Cardiovascular
[HYPERTENSION]
Introduction
Hypertension is defined by a systolic BP > 140 or a diastolic >
90. HTN is often an asymptomatic, chronic, age-related
condition that worsens and contributes to atherosclerotic
disease. In essential hypertension (primary hypertension) the
cause is idiopathic and independent of any one given risk
factor. This must be differentiated from secondary
hypertension - hypertension attributable to some hormonal,
structural, or metabolic condition. Essential is by far the most
common but other causes must be investigated.
Diagnosis
In order to diagnose hypertension there must be two blood
pressures taken at separate office visits that are greater than
140/90. Normal is 120/80. Pay attention to the severity/stage of
hypertension. Remember the “20, 10, symptom rule”. Start at
120/80, then add 20 to the systolic and 10 to the diastolic to
reach the next stage. Once at 180/120, the presence of end organ
damage pushes from urgency to emergency. It’s important at the
time of diagnosis to evaluate for acute end organ damage,
which’d thrust the patient into the emergent category.
Management
Treatment is dependent on the stage of hypertension. For prehypertension the renoprotective benefits of ACE/ARB doesn’t
decrease the number of events but does prevent progression of
hypertension. For stage I, diuresis is the name of the game. If
drugs are to be added, diuretics > ACE/ARBs > CCB. When it
comes to Stage II, many permutations exist with the expectation
that 2-4 medications will be required. If using β-Blockers
combined vasodilators (Carvedilol) are better than nonvasoactive (Propranolol). When using CCB be aware that
addition or increasing dose may take several days to see effect.
α-blockers (like clonidine) should be avoided until no other
options exist.
Secondary Hypertension
This is refractory hypertension caused by something. If the
kidneys are nor perfused (renovascular, CHF, cirrhosis) then
the kidney responds with an increased RAS (which means
ANGII = HTN). A primary aldosterone secreting tumor
produces aldosterone without renin. Pheochromocytoma causes
the release of catecholamines. Hyperthyroid causes an
increase in T3 metabolism. Even an isolated hypercalcemia can
cause hypertension by accelerating plaque formation. Each are
discussed in detail in other sections.
Goals
In general, the minimum goal is <140/<90. Every 20 point
systolic increase OR 10 point diastolic DOUBLES the risk of a
cardiovascular event. More stringent blood pressure control is
required for diabetics (<135/<85, some would even say
<130/<80).
Hypertension
Cavitation
Alarm Symptoms
180/120?
PO / IV
BP Control
Urgent /
Emergent
HTN
Age >20, Age <70
Refractory, ↑↑HTN
Secondary
HTN
Aldo:Renin
Renal Art U/S
CrCl
TSH
Ca
CXR
CBC
Essential
Stage
Normal
Pre-HTN
Stage I
Stage II
Urgency
Emergency
SYS
DIA
120
80
130
90
140
100
160
110
180
120
Alarm Sxs
Initial Tx
?ARB?
ARB
Thiazide > ACE > CCB
Comorbid Specific
PO Meds (Hydralazine)
IV Meds (Labetalol)
Alarm Sx = Stroke, MI, Papilledema, Proteinuria, ARF,
eclampsia, aortic dissection
Condition
CAD (pre-MI)
Angina
Post MI
CVA PPX
DM
CKD
Option
CCB + ACE > β-Blocker + Diuretic
β-Blocker
β-Blocker + ACE
ACE
ACE
ACE + Others
CCB = Calcium Channel Blocker = Amlodipine
β-Blockers = Propranolol, Labetalol, Carvedilol
ACE/ARB = Lisinopril, Captopril, Losartan, Candesartan
Type
Renovascular
History
DM or glomerulonephritis
ARF induced by ACE/ARB
Renal Bruit, Hypo K
Pheochromocytoma
Hyperaldo
Pallor, Palpitations, Pain,
Perspiration, Pressure
Refractory HTN or
HTN and HypoK
Weight Loss, Sweating,
Heat intolerance,
Palpitation,
Polyuria, AMS, “moans,
groans, bones, kidney
stones”
Hyperthyroid
Hypercalcemia
Workup
CrCl
BMP
Aldo:Renin < 10
U/S Renal Artery
24-Hr Urinary
metanephrines, CT
Aldo:Renin > 20
CT Pelvis
TSH, Free T4
Free Ca
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