How to recognize the different faces of Hypertension
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How to recognize the different faces of Hypertension Reena Kuriacose, MD. FACP. March 26,2012
description
How to recognize the different faces of Hypertension. Reena Kuriacose, MD. FACP. March 26,2012. Disclosures. No conflict of interest Not a specialist Statistical data varied. Resistant hypertension. BP above goal in spite of > 3 anti HTN meds All of these in optimal doses - PowerPoint PPT Presentation
Transcript of How to recognize the different faces of Hypertension
How to recognize the different faces of Hypertension
Reena Kuriacose, MD. FACP.March 26,2012
Disclosures
• No conflict of interest• Not a specialist• Statistical data varied
Resistant hypertension
• BP above goal in spite of > 3 anti HTN meds• All of these in optimal doses• Resistant HTN = Refractory HTN• Uncontrolled HTN = Resistant HTN Inadequate Rx Pseudo resistance
Pseudo resistance
• Attributed to other factors: - Inaccurate measurement - Poor adherence to Rx - White coat syndrome 20-30% (also more in resistant HTN: 37-44%)
• Suboptimal Rx: Only 18-27% uncontrolled get Rx with at least 3 anti HTN meds
Difficult to control HTN
• Higher baseline• Left Ventricular Hypertrophy• Older age• Obesity- lifestyle and diet• AA race• Chronic kidney disease• Diabetes• Medications and herbal supplements
Resistant HTN
• Prevalence: Not known- 8.9-16%• Pt with ≥ 3 BP meds 1994: 14% to 2004: 24%• 5–20% HTN- specific underlying disorder
I. Intravascular volume
• ↑ Na ↑ vascular vol ↑ cardiac output• Overtime ↑ Peripheral resistance• Non chloride Na salts have no effect on BP
• NaCl dependent HTN: - Intrinsic renal disease: ↓ capacity to excrete Na - ↑ Mineralocorticoid: ↑ tubular Na reabsorption - ↑ Neural activity to kidney: ↑ tubular Na reabsorption
ESRD 80% volume dependent and respond to dialysis
II. Autonomic Nervous System• Adrenergic receptors: α- activated by NE more than epinephrine β- activated more by epinephrine than NE
• α₁ - vasoconstriction,↑ Renal Na reabsorption• α₂ - inhibit NE release• β₁ - ↑ rate and strength of cardiac contraction
↑ CO; ↑ renin release from kidney• β₂ - vasodilatation
• Tachyphylaxis – sustained high levels of catecholamines ↓ response (orthostatic hypotension in pheo)
• C/c ↓ catecholamines temporary hypersensitivity to sympathetic stimuli (clonidine withdrawal)
• Sympathetic outflow: ↑ Obesity and OSA
III. Renin-Angiotensin-Aldosterone
• Angiotensin II Vasoconstriction Atherosclerosis
• Aldosterone Na retention
↓ NaCl in distal asc loop of Henle↓ pr. In afferent renal arteriole β₁ stimulation of renin secretionPharmacological blockade of a. ACE receptor b. Angiotensin II receptor
↓K ----------- ↓
Secondary Hypertension
• Severe or resistant hypertension• An acute rise in BP developing in a patient with previously stable values• Malignant or accelerated hypertension • < 30 years in non-obese, -ve FH, no other risk factors • >50 years
Secondary HypertensionResistant HTN with an identifiable cause:
1. Primary Aldosteronism2. Renal Artery Stenosis3. Chronic Kidney Disease4. OSA5. Pheochromocytoma6. Cushing’s Syndrome7. Aortic Coarctation
Primary Aldosteronism• 10 – 20% of resistant HTN• Peak: 30–60 years• Unexplained hypokalemia- 37% > 50% Normokalemic @ presentation Unprovoked hypokalemia : 40-50% primary aldosteronism• Renal Mag wasting mild hypomagnesemia
Primary Aldosteronism
• ↑ Aldosterone ↑ Na, ↓ Renin ↑ K excretion
• ↓ K ↓ Aldosterone synthesis correct K before eval for hyperaldosteronism
Primary Aldosteronism
• Resistant hypertension• Spontaneous or thiazide-induced hypokalemia• Serum K <3.1 mmol/L• Incidentaloma• FH of primary hyperaldosteronism
Primary Aldosteronism
• Adrenal adenoma: 60–70% Unilateral < 3cm• Unilateral/ bilateral adrenal hyperplasia• Adrenal carcinoma or an ectopic malignancy
e.g., ovarian arrhenoblastoma- rare
Primary Aldosteronism
• PAC:PRA ratio (ratio ≥ 20:1)• Plasma aldosterone concentration (PAC) (>416 pmol/L) (>15 ng/dL))• Sensitivity 90% , Specificity 91% for aldosterone-producing adenoma• Plasma renin activity (PRA) ↓
• 24 hr urine Na excretion, Creatinine clearance, aldosterone excretion
Primary Aldosteronism
• Medications that alter renin and aldosterone levels:-
Diuretics (especially spironolactone)- should be discontinued 4 weeks before ACE inhibitors, ARBs, β -blockers, Clonidine
• Calcium channel and α-receptor blockers can be used
Primary Aldosteronism
• Confirmed by demonstrating : - - Failure to suppress plasma aldosterone to isotonic saline - Failure to suppress aldosterone to oral NaCl load/ fludrocortisone/ captopril
Primary Aldosteronism
• High-resolution CT (90%) or MRI scanning
• Bilateral adrenal venous sampling for plasma aldosterone (sensitivity 95% and specificity 100%)
Primary Aldosteronism
• Hyperplasia- Aldosterone receptor antagonist
• Pts not willing for surgery Medical Rx (avoid extensive w/u)
Renal Artery Stenosis
• Atherosclerotic disease: 2/3 – older males OR• Fibromuscular dysplasia: 1/3- younger females
• Renal artery stenosis: 1–2% of hypertensive patients 10-45% of refractory HTN • Prevalence 60% in >70 years
Renal Artery Stenosis
• < 20; > 50 years• HTN is resistant to ≥ 3 drugs• Epigastric / renal artery bruits
• ↓ Renal perfusion pr → ↑ renin (over time secondary renal damage)
Renal Artery Stenosis
• Atherosclerotic disease of the aorta or peripheral arteries: - 15–25% of patients with symptomatic PVD in legs renal artery stenosis• Abrupt deterioration in kidney function (30%) after administration of ACE inhibitors• Episodes of pulmonary edema are associated with abrupt surges in BP
Renal Artery Stenosis
• BP meds can effectively control BP in many patients with renovascular HTN
• Screening is not recommended unless plan is to intervene if a significant stenotic lesion is found:
* Failure of medical therapy to control BP * Intolerance to medical Rx * Progressive renal failure * Young pt- to avoid life long Rx
Renal Artery Stenosis
• No ideal screening test for renal vascular HTN• Magnetic resonance angiography-
atherosclerotic • Spiral CT with CT angiography• Duplex Doppler ultrasonography- operator
dependant • Renal arteriography, the definitive diagnostic test
(suspicion is sufficiently high ) ---------------------------------------- * Renal insufficiency limits use of contrasts
OSA
• OSA seen in 71-85 % of resistant HTN referred
for sleep study• 45% OSA without HTN develop HTN in 4 years• Blunted/ No ↓ in nighttime BP• >50% OSA HTN (independent of obesity)
OSA
• Screen if: Obesity + snoring + daytime sleepiness
• CPAP (> 5.6 hr/night) Decreases both systolic and diastolic hypertension
Pheochromocytoma
• < 0.1% of all patients with hypertension • < 0.3% of Secondary hypertension • Incidence: 2-3/ million / yr autopsy: 250–1300/ million• Episodic HTN(90%) HA (80%) Diaphoresis (70%) Palpitation (60%)
Anxiety (50%) Tremor (40%)• 90% in adrenals; 98% in Abdomen
Pheochromocytoma
• Hyperglycemia 35% • Leukocytosis• ↑ RBC • Occa ↑ ESR• ↑ Ca
• PRA may be ↑ ed by catecholamines
• Meds: Tricyclic antidepressants, Antidopaminergic agents, Metoclopramide, and Naloxone- can ppt HTNsive crisis
Pheochromocytoma
• Plasma fractionated free metanephrines • Used in high risk pts- FH or personal h/o pheo• Sensitivity - 96% ; Specificity - 85%• N levels = end of w/u
• ↑ levels - Physical or emotional stress Sleep apnea MAO inhibitors,levodopa
Pheochromocytoma
• 24-hour urinary collection for catecholamines and metanephrines - Sensitivity - 87.5% ; Specificity of 99.7% - 2.2 mcg of total metanephrine /mg creatinine > 135 mcg total catecholamines /gm creatinine - Total u. metanephrine >1300mcg/24hr
• Lab values varies- Slightly +ve tests not significant• 2-3 times above Normal
• VMA is not required
Pheochromocytoma
• Noncontrast CT - followed by CT with nonionic contrast• MRI scanning • CT/ MRI - sensitivity ~ 90% for adrenal pheochromocytoma • Less sensitive - recurrent tumors, metastases, and extra-adrenal paragangliomas• I¹³¹ metaiodobenzyl guanidine if CT/MRI -ve
Cushing’s syndrome• 80% of spontaneous Cushing syndrome HTN• ↑ WBC > 11,000/mm3
• Hyperglycemia• Hypokalemic metabolic alkalosis : Cortisol renal mineralocorticoid receptor.
Cushing’s syndrome
• 40% of cases are due to Cushing "disease,“• ACTH hypersecretion by the pituitary- benign
pituitary adenoma (98% in ant pituitary)• 10% nonpituitary ACTH-secreting neoplasms
(eg small cell lung Ca) ↑ K & ↑ pigmentation• 15% ACTH source that cannot be initially
located
Cushing’s syndrome
• 30% of cases- autonomous secretion of cortisol by the adrenals
independently of ACTH• Benign adrenal adenomas (small) cortisol• Adrenocortical carcinomas (large) cortisol + androgens
Cushing’s syndrome
• Tests for diagnosis:
- 24 hr Urinary free cortisol level - 1mg dexamethasone suppression test - Evening serum and salivary cortisol level
Cushing’s syndrome
• Urine Cortisol: - 24-hour urine collection >3-4 times upper limit (>200 µg/24hr) 3 N urine free cortisol – excludes
• ↑ Free Urine cortisol: high fluid intake; preg, Carbamazepine and fenofibrate
Cushing’s syndrome
• Dexamethasone suppression test: 1 mg @11 pm cortisol @ 8 am; a cortisol level < 5 mcg/dL or < 2 mcg/dL• Phenytoin, Phenobarbital, Primidone, Rifampin,
Estrogens (preg / OC) - lack of dexamethasone suppressibility false +ve
• 8% of pituitary Cushing disease- also have suppression
Cushing’s syndrome
• Midnight serum cortisol level > 7.5 mcg/dL: - Same time zone for at least 3 days - Fasting for at least 3 hours - Indwelling IV line
• Late-night salivary cortisol test: consistently
> 0.25 mcg/dL (7.0 nmol/L)
Cushing’s syndrome
• Confirmation:
- Low dose Dexa suppression test: Dexa 0.5mg q6hrX 48hrs - Cortisol > 55.2nmol/L (2 µg/dL) Cushing syndrome
Etiology of Cushing’s
• To differentiate ACTH dependant vs ACTH independent • Plasma or serum ACTH: < 5pg/mL = adrenal tumor > 10-20 pg/mL = pituitary or ectopic ACTH- secreting tumors.
Etiology of Cushing’s
• To differentiate Pituitary ACTH vs ectopic ACTH: - 8mg Dexamethasone suppression test @ 11pm: OR - 48-hr Dexamethasone suppression test: 2mg q 6hr X 8
doses
- Cortisol suppression <50% of baseline = Pituitary ACTH - Sensitivity 80%; Specificity 70-80% - ↓ of 90% in U free cortisol ~ 100% specific for ant pit disease
Cushing’s syndrome
• MRI of the pituitary- pituitary lesion ~ 50% • Selective catheterization of the inferior
petrosal sinus veins +/- CRH adm• CT scan: chest (lungs, thymus) abdomen
(pancreas, adrenals)- 60% lesions found• 111In-octreotide (OCT, somatostatin receptor
scintigraphy) scan: occult tumors• Non-ACTH-dependent Cushing syndrome- CT
scan of the adrenals
Coarctation of Aorta
• 1-8/1000 live births• 30 % Subsequent HTN after surgical correction• Less severe lesions diagnosed in young adulthood
Coarctation of Aorta
• Diminished and delayed femoral pulses• Systolic pr gradient b/w R arm and legs / L arm• Blowing systolic murmur - posterior L interscapular areas• Chest x-ray and transesophageal
echocardiography
Other causes:• Renal: Polycystic kidney disease, Renin secretory tr, obstructive uropathy• Adrenal: 17α hydroxylase defi, 11β hydroxylase dehydrogenase defi• Preeclampsia/ Eclampsia• Neuro: psycogenic, polyneuritis, a/c ↑ICP• Hyperthyroidism (systolic HTN) Hypothyroidism (Mild diastolic HTN) ↑ Ca, acromegaly• Mendelian forms
