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CARDIOLOGY: Hypertension/Hypotension For pts with HTN, 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. st ACE inhibitors are the 1 line agent for HTN in pts with diabetes, chronic kidney disease, and CHF. st Beta blockers such as atenolol are indicated as 1 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. •
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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 certai n pressure that is dumped by elastic elas tic properties of t he aorta and major art eries. 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 duri ng the cardiac cycle also als o decreases. As a result of in creased arterial rigidi ty, 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. 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 t hat 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.
CARDIOLOGY: Hypertension/Hypotension For pts with HTN, 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. st ACE inhibitors are the 1 line agent for HTN in pts with diabetes, chronic kidney disease, and CHF. st Beta blockers such as atenolol are indicated as 1 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. •
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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 certai n pressure that is dumped by elastic elas tic properties of t he aorta and major art eries. 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 duri ng the cardiac cycle also als o decreases. As a result of in creased arterial rigidi ty, 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. 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 t hat 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 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 vasodil ating properties . They are also metab olically neutral, n ot affecting plasm a lipid profile. profil e. Beta blockers can worsen the symptoms of peripheral vascular disease. When pts have longstanding HTN HTN,, they can develop diastolic dysfunction (impaired ventricular relaxation) and then develop LV failure. They can get paroxysmal nocturnal dyspnea. Nitroglycerin 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 alleviat ing symptoms. sympto ms. 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 s ensitive to high hig h BP, that’s why wh y the values of s ystolic BP for these t hese pts should shoul d 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 Statins 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 includ ing 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 •
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antihypertensive therapy. When the BP is in the range of 140-159/90-99 (stage I HTN), single drug therapy should be attempted. Hydrochlorothiazide Hydrochloroth iazide 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; 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
Premature ventricular complexes: they have a wide QRS (>120msec), bizarre morphology, and compensatory pause. They can be seen in normal individuals, but are more common in patients with cardiac pathology. They often occur with increased frequency following a myocardial infarction. Though numerous PVC’s may indicate a worse prognosis, suppressing PVC’s with anti-arrhythmic meds has actually been shown to worsen survival . No tx is indicated if the patient is asymptomatic . nd Beta blockers are first-line therapy for symptomatic patients. Amiodarone is considered 2 line therapy for symptomatic PVC’s.
when a pt experiences recurrent vt , the first thing to do after stabilizing the pt is to search for an underlying cause. diuretics commonly cause cause hypokalemia and hypomagnesemia. hypomagnesem ia. if uncorrected these both can lead to v -tach. furthermore, hypok alemia potentiates potentiat es side efx of dig oxin, which includes in cludes arrhythmias such as v-tach. therefore, ordering serum electrolytes and serum dig (if pt is on digoxin) is a reasonable approach. In digitalis toxicity, the most specific arrhythmia for digitalis is atrial tachycardia with AV block . Digitalis can increase ectopy in the atria or ventricles, which can lead to atrial tachycardia. It is distinguished from atrial flutter by its somewhat slower atrial rate ( 150-250 bpm as opposed to 250-350 bpm). P-waves are present, but may appear different from the p-wavs normally seen when conduction originates in the SA node. In atrial tachycardia, the closer the ectopic focus is to the SA node, the closer the resemblance of its p-waves to normal p-waves originating from the SA node. In addition to causing ectopic rhythms, digitalis can also increase vagal tone and decrease conduction through the AV node, potentially causing AV block . Since it is rare for both ectopy and AV block to occur at the same time, when they do, the combination is fairly specific for d digitalis toxicity. Amiodarone : has many toxic effects. It can cause hypothyroidism . Thus pts should have their TSH followed regularly.TSH should also be checked before initiating treatment. It can also cause lung fibrosis and liver toxicity, and pts require regular assessments of pulmonary function and liver enzyme concentrations as well. Digoxin can cause nausea, vomiting, diarrhea, blurry yellow halo vision, and arrhythmias. Meto-prolol can cause impotence, bradycardia, and AV node blockade. Hydral-azine can cause salt retention, reflex tachycardia, and a lupus-like syndrome. Paroxysmal supraventricular tachycardia (PSVT) is the m.c paroxysmal tachycardia in people without structural heart disease . Attacks begin abruptly and are characterized by heart rates between 160 - 220 bpm. The m.c mechanism underlying PSVT is re-entry into the AV node. The goal of mechanical and medical therapy is to decrease AV node conductivity. vagal maneuvers, such as Valsalva, carotid sinus massage, and immersion in cold water increase vagal tone and decrease conduction through the AV node. This slows the HR and can often break the rhythm. Adenosine is a very short-acting AV nodal blocker that is often used as well. Vagal maneuvers do decrease SA node automatism, but SA node automatism is not the underlying problem in PSVT. In most cases, re-entrant pathways through the AV node are responsible. Thus, AV node suppression, not SA node suppression, will treat PSVT.
In a witnessed cardiac arrest, defibrillation within the first 4-5 minutes is of critical importance. For unwitnessed cardiac arrests, or in cases in which the defibrillator is not available within 5 minutes of cardiac arrest, a 2 minute trial of CPR prior to defibrillation improves survival.
