Block I: CV III Flashcards
what effect does the autonomic nervous system have on the heart?
- influences the rate of impulse generation (firing), depolarization, repolarization
- influences strength of ventricular contraction
- produces changes in heart and circulatory system faster than metabolic or humoral agents
what is the role of ACH
- decrease nerve firing rates
2. cholinergic vagal fibers stimulate membrane to become hyperpolarized (very negative)
what does ACH do on the molecular level in the myocardium
- increases K+ conductance of nodal tissue via M2 muscarinic receptors
- opens K+ channels to allow for repolarization (more negative environment inside cell)
- DECREASE HR
what effect does ACH have on M2 receptors?
decrease cAMP, inhibit Ca2+ from entering cell
-decrease HR
strong vagal stimulation may [] spontaneous discharge
abolish, halt
stimulation of sympathetic cardiac nerves [] depolarizing effect of Ih
speeds up, increase HR
spontaneous discharge [] upon sympathetic stimulation
increases
what hormone is released a sympathetic synapses
NE
what hormone is released at vagal/cholinergic synapses
ACH
what receptors does NE bind? what does this lead to?
- Beta-1
- increased intracellular cAMP
- facilitates opening on L calcium channels
- -increase ICa2+ and rapidity of depolarization phase
list catecholamines
- epi
- norepi
- dopamine
catecholamines bind receptors on target cells to [] muscle contraction
strengthen
what is the physiology behind catecholamines strengthening muscle contraction
- receptor couples with G protein
- G proteins activate adenyl cyclase
- concentrations of cAMP increase
- influx of calcium
- contraction strengthened because of increased intracellular calcium
sympathetic fibers [] the strength of myocardial contractoin
increase
[] arise in thoracic spinal cord and branch into superior, middle, and inferior cardiac nerves
-join at cardiac plexus, neural junction, at the root of the aorta in front of the trachea
sympathetic nerves
[] interact with beta-adrenergic receptors and pacemaker cells to
a. increase influx of Ca2 into cell
b. increase contractile stregnth
catechoalmines
increase HR and force contraction
what overall effects do catecholamines have on the heart
- increase strength myocardial contraction
- increase HR
- shorten conduction time through AV node
chronotropic changes describe []
heart rate
- decrease
+ increase
inotropic changes describe []
change in force myocardial contraction
-decrease
+ increase
this sympathetic hormone is released a post synpatic nerve endings
NE
this sympathetic hormones is released by adrenal medulla and reaches heart via the blood stream
epi
what does stimulation of beta receptors 1&2 cuase
- increase in heart rate (chronotropy)
and force (inotropy)
-pump more blood
what does stimulation beta 3 receptors cause
decrease myocardial contractiliy (- inotropic)
negative feedback
-safety mechanism to prevent overstimulation heart my sympathetic nervous system
what receptors provide negative feedback mechanisms to prevent overstimulation of heart
beta 3
parasympathetic [] the rate of contraction
decreases
i.e. rest and digest
where are parasympathetic fibers found
medulla oblongata
what nerve do parasympethic impulses travel by
vagus
the parasympatheric impulses travel by way of [] nerve and synapse in the []
- vagus
2. cardiac plexus
ACH [] conduction through the [] node
- slows
2. AV
which one sympathetic/parasympathetic have a bigger impact on mycardial cells and why
sympathetic, more synapses on base/myocardium
muscarinic receptors are primarily on the [] while nicotinic is on the []
- heart
2. skeletal muscle
what role does ACH have on nicotinic receptors
increase contractility of skeletal muscle via nicotinic receptors (opposite effect on heart)
[] is the volume of blood flowing through either systemic or pulmonary circut in L/Min
CO
[] is calculated by multiplying HR by stroke volume
CO
[] is calculated by subtracting ESV from EDV
stroke volume
what is a normal adult CO
5 L/min
[] is the amount of blood ejected per beat and is useally measured by echocardiograph
ejection fraction
what is a normal ejection fraction
55% or higher
how is ejection fraction calculated
stroke volume/edv
what is ejection fraction a good indicator of
ventricular function
[] is the pressure generated at the end is diastole
pre-load (end of diastole is BEFORE contraction)
pre-load is also called what
left ventricular end diastolic pressure
[] is determined by EDV, the amount of venous return to ventricle and blood left in ventricle after systole or ESV
pre laod
an increased preload normally increases
CO (think equation)
[] is resistance during systole
afterlaod
[] is dependent on arotic pressure and aortic valve function
afterload
aortic systolic pressure is a good index of [] in left ventricle
after laod
low aortic pressure leads to []
decreased afterload, heart contracts more rapidly
leads to increased CO (think equation)
remember this is supposed to be a high pressure system, so if pressure is low heart will work overtime to increase that pressure
high aortic pressure leads to
increased afterload
-slows contraction and increases workload
what are some determinants of the force of contraction
- changes in stretching of ventricular myocardium
caused by changes in ventricular volume (preload) - alteration of nervous system input to ventricles
- adequacy of myocardial oxygen supply
what are positive inotropic agents
- Ne from sympathetic nerves
2. Epi from adrenal cortex
what are some negative inotropic agents
- hypoxia
average HR
70 BPM
what is the carioexcitory and cardioinhibitory
- sympathetic speeds up HR
2. parasympathetic decreases HR, controls resting HR
what are some neural reflexes of HR
- sinus arrythmia
- baroreceptor reflexes
- brainbridge reflex
- hormones and biochemicals
sinus arrythmias change the heart rate during []
breathing
describe the baroreceptor reflex
when BP falls, HR increases and arterioles constrict
describe the bainbridge reflex
changes in heart rate form intravenous infusions, volume reveptors in atria innvervated by vagus nerve
describe some hormones and niochemicals that have an effect on hert rate
- epi/ne
2. thyroid hormones
describe the frank-starling law of the heart
- length-tension relationship of cardiac muscles
- volume of blood in heart at the end of diastole contributes to length of muscle fibers (Stretch(
- myocardial stretch determines force of contraction
- more stretch, more contraction - as contractility decreases, curve shifts down & to right to CO will also be decreased
- contractility contributes to stroke volume and cardiac output
describe Laplace’s law
- contractile force (wall distenction) within a chamber depends on the radius of chamber and thickness of wall
- small chambers and thicker chamber walls equal decreases contraction force (tension) - in ventriculat dilation, force needed to maintain ventricular pressure lessens available contractile force
- more difficult for ventricle to eject blood
*anneruysm formation, dispensability in blood vessels, effects ventriculat dilation -> heart failure