The Management of Patients With Hypertension, Pt. 2
This podcast series aims to highlight the prevention, diagnosis, and treatment of patients with diseases commonly seen in internal medicine. Host, Anil Harrison, MD, discusses patient cases with residents and with prominent experts to help educate clinicians in treating patients using a multidisciplinary approach.
In this podcast, Dr Harrison and Paul Shiu, DO, discuss how to evaluate a patient with newly diagnosed hypertension, pharmacological and non-pharmacological interventions available for patients with hypertension, resistant hypertension, secondary hypertension, and more.
For more hypertension content, visit the disease state hub.
For part 1 of this 3-part podcast, click here.
Anil Harrison, MD, is the Program Director and Chair of the Internal Medicine Residency Program at the University of Central Florida and HCA Florida West Hospital (Pensacola, FL). Dr Harrison is board certified in India and the United States.
Paul Shiu, DO, is a second-year internal medicine resident at St Joseph's Medical Center (Stockton, CA).
TRANSCRIPTION:
Speaker 1:
Hello everyone and welcome to Multidisciplinary Dialogue Clinical Rounds and case reviews with your host Dr Anil Harrison, who is the program director and chair of the Internal Medicine Residency Program at the University of Central Florida and HCA Florida West Hospital in Pensacola, Florida. Today, Dr Harrison and Dr Paul Shiu will discuss the management of patients with hypertension. Dr Shu is an internal medicine resident at St. Joseph's Medical Center in Stockton, California. The views of the speakers are their own and do not reflect the views of their respective institutions or the views of Consultant 360.
Dr Paul Shiu:
Good morning folks. We're back again for part two of our hypertensive series. Last time we were talking about hypertension, specifically how we measure hypertension, the proper procedure, the indications for 24-hour automated monitoring as well as organ damage or sequelae as a result of uncontrolled hypertension, as. Dr. Harrison illustrated for us all. So Dr Harrison, how are you doing this morning?
Dr Anil Harrison:
I am doing well, Paul. Thank you.
Dr Paul Shiu:
It's a beautiful day. The birds are chirping outside. We have our hot coffee.
Dr Anil Harrison:
I think we've had too much of the coffee.
Dr Paul Shiu:
Maybe. You can hear in my voice, right? Speaking of hypertension, caffeine intake folks. All right, Dr. Harrison. Without further ado, would you please tell us how you evaluate a patient with newly diagnosed hypertension?
Dr Anil Harrison:
Yeah, absolutely, Paul. So this would include a thorough history and physical while establishing if there is a family history of hypertension in the patient. Are there any reversible causes? Could there be a secondary cause for high blood pressure? And very importantly, conduct an ASCVD risk score, taking into consideration other risk factors for cardiovascular disease. It is also important to assess if there is any end organ damage and to identify any potential barriers to lifestyle modifications for lowering a person's blood pressure. I would recommend getting some baseline labs like a CBC, a serum creatinine with a GFR, a serum sodium, and a potassium and a serum bicarb. I would also get a hemoglobin A1c, a TSH, and of course a lipid panel. I would also get a urine analysis with microscopy looking obviously for protein, RBCs, and casts. If the patient is a diabetic, I would get a spot urine albumin creatinine ratio, also called ACR.
Dr Paul Shiu:
Wait, wait, wait, wait. Would you get an electrocardiogram too?
Dr Anil Harrison:
Yes, I would, to see if the patient might have LVH or left ventricular hypertrophy or a previous silent myocardial infarction.
Dr Paul Shiu:
Okay. Now you piqued my interest. What about an echocardiogram? When would you get that?
Dr Anil Harrison:
It isn't necessary, Paul. Now I would recommend getting an echo if the EKG shows left ventricular hypertrophy or the patient might have had an MI in the past, and I would think about getting an echocardiogram if you have somebody with white coat hypertension, which is that the patient's blood pressure measured at home is normal, however it is elevated consistently in the physician's office, or while examining while doing a cardiac exam, the apex is displaced on palpation or if one hears an LVS4 or an S4 gallop on auscultation. So those would be good reasons for getting an echocardiogram.
Dr Paul Shiu:
So we already touched upon the sequelae of uncontrolled hypertension in our prior episode. So this might seem like a silly question, but have there been studies actually done, conclusive studies, which review the benefits of actually treating hypertension?
Dr Anil Harrison:
Oh, absolutely, Paul. Clinical trials suggest that antihypertensive medication therapy can be associated with up to a 40% reduction in stroke, a 25% reduction in myocardial infarction and a 50% reduction in heart failure. Also, hypertension is one of the most significant but modifiable risk factors for cardiovascular disease, stroke, end-stage kidney disease, and overall mortality. And remember, systolic blood pressure is more important than diastolic blood pressure as an independent risk factor for coronary events, heart failure, stroke, and end-stage renal disease.
Dr Paul Shiu:
So, Dr Harrison, how common is secondary hypertension and when would you consider evaluating for secondary causes of hypertension?
Dr Anil Harrison:
Absolutely. So secondary hypertension occurs in about 10% of adults with hypertension, A specific and remediable cause can be identified. Diagnostic testing for secondary causes of hypertension can be pursued if a high clinical suspicion exists following a good history, a good physical exam, and initial laboratory testing. Evaluations for secondary causes of hypertension include, say if a person has hypertension before the age of 30 or has an abrupt onset or worsening blood pressure if previously well controlled, or the patient has drug-resistant hypertension or has clinical features indicating a secondary process or has presence of target organ damage, which is disproportionate to hypertension, duration or severity. Similarly, diastolic hypertension, especially if it occurs after the age of 65, and if you notice somebody has unprovoked or excessive hypokalemia. I would also consider looking for secondary causes for hypertension if the degree of hypertension or blood pressure does not correlate well with the findings of end organ damage.
Dr Paul Shiu:
Would you recommend taking lifestyle changes? And what exactly do you mean by that?
Dr Anil Harrison:
Yeah, so lifestyle modifications and cardiovascular risk factors should be addressed in all patients with hypertension. Several non-pharmacological interventions have been shown to have efficacy in reducing blood pressure. Evidence shows that the most efficacious interventions for blood pressure lowering effects are number one, weight loss, number two, the dietary approach to stop hypertension, which is the DASH diet, and number three, dietary sodium reduction. Having said that, weight reduction is the most efficacious, followed by sodium reduction when it comes to lifestyle modifications, although difficult to achieve a combination of lifestyle modifications such as the DASH diet combined with a low salt diet alone or in combination with weight loss, has blood pressure lowering effects that are much greater than or equal to those of a single drug therapy in patients with hypertension.
Other effective non-pharmacological interventions include potassium supplementation, preferably in your diet, increased physical activity, abstinence of or moderation in alcohol consumption, and regardless of effects on blood pressure, tobacco cessation should be encouraged given that smoking is a significant risk factor for cardiovascular disease. Studies evaluating meditation, yoga, and biofeedback had modest mixed or no consistent blood pressure-lowering effects. More data support efficacy of device-guided breathing than acupuncture among the non-invasive procedures and devices that were evaluated.
Dr Paul Shiu:
So as you alluded to Dr. Harrison, with blood pressures consistently greater than systolic of 130 and a [inaudible 00:08:15] of 80 with ASCBD score greater than 10%, and with stage two hypertension classified as blood pressures consistently increasing, how would you go about the management of hypertension?
Dr Anil Harrison:
Sure, you're absolutely right on that, Paul. The first-line medications for the management of hypertension are ACE inhibitors or ARBs, which stands for angiotensin receptor blockers, thiazide diuretics, and the dihydropyridine calcium channel blockers such as amlodipine. So those are the four first line anti-hypertensives. Beta-blockers can be considered as first-line, specially if the patient has a history of coronary artery disease or congestive heart failure. For the prevention of heart failure, initial therapy with a thiazide diuretic was more effective than a calcium channel blocker or an ACE inhibitor, and an ACE inhibitor was more effective than a calcium channel blocker.
The initial antihypertensive should include a thiazide diuretic or a calcium channel blocker. Now you can use loop diuretics. Loop diuretics are preferred in patients with symptomatic heart failure or CKD who have a GFR of less than 30. Even in the absence of edema, persistent intravascular expansion without any apparent edema can still contribute to hypertension that appears resistant to treatment. Potassium-sparing diuretics such as aldosterone receptor antagonist, spironolactone or eplerenone or epithelial sodium channel blockers such as amiloride are weaker diuretics. Additionally, short-acting amphetamine can be associated with increased mortality if used immediately after an acute MI because of profound hypotension and sympathetic activation. Finally, there may be an increased risk of myopathy if a calcium channel blocker, especially a non-dihydropyridine, is used concomitantly with a high-dose statin. We don't have enough trials comparing beta-blockers with central or peripheral acting alpha blockers, vasodilators, aldosterone, receptor antagonists, or loop diuretics to the four drug classes mentioned before.
Therefore, these drug classes are not recommended as first line therapy, but can be used in specific populations such as beta blockers for post-myocardial infarction, or if a patient has heart failure, aldosterone receptor blockers for folks who have heart failure, loop diuretics for advanced kidney disease or as an add-on for resistant hypertension. The 2017 ACC/AHA Blood Pressure Guideline recommends combination therapy with two first-line antihypertensive drugs of different classes for adults with stage two hypertension and an average of greater than 20/10 millimeters mercury above the blood pressure target, which is typically one 50 over 90 millimeters of mercury. Response to treatment should be assessed in a month. Generally, there is diminishing return in blood pressure lowering if the dose is titrated up 50 to a hundred percent of maximum. The other thing I'd like to mention is it is unlikely that increasing the dose from 50 to one hundred percent of maximum on a blood pressure medication will result in an additional greater than five-millimeter blood pressure reduction.
Dr Paul Shiu:
Sounds like a classic case of emission return. So with that being said, what are some targets for goal blood pressure control? And then we can elaborate on the terms white coat hypertension and resistant hypertension as well as any specific labs recommended when the patient is on a anti-hypertensive.
Dr Anil Harrison:
Absolutely. So the target systolic blood pressure goal for nons institutionalized ambulatory community-dwelling patients who are more than 65 years of age, should be less than 130 millimeters of mercury. The target blood pressure for patients with hypertension and diabetes or somebody who has chronic kidney disease should be less than 130 over 80. Studies evaluating meditation, yoga, and feed biofeedback, I think we've already discussed that, we've had inconsistent results with those. The prevalence of white coat hypertension is about 15 to 30%. Screening echo may also be considered to screen for left ventricular hypertrophy, the presence of which necessitates treatment with antihypertensives.
You asked about resistant hypertension. Resistant hypertension is defined as blood pressure that remains above goal despite concurrent use of three antihypertensive agents of different classes or a blood pressure at goal, but requiring four or more medications. One of these medications must be a diuretic. Now what is the prevalence? The prevalence for resistant hypertension is from two to 10% in the general population, but can be as high as 40% in folks who have chronic renal disease. Other risk factors include older age, male sex, black race, diabetes, a person who has a higher BMI. And trials support the efficacy of adding a low-dose aldosterone receptor antagonist, either spironolactone or eplerenone for the treatment of resistant hypertension. If additional agents are needed for blood pressure control or the patient is intolerant of the agents mentioned before, then using vasodilators such as hydralazine or minoxidil or alpha-blockers such as prazosin or dioxazine or even centrally acting sympathetic agonists such as clonidine could be added.
The recommendations are that kidney function and serum potassium should be assessed two to three weeks after the initiation of an ACE inhibitor or an ARB and increase in the serum creatinine of 25 to 30% is acceptable, but the dose may need to be lowered or medication discontinued if more severe the decline in kidney function is observed. In such cases, one wants to consider could this patient have bilateral renovascular disease?
Dr Paul Shiu:
So now we're talking about renovascular disease, some mention of it. Would you be able to also speak about some of the causes of secondary hypertension such as the aforementioned renovascular hypertension, primary hyperaldosteronism and pheochromocytoma?
Dr Anil Harrison:
Yeah, absolutely, Paul. So clinical suspicion might arise. You might start thinking, especially in folks who have severe hypertension after the age of 55 or who have recurrent flash pulmonary edema or who have refractory heart failure or who develop an AKI, an acute renal injury insufficiency after initiation of an ACE inhibitor or an ARB or an acute kidney insufficiency after control of blood pressure to target.
Similarly on imaging, if one notices asymmetry in the kidneys of more than a 1.5 centimeters or if one of the kidneys is less than nine centimeters should also increase the likelihood. Similarly, abrupt onset of hypertension at an age less than 35 might suggest fibromuscular dysplasia. Having said that, routine testing for renal vascular disease may not change management because as you know, recent data suggests that medical therapy may be as beneficial as invasive procedures, especially for those with atherosclerotic renal vascular disease.
Dr Paul Shiu:
Less is more, less is more. So with that being said when is less, not more? When do we need to bring out some surgical intervention, especially in the setting of renovascular hypertension?
Dr Anil Harrison:
Absolutely. So the recommendations are that if you've got stenosis that is more than 75% in one or both renal arteries or there is a greater than 50% post stenotic dilatation that suggests the diagnosis, and percutaneous angioplasty and stenting or surgical intervention include those with a short hypertension duration or with atherosclerotic renovascular disease that is refractory to optimal medical therapy, or if somebody has severe hypertension or recurrent acute flow flash pulmonary edema, or somebody develops an acute renal insufficiency follow treatment with an ACE or an ARB, or somebody who has progressive impaired kidney function thought to result from bilateral renovascular disease or unilateral stenosis affecting a solitary functioning kidney.
The other thing is that patients with advanced CKD who have a proteinuria of more than a gram in 24 hours are less likely to benefit from revascularization with primary hyperaldosteronism, aldosterone production cannot be suppressed with sodium loading is the most common cause of secondary hypertension in middle-aged adults and an important cause for resistant hypertension. And a triad of resistant hypertension, metabolic alkalosis and hypokalemia, including by the way in patients treated with lost-dose thiazide diuretics, should raise suspicion. And the recommendations are that screening is recommended if any of the following are present. Somebody who has resistant hypertension, hypokalemia, be it spontaneous, or if a person is on a diuretic. It doesn't matter.
Incidentally discovered a renal mass or somebody who has a family history of early onset hypertension or somebody who has moderately severe hypertension, which is a blood pressure greater than 160 over a hundred, or somebody who's had a stroke before the age of 40. So in those getting plasma aldosterone and a plasma renin levels, you do that because these are usually suppressed in other disorders with hypokalemia and hypertension, including pushing syndrome, syndrome of apparent mineralocorticoid, excess familial hyperaldosteronism type one and little syndrome. But in folks where you suspect primary hyperaldosteronism, the ratio of aldosterone to renin is very high and it's usually greater than 20 is to one. And after the diagnosis had confirmed, a dedicated adrenal CT should be performed to determine whether the hyperaldosteronism is caused by diffused hyperplasia as seen in about 75% of the patients and managed by an aldosterone receptor antagonist such as spironolactone versus an aldosterone-producing adenoma, which is amenable to surgical resection.
Dr Paul Shiu:
As with all good things, they must come to an end. We are concluding episode two of our hypertensive podcast. Please tune in for episode three of the hypertensive podcast series with Dr Harrison and me. We really do appreciate your support. We're about starting our second chapter, soon to be a third chapter in the coming weeks. Thank you everyone.
Dr Anil Harrison:
Thank you, Paul. Before I end, I just want to mention one thing. One of the residents asked me this question, how would you evaluate for primary hyperaldosteronism in a patient who's already taking an ACE inhibitor or an ARB? So I think in this scenario, getting a serum renin level would be helpful, because if the serum renin level is elevated, primary hyperaldosteronism can be safely ruled out. But I just wanted to mention that. Thank you everybody. Bye.
Dr Paul Shiu:
Bye-bye guys. Thank you.