6 Principles of Pharmacology - Hypertension & its Pharmacological Management
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Course
Pharmacology
Institution
Pharmacology
The object of the course is to teach students an approach to the study of pharmacologic agents. It is not intended to be a review of the pharmacopoeia. The focus is on the basic principles of biophysics, biochemistry, and physiology as to the mechanisms of drug action, biodistribution and metabolis...
Harvard-MIT Division of Health Sciences and Technology
HST.151: Principles of Pharmocology
Instructor: Prof. Keith Baker
1
Hypertension
& its Pharmacological Management
Keith Baker, M.D., Ph.D.
Department of Anesthesia and Critical Care, MGH
HST 151 – Spring 2005
What constitutes “hypertension?”
Systolic (mmHg) Diastolic (mmHg)
Normal <120 AND <80
Pre-hypertension 120-139 OR 80-89
Stage I (moderate) 140-159 OR 90-99
Stage II (severe) >160 OR >100
Hypertensive emergencies (malignant hypertension) are defined as severe hypertension
coupled with acute end-stage organ damage.
How common is hypertension?
Hypertension effects approximately 25% of the adult American population.
What are signs or symptoms of hypertension?
There are usually no symptoms or signs of hypertension, and thus it is called the “silent
killer”. Since humans are completely unaware of excessive blood pressure, it is only through
measurements that it becomes detected. The exception is malignant hypertension, which
can cause headache, congestive heart failure, stroke, seizure, papilledema, renal failure and
anuria.
What are consequences of long-standing hypertension?
Long-standing hypertension causes accelerated atherosclerosis, which in turns leads to all of
the biological fallout of this disease. Some consequences include: stroke, coronary artery
disease, myocardial infarction, aneurysmal and occlusive aortic disease. Long-standing
hypertension also causes the heart to remodel and undergo a process of hypertrophy (left
ventricular hypertrophy or LVH). Hypertrophy can lead to diastolic dysfunction, which can
lead to congestive heart failure (CHF) since the heart is too stiff to relax properly. (This will
be covered in more detail in the next lecture.) The stiffened heart requires elevated filling
pressures, and this can worsen the dysfunction. Long-standing hypertension can also cause
the heart to dilate and lose its ability to pump during systole (systolic congestive heart
failure). Lastly, the kidneys are injured by long-standing hypertension and this is a significant
cause of renal failure in the U.S.
What causes hypertension?
Over 90% of hypertension in the U.S. is “essential” or idiopathic hypertension, i.e., without
an identifiable cause. About 10% of hypertension is secondary to some identifiable cause
such as steroids, renal vascular disease, renal parenchymal disease, pregnancy related,
pheochromocytoma, Cushing’s syndrome, coarctation of the aorta or primary
hyperaldosteronism to name a few.
, 2
The physiological framework for understanding hypertension: Ventriculo-arterial coupling
ESPVR = Emax = Es
Pressure Ea
3 SV
ESP 2
EDPVR
1
4
LVEDP
LVEDV
Volume
Key:
1 = End diastole, just prior to LV contraction. The pressure at 1 is the left ventricular end
diastolic pressure (LVEDP) and the volume is the left ventricular end diastolic volume
(LVEDV)
(1 to 2 = isovolemic contraction)
2 = Opening of the aortic valve and beginning of ejection into the aorta
(2 to 3 is the volume ejected from the LV into the aorta which is the stroke volume
(SV))
3 = End systole. The pressure at 3 is known as the end-systolic pressure (ESP). The aortic
valve shuts just after 3.
(3 to 4 is isovolumic relaxation)
4 = Beginning of passive diastolic filling.
4 to 1 is diastolic filling along the dotted curve. This dotted curve is the end-diastolic
pressure volume relation (EDPVR).
ESPVR = End-systolic pressure volume relation. This also called Emax or Es which stand for
maximal elastance or elastance at end-systole, respectively. This characterizes the
strength of the LV irrespective of the systolic load it faces.
Ea = Effective arterial elastance. This is characterizes the arterial tree and the load it presents
to the LV during systole. Ea is primarily determined by arterial resistance but arterial
compliance effects it too.
Ea and ESPVR “Couple” to exactly determine the stroke volume. In essence, the volume
lost by one chamber is exactly equal to the volume gained by the other. The
elastance of each chamber (heart and vascular tree) determines the pressure. The
exact systolic and diastolic pressures that obtain are dependent on arterial
properties (Ea), ventricular properties (ESPVR) and the filling state (LVEDV).
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