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SHORT TERM REGULATION OF BLOOD PRESSURE - Coggle Diagram
SHORT TERM REGULATION OF BLOOD PRESSURE
CNS Ischemic Control of BP
CNS Ischemia Trigger
:
Caused by reduced cerebral blood flow (hypoperfusion).
Medullary Vasomotor Center
:
Located in the medulla oblongata, it regulates BP.
Sympathetic Activation
:
Ischemia activates the SNS, increasing norepinephrine release.
Vasoconstriction
:
Norepinephrine causes vasoconstriction, raising total peripheral resistance (TPR).
Increased Heart Rate & Contractility
:
SNS activation increases heart rate and contractility.
Renal Response
:
Reduced renal blood flow triggers renin release, activating the RAAS (renin-angiotensin-aldosterone system).
BP Elevation
:
Increased TPR and cardiac output elevate BP to restore cerebral perfusion.
Negative Feedback
:
Elevated BP alleviates ischemia, improving cerebral blood supply.
Baroreceptor Reflex*
Location
: Carotid sinus, aortic arch
Stimulus
: Changes in blood pressure (stretch of arterial walls)
Mechanism
:
Increased BP
: Baroreceptors increase firing → Activation of parasympathetic nervous system (PNS) → Decreased heart rate (via vagus nerve) → Vasodilation
Decreased BP
: Baroreceptors decrease firing → Activation of sympathetic nervous system (SNS) → Increased heart rate, contractility, and vasoconstriction (via norepinephrine)
Effect
: Restores BP to normal levels via HR, SV, and vascular tone adjustments.
Chemoreceptor Reflex
Location
: Carotid bodies, aortic bodies
Stimulus
: Low O₂, high CO₂, low pH
Mechanism
:
Hypoxia, Hypercapnia, or Acidosis
: Chemoreceptors signal to medulla → Increase sympathetic output → Vasoconstriction → Increased BP
Effect
: Ensures adequate perfusion of vital organs (especially brain and heart) during oxygen deprivation.
.
Vasovagal Syncope
Stimulus
: Stress, pain, sight of blood, or standing for long periods
Mechanism
:
Overactivation of parasympathetic response or withdrawal of sympathetic tone
Effect
: Vasodilation, bradycardia → Sudden drop in BP → Decreased cerebral perfusion → Fainting
Outcome
: Protective mechanism to restore upright posture and circulation to the brain.
*Bainbridge Reflex
Location
: Right atrium
Stimulus
: Increased venous return (e.g., exercise, fluid infusion)
Mechanism
:
Stretch of atrial walls → Activation of stretch receptors → Increased heart rate (via increased sympathetic activity)
Effect
: Increases heart rate to accommodate increased blood volume and prevent congestion.
Atrial Blood Flow (Frank-Starling Mechanism)*
Stimulus
: Increased blood volume or venous return
Mechanism
:
Increased atrial stretch → Increased force of ventricular contraction (due to length-tension relationship of muscle fibers)
Effect
: Ensures that the amount of blood entering the heart matches the amount leaving, stabilizing BP.
Role of Skeletal Muscles in Increasing Cardiac Output and Atrial Pressure
:
Muscle Pump Mechanism
:
Skeletal muscle contractions compress veins, aiding venous return to the heart.
Increased Venous Return
:
Enhanced venous return boosts preload (end-diastolic volume), which increases stroke volume.
Activation of Sympathetic Nervous System
:
Muscle activity stimulates the SNS, increasing heart rate and contractility (positive chronotropy and inotropy).
Increased Cardiac Output
:
Greater venous return and SNS activation elevate cardiac output.
Increased Atrial Pressure
:
Increased venous return raises atrial pressure, enhancing preload and further cardiac output.
This process, known as the "muscle pump," helps improve circulation, especially during physical activity.