical:
a. Heart failure (dilated thinned wall heart) or aneurysm
Preload
- Left ventricular preload is the pressure generated in the left ventricle at the end of diastole (ventricular filling).
- Preload = left end-diastolic pressure
What determines preload in healthy heart?
a. Left end-diastolic volume (Starling’s Law of Heart)
b. ↑ Left end-diastolic volume = ↑ preload = ↑ stroke volume/cardiac output
Healthy diastolic function
a. increased preload with increased stroke volume
b. “For all input there is corresponding output”
Diastolic dysfunction
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
Afterload
- The force the left ventricle must generate during systole to overcome aortic pressure to open the aortic valve.
- 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
Clinical- Afterload
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
Cardiovascular Control Centers (3)
- located in medulla (lower region of brainstem)
- synapse with sympathetic and parasympathetic pathways to the heart
- autonomic response at rest and during exercise
Autonomic response at rest and during exercise
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
Synapse with sympathetic and parasympathetic pathways to the heart
a. Sympathetic – increase HR and contractility
b. Parasympathetic – decrease HR and contractility
Arterial Baroreceptors
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
Atrial Receptors
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
Bainbridge reflex (stretch receptors in atria)
- ↑ 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
Myocardial Contractility
- Ability of ventricular walls to contract (force production)
- Two factors determine contractility
a. Sympathetic nervous input
b. Increased stretch of ventricle (in healthy cardiac muscle)
Starling’s Law of the Heart
(i) Increase preload = increase contractility of healthy cardiac muscle (i.e. ventricle)
2 Factors Determining Cardiac Output
A. CO = HR x SV
B. Examples:
1. Increased HR
a. increased sympathetics and decreased parasympathetics
- Increase stroke volume
a. ↑ venous return
• ↑ blood volume
• ↑ sympathetic activity to veins
b. ↑ end-diastolic volume
c. ↑ preload
