Exam 4 Flashcards
Length of cardiac muscle action potential and why is it important
250ms, therefore the refractory period is long and therefore under normal conditions the muscles cannot undergo tetanic contractions
Resting membrane potential of cardiac muscle
-90mv
General shape of the action potential of cardiac muscle
there’s a sharp depolarization and then the bulk is a plateau which then repolarizes quickly (not as quick as the depolarization)
SA node, how many action potentials per minute, and how many potentials make its way through the conduction system, how do the action potentials spread
sinoatrial node, pacemaker, near the cardiac sinus in the right atrium, automaticity; will undergo around 100 action potentials per minute under normal conditions; not every change in membrane will make its way through the rest of the conduction system and this is why the number isn’t the same as heart rate; potentials will spread through the rest of the atria due to cells being connected by gap junctions
Will conduction pass from the atria to the ventricles
no, due to the connective tissue it prevents the conduction to pass through
AV node
atrial ventricular node, connected to interventricular septum, sends conduction to the bundle of His
Automaticity
undergo regular patterns of action potentials independent of the nervous system
Interventricular septum
tissue that runs down the middle of the heart
Bundle of His
divides into two branches, the right branch innervates to myocardial tissue of the right ventricle, left branch innervates to myocardial tissue of the left ventricle, sends conduction to Purkinje fibers
Purkinje fibers
extensions of specialized myocardial cells that make their way throughout the myocardium of the right and left ventricle
P wave
atrial depolarization, point just before contraction of atrial muscle
QRS waves, why is this larger than P wave
ventricular depolarization; due to the increased amount of myocardial tissue in the ventricles
T wave
ventricular repolarization
Missing EKG wave
atrial repolarization, is overshadowed by ventricular depolarization
Nodal cell resting membrane potential
-55 to -60
Where and why is there thin myocardium
the left ventricle has thicker myocardium than the right ventricle due to the left ventricle moving blood into the systemic circuit while the right ventricle moves blood into the pulmonary circuit; myocardium in the atrium is not as thick as in the ventricles because the atria don’t do much work moving blood into the ventricles, the pressure of blood entering the chambers is almost always enough to push blood down into the ventricles , the atria gives it the final push
Ventricular myocardial action potential length and corresponding EKG waves, regulated by what
is 250-300ms long; depolarizes from -90 to +20mv corresponds to depolarization of ventricles QRS, repolarization corresponds with the T wave; regulated by changes in permeability of sodium, calcium, and potassium
What causes the gradual repolarization of ventricular myocardial action potentials
decrease in potassium permeability meaning that the potassium efflux is decreased and positively charged potassium stays within the cell, the increase of permeability of calcium due to T type calcium channels opening, f type sodium channels will pen when the cell is in its most hyperpolarized state
What leads to repolarization of myocardial cells
decrease of calcium permeability and increase of potassium permeability
Central nervous system
brain and spinal cord
Peripheral nervous system
everything else connected to brain and spinal cord, somatic and autonomic, sympathetic and parasympathetic, acramine
Acramine parasympathetic nervous system
salivation, lacrimation, urination, digestion, defecation
Sympathetic and parasympathetic activity
are always active but one could overpower the other
Cardiac output
HR*SV, average cardiac output is 5L/min
Stroke volume
the amount of blood ejected from the ventricles at each contraction, around 70mL, this can increase through increasing the contractibility of the ventricles
End diastolic volume
how much blood does the ventricles fill with, could be caused by an increase of antria contractibility, can be increased due to an increase of bp which will increase the amount of blood returning to the heart
Sympathetic effects cardiac output
releases norepinephrine onto beta-1 adrenergic receptor along with epinephrine released by the adrenal medulla which has been acted on by the sympathetic nervous system increasing activity of the SA node and increasing conduction rate to the AV node, has input to the atrial and ventricular muscles effecting end diastolic volume
Adrenergic receptor
acts on norepinephrine, first discovered on the adrenal glands, there’s beta-1, beta-2, alpha-1, and alpha-2
Parasympathetic effects cardiac ouput
there’s no parasympathetic input to the ventricles therefore there’s no significant effect onto ventricular contraction therefore not effecting end diastolic volume, decreases heart rate and conduction rate of AV node and decreases activity of the SA node through releasing acetylcholine
Muscarinic receptor
binds acetylcholine on cardiac muscle
Beta-1 adrenergic receptors mechanism
g coupled receptor whose alpha subunit will activate adenylyl cyclase to create cAMP, cAMP will change an inactive cAMP dependent protein kinase to an active cAMP dependent protein kinase
What does an active cAMP dependent protein kinase do
lowers the sensitivity of L type calcium channels which will increase cytosolic calcium and lead to the nodal cells working faster and better and ventricular cells will contract with a greater force; makes it easier for ryanodine receptors to open within the sarcoplasmic reticulum and will be open longer when calcium is bound to it allowing for more calcium to come from the sarcoplasmic reticulum (calcium induced calcium released); the increased amount of calcium within the cytosol will allow for more binding to troponin and an increase of cross bridge cycling; makes troponin more sensitive to calcium; makes it difficult for some transporter protein calcium ATPase to operate and some will be induced, by blocking ATPase calcium will stay within the cytosol, by promoting activity the calcium gradient will increase as the concentration of calcium within the SR will increase leading to a larger current of calcium out the SR
Blood pressure
is due to cardiac output along with peripheral resistance
Peripheral resistance
how open the vessels are
Blocking beta-1 adrenergic receptors
most common treatments of high bp, ex/ atenolol which will bind to the receptor and lower cardiac output
Force of ventricular contraction
end diastolic volume can be the same while stroke volume increases leading to the ventricles needing to squeeze more, the force that develops during contraction during sympathetic stimulation is larger and occurs over a shorter period of time which will increase heart rate
Pericardium
outer layer with two layers separated by fluid
Epicardium
layer directly over the heart, also known as the visceral pericardium
Pericardium
outside layer, known as the parietal pericardium
Visceral membranes
membranes that directly cover organs
Parietal membranes
membranes that line cavities
Endocardium
layer of the heart that is in contact with the blood
Valves
separate chambers of the heart and vessels leading from the chambers, also found within veins, lymphatic system, prevent retrograde flow
Chordae Tendinae
tough fibrous strings that are attached to papillary muscles within the left and right ventricles
Papillary muscles
extensions of the myocardia within the left and right ventricles
How are the valves kept shut
papillary muscles remain rigid which leads to the chordae being taught
Pathway of blood through the heart (beginning with left atrium)
left atrium, left bicuspid AV valve, left ventricle, aortic semilunar valve, aorta, arteries, arterioles, capillaries, venules, veins, vena cavae, right atrium, right tricuspid AV valve, right ventricle, pulmonary semilunar valve, pulmonary trunk, pulmonary arteries, capillaries of lungs, pulmonary veins
How can you detect a valve defect
detected using a stethoscope not making the “lub” “dub” sound, the sounds refer to the shutting of valves and blood pushing against the valves, lub is arterial ventrial valves closing, dub is the semilunar valves closing
Sphygomanometer
measures pulse pressure
Systole
ventricles contract and move blood, compliance of vessels based on ventricular contraction that allows blood to apply pressure on the walls
Diastole
ventricles relax and fill with blood, the pressure of the blood within the vessels during ventricular repolarization
Mean arterial pressure
(systolic + 2diastolic) / 3
Normal mean arterial pressure
93.3 given with an arterial pressure of 120/80
How do we know what baroreceptors pick up on
120/80 and 130/70 yield similar mean arterial pressures but the firing rates of baroreceptors are not the same
What do baroreceptors pick up on
changes in pulse pressure, the greater the difference the greater the firing rate
Pulse pressure
difference between systolic and diastolic
Smooth muscle in the arterials and in the veins
it’s more pronounced within the arteries and arterials but not as pronounced in veins
Sympathetic constriction of veins leading to
increase venous pressure, increase venous return which will effect the amount of blood entering the atria and effecting the end diastolic volume
Sympathetic increasing discharge to arterials
this is what we’re talking about when measuring blood pressure, arterials constrict and increase total peripheral resistance
Total peripheral resistance
arterial pressure / cardiac output
How much blood do the ventricles normally pump out
60% of the blood that fills it
Systolic dysfunction
primarily caused by ischemia, occurs during a myocardial infarction, cardiac muscles can survive without oxygen for about 20 minutes, if there isn’t as much myocardia as before then the ventricles can’t pump out a much blood as normally, ventricles pump about 40-50% of blood
Ischemia
loss of oxygenated blood to the myocardium
Diastolic dysfunction
ventricles don’t have enough space to fill with blood normally, it’s one of the primary things associated with hypertension that hasn’t been treated for a long period of time (silent disease), if the heart can’t move blood into the systemic circuit and if there’s already hypertension in the arteries this can cause arteries to bulk up through hypertrophy of the ventricles losing space and compliancy of the myocardia,
Cadiac failure
reduced cardiac output due to loss of myocardia or due to ventricular hypertrophy, the left ventricle can’t keep up with the right ventricle as it has the harder job of pushing blood throughout the systemic circuit
Congested heart failure
happens before heart failure, blood can become congested and stay within the pulmonary circuit and lead to pulmonary edema leading to respiratory failure and cardiac arrest
How to treat cardiac failure
reduce sympathetic nervous system function (atenolol), antagonists for alpha adrenergic receptors on the smooth muscle lining leading to reduction of cardiac output and peripheral resistance as blood vessels are vasodilated, promote parasympathetic activity, block ADH via antibiotics working as antagonists for it, give a diuretic
What’s a side effect if cardiac failure goes untreated
people gain water weight very quickly, edema, one of the huge problems associated to heart failure
Heart failure in the context of baroreceptor reflex
if there’s a drop in cardiac output (regardless of whether due to systolic or diastolic dysfunction), sympathetic activity will increase increasing water retention
What happens with sustained hypertension and diastolic dysfunction
cardiac output will increase due and the diastolic dysfunction will help in keeping the heart in homeostasis
Drugs to treat heart failure
diuretics, cardiac inotropic drugs, vasodilators, vasodilation promoters, beta adrenergic receptor blockers
Diuretics
most important drug to treat heart failure, increase urinary excretion of sodium and water
Digitalis
cardiac inotropic drugs, increase contractility of ventricles which doesn’t make sense because it stresses the heart that’s already overworked, increased contractibility of the remaining myocardial tissue, increases quality of life but not life span
Alpha blocker
vasodilator, block norepinephrine and epinephrine at alpha-adrenergic receptors
Renin-angiotensin-aldosterone system
There’s a drop in arterial pressure and ultimately a drop in oxygen delivery to the body or an increase in sympathetic discharge, the kidneys secrete renin which travels through the blood and takes angiotensinogen which is made by the liver and converts it to angiotensin I which will be converted to angiotensin II by angiotensin conversion enzyme (ACE), angiotensin II is a potent vasoconstrictor and promote the release of aldosterone from the adrenal cortex which will promote sodium reabsorption which will increase blood volume and blood pressure
Angiotensin I
by itself it will not do anything, converted from angiotensinogen by renin
Angiotensin conversion enzyme
found in the membranes of endothelial cells that line capillaries, especially those that are found in the lungs
Angiotensin II
binds to vascular smooth muscle to vasoconstrict the vessel
Sodium reabsorption
sodium will be lost via the urine in the lumen of kidney tubules, sodium within the kidney tubules will be moved back into the blood, by increasing sodium reabsorption water reabsorption has to increase
ACE inhibitor
vasodilator, inhibits the conversion of angiotensin I to angiotensin II therefore dilation of vessels is promoted and aldosterone is not released
Angiotensin blockers
blocking the receptor leads to vasodilation being promoted and aldosterone is not released
Tunica intima
inner layer of the artery, synonymous with epithelium, blood makes contact with this layer, made of simple squamous epithelium and is found wherever the need for diffusion is high
Endothelial cell functions
create a barrier, prevent blood loss, blood doesn’t normally adhere to it
How does endothelial cells prevent blood loss
produce growth factors in response to damage, makes nitric oxide to vasodilate and endothelin to vasoconstrict, synthesizes active hormones such as angiotensin II from inactive precursors
Atherosclerosis
hardening of the arteries through thickening and narrowing of the blood vessel due to build up of plaques typical cause of heart attacks, stroke, and peripheral vascular disease; injured endothelial cells release inflammatory cytokines (C-reactive protein), release less nitric oxide, secrete more vasoconstrictors (vascular endothelial growth factor, platelet-derived growth factor, endothelin-1); macrophages attach to the spot of injury via adhesion molecules (VCAM-1) and release enzymes and oxygen free radicals to create oxidative stress, oxidizing LDL and resulting in further injury to the vessel wall; oxidized LDL activates inflammatory and immune responses to promote superoxide production, decrease nitric oxide production, and smooth muscle cell proliferation; oxidized LDL will then move into the intima of the arterial wall and become engulfed by foam cells (macrophages); as these cells accumulate they form a lesion called a fatty streak; fatty streaks trigger further immunologic and inflammatory responses leading to vessel damage and vasoconstriction; macrophages stimulate smooth muscle proliferation causing collagen to form and move over the fatty streak forming a fibrous plaque; this plaque can become calcified and protrude into the lumen of the vessel and restrict blood flow (not all do this); plaques can rupture or ulcerate to cause sheer forces, microphage derived collagenases, elastases, matrix malloproteinases, cathepsins, and apoptosis of the cells at the edge of the plaque
Atherosclerosis mechanism
injury to endothelial cell,
How can endothelial cells be damaged
genetics, chemicals, failure of cholesterol regulation, autoimmune disorder, infection with bacteria (H. pylori), hypertension which is the main causer, age which can lower vessel wall compliance increased by sheer forces
Resorption
absorbing a substance from a reservoir
Reabsorption
substances that were eliminated and then absorbed
Absorbed
substances taken from ingested material
VCAM1
vascular cell adhesion molecule-1 will draw macrophages to a particular spot
Oxidative stress
macrophages releasing oxygen free radical (superoxide) binding to LDL (phospholipids) causing damage, linked to increased levels of angiotensin II
What happens to ruptured plaques
platelets will adhere to the surface of the ruptured or ulcerated area, coagulation cascade is initiated and a thrombus will begin to form which can create a blood clot (completely obstructing the lumen) ending with the arteries that are narrow and susceptible to vasoconstriction and thrombus formation
Tunica media
middle layer of the artery, made of sooth muscle that’s interspersed with collagen
Tunica externa/ adventitia
outer layer of the artery made of connective tissue
Vein layers
has all the layers of the artery but the tunica media is not as pronounced leading to a larger diameter lumen
How to increase venous pressure and what results
smooth muscle of the veins constrict, increasing venous return to increase end diastolic volume which increases stroke volume
Varicose veins
breaking down of valves within the veins causing pooling of blood which can distort the veins and swell, occurs with age
Arteriole
small diameter artery, has tunica intima and tunica media (which is only smooth muscle)
Venule
small diameter vein with an endothelium
Capillary
has simple squamous epithelium, contains psuedo-fenestrations allowing diffusion through the junctions and allow large molecules to move out
Law of Laplace
talks about the thickness diameter of the vessel, there’s a certain pressure inside and pressure outside, the pressure is divided by the radius which gives an idea of how much pressure there is on the spot
Aneurism
weakening of the vessel wall, could be balloon like dialation or the entire vessel, could be due to artherosclerotic plaques, when the wall burts it leads to hemorrhage
Commonly accepted hypertension bp and AHA bp
140/90; 130/80
Primary hypertension
is 95% of cases of high bp, due to unknown origins
Secondary hypertension
associated with diabetes mellitus, glucose is high within the plasma and water has to balance this concluding with an increase blood volume
Neurons releasing nitric oxide
neural control of blood pressure will lead to vasodilation of smooth muscles; nitric oxide activate guanylyl cyclase to create cGMP leading to decrease in calcium influx and increase in potassium deflux
Vasopressin aka ADH
hormonal control of bp, made by supraoptic nucleus of the hypothalamus released a tthe posterior pituitary, resting of water increasing blood volume
Hormonal vasoconstriction controls of bp
vasopressin, epinephrine, angiotensin II
Arterial natriuretic peptide
hormonal controls of bp, made by the atria of the heart, promotes excretion of sodium, when you get rid of sodium you get rid of water lowering blood volume
Myogenic response
local control of bp, when blood is damaged it will first constrict
Endothelin
local control of bp, made by endothelial cells, very potent vasoconstrictor
Eicosanoids
local control of bp, prostaglandin or a form of it is made by epithelial cells to vasodilate
Treatments for hypertension
lifestyle changes, medications
