Exam 1, lecture 2 Flashcards
Cardiac ischemia
Insufficient coronary blood flow to meet the needs of the myocardium
Elevated CK-MB suggests what?
Recent acute myocardial infarction
Myocardial infarction
Death of cardiac muscle cells, from severe cardiac ischemia
AMI stands for
Acute myocardial infarction
Pressure volume loop
Area enclosed by loop is stroke work
Ees represent what in the pressure volume loop
Slope of the end systolic pressure volume relationship= ventricular elastase= ESP/ ESW
STEEPER SLOPE EQUALS GREATER CONTRACTIBILITY
Ea represents what on pressure volume loop
Efferent atrial elastance= esp/sv
Pressure developed in the arteries for a given stroke volume
Pressure dependent of elastance and outflow resistance
Laplaces law states
Estimates wall stress, wall tension from intraventricular pressure and radius and wall thickness
Wall tension is proportional to pressure inside vessel and to its radius
Wall stress is (eq)
Wall stress is wall tension divided by wall thickness
Laplaces law and the failing heart
In congested heart failure, dilation of ventricles and increase in EDV coupled with a reduction of EJF
Stroke volume and cardiac output usually maintained
What is maintaining stroke volume at the cost of?
Even though EJF is reduced, increase in EDV can maintain stroke volume. This means Elevated wall stress, and this means more oxygen demand and maintains stroke volume is a high metabolic cost
This leads to hypertrophy of the ventricle, compensation for wall thickness to renormalize wall stress
Wall stress
Pressure x radius/ ( wall thickness)
Pressure x radius is wall tension.
T/ wall thickness
Things and could increase pressure and volume work in heart ( usually occur together)
Increased pressure work (hypertension)
Aortic stenosis (increase pressure)
Increase volume work ( elevated preload)
Increased volume work ( aortic insufficiency from regurgitation)
Myocardial oxygen consumption cardiac work and cardiac efficiency
The lower the cardiac work, the higher the cardiac efficiency
So the less oxygen that is consumed for given level of cardiac work, higher the cardiac efficiency
Pressure work demands more oxygen, therefore less efficient work
Increase in pressure work places a higher demand on a coronary blood flow than an increase in volume work
Pain of angina is from
Insufficient supply if oxygen to the myocardium via coronary circulation
Common in aortic stenosis
Difference between aortic stenosis and aortic insufficiency
Aortic stenosis: pressure required to deliver Norma l cardiac output is higher than normal because of stenotic aortic semilunar valve
Aortic insufficiency: diastolic regurgitation of blood pressure an increase in stroke volume with a smaller change in resistance to ejection
Aortic regurgitation results in what kind of work?
Volume. Isovolumic relaxation does not occur. Blood is continuously entering the ventricle from aorta and increasing ventricular volume
EDV is increased
No true isovolumic contraction occurs
When ventricular pressure exceeds aortic diastolic pressure, blood starts being ejected into the aorta, elevating preload, increasing force of contraction and increasing systolic pressure and stroke volume
Aortic stenosis represents.
Pressure work
Increase peak of ventricular systolic pressure because large pressure gradient on narrowed aortic valve
After load and ESV increased
SV and EJF decrease
Increased EDV because of incoming venous return
Slow ventricular hypertrophy in response to elevated after load
Force of contraction is increased
Preload is
Degree to which ventricle are distended after diastole filling at onset of ventricular systole
EDV, stretching of walls in ventricles
Four major determinants of cardiac output are
1 preload
2 cardiac inotropic state
3 heart rate
4 myocardial contractability
After load
Ventricular wall tension that must be developed to open the semilunar valves and eject blood into the pulmonary trunk and aorta, or myocardial wall tension during systole
Starlings law ( heterometric autoregulation)
Heart behaves as a a self- regulating pump, so insures pumps out what gets from vena cavae into the aorta. The Greater the stretch of ventricular myocardium the greater force generated during systolic and greater is the stroke volume. So consequently stroke volume of each ventricle increases with diastolic filling
Depends on varying lengths of cardiac muscle fibers prior to contraction
Elements of preload
Length if ventricular muscle fibers at onset of ventricular systole
End diastolic volume
Central venous pressure, atrial pressure
Elevated preload affects
Force in contraction but NOT myocardial contractability
MC is related to force developed by contrasting myocardium for a give muscle fiber length ( homeometric regulation)
Manipulable elements of preload
Blood volume and venous capacity
Increased capacity is equivalent in effect to a reduced blood volume and vice versa
explains starlings law for a missed beat
heart continues to fill, by the next hear beat the EDV is roughly double its normal value and heart contracts more, expelling extra blood into the aorta and compensating for the missed beat.Second beat is an extra-systole or premature beat, this creates less filling time and EDV is smaller and the beat is weaker, expelling smaller stroke volume. The next beat there is a delay, and extra filling time EDV is larger, beat stronger and expels more. AVERAGE CARDIAC OUTPUT STAYS THE SAME
mean filling pressure
pressure within the cardiovascular system
what can increase afterload in the left ventricle
- mean aortic pressure,
- total systemic resistance (a change in total perpheral resistance doe not affect mean filling pressure but does affect the slope of the vascular function curve
- aortic or pulmonary valve resistance: resistance increased if valve orifice is narrowed
consequence of increased afterload
increases amount of high cost pressure work and therefore myocardial oxygen demand, placing greater demands on coronary circulation
heart rate
heart rate and stroke volume determine the cardiac output. Determined by sympathetic and parasympathetic input into the SA node
severe drop is stroke volume can cause
impair cardiac output, for example during pathological ventricular tachycardia
what does myocardial contractability effect
ESV. increased myocardial contractility the end systolic volume is decreased from ESV to ESV’. If the EDV remains the same, the stroke volume is increased
MC depends on what
intracellular calcium ion concentration, which affects the number of available myosin binding sites on actin filament
What does extracellular calcium concentration lead to
increased intracellular calcium ion concentration and increased MC
Heart rate in relation to MC
increasing heart rate can increase MC due to accumulation of intracellular calcium (force-frequency relationship)
what is positive inotropic agents
NE and E:
and cardiotonic drugs like digitalis (dogxin)
what does NE and E do to calcium concentration
increase calcium current during cardiac action potential and there increase intracellular calcium ion concentration. Sympathetic origin. Dopamine acts similarly (beta-adenergic receptors) Drug dobutamine binds beta adenergic receptors
what does Digitalis do to calcium levels
increases intracellular calcium ion concentration. impairs sodium-potassium exchange pump in sacrolemma, therefore reducing transmembrane sodium gradient and reduces driving to sodium-calcium exchange pump-» internal calcium rises
negative inotropic agents
calcium channel blockers: MC is reduced by calcum channel blockers because prevent calcium from entering the myocardial cell
myocardial ischemia leads too
heart failure-> depresses MC and starlings law response
two major NT of the ANS
acetylcholine and NE
which receptors do sympathetic and parasympathetic use?
cholinergic
which receptors do postganglionic neurons use
cholinergic
which receptors do sympathetic neurons use
adrenergic, except sympathetic in eccrine sweat glands is cholinergic
Sympathetic effect on cardiovascular system
vasoconstriction
Acetylcholine receptors
Nicotinic and muscarinic receptors
Nicotinic receptors
also bind nicotine, which is an agonist of acetylcholine (same effect).
Muscarinic receptors
toadstool toxin called muscarine and acts as agonist (pacemarker cells)
alpha-adrenergic receptors
bind both NE and E. walls of vessels, alpha 1 adrenegeric receptors mediate vasoconstriction. Alpha 2 inhibit NE release from sympathetic nerve endings
beta-adrenergic receptors
bind NE and E. beta 1 group, Pacemarker cells of the myocardium. increasing heart rate and force contraciton. Beta 2 are found in walls of blood vessels and are involved in vasodilation
medulla
can increase heart rate or decrease, vasomotor center
hypothalamus
controls autonomic motor system, can change heart rate dramatically
thalamus
can produce tachycardia
What area does the parasympathetic not innervate in the heart
ventricles
SA and AV node innervation
left vagus nerve does AV, and right vagus nerve does SA.
NE binds beta 1 adrenergic receptors, causes
G coupled receptors-> activate G stimulatory adenylyl cyclase, which converts ATP and cAMP-> activation of protein kinase A-> phosphorylation number or proteins, including L-type voltage-gated calcium channels, ryanodine receptor and phosphorlamban
stimulation of beta 1 adrenergic receptors in heart
- positive inotrpic (increase C) phosphorylation of calcium channel proteins-> open during action potential and permitting larger calcium flux into the cell. Facilitation of calcium release from sacroplasmic reticulum via ryanodine receptors, sensitization of troponin c calcium
- chronotropic: accelerated firing of pacemaker cells-> accelerated heart rate.
- dromotropic: increase rate of conduction thru AV)
- ) lusitropic: phosphorylation of phospholamban
beta-blockers
block sympathetic stimulation
parasympathetic receptors
cholinergic receptors muscarinic and nictoinic, G inhibitory proteins, decrease cAMP in cell
parasympathetic effect on cardiovascular system
release of acetycholine and slow heart rate and reduce rate of the conduction of thru AV node
Atropine
blocks acetylcholine, and binds muscarinic receptor, abolishes parasympathetic tone, increases heart rate
what keeps the intact innervated heart rate normal?
parasympathetic tone with some degree by a weaker sympathetic tone
Propranolol
blocks beta 1 and beta 2 adrenergic receptors, abolishes sympathetic tone and small drop in heart rate
sympathetic mainly cause vasoconstricition where?
skin and abdominal viscera NOT coronary or cerebral circulations
what governs resistance
arterioles
what governs capacitance
veins and muscular venules
How does sympathetic nervous system play a role in survival after hemorrhage
drop in mean arterial pressure produces strong sympathetic nervous system via baroreceptor reflex
sympathetic role during hemorrhage causes what
- increased MC->reduces ESV, increases stroke volume-> boosts cardiac output
- increased heart rate couple with positive lusitropic effect-> boosts cardiac output
- vasoconstriction
increased vasocontriction in arterioles does what?
increases total peripheral resistance and increases mean arterial pressure
vasoconstriction in veins and muscular venules?
reduction in capacity of cardiovascular system, which increases mean filling pressure nd causes increase in preload, boost cardiac output according to starlings law
