ICL 3.3: Cardiac Physiology, Vascular Physiology & Autoregulation Flashcards
what is the purpose of homeostasis?
to provide adequate blood to the tissues
ex. during exercise the blood flow to skeletal muscles increases while GI decreases!
what are the 3 primary mechanisms through which homeostasis is achieved?
- autoregulation
- neural and endocrine mechanisms
- organ-specific regulations
what branch of the nervous system controls peripheral blood flow?
peripheral blood flow is under dual regulation of the CNS anddddd local!
whereas the heart is mainly just under CNS regulation
what is autoregulation?
maintenance of a constant blood flow to an organ in the face of changing arterial pressure/resistance
if you change the BP to double, the blood flow will not change! this is due to autoregulation!
this mechanisms is mainly driven by local factors –> so it’s based on the intrinsic ability of the organ and isn’t based on neural or hormonal effects!
which organs have strong autoregulation? weak? non?
STRONG
- kidney
- brain
- coronary
WEAK
- skeletal muscle
- splanchnic circulation
NONE
1. cutaneous circulation
how is autoregulation achieved?
CO = P/TPR
P = CO X TPR
= HR X SV X TPR
= HR X (EDV-ESV) X TPR
short term regulation of MAP principally involves the sympathetic nervous system and the regulation of HR and TPR
if you increase the perfusion pressure, you will have an increase in flow! if you decrease perfusion pressure, you will have a decrease in flow!
however, when there’s autoregulation, if there is a decrease in perfusion pressure, the autoregulation will maintain constant flow by decreasing resistance via vasodilation of the arterioles
arterioles are the major resistance controlling vessels!!
what is perfusion pressure?
the pressure difference between the arterial and venous pressure of an organ/tissue
what is the myogenic hypothesis?
increased perfusion pressure = increased blood flow and also increased stretch of arteriolar smooth muscle
this stretch is followed by a reflux that causes increased constriction of the arterioles and increased resistance which then causes a decrease in flow aka negative feedback! this is autoregulation and ultimately keeps the blood flow consistent even though perfusion pressure increased
again, if you decrease perfusion pressure then blood flow decreases and there is less stretch of the arterioles –> this causes vasodilation, decreased resistance and ultimately increased flow!
CO = P/TPR
what is reactive hyperemia-increased blood flow?
reactive increased blood flow that happens during ischemia
if you put on a tourniquet you cause an ischemia in your lower arm – when you take it off you expect it to go back to steady state immediately, there is a huge increase in blood flow in the lower arm! this transient increase in blood flow is called reactive hyperemia!
so it’s increased flow in response to a prior decrease in blood flow and it’s controlled by metabolites
this is totally controlled by the autoregulation mechanism
what is active hyperemia-increased blood flow?
when you’re exercising there’s an increasing demand for blood flow so more blood is flowing but it’s over a longer period of time
when you exercise you have lactic acid production which decreases pH and is a vasodilator and facilitates blood flow –> so there’s CNS activation increasing heart contractility and metabolic control decreasing pH
this is controlled by autoregulation and SNS control so we don’t talk about it as much in terms of autoregulation since it’s a mix
what is the metabolic hypothesis?
the blood flow is connected to the metabolic state of the tissue
hypoxia leads to vasodilation everywhere except for in the lungs where it’s a vasoconstriction
adenosine, NO, CO2, H and K lead to vasodilation
which natural molecules in the blood cause vasodilation?
- low O2
- adenosine
- NO
- CO2
- H+
- K+
which vasoactive compounds are vasoconstrictors?
- angiotensin II
2. vasopressin (ADH)
what are the 2 classes of receptors that help regulate blood flow?
- baroreceptors
2. chemoreceptors
what are baroreceptors?
clusters of nerve ending in blood vessel wall that respond to stretch that is exerted by the blood pressure
when we increase pressure on arterial wall there’s a natural reflex vasoconstriction
what are the 2 types of baroreceptors?
- arterial = high pressure
found in the aortic sinus (CN 10) and carotid sinus (CN 9) which then feed into the brain stem to elicit a response
- cardiopulmonary = low pressure (volume-sensitive-induced stretch)
found in the right atria/ventricle and the pulmonary artery/vein –> signals are transferred via the vagus nerve to the brainstem to regulate HR and blood volume via the kidney
right atria/ventricle release ANP and BNP which are both vasodilators
what is the mechanism behind baroreceptors?
baroreceptors are always firing!
when there’s an increase or decrease in blood flow it’ll cause a parasympathetic or sympathetic reaction
they’re mechanically gated receptors so when there’s stretch there’s increased opening of channels to CN 9 and 10 and when there’s relaxation, there’s decreased opening of channels and less firing to CN 9 and 10
what are ANP and BNP?
- ANP = atrial natriuretic peptide
released from atrial myocytes
- BNP = brain-type-natriuretic peptide
released from ventricular myocytes
both cause vasodilation and are usually secreted as inactive forms and they have to be activated
in CHF where there is increased NaCl and water by RAS, ANP and BNP will increase because more volume, more ventricular and atrial filling = more ANP and BNP to cause vasodilation and decrease BP
how does vessel diameter try and compensate for an increase in BP?
increase in BP increases arterial wall stretch which increases baroreceptor during and decelerates HR
this means there’s an increase in the parasympathetic nervous system and decrease in the SNS that’s causing a decrease in HR and TPR
this leads to vasodilation and a decrease in BP
what happens when there’s carotid massage?
increase pressure on carotid artery = increased stretch = increased baroreceptor during = decreased HR
what are the 2 types of chemoreceptors?
- peripheral = aortic body and carotid body
detect O2 concentration, CO2 concentration and pH
- central in the medulla oblongata
detect CO2 concentration and pH; don’t detect O2
so both their primary effect is on respiration! when you’re at high altitudes you increase depth of breathing because there’s decreased O2
they have a minor effect on vasomotor activity in comparison to baroreceptor activity
what happens when there’s increased CO2 in the blood
CO2 is quickly metabolized into H2CO3 which decreases pH in blood and cerebrospinal fluid which activates central chemoreceptors
then arteriolar and venous constriction happens to get more blood to the brain
this results in increased TPR and BP so you’re hypertensive because of the constriction!
when the BP > CSF then this will cause increased intracranial pressure and will lead to Cushing reflex
what is the Cushing Reflex?
it’s an ischemic response when there’s increased intercranial pressure and decreased blood flow to the brain
when there’s less oxygen in the CNS that means more CO2 is accumulating which activates the SNS and cause vasoconstriction, more HTN = increased CO
then your body tries to restore your arterial pressure so the baroreceptors in the carotid bodies are stimulated which slows down the HR and reduces perfusion
the Cushing reflex helps save brain tissues during periods of poor perfusion
how does oxygen regulate MAP?
peripheral chemoreceptors are vascular bodies in the region of aortic situ and the carotid sinus –> low pO2 activates afferent signals that stimulate nucleus solitaires tract and vasomotor area to cause vasoconstriction and tachycardia
central chemoreceptors in the medulla primarily detect pCO2 and activate the vasomotor area to produce vasoconstriction
so hypoventilation or diffusional problems lower pO2 and raise pCO2 causing reflex vasoconstriction and bradycardia
with increased blood volume, what will happen to HR?
if you give an infusion, you’ll have increased CO –> increased arterial pressure –> increased baroreceptor reflex –> decrease in HR
but what actually happens is the bainbridge reflex: infusion –> increased RA pressure –> atrial receptors stimulated –> bainbridge reflex –> increased HR
so at high volumes, bainbridge reflex predominates over the baroreceptors
but the baroreceptor reflex prevails over the bainbridge reflex when the blood volume is normal or decreased
what is the effect of SNS activation on vessel diameter?
vasoconstrictor
is it an alpha 1 or B2 response?
SNS response releases epinephrine and NE –> NE is a constrictor when it acts on alpha1
when it’s epinephrine via alpha1 it’s vasoconstriction BUT if it’s B2 then it’ll cause vasodilation
what happens when there’s decreased firing of high pressure baroreceptors?
HPBR = aortic and carotid sinus
when there is decreased MAP, there will be a decreased firing rate of HPBR and less activation of nucleus solitaires tract –> inhibition of PNS and activation of SNS
this leads to an increase in TPR, HR, cardiac contractility and CO
what is the endocrine mechanism?
- Epi and NE are released from medulla and enhance sympathetic response by increasing HR and contraction
- antidieretic hormone is secreted from the hypothalamus and is triggered by blood loss or increased osmolarity –> leads to increased water retention and increased blood volume and increased CO
- renin-angiotensin-aldosterone system (RAAS)
what is the RAAS system?
vasoconstriction response!
angiotensinogen is released from the liver and gets cleaved into angiotensin I by renin from the kidney
angiotensin I goes to the lungs which have enzymes to cleave angiotensin I into II which is a vasoconstrictor and increases CO!
angiotensin II also leads to aldosterone production which allows for Na+ retention and hence H2O retention to increase BP and blood volume
what regulates arterial pressure long term?
as the HPBR adapt after prolonged change in MAP like in someone with chronic HTN, the baroreceptor will adapt to the new normal and not cause any change in the BP! so they really only have a short term effect on BP
BUT the RAAS system has a long term effect on blood pressure and is able to control it even with persistent elevated BP
what happens when there’s venous pooling?
venous pooling decreases preload which decreases EDV
this decreases SV, CO and BP
this means there will be a decrease in HPBR firing which means SNS will be activated and cause vasoconstriction and tachycardia
what happens to SNS activation during exercise?
SNS is activated and Increased cardiac contractility rotates the CO curve upwards and to the left and venous return also increases!
as the exercise progresses the local muscular beds dilate due to accumulating metabolites (e.g. adenosine) –> this vasodilation shifts the VR curve further upwards and the CO curve also rotates further up and to the right
what happens to cardiac contractility during CHF?
CO is decreased and Na retention compensates by increasing blood volume
A 27-year-old man is involved in amotor vehicle accident and sustains massive blood loss. He is promptly brought to theemergency department. Initial survey shows an agitated, pale,diaphoretic young man. His initialblood pressure is holding steady at 100/70mm Hg, but the trauma team is concerned about developing shock. Which of the following pathways is involved in the afferentlimb of thephysiologic response maintaining this patient’sblood pressure
A. Aortic body transmits via vagus nerve to medulla.
B. Aortic arch transmits via vagus nerve to medulla
C. Carotid body transmits via vagus nerve to medulla
D. Carotid body transmits via glossopharyngeal nerve to medulla
E. Carotid sinus transmits via glossopharyngeal nerve to medulla
E. Carotid sinus transmits via glossopharyngeal nerve to medulla
carotid sinus = baroreceptor
carotid body = chemoreceptor
