Wk 2 HTN Flashcards
Renin Angiotensin Aldosterone System (RAAS)
regulates long term blood pressure and extracellular volume
Angiotensinogen
released by liver in response to low blood pressure and changes in blood volume (sodium/Na level)
-sinogen
hormones or chemicals in body
- precursor to something
LFV (serum Na) stimulates…
the KIDNEY to release RENIN which causes the liver to convert angiotensinogen to ANGIOTENSIN I
Angiotensin I travels to…
the LUNG where it is converted to ANGIOTENSIN II by ACE (angiotensin converting enzyme)
Angiotensin II acts on the…
ADRENAL GLANDS to cause release of ALDOSTERONE which causes the fluid retention to increase BP
Angiotensin II is
POTENT vasoconstrictor, tightens vascular system to increase BP
RAAS ultimately causes…
the nephron in the kidney to retain fluid and BP goes up
Decreased renal perfusion
RAAS activated
- release of renin -> liver converts angiotensinogen to angiotensin I -> angiotensin I to angiotensin II by ACE from the lungs
RAAS pathologic way
problem
- hypersensitivity to angiotensin II OR
- high secretors of renin
RAAS + stress
can elevate angiotensin II
- chronic stress stimulates renin and sets off RAAS
Arterial baroreceptors
affect BP
- receptors in the carotid sinus, aorta, and left ventricle that can sense BP, can alter BP by altering HR
- can also impact vasodilation and vasoconstriction
Vascular Autoregulation
helps maintain consistent levels of tissue perfusion
- regulates based on mean arterial pressure (MAP)
- alters the resistance (diameter) in arterioles (small vessels)
- helps keep CONSISTENT BP at the tissue levels despite changes that are occuring in other mechanisms
Normal BP
systolic = < 120
AND
diastolic = < 80
Elevated BP
systolic = 120 - 129
AND
diastolic = < 80
HTN stage 1
systolic = 130 - 139
OR
diastolic = 80 - 89
HTN stage 2
systolic = 140+
OR
diastolic = 90+
Hypertensive Crisis, consult your doctor immediately
systolic = 180+
AND/OR
diastolic = 120+
Primary hypertension
90-95% of cases in US
- also called “essential htn”
- occurs when there is NO SPECIFIC KNOWN CAUSE of HTN
- absence of underlying disease process
- idiopathic most common = no known cause
Why does primary htn occur?
Complicated interactions of genetics and the environment, and involving several neurohormonal effects that affect our
- SNS
- RAAS
- natriuretic peptides
Overactive SNS
increased HR, increased systemic vasoconstriction
Overactive RAAS
associated with remodeling of blood vessels, which can cause permanent increases in peripheral vascular resistance (target of most htn meds)
Natriuretic peptides
help control sodium excretion by the kidneys, helps with salt and water retention
- interruption in these can cause increased blood volume
Risk factors for primary HTN
smoking
excess sodium intake
sedentary lifestyle
HLD
stress
family hx + genetics
obesity
age > 60 (males at 55)
insulin resistance
high alcohol consumption
Secondary Hypertension
HTN with a known cause
- related to underlying disease or disorder
- treat the underlying cause, treats HTN
Secondary htn causes
- renal disorder/disease
- adrenocortical tumor
- adrenomedullary tumors (pheochromocytoma)
- drug induced -> oral contraceptives, corticosteroids, antihistamines, cocaine, amphetimines
S/S of HTN
NONE
“silent killer”
- must look for signs of END-ORGAN damage
End-organ damage
chest pain -> heart
headache -> brain
visual changes -> eyes
weakness/pain in the extremities -> brain/stroke
Long-term cardiac outcomes of HTN
increased left ventricular work
- hypertrophy = enlargement of the left ventricle
– due to pressure it has to exert to pump blood out and myocardial oxygen demand
- accelerated progression of atherosclerosis
- increased risk for aortic aneurysm (weakened vessel walls)
Long term kidney outcomes of HTN
primary cause of end-stage renal disease
Long term brain outcomes of HTN
higher risk for stroke, aneurysm, hemorrhage
Long term eye outcomes of HTN
retinopathy and blindness
Long term lower extremity outcomes of HTN
gangrene, intermittent claudication
Hypertensive Crisis
acute issues
- rapidly progressive hypertension in which systolic BP is > 180 AND/OR diastolic BP > 120
- occurs more commonly in those with PRIMARY HTN
2 types of hypertensive crisis
hypertensive urgency
hypertensive emergency
Hypertensive urgency
- No S/S of end-organ damage
- BP > 180/120
- treat with oral agents and GRADUALLY reduce BP
- causes: anxiety, pain, abrupt withdrawal
Hypertensive emergency
- Uncontrolled BP that leads to end-organ damage
- BP > 180/120
- symptoms of organ damage = headache, blurry vision
- can lead to stroke, brain hemorrhage, chest pain, acute coronary syndrome, heart dysfunction
- AGGRESSIVELY lower BP in minutes to hours (IV meds)
- risk of lowering BP and “bottoming out” is lower than risks of end-organ damage
Medications to treat HTN
- diuretics
- sympathetic nervous system blockers
- beta blockers
- calcium channel blockers
- vasodilators
Diuretics
potassium-sparing: mild
Thiazide (thiazide-like): mild
Loop: moderate to profound
Sympatholytics
- alpha-adrenergic blockers
- centrally acting alpha2 agonists
- beta adrenergic blockers
RAAS Blockers
- ACE inhibitors
- ARBs
- Renin Inhibitors
