Presentation is loading. Please wait.

Presentation is loading. Please wait.

Resistant and Secondary Hypertension

Similar presentations

Presentation on theme: "Resistant and Secondary Hypertension"— Presentation transcript:

1 Resistant and Secondary Hypertension
Oliver Z. Graham, MD “Hypertension Specialist” Department of Internal Medicine

2 What I am going to talk about
Why BP control is important Initial workup of newly diagnosed HTN Secondary hypertension Sleep apnea Primary Hyperaldosteronism Renal Artery Stenosis White coat HTN Tips for improving adherence Resistant hypertension and diuretic use

3 Benefits of Lowering BP
Antihypertensive therapy has been associated with: 35-40% reduction in stroke 20-25% reduction in MI 50% reduction in heart failure One of the things I want to first talk about is why we care about HTN in the first place. We are all busy cliincians, and in the setting of a hectic clinic it is easy to blow off a moderately high blood pressure value. But what I would like to reintroduce is the data with regard to HTN and hard outcomes. So here are some numbers….

4 Treating HTN – A Clear Reduction in MORTALITY
If patient with BP /90-99, (and other cardiac RF) achieving a 12 mm Hg decrease in SBP over 10 years will prevent one death for every 11 patients treated!! In the presence of CVD or target-organ damage, same tx will prevent one death for every 9 patients treated!! So lets look at the hardest endpoint available – mortality. What you can see is the following: So, in summary, as a doctor treating adults, this is one of the very most important evidence based things you can do in clinic to reduce mortality. There are very few other things – perhaps only statin use and propylactic asprin, that have this kind of compelling data to support treatment.

5 Another way of evaluating hypertension therapy is to look at the realative “bang for your buck” of treating one disease process versus another. Although there is a lot of discussion about the importance of tight glycemic control, it is helpful to refer to the literature with regard to the relative benefit glucose control provides compared to blood pressure control. This is data from the UKPDS study, one of the largest studies on the impact of glucose and blood pressure control in type 2 diabetics. They enrolled 1100 patients and followed them over 8 and a half years. What this showed was that when we compare tight glucose control, HbA1c=7% (achieved was 8.2%) vs tight blood pressure control <150/85 mmHg (achieved 144/82 mmHg) you would get a lot more bang for your buck by concentrating on blood pressure control. As you can see here, your risk of stroke, death, and microvascular complications are reduced by both intereventions, but more significantly by the blood pressure reduction. Again, looking at your hardest endpoint, that is, death, you get a 10% reduction with glucose control vs a 32% reduction with bp control. So just to state again, one could argue that your time is better spent getting someone’s blood pressure down 10 points rather than an a1C down by one point. And in most situations, blood pressure control is a lot easier.

6 A Case Study… A 55 year old Hispanic man comes to your clinic for a first visit. He recently immigrated from Mexico several years ago, he was on some medications for blood pressure previously but has not taken anything for several years. PE 5’ 8” 190 pounds BP 172/105 HR 82 What are you looking for on PE? What kind of screening labs do you order?

7 New Hypertensive Patient – The Physical Examination
Test accuracy of reading (check cuff size, check other arm, repeat office reading or home reading) “fundoscopic evaluation” Thorough exam heart/lung/JVP Auscultate for abdominal bruit (renal artery stenosis?) Femoral pulses (coarctation?) LE edema So first you want to make sure you get an accurate blood pressure. So many times someone is rushed into the triage area and the concomitant hustle and bustle leads to a falsely high BP value. My nurses are always laughing at me because I often drag the manual BP cuff with me and integrate the blood pressure into my physical examination, ensuring that the patient is relaxed and the blood pressure cuff is large enough. Its not uncommon that I get a referral for resistant hypertension solely on automated blood pressure values, and when I take the BP myself I get a normal value. Other things that are recommeded are a fundoscopic evaluation, although I can tell you with all honesty I am not skilled enough at this for it to be of any practical value. Its important to listen to the heart and lung and try to assess JVP. Listening to the belly for a bruit can help clue you into renal artery stenosis. Deminished femoral pulses can indicate coarctation, and LE edema can suggest CHF or nephrotic syndrome.

8 Diagnosis of HTN: Initial Workup
The “cheap screening for secondary hypertension” labs: Creatinine Sodium, Potassium (hyperaldosteronism) U/A (nephrotic syndrome, nephritic syndrome) Calcium (secondary hyperparathyroidism) CBC (polycythemia) UTox (CCRMC special) Consider TSH (both hyper and hypothyroidism associated with hypertension) So when you get a new hypertensive patient there are some cheap screening labs that you should probably order. They include

9 Diagnosis of HTN: Initial Workup
The “Cardiovascular Risk” labs: EKG (get as baseline + evaluate for LVH, prior MI) Lipid panel Fasting glucose Other recommended labs are not necessarily to help with the diagnosis of hypertension per se, but to assess their overall cardiovascular risk.

10 Back to case study…. Repeat SBP 182/96, Obese (BMI 35). CV/lungs WNL. No abd bruit. No edema. Na 141 K 4.2 Creat 1.2 U/A neg, except 30 protein. Spot urine protein 0.14 g/24 hours. EKG – LVH. CBC, Calcium, TSH, WNL. Utox neg. Fasting Glucose 145, HA1c 8.1 Would you do a secondary HTN workup? If so, what would you focus on?

11                                                                                  This is a nice algorithm I found in the American Acadamy of Family Practice journal. Lets walk through this algorithm:

12 Risk factors for secondary hypertension
Poor response to therapy An acute rise of BP over a previously stable value Confirmed onset of hypertension before 20 or after 50 years (need accurate hx) Age < 30 in non-obese, non-black patients with a negative family hx Stage 3 HTN (>180/110) So these are the risk factors for secondary hypertension. Put another way, if the patient as some of these clinical features, you may consider a search for a secondary cause

13 Prevalence of Secondary Causes of Hypertension
COMMON (prevalence) RARE (prevalence) Sleep Apnea (? Really Common ?) Pheochromocytoma (<0.5%) Renal Disease (1-8%) Coarctation of Aorta (<1%) Hyperaldosteronism (1.5-15%) Cushing’s Syndrome (0.5%) Renal Artery Stenosis (3-4%) Acromegaly Thyroid disease (1-3%) Carcinoid Syndrome Hypercalcemia So assuming the patient has risk factors for secondary hypertension, what kinds of things do we need to look for? This is a table that illustrates the prevalence of different types of secondary hypertension. On the left are the relatively common ailments that contribute to hypertension, on the right are the rarer conditions. When you do your assessment for secondary hypertension, I would ask that you first assess the conditions on the right, as they are much much more common. They are: Now lets talk about some of these more common causes of secondary hypertension.

14 Obstructive Sleep Apnea
In one study, 83% of those with resistant HTN had sleep apnea Intervention Studies (using CPAP in pts with sleep apnea + resistant HTN): Two studies show decrease SBP 10-15 Other studies showed little or no reduction after CPAP administration BOTTOM LINE: Reasonable to screen those with resistant hypertension, especially if with risk factors (obesity, daytime somulence, apnea history) The first syndrome, and I think arguably one of the most important in terms of therapy, is Sleep apnea. It is now becoming increasingly recognized that resistant hypertension and sleep apnea are related, but how much one contributes to the other is not fully elucidated. It is, however, very very common. In fact, in one study, 83% of those with resistant hypertension had sleep apnea. Now when you look at intervention studies, that is, using CPAP in patients with sleep apnea and resistant hypertension, the results are somewhat mixed. Two studies are fairly compelling, that is, they show a decrease of systolic pressure of with CPAP treatment. Other studies, however, are not so compelling. So the bottom line is this:

15 Primary Hyperaldosteronism and Hypertension
Now the next relatively common cause of secondary hypertension is something that is not discussed that frequently, that is, primary hyperaldosteronism. I just briefly want to go into the pathophysiology for a moment because it is a little confusing. Basically in primary hyperaldo you get excessive secretion of aldosterone from an adrenal tumor or hyperplasia. This leads to salt retention which in turn increases one’s blood pressure Primary hyperaldo – excessive secretion aldosterone from tumor or Hyperplasia  salt retention  increase blood pressure

16 Primary Hyperaldosteronism
May be present in % those with resistant hypertension Etiologies Adrenal adenoma Bilateral adrenal hyperplasia Clinical features Hypokalemia (although normal K in 30%) Hypernatremia Metabolic alkalosis Workup – AM plasma renin and aldosterone levels, go to Uptodate Now primary hyperaldosteronism may be common or rare, depending on the study you look at. Its described in the literature as being present in % of those with resistant hypertension. The etiologies include an adrenal adenoma or bilateral adrenal hyperplasia. The most consistant clinical feature is hypokalemia, although recent data suggests that folks can have a normal potassium in 30% of the time. Other clinical features include hypernatremia and metabolic alkalosis. One would start the workup with an Am plasma renin and aldosterone level, then what I do is go to uptodate, because where to go from there is pretty complicated and they have a good algorithm.

17 Hypertension and renal artery stenosis
less blood flow Now lets talk about the pathophis of renal artery stenosis for a moment. This is the same graphic, with my careful addition. First what happens is that you get decreased blood to the kidney Decreased blood to kidney  kidney “senses” diminished BP Activation renin/angiotension system  vasoconstriction Aldosterone secretion  salt retention

18 Renal Artery Stenosis – Etiologies
Fibromuscular dysplasia (young women) Atherosclerotic (HTN/DM/lipids/FH etc) Suspect in resistant hypertension and: Elevation Cr with admin ACE/ARB Unilateral small kidney on imaging Abdominal bruit Repeated episodes flash pulmonary edema Acute rise in BP over previously stable value Now the thing to keep in mind with renal artery stenosis is that there are essentially two major etiologies for this condition, and its very important to make the clinical distinction because the treatment between the two are different. The first, and less common, is fibromuscluar displasia. Typically the syndrome for this would be a young woman who is otherwise well and presents with unexplained hypertension. The more common etiology is athrosclerosis, and that occurs in those with traditional risk factors for vascular disease like HTN/diabetes etc. The time when you suspect it would be in the following clinical situations:

19 Renal Artery Stenosis and Resistant HTN – Does Dx/Intervention matter?
RAS from fibromuscular dysplasia responds well to angioplasty (HTN improved in 20-80%) RAS from atherosclerosis: sustained response to intervention “unusual” (lesions usually too diffuse) NEJM study: pts randomized to angioplasty vs med tx. No difference in BP control or renal insufficiency noted at 1 year No good studies using angioplasty + stents Complications from intervention include atheroembolism  dialysis Now the next question becomes, if you identify it, does it really make any difference in treatment? The answer is – it depends on what the etiology of the stenosis is. If the stenosis is from dysplasia, it is usually from a focal lesion which is easily angioplastied. And the results from intervention in dysplasia are not bad – an improvement in blood pressure in 20-80% This is in contrast to RAS from atherosclerosis. Looking at the trials, review articles describe that a sustained response to intervention is “unusual” and that is because the lesions are usually too diffuse. For example, in one NEJM study This is still an open question and a moving target, especially with stents, and literature is difficult to interpret. But an important thing to keep in mind is that it is a procedure that is not without its complications, one of the most serious would be flicking off a plaque while angioplasting, that goes to the kidney and leads to renal failure and dialysis.

20 Renal Artery Stenosis and Resistant HTN – Does Dx/Intervention matter?
BOTTOM LINE: If you suspect RAS, people who may benefit from intervention: Young women (may have dysplasia) Suspicion for atherosclerotic RAS + any of the following: HTN not responsive to treatment, esp if severely elevated over stable value Progressive renal failure Repeated episodes flash pulmonary edema Age < 60 Workup: At our institution, order MRA So the central issue is if you clinically suspect RAS whether you should do an evaluation at all. And that is where I differ from the guidelines. The guidelines say that if you think this may be going on you get an MRA and ask questions later. I would offer that you would only look for RAS in those who you would consider sending for a intervention, as you don’t want to send someone to an intervention with potential morbidity and no efficacius benefit. The folks that you would strongly consider workup would be the following: Young women…

21 Screening for the rare stuff – Reasonable to go by Hx/PE
Pheochromocytoma Paroxysmal elevations in BP, HA, Palpitations, sweating Cushings disease Moon facies, central obesity, striae, inc glucose Coarctation of aorta Hypertension in arms but not legs, decreased femoral pulse, abnl murmur/bruits Acromegaly Looks like they have acromegaly Now what about the rare stuff? In uptodate they recommend routine screening for pheochromocytoma in all those with resistant hypertension. That is not evidence based, but one would clearly screen if you had Cushings disease would be suggested by Coarctation


23 Height: 5’11” Weight: 129 My BMI, circa 1991: 17

24 Back to our patient… His blood pressure is 182/96.
How many agents would you start him on?

25 “The Rule of 10’s” Each BP med will reduce SBP by about 10 mmHg
Per JNC recommendations: If BP > 20/10 of goal, consider initial treatment with TWO agents (one should probably be diuretic) There is a helpful concept with regard to hypertension management called the “rule of 10’s” what that means is that each So because of that, the JNC recommends that…

26 Case continued So you start the patient on lisinopril 10 mg daily + HCTZ 25 daily When should you check his potassium and creatinine?

27 Recommended intervals for Monitoring Creatinine/K in ACE/ARB tx
GFR > 60 GFR 30-59 GFR < 30 After initiation or change of ACE/ARB dose 4-12 weeks 2-4 weeks <2 weeks After dose is stable 6-12 months 3-6 months 1-3 months

28 Back to our patient… A sleep study was ordered given the patient’s obesity. He comes back for followup, and is on HCTZ 25 daily, Lisinopril 20 daily. His BP in office is 174/96 What are some other features that may be contributing to the patient’s hypertension?

29 White Coat Hypertension
May be responsible for 30% those with resistant hypertension Appears that BP values obtained at home correlate better with target organ involvement If a consideration – have patient check BP at home, have therapy target those values A very common condition is that of white coat hypertension, and it may be responsible for up to 30% of those with resistant hypertension. One thing to keep in mind is that ….. So because of this, if you suspect the patient has white coat HTN,

30 Medication Adherence – Possibly helpful tips
Appropriately educate patient/family about benefits of good BP control Have patient check BP at home periodically and bring in logbook Use “Rule of 10’s” to guide expectations Tell patient: “You will likely need 2 or more meds to get your BP under control” Adherence is a huge issue, especially in our population. There are no silver bullets to help magically make all hypertensive patients take their medicine, but I do have some tips which could possibly be helpful. Whenever I start a patient on blood pressure medicines, I try to probe them for their understanding of why blood pressure control is important. Many times they say stuff like “I take medicines because doctors tell me to” If this is the case, then talking to them about the reasons for treatment may improve adherence. Another thing to do is to get them involved in their care by getting them a BP machine at home and bring in a logbook, much the same as diabetes. A third suggestion is to use the rule of 10s to guide expectations. That is, if they are diabetic with a BP of 170, you should tell them at the onset that they will need to be on at least 3 agents to get their BP under control.

31 Medication Adherence – Possibly helpful tips
Write on prescription: “take 1 tablet daily to get blood pressure less than 140/90” Use fixed-dose combinations Benazepril/HCTZ combo on both CCHP and MediCal formularies Another way to get patients involved in their care is to get them to understand the goals of therapy. For this reason, a lot of times I write on the prescription: Another underutilized therapy which has been shown to improve adherence is fixed dose combinations. For example, Benazapril/HCTZ combination pills are on both CCHP and medical formularies

32 Other things that can increase Blood Pressure
Medications NSAIDS (inc SBP by approx 4 mmHg) Cocaine, Amphetamines Phenylephrine Anabolic Steroids Erythropoietin Oral Contraceptives Excessive EtOH (>3-4 drinks/day) High Salt Diet Obesity And these are some other things that can lead to resistant hypertension


34 Another patient comes in….
A 65 YO woman is seen in your clinic for f/u of longstanding HTN. She is on HCTZ 12.5 mg, Toprol XL 200 mg daily, amlodipine 10 daily, lisinopril 40 daily. Her BP is 162/94. Creat 1.4 (GFR 45), no protienuria. Utox neg. She emphatically states that she takes her medications as directed. What is your next step in managing her HTN?

35 Diuretics – Cornerstone of HTN therapy
Most patients with resistant hypertension have inappropriate sodium/fluid retention  EFFECTIVE DIURETIC THERAPY ESSENTIAL for HTN control 60% of those with resistant HTN improve BP by add/increasing diuretic therapy So when you have this patient in mind, it is important to recognize that most patients…. In fact, studies show that 60% of those with reistant HTN….

36 What is the proper HCTZ dose?
In uncomplicated patients without resistant HTN or renal disease, no real benefit in HTN control with increase from 12.5 vs 25/50 daily Those with resistant HTN and normal renal function – may need increase in HCTZ 12.5  25  50 So the next question becomes what is the proper dose of HCTZ. In most patients with controlled hypertension, studies show that 12.5 mg daily is fine. ON the other hand, if someone has normal renal function but resistant hypertension, one could consider increasing the HCTZ to 25 or 50 daily

37 What about resistant HTN with GFR < 50?
HCTZ may not be not effective Options: Substitiute another thiazide: Metolazone 2.5 – 10 daily Substitute for loop diuretic: Lasix BID or Bumex BID (Dosed BID because of short half life) Toresemide 2.5 – 5 daily (longer half life, more expensive) Now if you have renal insuffiecincy, it may be that HCTZ will not be effective at all as a diuretic. If this is the case, you have several options:

38 Resistant HTN and Diuretics
And here is an algorithm from a good review article in NEJM, a copy of which is in your handout.

39 Spirinolactone for Resistant Hypertension
Study  patients with uncontrolled HTN and on 4 agents were given spirinolactone mg daily Avg BP reduction at 6 months: 25/12 (!!) Degree of antihypertensive benefit similar in subjects with and without primary hyperaldosteronism **Follow K very closely, esp in renal failure Probably avoid in Creatinine > 2 I just wanted to conclude on another exciting therapy that is emerging for resistant hypertension. One study used daily spirinolactone to folks with uncontrolled HTN and on 4 agents. At six months the degree of blood pressure reduction was an average of 25 mm mercury. Interestingly, the degree of antihypertensive benefit was independent of what the patients aldosterone levels were. Now if you embark on this, it is very critical that you follow the potassium very carefully, and probably should not be given for creatinines greater than 2.

40 My bullet points… Blood pressure control is a worthwhile endeavor and improves mortality more than most other stuff you do in clinic Strongly consider sleep apnea screening in hypertensive patients Think of primary hyperaldosteronism in those with hypertension and low K Renal artery stenosis relatively common, but unclear if invasive procedures work

41 My bullet points, continued
“Rule of 10’s” guideline helpful for guidance tx OK to follow home BPs if patient with white coat HTN Try combination medication and writing BP goals on prescription to improve adherence If patient has resistant hypertension, ensure s/he is on proper diuretic dose HCTZ may not work at GFR < 50 Spirinolactone may be really great


Download ppt "Resistant and Secondary Hypertension"

Similar presentations

Ads by Google