BP Control Flashcards
ANS control
Baroreceptors
Chemoreceptors
Low-Pressure receptors
CNS ischemic response
ACUTE CONTROL
Renin-Angiotensin-Aldosterone-System (RAAS)
Slow: takes 20 minutes to take effect
Activated when faster mechanism fail to regulate BP
Also responsible for maintaining normal BP despite wide variation in salt intake
Long-term control
Sympathetic > Parasympathetic
To increase BP via ANS:
- arteriolar vasoconstriction-> increase TPR -> increase BP
- venous vasoconstriction-> increase VR -> increase CO -> increase BP
- increase HR & SV via B1 receptors of the Heart -> increase CO -> increase BP
ANS
center responsible for regulation of HR and BP
Found in the Medulla:
Lateral Portion: Excitatory Area (increases HR & BP)
Medial Portion: Inhibitory Area (decreases HR & BP)
Controlled by the Hypothalamus and other higher nervous centers
VASOMOTOR AREA OF THE MEDULLA
Could also induce changes in BP
Responds to low O2, high CO2 concentation whenever BP increased TPR-> increased BP
CHEMORECEPTORS
Low-pressure receptors (Cardiopulmonary Baroreceptors)
In the atria and pulmonary arteries
Detects “fullness” of vascular system (increased intravascular volume)
In response to increased intravascular volume:
- INCREASES ATRIAL NATRIURETIC PEPTIDE (ANP)
- DECREASES ANTI-DIURETIC HORMONE (ADH)
- RENAL VASODILATION (increases urine output)
- INCREASES HEART RATE (Bainbridge Reflex) [helps match VR with CO]
CNS ISCHEMIC RESPONSE
The VASOMOTOR CENTER itself responds directly to the ischemia during low BP
Starts at BP
CUSHING REACTION or CUSHING REFLEX
Occurs in response to increased intracranial pressure
Triad: HPN, BRADYCARDIA, IRREGULAR RESPIRATIONS
Mechanism:
Increase ICP ➡️ ICP > MAP ➡️ compression of blood vessels ➡️ decreased cerebral perfusion ➡️ increased PCO2 ➡️ CNS Ischemic Response ➡️ powerful sympathetic vasomotor response ➡️ inc BP and HR ➡️ ICP
