Hypertension

Report
Hypertension
Mike Clark, M.D.
• Hypotension – blood pressure less than
90/60mmg or MAP of 60mmg or less
• Hypertension – blood pressure of 140/90 or
greater
• Primary Hypertension – also called Essential
Hypertension - no actual cause can be
identified for this type of hypertension (90 –
95% of patients have this type)
• Secondary Hypertension – a cause can be
identified
Symptoms
• General no symptoms
• Sometimes with accelerated there are
headaches, somnolence, confusion, visual
disturbances, and nausea and vomiting.
In Primary Hypertension there are no direct
causes, there are many risk factors such as
sedentary lifestyle, obesity (more than 85% of
cases occur in those with a body mass index
greater than 25), salt (sodium) sensitivity,
alcohol intake, and vitamin D deficiency. It is
also related to aging and to some inherited
genetic mutations. Family history increases
the risk of developing hypertension.
Secondary hypertension is by definition
results from an identifiable cause. This type is
important to recognize since its treated
differently than essential type by treating the
underlying cause.
• Adrenal
Cortex (cortisol, aldosterone)
Medulla (increased epinephrine and
norepinephrine)
• Renal
• Cardiac
Hypertension Workup
• The workup attempts to find if the
hypertension is primary or secondary. If
secondary, then the type of secondary is
sought.
•
•
•
•
•
History
Physical Exam (Cardiac exam)
Lab Test (Urine and Blood)
EKG
Radiology – chest other studies
The cause of hypertension is caused by some change in
a component of MAP. Many times that component is
not found – thus primary hypertension.
MAP = CO x SVR
• CO = HR x SV
• SV = EDV – ESV
• (EDV concerned with blood volume and ESV
concerned more with inotropic effect)
• SVR = ∑R₁ + R₂ + 1/R₃ + 1/R₄ …..
• R = 8ŋL/∏r⁴
• In order to live – the body compensates by
increasing the actions of the organs not
affected (homeostasis – negative feedback)
Lifestyle activities that decrease hypertension
• Weight reduction and regular aerobic exercise (e.g., walking) are
recommended as the first steps in treating mild to moderate
hypertension. Regular exercise improves blood flow and helps to reduce
resting heart rate and blood pressure.
• Reducing dietary sugar intake.
• Reducing sodium (salt) in the diet may be effective: It decreases blood
pressure in about 33% of people (see above). Many people use a salt
substitute to reduce their salt intake.
• Additional dietary changes beneficial to reducing blood pressure includes
the DASH diet (dietary approaches to stop hypertension), which is rich in
fruits and vegetables and low-fat or fat-free dairy foods.
• Discontinuing tobacco use and alcohol consumption has been shown to
lower blood pressure. Note that coffee drinking (caffeine ingestion) also
increases blood pressure transiently but does not produce chronic
hypertension.
• Reducing stress, for example with relaxation therapy, such as meditation
and other mind-body relaxation techniques, by reducing environmental
stress such as high sound levels and over-illumination can be an additional
method of ameliorating hypertension.
Medications
•
•
•
•
•
•
Diuretics
Calcium Channel Blockers
Angiotensin Converting Enzyme Inhibitors
Direct Renin Inhibitors (Aliskiren)
Alpha Blockers
Beta Blockers
•
•
•
•
•
•
•
•
•
•
Diuretics
Potassium-sparing diuretics
These are diuretics which do not promote the secretion of potassium into the urine;
thus, potassium is spared and not lost as much as in other diuretics. The term
"potassium-sparing" refers to an effect rather than a mechanism or location;
nonetheless, the term almost always refers to two specific classes that have their effect
at similar locations:
Aldosterone antagonists: spironolactone, which is a competitive antagonist of
aldosterone. Aldosterone normally adds sodium channels in the principal cells of the
collecting duct and late distal tubule of the nephron. Spironolactone prevents
aldosterone from entering the principal cells, preventing sodium reabsorption. A similar
agent is potassium canreonate.
Epithelial sodium channel blockers: amiloride and triamterene.
Calcium-sparing diuretics
The term "calcium-sparing diuretic" is sometimes used to identify agents that result in a
relatively low rate of excretion of calcium.
The reduced concentration of calcium in the urine can lead to an increased rate of
calcium in serum. The sparing effect on calcium can be beneficial in hypocalcemia, or
unwanted in hypercalcemia.
The thiazides and potassium-sparing diuretics are considered to be calcium-sparing
diuretics
Osmotic diuretics
Compounds such as mannitol are filtered in the glomerulus, but cannot be reabsorbed.
Their presence leads to an increase in the osmolarity of the filtrate. To maintain osmotic
balance, water is retained in the urine.
Figure 9.27
Classes of Calcium Channel Blockers
Dihydropyridine calcium channel blockers are often used to reduce
systemic vascular resistance "-dipine".
Amlodipine (Norvasc)
Nifedipine (Procardia, Adalat)
Phenylalkylamine
Phenylalkylamine calcium channel blockers are relatively selective for
myocardium, reduce myocardial oxygen demand and reverse coronary
vasospasm, and are often used to treat angina. They have minimal
vasodilatory effects compared with dihydropyridines and therefore cause
less reflex tachycardia, making it appealing for treatment of angina.
Therefore, as vasodilation is minimal with the phenylalkylamines, the
major mechanism of action is causing negative inotropy.
Phenylalkylamines are thought to access calcium channels from the
intracellular side, although the evidence is somewhat mixed.
Verapamil (Calan, Isoptin)
Gallopamil (Procorum, D600
Benzothiazepine
Benzothiazepine calcium channel blockers are an intermediate class between
phenylalkylamine and dihydropyridines in their selectivity for vascular calcium channels.
By having both cardiac depressant and vasodilator actions, benzothiazepines are able to
reduce arterial pressure without producing the same degree of reflex cardiac
stimulation caused by dihydropyridines.
Diltiazem (Cardizem)
Angiotensin Converting Enzyme Inhibitor
ACE inhibitors or angiotensin-converting enzyme inhibitors, are a
group of pharmaceuticals that are used primarily in treatment of
hypertension and congestive heart failure, in some cases as the
drugs of first choice.
ACE inhibitors can be divided into three groups based on their
molecular structure:
Sulfhydryl-containing agents
Captopril (trade name Capoten), the first ACE inhibitor
Zofenopril
Dicarboxylate-containing agents
This is the largest group, including:
Lisinopril (Lisodur/Lopril/Novatec/Prinivil/Zestril)
Benazepril (Lotensin)
Phosphonate-containing agents
Fosinopril (Monopril) is the only member of this group
Alpha Blockers
•
•
•
•
•
•
•
•
•
Classification
α1 blockers or antagonists act at α1-adrenoceptors
α2 blockers or antagonists - act at α2-adrenoceptors
When the term "alpha blocker" is used without further
qualification, it sometimes refers to α1 blockers, and
sometimes refers to agents that act at both types of
receptors.
Non-selective α-adrenergic blockers include:
Phenoxybenzamine
Phentolamine
The agents carvedilol and labetalol are both α- and βblockers.
Alpha 2 Blockers used to treat depression
Beta Blockers
•
•
•
•
•
•
•
•
•
β1-Selective agents
Acebutolol (has intrinsic sympathomimetic activity)
Atenolol
Betaxolol
Bisoprolol
Celiprolol
Esmolol
β2-Selective agents
Butaxamine(weak α-adrenergic agonist activity) - No common clinical utility, used in experimental
situations.
•
•
•
•
•
•
•
•
•
•
•
Non-selective agents
Alprenolol
Bucindolol
Carteolol
Carvedilol (has additional α-blocking activity)
Labetalol (has additional α-blocking activity)
Nadolol
Penbutolol (has intrinsic sympathomimetic activity)
Pindolol (has intrinsic sympathomimetic activity)
Propranolol
Timolol

similar documents