Chest Pain II Flashcards
Rate-pressure product (RPP)
RPP = HR x SystolicBP
Coronary circulation regulated by?
mostly local control - tissue metabolites such as adenosine and NO cause vasodilation
some autoregulation/myogenic control
Blood flow through coronary arteries occurs when?
During diastole, because vessels are compressed during systole
Blood flow through coronary arteries moves in what direction?
Epi to myo to endocardium
Heart extracts what % of oxygen?
75-80% vs 25% in the tissues
Treatment options for angina
1) increase blood flow/oxygen supply (but not really able to do this practice because local regulators have already vasodilated to max)
2) decrease oxygen demand through decreasing HR, inotropy, or afterload
How is splanchnic circulation oriented?
in both series (hepatic portal system) and parallel
Splanchnic circulation receives high or low percentage of CO at rest?
high 25%
Splanchnic circulation regulated by?
Local and CNS mechanisms, when body is under stress and SNS is activated this will decrease blood flow to splanchnic circulation
Counter-current exchange in intestinal villi
Venules steal oxygen from ascending arterioles and under normal conditions there is enough oxygen left to nourish the villi, but during low blood flow, can cause anoxic damage to villi
Body’s major thermoregulatory organ?
Skin
How does cutaneous circulation play role in thermoregulation?
1) temperature gradient between skin and environment
2) capillaries increase SA for heat exchange
3) slow velocity of blood flow allows for max time for heat exchange
Apical skin
hands, feet, ears, nose, some face
AV anastomoses for heat exchange, caps for nutrient delivery
stimulation of sympathetic adrenergic fibers control BF via vasoconstriction, no heat exchange at AV anastomoses
Hypothalamic control of apical skin
increased body temp, Hypothalamic decreases sympathetic outflow leads to passive vasodilation and heat exchange
Nonapical skin
NO AV anastomoses, sympathetic neurons release Norepi leading to vasoconstriction, no heat exchange, other sympathetic neurons release ACh at sweat glands causing active vasodilation via bradykinin
Bradykinin
released from sweat glands causes active vasodilation of cutaneous capillaries and heat exchange
Cutaneous vasodilation vs vasoconstriction
Vasodilation - heat exchange
Vasoconstriction - heat retention
Skeletal muscle circulation regulated by?
CNS - sympathetic NS vasconstrict
Local mediators - vasodilate
Reactive hyperemia
No flow to skeletal mm leads to buildup of vasodilating metabolites, when flow is resumed, flow is increased due to dilation to wash out metabolites
Cerebral sympathetic stimulation to shut down blood supplies to other organ systems can be overridden by?
Skeletal mm and coronaries
BBB contains what kind of junctions?
tight junctions, lipid sol molecules can pass (oxygen, carbon dioxide, alcohol) most other mols. are excluded, glucose/GLUT1 transporter are exceptions
Autoregulation range for cerebral blood flow
60-130mmHg, range can be shifted by HTN to protect brain from high pressures
Cerebral BF is dept on partial pressure of?
Carbon dioxide and lesser extent oxygen
Eq for cerebral perfusion pressure
CPP = MAP - ICP
Renal circulation regulated by?
Autoregulation (afferent arterioles) and sympathetic control
Blood flow in kidney
Afferent arterioles > Glomerular capillaries > Bowman’s capsule > Efferent arterioles > Peritubular capillaries
Effect of decreasing resistance at afferent arterioles?
Increases pressure in both capillary beds (glomerular and peritubular), increase flow
Effect of increasing resistance at afferent arterioles?
Decreases pressure in both capillary beds (glomerular and peritubular), decrease flow
Effect of decreasing resistance at efferent arterioles?
Decreases pressure at GC, increases pressure at PC, increase flow
Effect of increasing resistance at efferent arterioles?
Increases pressure at GC, decreases pressure at PC, decrease flow
Parasympathetic and sympathetic pre/postganglions
Para: long pre, short post (ACh)
Symp: short pre, long post (NE)
Nicotinic vs muscarinic receptors
Both use ACh, nicotinic is pregang, muscarinic is postgang
Termination of parasymp AP
Acetylcholinesterase
Muscarinic receptor locations
M1 - CNS
M2 - cardiac
M3 - smooth MM, secretory glands, endothelium
M4+M5 - CNS
NE is effector junction neurotransmitter for?
Sympathetic actions on both alpha and beta adrenergic receptors EXCEPTION: ACh for sweat glands
Termination of symp AP
Reuptake of neurotransmitter and degradative enzymes (MAO)
Alpha 1
NE/E, radial muscles of eye, sympathetic synapse in blood vessels, increases Ca++
Alpha 2
NE/E, presynaptic, decreases cAMP and inhibits NE release
Beta 1
NE/E, heart, increases cAMP, HR, FOC
Beta 2
E, bronchi, blood vessel wall, liver, skeletal mm, ciliary, increase cAMP causing relaxation
Choline acetyltransferase
makes ACh from choline and acetate, ACh is stored in vesicles and released upon Ca influx
Dopamine-beta-hydroxylase
converts Dopamine to NE (NE can then be converted to E in adrenal medulla)
Para/Symp actions on Bronchioles
b2 symp - increase radius
M3 para - decrease radius
Para/Symp actions on Heart
b1 symp - increase HR, inotropy, dromotropy
M2 para - decrease HR, inotropy, dromotropy
Para/Symp actions on blood vessels
a1 symp - decrease vessel radius, increase TPR
b2 symp - increase vessel radius in skeletal mm
No para actions
Para/Symp actions on liver
b2 symp - increase glycogenolysis/glucoNEO
No para actions
Short-term mechanisms for pressure change
Baroreceptors, monitor hr-hr, min-min changes, changes occur on the time course of second-minutes
High pressure baroreceptors
Arterial baroreceptors at carotid sinus (brain BF, more sensitive, signals through 9th cranial nerve) and aortic baroreceptors (body BF, signals through 10th cranial nerve)
Low pressure baroreceptors
In cardiac atria and pulmonary artery provide info on venous return, CVP, BV, A receptors (report HR), B receptors (report atrial volume)
Chemoreceptors
at carotid fork and arch of aorta, sense CO2 and O2 levels, regulate breathing
Firing of baroreceptors is proportional to?
Pressure
Cardiovascular center
Nucleus tractus solitarius (NTS) integrates signals, contains vasomotor center and cardioinhibitory center
Vasomotor center
activates SNS leads to vasoconstriction and positive chronotropic/inotropic response, receives INHIBITORY signal from NTS
Cardioinhibitory center
activates PNS leads to vasodilation and negative chronotropic/inotropic response, receives STIMULATORY signal from NTS
Factors that reset baroreceptor ranges
hypertension increases receptor range so that the reflex is sensitive over a wider range
Humoral control
modulates BP over longer time period, includes vasoactive substances and nonvasoactive substances
Vasoactive substance
released into the blood, affect vascular smooth muscle, modulates pressure and distribution of BF
Nonvasoactive substances
targets organs outside CV system, modulates effective circulatory volume
Epinephrine
binds a1 on smooth MM - vasoconstriction, binds b2 on cardiac MM, liver, skeletal muscle - vasodilation
Serotonin
5-HT, vasoconstriction, local mediator
Histamine
from mast cells, vasodilations
Angiotensin II
vasoconstriction, regulated by RAS
Atrial natriuretic peptide
ANP, vasodilator, release by atrial myocyte in response to stretch sensed by cardiopulmomary receptors, low pressure baroreceptors
Vasopressin
AVP/ADH, vasoconstrictor at high concentrations
Endothelins
ET, vasoconstrictor
RAS
1) low P or SNS stimulation triggers release of renin
2) renin hydrolyzes angiotensinogen (made in liver) to angiotensin I - weak vasoconstrictor
3) I converted to II - potent vasoconstrictor
4) II converted to III - weak
Ang II functions
vasoconstriction, stimulate thirst, ADH release, and aldosterone synthesis and release
NET EFFECT: increase arterial pressure by increase TPR and BV
Vasopressin/ADH functions
stimulates renal collecting ducts to insert more AQP2
ANP functions
relaxes smooth MM, arterioles of kidneys to increase filtration and reduce renin release, inhibits aldosterone secretion, Na+ reabsorption, secretion of ADH
NET EFFECT: decrease effective BV
Aldosterone function
released in response to increase AngII, acts on distal tubules of kidney to retain water by absorbing Na++ back into blood
NO function
sheer stress, bradykinin and ACh stimulate NO synthesis, which activates cGMP formation, PKG activation, and inhibits MLCK and activates SERCA pump which lead to vasodilation
Clinical relevance of NO
1) septic shock - toxins increase NO, causing systemic drop in TPR and BP
2) nitrates used to treat angina dilates resistance vessels and decreases TPR and afterload, as venodilator it decreases preload, SV and O2 demand
Does venoconstriction increase pressure?
Not substantially, usually only allows for faster blood flow
Orthostatic reflex
AoP - systolic decreases, diastolic increase
CVP decreases
CO decreases
HR increases
**all return to normal when walking, except HR which increases
Positive inotropic agents:
SNS, drugs
Negative inotropic agents:
CHF, MI, drugs
Cardiac function curve
function of heart as pump, starling curve, changes with inotropy, show CO for changes in venous pressure, direct relationship
Vascular function curve
how venous system responds to CO, inverse relationship, increases/decreases in BV (hyper/hypovolumia) moves curve upwards/downwards, changing arteriolar tone (TPR) has not effect on MCP but changes slope of curve
Respiration effect on CVP
Inhalation increase PL and SV in right heart and decreases them in the left
Exhalation increases PL and SV in left heart and decreases them in the right
Vasodilation leads to?
Increases cap permeability, cap hydro pressure, cap filtration rate, interstitial hydro pressure, and lymph flow
Atherosclerosis leads to?
decrease arterial compliance, leading to increased systolic pressure and pulse pressure
PP is dependent on?
directly proportional to SV and inversely proportional to arterial compliance
Pulmonary cap. pressure?
8mmHg
Systemic capillaries pressure?
25mmHg
Pulmonary art. sys+dias
25/10
Aorta sys+dias
130/80
Right ventricle sys+dias
25/5
Left ventricle sys+dias
130/10
Aortic Stenosis vs aortic regurgitation in terms of PP, SBP, SV?
Aortic stenosis decreases all
Aortic regurgitation increases all
