Cardio Module 3 Flashcards
What are the Cardiac layers?
Endocardium Myocardium Epicardium (visceral pericardium) Parietal space (pericardial cavity) Parietal pericardium Fibrous pericardium
Describe the endocardium
The smooth frictionless surface (inner) layer of the heart
Describe the Myocardium
The middle layer of the heart that has contractile tissue made up of cardiac muscle cells
Describe the Epicardium
The outer layer of the heart that is made up of connective tissue.
Epicardium is also known as
Visceral pericardium
Describe the pericardial space/cavity
Between the Parietal and Fibrous pericardium. It contains pericardial fluid to reduce friction during heart movement.
Describe the Parietal pericardium
The connective tissue layer insulating the heart
Describe the Fibrous pericardium
the Fibrous space that ‘contains’ the heart
Which is thicker the Right or left ventricle (why?)
the Left is thicker. Because higher contractile forces are required in the LV (has to crank out forces to overcome 120-140 mm of mercury)
Which side of the heart would be more effected by a pericardial effusion (why?)
The right side. If you have an increase of fluid and the left side is stronger and working harder, the weak side will be ‘squished’ the most
Name 3 of the more common cardiac markers
1) Troponin I and T (TnI and TnT)
2) Creatine kinase (MB)
3) Myoglobin
When would you find cardiac markers
During necrosis of cardiac muscle possible due to ischemia or an MI (proteins from necrosis leak from muscle cells and into the blood)
All muscle cells have
Triponin (the I and T forms are more specific to cardiac muscle)
What is the hierarchy of myocardial cells (from largest to smallest)
1) Muscle fibers
2) Sarcolemma
3) Myofibrils
4) Myoflimament - (Myosin and Actin)
What is a muscle fiber composed of
Many myofibrils, a single nucleus, mitochondria, sarcoplasmic reticulum and cytoplasm (wrapped up by the plasma membrane called the sarcolemma)
What is the job of the sarcolemma
It spreads the action potential down throughout the muscle fiber, allows for a rapid transmission of action potential
Describe the sarcolemma
The cell/plasma membrane of the muscle fiber, it surrounds the myofibrils and also penetrates into them with invaginations called T tubules
Myofibrils are composed of
Myofilaments
What do myofilaments do?
They are protein filaments that provide mechanical shortening/lengthening of the muscle fiber (for contraction)
What are an arrangement of myofilaments called
Sarcomeres
What is essentially needed for cross bridge cycling to happen in cardiac muscle
calcium
What are myofilaments composed of…
Protein chains known as actin and myosin microfilaments
Describe myocin
The ‘thick’ microfilament
What is myocin’s role in the sacromere
Each has a globular head that bind to actin and swivel causing a mechanical shortening of the sarcomere (leading to a contraction)
What does the head of a myocin microfilament contain?
the head contains 1) A binding site for actin and 2) a receptor for ATPase.
Describe actin
The ‘thin’ microfilament
What two chains of molecules wrap around each actin to form an actin microfilament
1) Tropomyosin - A protein wrapped around the length of the actin microfilament
2) Troponin - A protein attached intermittently along the length of the tropomyosin
What are the roles of troponin and tropomyocin
When calcium comes down it binds to the troponin which alters the tropomyosin that exposes the binding site on actin for the myosin globular head which allows the muscle fiber to mechanically contract. If the binding site is covered the sarcomere can’t contract.
What are the 3 sub-components for troponin
1) Troponin T
2) Troponin C
3) Troponin I
What is the role of Troponin T (where it is found)
Binds the troponin to the tropomyosin and actin. Specific to cardiac muscle
What is the role of Troponin C (where it is found)
Contains a binding site for calcium. Similar in both cardiac and skeletal muscle
What is the role of Troponin I (where it is found)
Inhibits ATPase (ATP is needed to fuel the contraction). Specific to cardiac muscle
What is essentially needed for cross bridge cycling to happen in cardiac muscle
calcium (serves as the on/off switch)
What is the role of Troponin I (where it is found)
Inhibits ATPase (ATP is needed to fuel the contraction). Specific to cardiac muscle
Muscle contraction is a result of
Muscle fiber shortening
Describe the ‘cross-bridge theory’
The molecular events that cause a muscle fiber to shorten.
Besides calcium what is also required for a fiber to shorten (cross bridge theory)
ATP
How is calcium released for muscle contraction
The action potential travels down the sarcolemma and down the T-tubules and reaches the sarcoplamsa reticulum (which stores the calcium) and signals its release. It diffuses into the microfilaments and binds to Troponin-C which exposes binding site for the myosin head
What is the process called of an action potential travelling from cell to cell
Syncytium
What is the attachment site between muscle fibers that allows for the action potential to travel from cell to cell
Intercalated discs
What attaches each cardiac muscle to the next
Desmosomes
What is a gap junction
A small space (looser area) in the intercalated disc that allows the electrical action potential to spread through the intercalated disc from one fiber to the next
Define Frank Starling’s Law of the Heart
In healthy cardiac muscle, the length of cardiac muscle fiber (sarcomere) is directly related to the force generated by the muscle fiber
How does Frank Starlings law apply to ventricle contraction
The end diastolic volume (filling of the ventricles) determines the amount of stretch on the cardiac muscle fibers. The more stretch (increased end diastolic volume) the more increased contractility which means an increased stroke volume/cardiac output
How does Frank Starling’s law apply to an unhealthy heart?
When cardiac muscle is damaged or dilated the sarcomeres are lengthened too far that affect and lowers stroke volume/cardiac output, Too close you can’t have enough cross bridge cycling
Define LaPlace’s law
Wall tension (contractile force) is directly related to the product of intraventricular pressure x internal radius (ventricular volume) and inversely related to wall thickness
How does Laplace’s law related for heart failure
Heart failure which generally has a dilated thin walled ventricle. When it is full of blood it requires more time to generate a contraction force (wall tension) strong enough to generate the intraventricular pressures needed to eject the blood from the heart. That makes for poor cardiac output and performance
What is left ventricular preload?
The pressure generated in the left ventricle at the end of diastole (ventricular filling). Used hand in hand with end diastolic volume.
What determines preload in a healthy heart?
The integrity of the ventricle wall
What is afterload?
The force the left ventricle must generate during systole to eject the stroke volume. Increased pressure, stroke volume will decline. An unhealthy wall can’t push out an adequate SV.
What determines a healthy diastolic function
The ability for the ventricle walls to be able to stretch to allow for adequate filling
What determines a healthy systolic function
The ability for the ventricles to be able to generated an appropriate contraction in response to ventricular filling (Frank Starling’s law)
What are some causes of diastolic dysfunction
Inadequate filling of ventricles in the presence of normal systolic function (can’t stretch enough/thick ventricle wall). The ejection fraction is normal but stroke volume is reduced. It’s caused by reduced ventricular compliance and ventricular hypertrophy and can lead to inadequate ventricular filling and congestive back up (diastolic heart failure
What are some causes of systolic dysfunction
The ventricle is unable to generate sufficient force to eject stroke volume. Less contractility leads to reduced ejection fraction. It can be caused by any pathology that can lead to the dilation of the left ventricle
What are factors that increase ventricular filling and preload
1) Increased central venous pressure (for decreased venous compliance)
2) Increased ventricular compliance (expansion)
3) Increased atrial contraction (sympathetic stimulation)
4) Reduced HR
5) Increased Aortic pressure (increases afterload on ventricle)
What are the factors that decrease ventricular filling and preload
1) Decreased venous blood pressure (reduced blood volume or gravity causing blood to pool in LE)
2) Impaired atrial contraction
3) Increased HR (reduces ventricular filling time)
4) Decreased ventricular afterload
Where in the brain is the Cardiovascular Control center located?
In the medulla (lower region of the brainstem)
What is the autonomic nervous system response of the heart 1) at rest 2) during easy exercise and 3) during intensive exercise
1) Rest - Parasympathetic dominates at the SA node
2) Easy Exercise - Removal of parasympathetic influence on SA node
3) Intensive Exercise - Increase sympathetic influence on SA node
What are the two neural reflexes (stretch receptors)
1) Arterial Baroreceptors - High pressure receptors
2) Atrial Receptors - Low pressure receptors
Where are the Arterial Baroreceptors located
At the aortic arch and the carotid sinus
What will the stimulation of arterial baroreceptors do to the heart
When they stretch It will decrease HR and lower BP
Where are the Atrial receptors located
In both the R/L atria.
What do the Atrial receptors do to the heart?
They will stimulate blood volume control. It will release ANP from the atria which stimulates kidneys to excrete urine and Na+ to reduce blood volume and Increase HR (to push out volume)
Which has the more dominant role in maintaining HR atrial receptors or arterial baroreceptors
Arterial baroreceptors
What is the Bainbridge reflex
If you artificially put too much fluid volume (like with an IV) in the blood you are going to increase HR by stimulating the atrial stretch receptors which will stimulate the sympathetic influence to the heart. HR is increased to push volume out quicker.
Two factors that determine myocardial contractility
1) Sympathetic nervous input
2) Increased stretch of ventricle (Frank Starling’s Law of the Heart)
