Autorhythmic Cells
What is the resting membrane potential and threshold in autorhythmic cells?
RMP = -60
Threshold = -40
What is the resting membrane potential and threshold in myocardial cells?
-90 and -70
Starting with Elastic Arteries, what are the types of blood vessels and what order would blood flow through them?
Elastic arteries-> Muscular arteries-> Arterioles-> Capillaries-> Venules-> Small/Medium Veins-> Large Veins
Describe blood flow through the heart
Be as specific as possible
yeah that's pretty much it
What hormone upregulates NE receptors?
T1-T4
What ion leaks to begin depolarization, in what direction, and through what type of channel?
Sodium (Na+) leaks into the cell through funny channels
What ion leaks first during an action potential in myocardial cells and how is that AP initiated?
Sodium (Na+)
A current sent from the SA Node allows the cells to reach threshold very quickly and begin the influx of sodium.
What are the 3 types of capillaries and why is it important to have different types?
Continuous Capillaries are found in capillary beds most everywhere in the body and have "cracks" on them that allow for exchange (of gases, nutrients, waste) of the smallest molecules such as much of the makeup of plasma (except proteins)
Fenestrated capillaries have cracks but are also are full of "holes" and found in places where large amounts of materials need to be filtered, released, or absorbed (such as the kidneys)
Sinusoid capillaries have incomplete basement membranes and large gaps in the lining of the lumen. These allow for large molecules (e.g. large proteins) and entire formed elements (e.g. red blood cells) to pass through which is vital for function in places such as red bone marrow where formed elements enter the blood stream, the liver where erythrocytes are removed from the blood stream to be recycled/phagocytized and large proteins such as albumin enter that stream, and the spleen where reservoirs of blood are held.
Reservoirs for blood that can assist with venous return are found in ____ and ____
Spleen and Inferior Vena Cava
There are sensory receptors detecting blood pressure and O2/CO2. They can be found in the ____ and the ____. They communicate with the cardiovascular control center (CVCC) through what nerve pathways?
Carotid Sinus and the Aortic Arch
Cranial Nerve 9 (Glossopharyngeal) & 10 (Vagus)
Autorhythmic cells are primarily found in the ____ and ____ where action potentials can be created spontaneously. This is thanks to the autorhythmic cells having leaky channels that create a ______ potential.
SA Node & AV Node
Pacemaker Potential
What ion is primarily responsible for repolarization of myocardial cells? The ion moves (into/out of) the cell, initially through ___ channels and then largely through ____ channels that close at ____. Repolarization is slowed during the ____ phase which lasts _____ msecs
Potassium
out of
t-type
voltage gated
threshold
plateau
250
What is the normal healthy range for MAP? Why is this range vital? What factors determine MAP and how might they compensate for each other?
70-110mmHg
Key to maintaining homeostasis, MAP will be an important factor in Bulk Flow and exchange.
Cardiac Output, Blood Volume, and Total Peripheral Resistance. If your CO is low, you might vasodilate to decrease TPR and/or increase your blood volume to increase blood flow and preload.
What mechanisms are involved in making sure backflow is prevented?
The SA Node's charge is sent through internodal pathways causing the atria to contract before the AV Node can relay the signal further assuring the ventricles contract only after the atria have fully contracted. This planned delay also ensures the pressure within the heart's chambers is greater in a foremost chamber. The chordae tendineae attach to papillary muscles and the atrioventricular valves to reinforce them and only allow them to open in one direction.
What are the 3 types of receptors the CVCC will send signals to? What neurotransmitters attach to those receptors? What is the expected response to each of those signals?
Muscarinic, Beta 1 Adrenergic, Alpha 1 Adrenergic
Acetylcholine, Norepinephrine
Muscarinic receptors will slow down heart rate, Beta1 will speed up heart rate and increase stroke volume, Alpha1 will increase preload and therefore stroke volume
What channel is open from -50 to -40 membrane potential? What kind of channel is it?
Transient-type Calcium channel
What is the most important ion for myocardial cell function and why? What is the intracellular reservoir for this ion and how is it activated to release it's stores?
Calcium (Ca++) increases force of contraction, is responsible for the plateau phase which allows for a full and strong contraction, and calcium binds to troponin as part of excitation-contraction-coupling which initiates the cross-bridge-cycling we recognize as muscle fibers shortening/contracting.
The sarcoplasmic reticulum holds a large quantity of calcium so it's not free floating in the cells and is opened by calcium moving in from L-type channels and attaching to ryanodine receptor gates.
Net Filtration Pressure determines if the end result at an exchange site is a net filtration (leaving the bloodstream) or a net reabsorption (entering the bloodstream). We calculate NFP by examining opposing forces. What are those forces and what are they driven by?
Hydrostatic pressure within the bloodstream is analogous to blood pressure and pushes outward acting as the main driving force for filtration. Conversely, hydrostatic pressure in the interstitial fluid is an opposing push that promotes reabsorption.
Colloid Osmotic Party within the bloodstream attracts water and pulls inward acting as the main driving force for reabsorption. Albumin in the plasma is the largest contributor to this force. COP in the interstitial fluid is the weakest force in determining NFP but acts as the opposing pull, attempting to drive filtration.
What vessels make up the coronary circulation and why are they so important? What makes them vulnerable?
left coronary artery, anterior interventricular artery, circumflex artery, right coronary artery, posterior interventricular artery, marginal artery, coronary sinus, great cardiac vein, middle cardiac vein
These vessels deliver oxygen to the myocardial cells and remove waste. These pathways can more easily become blocked and quickly cause damage through oxygen deprivation that will weaken the heart, further compounding the damage.
What are the two types of receptors that can be found on blood vessels? What pathway must a molecule take to attach to each? What is the expected response when those receptors are activated?
Alpha 1 Adrenergic Receptors are activated by NE delivered by the Sympathetic Nervous System and will cause vasoconstriction.
Beta 2 Adrenergic Receptors are activated by NE delivered through the bloodstream as part of the Endocrine System and will cause vasodilation
Some channels start closed but open at threshold. What ions are they permeable to, what kind of channel are they, what direction do they leak, do they drive the membrane potential more positive or negative, and what are the key difference between them?
Calcium (Ca++) voltage-gated Long-type channels allow calcium to flow into the cell driving the membrane potential more positive.
Potassium (K+) voltage-gated Long-type channels allow potassium to flow out of the cell driving the membrane potential more negative.
The calcium channel opens quickly and closes once the membrane potential passes neutral membrane potential. The potassium channel opens and closes slowly when reaching threshold.
Define the Frank Starling Law of the Heart and it's importance in heart function. Think about preload and how it affects Cardiac output.
The frank starling law defines the relationship between actin-myosin head overlap and force of contraction. A sarcomere extended further will contract with more force. Thanks to the heart's elasticity, more preload-> more stretch-> the stronger the hearts chambers will contract-> increasing stroke volume.
How do these controls affect MAP and how do they create that effect?
Renin, Angiotensin II, Aldosterone, ADH, ANP, NE, Epi, Nitric Oxide
Renin initiates RAAS and converts angiotensinogen into angiotensin I
Angiotensin II is a potent vasoconstrictor throughout the whole body and acts as a long lasting control for increasing MAP. ANGII also activates release of aldosterone from the Adrenal Glands and ADH from the posterior pituitary, which can both help bolster this effect.
Aldosterone acts on the kidneys mainly but can affect many sites to increases sodium retention which will increase colloid osmotic forces that draw water back into the bloodstream, thereby increasing blood volume.
ADH is a potent vasoconstrictor by acting on smooth muscle on blood vessels. It also promotes water retention by increasing aquaporin expression in the kidneys which will increase blood volume.
Atrial Natriuretic Peptide is release when stretch in the atria of the heart is detected and stimulates water excretion, vasodilation of blood vessels, and inhibits renin secretion which prevents the cascade from RAAS
NE is a prominent neurotransmitter used by the SNS to vasoconstrict, so much so that SNS Tone inhibition is also an effective vasodilator
Epi is a prominent endocrine control to vasodilate
Nitric Oxide is a potent local vasodilator
What are the frequencies and delays starting at the SA Node? How do these affect ESV, EDV, Stroke Volume and Ejection Fraction? What are those volumes representative of and how do changes to them affect Cardiac Output?
SA Node 100 action potentials per minute (without PNS tone), SA Node 70-80 (normal), AV Node 40-60, Bundle of His and Purkinje Fibers 20-40
A higher amount of action potentials will increase heart rate but abnormally/dangerously high heart rate will not give the ventricles enough time to fully refill (lowering EDV) or fully contract (lowering Stroke volume and increasing ESV). Lowering EDV, ejection fraction, stroke volume, or increasing ESV can decrease Cardiac Output.
Be as specific as possible
Describe HOW signals from the CVCC are creating chronotropic and inotropic effects.
refer to Dr. H's flow chart and expand