CARDIOLOGY:
Hypertension/Hypotension
For pts with HTN, in the absence of a specific indication or contraindication, diuretics and beta
blockers are still recommended as the initial drug treatment.
- diabetics and pts with reduced lv systolic dysfunction should always be started with an aceinhibitor first.
- post-mi patients should be on a beta blocker and an ace inhibitor..
- studies have shown that black patients respond better to diuretics and calcium channel
blockers. - Hydralazine should not be used as a first-line therapy for HTN because it requires up to 4 times
daily dosing. - ACE inhibitors are the 1st
line agent for HTN in pts with diabetes, chronic kidney disease, and
CHF. - Beta blockers such as atenolol are indicated as 1st
line antihypertensive in pts with angina,
status post MI, or low ejection fraction. - If they have intermittent claudication and other stenotic issues throughout their body, the best
initial choice for tx of HTN in this pt seems to be a dihydropyridine calcium channel blockers,
ie amlodipine. They are also metabolically neutral, not affecting plasma lipid profile.
Beta blockers can worsen the symptoms of peripheral vascular disease - In pts with benign essential tremors use propranolol as anti hypertensive
- In pts with aortic dissection, lower the BP using Beta Blockers. Don’t use vasodilators like
hydralazine,CCBs,Nitrates etc because they cause reflex tachycardia. - Pt with ANGINA and HTN, give Beta blockers. . If the effect of a beta blocker is not
satisfactory, a nitrate can be added to the regimen.
Isolated systolic HTN is an important cause of AHN in elderly patients. The mechanism leading to this is
believed to be decreased elasticity of the arterial wall, which leads to an increased systolic BP, without
concurrent increase (and even decrease) in diastolic BP. Normally during systole, the heart ejects the
blood under a certain pressure that is dumped by elastic properties of the aorta and major arteries. Then,
this elastic recoil of the arterial wall contributes the diastolic flow of the blood and diastolic pressure.
When elastic properties of the arterial wall diminish and arteries beome more rigid, this “dumping” of
pressure changes during the cardiac cycle also decreases. As a result of increased arterial rigidity,
patients with ISH have a widened pulse pressure (the difference between systolic and diastolic pressure).
Widened pulse pressure was recently recognized as an important cardiovascular risk factor.
Therefore it should be treated appropriately, in spite of the fact that diastolic pressure is not
elevated sometimes. HCTZ is considered to be the drug of choice for this condition.
Peripheral artery disease.
Measurement of the ankle-brachial index (ABI) is the first step in diagnosing PAD. The ABI is
calculated by dividing the systolic blood pressure obtained by Doppler in the posterior tibial and dorsalis
pedis arteries by that in the brachial artery. Ratios of 1 to 1.3 are considered normal. An ABI less than
0.9 is highly sensitive and specific for greater than 50% occlusion in a major vessel. ABI less than 0.4
is consistent with limb ischemia. After PAD is diagnosed by ABI, a number of different imaging studies
may be performed to more accurately identify the occluded vessel.
In pts with HTN, look at other symptoms. If they have intermittent claudicating that significantly restricts
their daily activities and other stenotic issues throughout their body, the best initial choice for tx of HTN
in this pt seems to be a dihydropyridine calcium channel blockers, ie amlodipine. They have a good
peripheral vasodilating properties .They are also metabolically neutral, not affecting plasma lipid profile.
Beta blockers can worsen the symptoms of peripheral vascular disease.
When pts have longstanding HTN, they can develop diastolic dysfunction (impaired ventricular
relaxation) and then develop LV failure. They can get paroxysmal nocturnal dyspnea. Nitroglycerin,
either IV, sublingual, or topical, relieves the dyspnea and tachycardia associated with cardiogenic
pulmonary edema by rapidly reducing preload. Stuies have suggested that it works quicker than
morphine or loop diuretics. NTG is not part of the long-term management for patients with heart failure
but can be beneficial in acutely alleviating symptoms. It should be cautiously in pts with hypotension.
Beyond NTG, loop diuretics are the mainstay of therapy for decompensate heart failure and principally
work by reducing total body volume.
Beta blockers are relatively contraindicated in pts with obstructive lung disease such as asthma or COPD
but can be used in restrictive lung disease.
In systemic HTN, lifestyle modification can help. Weight loss is the most beneficial lifestyle intervention
for obese individuals. Every 10kg reduction in weight can decrease the systolic blood pressure by 5-20
mmHG.
Regular aerobic exercise (at least 30mins per day on most days of the week) can decrease systolic BP by
4-9.
Smoking will not significantly decrease BP but will markedly decrease a pts overall cardiovascular risk.
Improved glycemic control will decrease the risk of developing micro vascular disease (neuropathy,
nephropathy, and retinopathy). But it will not improve BP control, however.
Limiting alcohol ocnsumption to no more than 2 drinks per day for a man or 1 drink per day for a
woman will decrease systolic BP by 2-4mmHG.
Restricting the daily sodium intake to no more than 2.4g daily will decrease the systolic BP by 2-8mmHg.
Traditionally a goal blood pressure is considered to be below 140/90 mmHg. But it is recently recognized
that BP needs more tight control in diabetics and patients with chronic renal failure. These 2 groups of
pts are especially sensitive to high BP, that’s why the values of systolic BP for these pts should be kept
lower than 130mmHG and diastolic BP lower than 80 mmHG to prevent end organ damage.
Statins are known to cause increased liver enzymes and sympathy. They inhibit HMG-CoA reductase, a
rate-limiting enzyme in the synthesis of cholesterol that converts HMG-CoA to mevalonate.
Mevalonate is used not only for the synthesis of cholesterol, but also for the production of several other
products including dolichol and CoQ10. Reduced CoQ10 production has been implicated in the
pathogenesis of statin-induced myopathy; therefore the decrease in the synthesis of such products
may be responsible for some adverse effects of statin therapy.
The dx of HTN requires at least 3 separate blood pressure readings greater than 140/90 mmHg,
preferabley measured over a period of months. Once the dx is made, the goal of therapy is to maintain
BP below 140/90 in patients with uncomplicated HTN and below 130/80 in patients with DM or
renal disease. - For pts ranging from 120-139/80-89, (pre-HTN), lifestyle modification in the form of weight
loss, exercise, and decreased salt intake is recommended. - Patients with a BP in excess of 140/90 should also undergo a trial period of lifestyle
modification, and if the BP still remains elevated, then it is appropriate to initiate
antihypertensive therapy. - When the BP is in the range of 140-159/90-99 (stage I HTN), single drug therapy should be
attempted. Hydrochlorothiazide is the most common first-line agent, and like calcium channel
blockers, is particularly effective in elderly patients and blacks. - Two-drug combinations are appropriate when the BP exceeds 160/100 (stage II HTN).
Continuous (systolic and diastolic) murmur in the per umbilical area, or in the flanks, is characteristic of
renal artery stenosis; the diastolic component makes this murmur more specific, compared to the
systolic component alone. If you carefully auscultate the per umbilical area of such a pt with advanced
atherosclerosis and resistant HTN, you have a good chance to arrive at a correct dx.
Nor epinephrine has alpha-1 agonist properties which cause vasoconstriction; this property is useful
when trying to increase the blood pressure of hypotensive patients. However, in some patients with
decreased blood flow, vasoconstriction can result in ischemia and necrosis of the distal fingers and toes.
A similar phenomenon can occur in the intestines (resting in mesenteric ischemia) or kidney (causing
renal failure).
Orthostatic hypotension Defined as a postural decrease in blood pressure by 20mmHg systolic or
10mmHg diastolic (sometimes accompanied by an increase in HR) that occurs on standing. In
general, it results from insufficient constriction of resistance and capacitance blood vessels in the LE on
standing, which may be due to a defect in autonomic reflexes, decreased intravascular volume, or
meds. Some baroreceptor sensitivity is lost as a normal part of aging. Arterial stiffness, decreased
norepinephrine content of sympathetic nerve endings, and reduced sensitivity of the myocardium to
sympathetic stimulation all contribute to a tendency toward orthostatic hypotension with age.
Remember that beta blockers may worsen Peripheral vascular disease and are therefore relatively
contraindicated in some settings. The mechanism is thought to involve beta2mediated vasoconstriction
of peripheral arteries. The first step in management is to switch the metropolis to a different
antihypertensive.
Rhythm defects
Prolonged, tachysystolic atrial fibrillation causes significant left ventricular dilation and a depressed
EF. LV dysfunction results from tachycardia, neurohumoeral activation, absence of an atrial
“kick” (that accounts for up to 25% of LV end-diastolic volume), and atrial-ventricular
desynchronization. Controlling the rhythm in such patients usually improves the LV function
significantly.
Ventricular tachycardia: it is a regular, wide complex tachycardia. The most common cause of vtach is due to coronary artery disease. The best tx for a pt who has no homodynamic compromise is
loading with either lidocaine or amiodarone. Either of these 2 agents will aid in the conversion to
normal sinus rhythm. However, amiodarone has become the drug of choice.
In the presence of a ventricular tachycardia, digitalis should never be administered as the
arrhythmia can worsen. Digoxin is only used to treat atrial arrhythhmias.
Cardio version is an option for sustained v-tach with hemodynamic compromise.
IV diltiazem should not be used for ventricular arrhythmia. Its only indicated only for atrial
arrhythmias.
Carotid massage is useful for SVT (narrow complex), not for ventricular tachycardia. It has
no role in the management of ventricular tachycardia. It carries the risk of releasing emboli from the
carotid plaques to the brain and is no longer a recommended technique