PHYSIOLOGY CR2 Flashcards
THE DRIVING FORCE FOR TISSUE PERFUSION
ARTERIAL PRESSURE
–WHICH DEPENDS ON THE COORDINATION OF THE CARDIAC OUTPUT AND TOTAL PERIPHERAL RESISTANCE-WHICH MEANS IT IS HIGHLY REGULATED BY THE AUTONOMIC NERVOUS SYSTEM!!
EFFECTIVE CIRCULATING VOLUME
THIS IS THE VOLUME OF BLOOD THAT IS REQUIRED TO MAINTAIN PERFUSION -
-IT HELPS TO KEEP THE SYSTEM OPERATING AT A SPECIFIC PRESSURE THAT WILL ALSO MAINTAIN PERFUSION
WHAT EFFECTS MOMENT TO MOMENT CHANGES IN THE ARTERIAL PRESSURE?
-BAROREFLEX
MAP EQUATION
MAP= CO X HR MAP= 1/3PP +DIASTOLIC PRESSURE
PP (PULSE PRESSURE)
HIGHEST SYSTOLIC PRESSURE - THE LOWEST DIASTOLIC PRESSURE
BARORECEPTOR RELFEX ARC
- RECEPTORS SENSE STRETCH AS IT CHANGES WITH PRESSURE AND CONVERT IT TO A CHEMICAL SYNAPSE
- ACT ON THE AFFERENT NERVES (VAGUS OR GLOSSOPHARYNGEAL NERVE)
- TAKEN TO THE NUCLEUS SOLITARIOUS IN THE MEDULLA
- EFFERENT NERVES GO OUT TO EFFECTOR ORGANS IF AN ERROR SIGNAL IS DETECTED
BARORECEPTOR EXAMPLE (DECREASE IN BP)
- DECREASE IN PRESSURE WILL CAUSE THE BARORECEPTORS TO FIRE AT APs AT A HIGHER FREQUENCY
- INFORMATION IS SENT TO THE MEDULLA VIA AFFERENT NERVES
- THE MEDULLA SENDS EFFERENT SIGNALS TO THE EFFECTOR ORGANS
3A. SYMPATHETICS INCREASE
3B. PARASYMPATHETIC DECREASE
THE SYMPATHETIC NERVOUS SYSTEM DOES WHAT TO TPR, CONTRACTILITY, AND BP
- INCREASES THE TOTAL PERIPHERAL RESISTANCE
- INCREASES CONTRACTILITY
- INCREASE BP
BARORECEPTOR REFLEX
- THIS IS THE REFLEX ARC RESPONSIBLE FOR THE SHORT TERM (SEC, MINUTES, HOURS) REGULATION OF OUR BLOOD PRESSURE
- NEGATIVE FEEDBACK LOOP!!
- 15-20 SECONDS TO RESPOND-RESPONDS FASTER THAN ANYTHING ELSE
HOW LONG DOES IT TAKE THE KIDNEYS TO RESPOND TO CHANGE IN BP
DAYS!!
CAROTID SINUS
- THE CAROTID SINUS IS A DILATION OF THE INTERNAL CAROTID ARTERY
- HAS A SINUS NERVE THAT
- SYNAPSES ONTO THE GLOSSOPHARYGEAL NERVE
- WHICH SYNAPSES ONTO THE MEDULLA’S NUCLEUS SOLTARIOUS
- Receptors here are tonically active and most sensitive
EFFECTOR ORGANS OF THE Baroreceptor reflex
- SA node (frequency)
- Cardiac muscle (cardiac output)
- venous smooth muscle (capacitance)
- Arterioles (TPR)
- Adrenal Gland
- all effect cardiac output
Baroreceptor locations
- carotid sinus (highest sensitivity)
- Atrial (sense stretch in the atrium which is reflected to the atria through the distension of the vessels)
- aortic arch, subclavian, common carotid (aortic arch receptors)
Aortic arch receptors
- synapse on to the vagus nerve
- not as sensitive
- more rigid
Venoconstriction and its effect on the MAP and CO
-sympathetics act on the venous system by constricting its smooth muscle wall =
this pushes the venous blood to the arterial side helping to maintain BP and increases cardiac output
sinus nerve
-just a part of the glossopharygeal (CN 9)
Baroreceptors (what are they)
- receptors branched and buried into the elastic walls of arteries
- the are “stretch receptors”
- because they sense stretch of the artery walls (which happens due to increases in pressure)
- the higher the magnitude of the pressure the more frequently the baroreceptors fire (and vice versa)
Baroreceptor sensitivity
- 50-200mmHg = range of sensitvity
- optimal range of sensitivity is where the slope of the pressure impulse curve is the steepest (getting the biggest amount of firing per incremental change in bp)
Baroreceptor Sensitivity Shift
- When you chronically elevate your bp the baroreceptors will shift their optimal sensitivity so that whatever your average bp is that is where their optimal sensitivity lies
- chronic increase resets and shifts curve to right (decrease shifts to left)
- Until a certain point— at 200mmHG baroreceptors will cease shifting and just continuously fire??
Tonic firing
magnitude of BP encoded by frequency of AP ellicited by the baroreceptor
-the higher the frequency the higher the bp
Phasic Firing
- detects rate of change of Bp
- ??
Central Integration in the nucleus solitarius of the medulla
- involves a pressor center and a depressor center that interacts with the system to adjust peripheral resistance
- also involves a cardiostimulatory and cardioinhibitory center that interacts to regulate cardiac output
Pressor center
- tonically active (always on)
- controls sympathetic outflow to changes TPR
depressor center
- not tonically active
- modulates the pressor center
- indirectly affects TPR
Pressor and Depressor example (increase in arterial
pressure does what to the BP )
- increase in BP
- Increase in signaling from the baroreceptors
- Pressor center is inhibited decreasing sympathetic outflow
- the depressor center is stimulated to inhibit the pressor center even further
- decrease vasoconstriction and veno. to bring down BP -Be able to do the reverse of this!!
Cardioinhibitory center
-tonically active
-controls the parasympathetic output to the heart
-
cardiostimulatory center
- tonically active
- controls sympathetic output to the heart
The cardioinhibitory center/ stimulatory center
-example: pressure goes down
- pressure decreases
- less input from the baroreceptors
- decrease the stimulation of the cardioinhibitory center which decreases the parasympathetics
- more stimulation of the cardiostimulatory center = increase of sympathetics to the hearts
Hypothalamus
- low pressure baroreceptors in the right atrium and pulmonary artery
- changes in central venous pressure relayed to hypothalamus and mediated by the cardiostimulatory /inhibitory center
Thermoregulation
- changes in body temperature alter blood distribution
- and therefore BP
Emotional stimulus effect on BP
- extreme fear, anxiety, embarrassment alters efferent output
- can lead to syncope
Painful stimulus
-can evoke a powerful sympathetic stimulation originating in the spinal cord
Other mechanisms that effect BP
- Pain
- Emotion
- Temperature
can overwhelm your body’s methods of maintaining your BP and cause syncope/ unconsciousness
Decreased MAP and baroreceptor reflex
- cardiac function (increases)
- vasoconstriction (increases)
- venoconstriction (increases)
- SO increased CO and decreased R atrial pressure/ Central venous return
Orthostatic changes in BP
- results from the effect of gravity on distribution of blood volume
- acute and chronic orthostatic hypertension
- body normally compensates with myogenic contraction and we do not pass out
Acute orthostatic hypertension
-anti-hypertensive drugs
or volume depletion
Chronic Orthostatic Hypertension
-disease like diabetes that cause vascular dysfunction
-i.e. peripheral neuropathy
OR CNS degeneration!
increased Gravitational Forces and their effect on BP
- ex) high performance flying
- blood will pool in the bottom of your feet
- and the blood flow to your brain will be decreased
- there are automatic pressure suits that will compensate for this!!
Decreased G forces
- eliminates the normal effect of gravity on volume
- going into space= example
- body perceives this as hypervolemia while in space and the excess volume is excreted (pee)
- But then when they return to earth they are hypovolemic because have been excreting salt and water for days so much that body has trouble maintain the BP
Chronic hypertension
- resets baroreceptors so they are functioning normally
- BUT structural changes result = hypertrophy of vascular smooth muscle in the arteries, and ventricles
- decreases capillary number (vascular rarefaction)
vascular rarefaction
-decrease in capillary number
