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LONG TERM CONTROL OF BLOOOD PRESSURE - Coggle Diagram
LONG TERM CONTROL OF BLOOOD PRESSURE
Pressure Diuresis*
Definition
: Increased urine output in response to elevated arterial pressure.
Mechanism
:
High arterial pressure → Increased renal perfusion → Increased glomerular filtration rate (GFR)
Increased GFR → More fluid excretion (diuresis) → Reduction in blood volume → Decrease in blood pressure
Pressure Natriuresis*
Definition
: Increased sodium excretion in response to elevated arterial pressure.
Mechanism
:
High arterial pressure → Increased renal perfusion → Increased GFR
Increased sodium filtration → Reduced sodium reabsorption → Sodium excretion increases
Reduced sodium reabsorption → Decreased blood volume → Decreased blood pressure
Increased Fluid Volume Elevates Arterial Pressure*
Cardiac Output (CO)
:
Fluid retention → Increased venous return → Increased stroke volume → Increased cardiac output
Increased CO → Elevated arterial pressure
Total Peripheral Resistance (TPR)
:
Fluid retention → Increased blood volume → Increased arterial pressure → May increase vascular resistance
Importance of Salt in Renal-Body Fluid Schema for Arterial Pressure Regulation*
Salt intake
:
Increases extracellular fluid volume
Increases blood volume and pressure
Renal Excretion of Salt
:
Kidneys excrete salt to balance pressure
Sodium retention → Increased blood volume → Elevated pressure
Sodium excretion → Decreased volume → Reduced pressure
One Kidney Goldblatt Hypertension*
Mechanism
:
Renal artery stenosis (reduced kidney blood flow) → Activation of RAAS → Increased sodium and water retention → Elevated blood pressure
Effect
:
High blood pressure in one kidney, but normal pressure in the contralateral kidney
Two Kidney Goldblatt Hypertension*
Mechanism
:
Bilateral renal artery stenosis → RAAS activation → Sympathetic nervous system activation → Increased sodium and water retention → Elevated blood pressure
Effect
:
Systemic hypertension with elevated blood pressure in both kidneys
Role of the Renin-Angiotensin-Aldosterone System (RAAS) in Arterial Pressure Control*
Renin Release
:
Low renal perfusion → Juxtaglomerular cells release renin
Angiotensin II Production
:
Renin → Converts angiotensinogen → Angiotensin I → Angiotensin II (via ACE)
Effects of Angiotensin II
:
Vasoconstriction → Increased total peripheral resistance (TPR)
Stimulates aldosterone release → Increases sodium retention → Increases blood volume → Elevated blood pressure
Stimulates ADH release → Increased water reabsorption → Elevated blood pressure
Primary Hypertension*
Definition
: Hypertension without identifiable secondary cause (essential hypertension).
Etiology
:
Genetic factors
Environmental factors (diet, lifestyle)
Renal sodium handling, RAAS activation
Mechanism
:
Increased vascular resistance, cardiac output, or both
Primary Hypertension*
Definition
: Hypertension without identifiable secondary cause (essential hypertension).
Etiology
:
Genetic factors
Environmental factors (diet, lifestyle)
Renal sodium handling, RAAS activation
Mechanism
:
Increased vascular resistance, cardiac output, or both
Secondary Hypertension*
Definition
: Hypertension caused by an underlying condition.
Common Causes
:
Renal artery stenosis
Hyperaldosteronism
Pheochromocytoma
Cushing's syndrome
Coarctation of the aorta
Sleep apnea
Treatment of Essential Hypertension*
Lifestyle Changes
:
Diet (low salt, DASH diet)
Exercise
Weight loss
Alcohol reduction
Stress management
Pharmacological Treatments
:
Diuretics
: Reduce fluid volume and blood pressure
ACE Inhibitors/ARBs
: Block RAAS activation
Calcium Channel Blockers
: Reduce vascular resistance
Beta-blockers
: Reduce cardiac output
Alpha-blockers
: Lower vascular tone
Monitor and Adjust
:
Blood pressure monitoring
Medication titration