cvs 4 previous semester Flashcards
BF to an organ is proportional to its metabolic activity. IE more blood flow to exercising muscles is an example of
active hyperemia
is an increase in blood flow to an organ to occurs after a period of occlusion of flow
reactive hyperemia
what three organs exhibit auto-regulation
heart, brain, kidneys
blood flow to an organ remains constant over a wide range of perfusion pressures- this is called
auto regulation
what is used to explain autoregulation
myogenic hypothesis
vascular smooth muscle contracts when it is stretched
myogenic hypothesis
example of myogenic hypothesis
increase perfusion pressure to an organ increases stretch of vascular smooth muscle leads to contraction. the resulting vasoconstriction will maintain a constant flow.
tissue supply of 02 is matched to tissue demand for 02
metabolic hypothesis
in metabolic hypothesis vascular metabolites are produced as a result of metabolic activity in tissue. what are the vasodilators
c02
H+
K+
adenosine
during exercise the increase metabolism leads to what
increase production of vasodilators, increase blood flow, increase 02 delivery to the tissue
increase sympathetic tone causes
vasoconstriction
decrease sympathetic tone causes
vasodilation
what is bradykinin similar to
histamine
what causes arteriolar constriction helps to prevent blood loss
serotonin 5-ht
what is implicated in the vascular spasm of migraine headache
serotonin 5ht
what are the effects of histamine
arteriolar dilation and venous constriction leads to increased capillary hydrostatic pressure and increased filtration out of the capillaries resulting in local edema
how does histamine create local edema
artery dilation venous constriction
increase cap hydrostatic pressure
increased filtration out of the capillaries
prostacyclin is a
vasodilator
thromboxane A2 is a
vasoconstrictor
what do baroreceptors do
alerts brain in case of low blood pressure
what are baroreceptors
stretch receptor
where are baroreceptor located
carotid sinus near the bifurcation of common carotid arteries
what is responsible for the minute to minute regulation of arterial BP
baroreceptor
what accounts for vasomotor tone and produces vasoconstrictor activity tonically
baroreceptor
what controls circulation
sympathetic nervous system
what controls the heart function via vagus nerve
parasympathetic nervous system
where does the vasomotor center transmit its impulses
down the cord to almost all blood vessels
where is the VMC located?
bilaterally in the reticular substance of the medulla and the lower third of the pons
what is the vmc composed of
a vasoconstrictor area, vasodilator area, and sensory area.
decrease stretch on the baroreceptors - what happens
the firing rate of the carotid sinus nerve hering nerve, CN IX, which stimulates the VMC in the brain
The responses of VMC to a decrease MAP are:
Decrease parasympathetic (vagal) outflow to the heart
Increase sympathetic outflow to the heart and blood vessels
The following four effects attempts to increase the arterial pressure to normal
increase Heart rate ,resulting from decrease parasympathetic tone and increase sympathetic tone to the SA node
increase Contractility and SV which produces increase in cardiac output
increase vasoconstriction of arterioles; as a result TPR will increase , increasing arterial pressure
increase vasoconstriction of veins resulting increase venous return
A decrease in renal perfusion pressure causes the juxtaglomerular cells to secrete
renin
ACE catalyzes the conversion of angiotensin I to angiotensin II in the
lungs
ace inhibitors
e.g. captopril) blocks the conversion of angiotensin I to angiotensin II and therefore, BP
arb action
Angiotensin receptor (AT1) antagonist (e.g. Losartan) block the action of angiotensin II at its receptor and decrease blood pressure.
what does angiotensin 2 have for effect on aldosterone
synthesis and secretion of aldosterone by the adrenal cortex
aldosterone increases what to be reabsorbed
Na+ reabsorption by the renal distal tubular, thereby increasing extracellular fluid volume
increase HR= means? treatment?
increase 02 consumption
decrease coronary blood flow
give beta blockers
increase BP
increase Wedge
increase afterload
increase work of heart
increase 02 consumption
increase depth of anesthesia
nitroglycerin
decrease blood pressure
decrease or normal wedge
decrease TPR
decrease BP and coronary blood flow
decrease anesthesia
fluids
phenylephrine to improve BP and coronary circulation
decrease BP
increase wedge
heart is failing
intros
phenylephrine
nitroglycerine
normal hemodynamics
ng and CA channel blockers
Loss of circulating volume %
< 20 %
Skin changes
BP normal
Thirsty , cold , wake and alert
20-40%
Oliguria (20 ml/hr)
Restlessness
decrease BP, weak pulse >120
Confusion
> 40 %
Very low BP, no pulse >140
EKG changes
Lethargic, coma
No urine output
Coronary Circulation %
5% of cardiac output (250 ml/min)
Coronary Circulation
vasodilation
hypoxia and adenosine
Bainbridge Reflex
Increase in atrial pressure increases heart rate
Stretch of atria sends signals to VMC via vagal afferents to increase heart rate and contractility.
Prevents damming of blood in veins atria and pulmonary circulation.
Cushing reaction:
increased ICP causes compression of cerebral blood vessels leading to cerebral ischemia and increase cerebral PCO2 .The VMC directs an increase in sympathetic outflow to the heart and blood vessels, which cause a profound hypertension, bradycardia and irregular respiration (Cushing triade; opposite to shock !)
Cerebral ischemia
Cerebral ischemia
When the brain is ischemic the conc. of CO2 and H+ in brain tissue increases
Chemoreceptor in the VMC respond by increasing sympathetic flow to heart and blood vessel
Constriction of arterioles causes intense peripheral vasoconstriction and increase TPR
Blood flow to other organs (e.g. kidneys) is significantly reduce in an effort to keep blood flow to brain
MAP can increase to life-threatening levels
Angiotensin II has four effects
It stimulates the synthesis and secretion of aldosterone by the adrenal cortex
Aldosterone increases Na+ reabsorption by the renal distal tubule, thereby increasing extracellular fluid volume, blood volume and arterial pressure
This action of aldosterone is slow because it requires new protein synthesis
It increases Na+-H+ exchange contraction alkalosis
It increases thirst
It causes vasoconstriction of the arterioles, thereby increasing the TPR and MAP
Steps in the renin-angiotensin-aldosterone system
A decrease in renal perfusion pressure causes the juxtaglomerular cells to secrete renin
Renin catalyzes the conversion of angiotensinogen to angiotensin I in plasma
ACE catalyzes the conversion of angiotensin I to angiotensin II in the lungs
ACE inhibitors (e.g. captopril) blocks the conversion of angiotensin I to angiotensin II and therefore, BP
Angiotensin receptor (AT1) antagonist (e.g. Losartan) block the action of angiotensin II at its receptor and decrease blood pressure.
Renin-angiotensin-aldosterone system
Is a slow, hormonal mechanism
Is used in long-term blood pressure regulation by adjustment of blood volume
Renin is an enzyme that catalyzes the conversion of angiotensinogen to angiotensin I in plasma
Angiotensin I is inactive
Angiotensin I is converted into Angiotensin II by ACE in lung
Angiotensin II is physiologically active
Valsalva maneuver
expiring against a closed glottis)
Tests the integrity of baroreceptor mechanism
Causes intrathoracic pressure which venous return
The venous return causes in cardiac output and arterial pressure (Pa)
If the baroreceptor reflex is intact, the decrease in Pa is sensed by the baroreceptor, leading to in sympathetic flow to the heart and blood vessels. In the test, in heart rate would be noted.
When the person stops the maneuver, there is a rebound increase in venous return, cardiac output and Pa. The in Pa is sensed by the baroreceptor, which direct a in heart rate.
