I. Management of hypertension: What every physician needs to know
Hypertension is THE disease. It is present for all to consider and deal with regardless of the specialty. However, it is the quintessential internist’s dilemma.
To date, the proposed surgical remedies for hypertension have only had paltry results and serve such a small fraction of the population afflicted, that medical therapy remains the cornerstone of management.
There are multiple causes of hypertension. No single genetic defect explains the etiology of “essential hypertension” (though genetic disorders leading to hypertension are known), and no single pathophysiologic mechanism explains how hypertension develops; hence the numerous available therapies that target these varied mechanisms. Nevertheless, hypertension cannot be treated out of context.
For example, hypertension in renal disease is very different from hypertension with “normally” functioning kidneys. As such, consideration must be given to the co-existing conditions that may alter the disease itself, or the desired control in order that the co-existing condition does not worsen. This review will outline the essential components of hypertension management within the context of established coronary artery disease.
II. Diagnostic Confirmation: Are you sure your patient has hypertension?
Hypertension is defined, as according to the Joint National Commission for the Diagnosis, Prevention, and Treatment of Hypertension 7 (JNC-7), as:
systolic blood pressure (SBP) greater than or equal to 140 mmHg, or
diastolic blood pressure (DBP) greater than or equal to 90 mmHg, or
the requirement of antihypertensive therapy.
This diagnosis should be repeated, if a new diagnosis, over three readings at separate visits. However, if a patient presents with hypertensive emergency, hypertension may be diagnosed until proven otherwise as many individuals who present with hypertensive urgency or emergency have underlying hypertension.
A. History Part I: Pattern Recognition
As mentioned above, hypertension is a common occurrence among the medical population. The availability of blood pressure readings is ubiquitous, and if results surpass the criteria as above, they should be considered as suggestive or confirmative of the diagnosis.
However, the co-existence of glucose intolerance or diabetes, obesity (especially central), and elevated lipids with hypertension should be recognized as metabolic syndrome. This is a critical recognition as the individual components need to be managed aggressively to ultimately reduce the cardiovascular risk of the patient.
B. History Part 2: Prevalence
Hypertension is one of the most common conditions in modern society. Nearly 25% of the US population meet current diagnostic criteria for hypertension.
In individuals <50, of the blood pressure components, DBP is most closely linked to ischemic heart disease.
In individuals >60, SBP is most closely linked.
In addition, DBP demonstrates an inverse relationship to cardiovascular mortality among individuals >60.
C. History Part 3: Competing diagnoses that can mimic hypertension
Identify important secondary causes of hypertension:
Renal artery disease (especially if hypertension is uncontrolled with four medications including a diuretic [so-called resistant hypertension], there are episodic surges of blood pressure with symptoms, or renal function rapidly worsening with attempted therapy [especially with initiation of renin-angiotensin-aldosterone axis inhibition].
Hyperaldosteronism: Hypokalemia with metabolic alkalosis (out of proportion for what is expected with a diuretic), difficult to manage hypertension, family history.
Chronic kidney disease.
Obstructive sleep apnea – untreated.
Untreated hypo- or hyperthyroidism.
Untreated psychiatric condition (especially depression or anxiety).
Pheochromocytoma: episodic surges of hypertension, with flushing, diaphoresis or both. Use a 24-hour urine metanephrines, catecholamine test for highest sensitivity. Plasma metanephrines have lower sensitivity.
D. Physical Examination Findings
The signs of malignant hypertension
Modified Scheie Classification of Hypertensive Retinopathy
Grade 0: No changes.
Grade 1: Barely detectable arterial narrowing.
Grade 2: Obvious arterial narrowing with focal irregularities.
Grade 3: Grade 2 plus retinal hemorrhages, exudates, cotton wool spots, or retinal edema.
Grade 4: Grade 3 plus papilledema.
The signs of chronic arteriosclerotic hypertension
Stage 1: Widening of the arteriole reflex.
Stage 2: Arteriovenous crossing sign.
Stage 3: Copper-wire arteries (copper colored arteriole light reflex).
Stage 4: Silver-wire arteries (silver colored arteriole light reflex).
Listen for carotid bruits to search for other arterial disease.
Estimate jugular venous pulsation to estimate diuretic needs.
Listen for pulmonary edema.
Palpate the heart impulse to see if displaced.
Listen for S4 gallop.
Listen for abdominal bruits.
Complete volume assessment by looking for edema. Examine peripheral pulses. Ankle brachial index.
E. What diagnostic tests should be performed?
Repeated blood pressure measurements. Depending on suspicion of secondary causes, certain laboratory and imaging tests may be considered.
1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
At least a baseline basic metabolic panel (provides sodium; potassium; chloride; bicarbonate; blood, urea, nitrogen [BUN];creatinine, glucose, and often calcium).
Information on individual elements
Baseline hyponatremia, especially if chronic, should give pause in using thiazide type diuretics.
Presence of hypokalemia, especially in conjunction with alkalosis, should prompt a search for aldosterone-mediated hypertension, or apparent mineralocorticoid excess-mediated hypertension. Presence of hyperkalemia may indicate either a limitation of the ability to use ACEI/ARB/mineralocorticoid antagonists/renin antagonists, or, rarely, the presence of Gordon syndrome (pseudohypoaldosteronism type II: hyperkalemia, acidosis, and hypertension).
Hypochloremia typically accompanies hyponatremia.
Either primary metabolic alkalosis or compensation for a respiratory acidosis: Primary metabolic alkalosis (as in potassium section); primary respiratory acidosis with compensation – may need caution when using beta blockers, especially those that are beta-non selective.
Either primary metabolic acidosis or a compensation for a respiratory alkalosis: Primary metabolic acidosis (as in potassium section); primary respiratory alkalosis with compensation – possible anxiety component to hypertension.
Blood, urea, nitrogen/Creatinine
More reliable to monitor estimated glomerular filtration rate (eGFR), which is a routinely provided measure from most clinical laboratory services. Low eGFR indicates a possible contribution of chronic kidney disease (CKD) to the hypertension. In addition, monitoring of potassium and further worsening of renal function needs to be considered when using diuretics, or renin-angiotensin-aldosterone antagonists.
Urine for microalbumin and, if not part of the microalbumin order at your facility, creatinine to calculate the albumin-to-creatinine ratio (ACR).
If potassium, bicarbonate, or both suggest aldosterone excess, the following tests should be ordered:
Plasma renin activity
Plasma aldosterone (preferably done off of antihypertensives, but not imperative)
If history is suggestive of catecholamine excess (sudden onset of severe hypertension, especially if associated with flushing, diaphoresis, and palpitations):
24-hour urine for catecholamines, fractionated metanephrines, and creatinine (to confirm adequate collection).
May also consider plasma fractionated metanephrines.
All patients should have additional risk factor modification values assessed – fasting lipid profile as per lipid management section; as well as presence of diabetes.
Thyroid function with screening TSH.
2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
Renal artery imaging
If the clinical scenario is suggestive (acutely elevated creatinine on ACEI/ARB; elevated renin and aldosterone on plasma testing; discordant size of kidneys on renal ultrasound [especially if >2 cm difference]).
Major pitfall: Studies do not demonstrate improved outcomes following renal artery intervention.
The gold standard is renal arteriogram. Pitfall: It is an invasive test and the selection of patients for renal intervention is challenging (estimating physiologic relevance of identifiable lesions).
Renal arteriogram not available: CT angiography or MR angiography. Limitations: Interpretation of findings is dependent on the experience of the reading radiologist.
Additional limitation: All iodinated contrast agents carry a risk of contrast induced-acute kidney injury (CI-AKI). Need to follow standard CI-AKI prophylaxis guidelines. However, patients at high risk for CI-AKI should not receive iodinated contrast agents.
Patients with eGFR <30 should not receive gadolinium contrast agents for MRI due to the risk of nephrogenic systemic fibrosis.
The goal of management is to:
target a blood pressure goal, and
utilize medications that have proven efficacy in improving outcomes following an acute coronary event.
A. Immediate management
In the setting of CAD emergency, the height of the blood pressure with acute coronary syndrome (ACS) presentation may be referred to or simply the presence of hypertension with ACS.
Initially, therapy in ACS requires treatment of symptoms, which typically involves the use of nitrates. Sublingual or transdermal are the preferred routes of administration for nitroglycerin during ACS. This will lower blood pressure as well. The therapeutic target of BP during ACS presentation should focus on the prevention of hypotension. Hence, BP management should be performed after symptoms of ACS are well-managed. Hypertension should be addressed as soon as symptoms are controlled and patients demonstrate stability given the need for antiplatelet and anti-coagulant therapy.
Choice of therapy in the ACS setting should involve intravenous therapy utilizing a beta blocker or ACEI.
Stable angina or history of MI:
Beta-blockers (carvedilol, metoprolol, or bisoprolol).
ACEI (lisinopril, ramipril, perindopril, trandolapril)
ARB (valsartan, telmisartan, losartan)
Thiazide-type diuretics (chlorthalidone, hydrochlorothiazide, indapamide).
The goal of therapy should be less than 140/90. Care should be taken not to lower DBP to <60. Diabetics, and those >60 years of age are at particularly high risk of adverse cardiovascular events with excessive DBP lowering.
Starting at the lowest doses and titrating up slowly is the recommended approach.
Individuals can be trialed and subsequent medications may be added on.
For patients intolerant of beta-blockers, use non-dihydropyridine CCB (verapamil or diltiazem). These agents should not be used in the setting of LV dysfunction.
For patients intolerant of ACEI, use ARB.
For patients with inadequate BP control after the addition of the above agents, use dihydropyridine CCBs (amlodipine, nifedipine).
CCBs have been associated with adverse outcomes in the setting of ACS so they should be avoided if possible.
B. Physical Examination Tips to Guide Management
Blood pressure lowering needs to be monitored closely. In addition, specific side-effects of therapy need to be monitored. ACEIs have been associated with angioedema. Dihydropyridine CCBs have been associated with lower extremity edema.
Orthostatic hypotension (postural drop in SBP >20 mmHg, DBP >10 mmHg or rise in heart rate >20 beats per second) is an important physical exam finding that should be evaluated, especially in the elderly. In patients found to have orthostatic hypotension, we opt to use the standing blood pressure as the target of therapy. This is based on the theory that excessive drops in standing BP is associated with falls and worsening cardiovascular outcomes.
C. Laboratory Tests to Monitor Response to, and Adjustments in, Management
ACEI/ARB: Monitor potassium (for rise > upper limit of normal for your laboratory); monitor serum creatinine (for rise >30% from baseline).
Diuretics: Monitor potassium (for fall to < lower limit of normal); monitor calcium; monitor sodium, especially when using thiazide-type diuretic.
D. Long-term management
Long-term management of hypertension in individuals with CAD should include all of the agents listed above. There is good evidence for beta blockers for at least 3 years post MI. Use of ACEI has been shown to improve left ventricular modeling and prevention of extension of infarct size.
Maintenance of adequate BP control is critical: <140/90 is the goal for the majority of patients. Patients with diabetes, chronic kidney disease, and LV dysfunction may benefit from lower targets: 130/80 or less. Lifestyle modifications are critical to the maintenance of benefits obtained. Continued emphasis on weight loss (adequate weight maintenance), proper diet (especially low sodium chloride intake, and increased potassium in the form of fruits and vegetables), smoking cessation, and moderation of alcohol intake is advised.
E. Common Pitfalls and Side-Effects of Management
Important monitoring points on the excessive lowering of DBP: avoid lowering DBP <60 mmHg, especially in the elderly or diabetics.
Lisinopril 5-40 mg (once or twice daily dosing)
Perindopril 4-8 mg (once or twice daily dosing)
Trandolapril 1-4 mg (in 0.5 mg intervals daily)
Ramipril 2.5-20 mg (once or twice daily dosing)
Losartan 12.5-50 mg (daily)
Valsartan 40-320 mg (one once or twice daily dosing)
Irbesartan 150-300 mg (daily)
Metoprolol 25-400 mg (daily, in divided doses)
Carvedilol 3.125-50 mg (daily, in divided dosing)
Bisoprolol 5-20 mg (daily)
Hydrochlorothiazide12.5-50 mg (daily, in divided dosing)
Chlorthalidone 6.25-25 mg (daily)
Indapamide 2.5-5 mg (daily)
IV. Management with Co-Morbidities
Peripheral arterial disease
No specific drug has proven to be preferential in the treatment of hypertension in peripheral arterial disease.
Glycemic control is important. As mentioned above, monitor DBP. In addition, orthostatic hypotension is not uncommon in this population. Monitor for low standing SBP/DBP, especially in the presence of orthostatic hypotension with controlled seated BP. Targeting control of the standing BP is our preferred method of management of these patients.
Diabetes itself is not an absolute contraindication to the use of beta blockers. However, those patients who are brittle diabetics may experience asymptomatic hypoglycemia when beta blockers are used. Caution should be taken when using beta blockers in brittle diabetics (if at all).
If hypoglycemia develops while on beta blockers, consider cessation of therapy with beta blockers.
Chronic kidney disease
Use of ACEI/ARB is beneficial especially in the setting of albuminuria/proteinuria. Impairment in renal function will limit the use of ACEI/ARB due to the potential of worsening renal function or hyperkalemia. Avoid the use of ACEI/ARB if potassium is >5.0 at baseline (especially if diuretics are already on board). Creatinine limitations are more relative. Most providers are comfortable with using an ACEI or ARB if the creatinine is <2. If the creatinine is higher, consider referral to a nephrologist for close monitoring and a trial of therapy. Combination therapy with isosorbide/hydralazine may be considered in the management of hypertension or LV dysfunction, especially in African Americans.
If the serum creatinine rises >30% from baseline after the start of ACEI or ARB, then strong consideration should be given toward cessation of therapy. Similarly if hyperkalemia (persistent serum potassium > 5.5) is uncontrolled despite the use of diuretics and dietary discretion, then ACEI or ARB should be stopped.
Chronic obstructive pulmonary disease/Asthma
With the use of cardioselective beta blockers, the incidence of bronchospasm is very low. Nevertheless, exacerbations of underlying lung disease may happen. Use of CCBs may be considered, in the chronic CAD setting, if beta blockers are not tolerated due to bronchospasm.
If bronchospasm is exacerbated, consider transition to non-dihydropyridine CCBs instead of beta blockers.
Use of diuretics, especially loop diuretics, in the elderly may result in increased nocturia or urinary incontinence. This could also lead to falls in those who are unsteady at baseline. Anticipation of increased urination should be made. Home modifications may be appropriate such as bedside commodes or urinals.
Reduce dose of diuretics or switch to thiazide diuretics to avoid excessive urination or volume depletion.
Prognosis and patient counseling
Uncontrolled hypertension is a strong predictor of recurrent ischemic heart disease. In addition, the risk for additional vascular events increases. For example, stroke risk is increased with every 10/5 increase in SBP/DBP over normal. Salt limitation is critical to controlling blood pressure as well. Maintaining an intake <3000 mg daily should be the goal.
V. Patient Safety and Quality Measures
A. Appropriate Prophylaxis and Other Measures to Prevent Readmission
Maintain appropriate weight
Limit salt intake
Increase fruit and vegetable intake
Limit alcohol intake
Limit NSAID use
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- I. Management of hypertension: What every physician needs to know
- II. Diagnostic Confirmation: Are you sure your patient has hypertension?
- A. History Part I: Pattern Recognition
- B. History Part 2: Prevalence
- C. History Part 3: Competing diagnoses that can mimic hypertension
- D. Physical Examination Findings
- E. What diagnostic tests should be performed?
- 1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
- 2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
- III. Management
- A. Immediate management
- B. Physical Examination Tips to Guide Management
- C. Laboratory Tests to Monitor Response to, and Adjustments in, Management
- D. Long-term management
- E. Common Pitfalls and Side-Effects of Management
- IV. Management with Co-Morbidities
- V. Patient Safety and Quality Measures
- A. Appropriate Prophylaxis and Other Measures to Prevent Readmission