dr. ali-akbar tavassoli. bp stagesbp mmhgdbp mmhg normal< 120< 80 prehypertension120-13980-89...

History, signs and symptoms of Hypertension

Dr. Ali-Akbar Tavassoli

Definition and classification of BP levels (mmHg)

BP stage SBP mmHg DBP mmHg

Normal < 120 < 80

Prehypertension 120-139 80-89

Stage1 hypertension 140-159 90-99

Satge2 hypertension ≥ 160 ≥ 100

Isolated Systolic Hypertension ≥ 140 > 90

White-coat hypertension◦ Physician measurement higher than BP taken by

patients, nurses, technicians and home measurements

◦ 24 ambulatory BP monitoring may be helpful resolve this issue

◦ Night dip

Source of Errors of BP Measurement

Auscultatory Gap:◦ A period of silence after

phase I and reappearing of Korotkoff sounds that causes missing phase II

◦ This period is usually short but may be over 40mmHg

◦ May be seen in elderly, fat arm, inflation too slow or inadequate, low intensity of Korotkoff sounds and venous congestion of upper extremity

Source of Errors of BP Measurement (cont.)

Auscultatory gap solution:◦ Rapid and adequate inflation (SBP estimated by

palpation method first)◦ Increase the intensity of Korotkoff sounds by some

maneuvered Rapid inflation Hold arm straight up during the inflation Open and close fist 10 times during the inflation 2nd measurement at least 1-2 minutes after the 1st

Source of Errors of BP Measurement (cont.)

Pseudohypotension:◦ Seen in patients with low cardiac output and

shock state◦ High peripheral vascular resistance tightens the

arteries to a point that generation of Korotkoff sounds is severely impaired and the sounds are too weak for accurate measurements of SBP or DBP and may lead to gross underestimation of BP

Source of Errors of BP Measurement (cont.)

Occurs in elderly patients who have rigid arteries and should be suspected in elderly patients with high BP and no evidence of target organ damage

Osler’s maneuver may be beneficial In elderly patients auscultatory gap is more

frequent

Psudo-hypertension

A fall in SBP more the 20mmHg or DBP more 10mmHg in response to moving from supine position to a standing position within 3 minutes

Normally in erect position:◦ DBP never drops or rises slightly◦ SBP may decrease slightly ◦ Mean BP doesn’t drops more a few mmHg◦ HR increases (except in neuropathy or using heart

rate-slowing agent) If HR increases, the 1st cause is hypovolemia

Orthostatic Hypotension

Normally SBP decreases in inspiration if inspiratory decreases > 10mmHg, we call

it Pulsus Paradoxus! Major causes:

◦ Pericardial tamponade ◦ Status asthmaticus and obstructive lung disease

Pulsus Paradoxus

Family and clinical history 1. Duration and previous level of high BP 2. indications of secondary HTN 3. Risk factors 4. Symptoms of organ damage 5. Previous antihypertensive therapy

(efficacy, adverse events) 6. Personal, family, environmental factors

Diagnostic evaluation: medical and physical examination

1. Signs suggesting secondary HTN 2. Signs of organ damage 3. Evidence of visceral obesity

Physical examinations:

Risk factors for cardiovascular disease Levels of SBP and DBP Age- men>55; women>65 Smoking Family history of premature cardiovascular

disease Abdominal obesity Diabetes CRP >= 1mg/dl

Risks influencing prognosis in patients with hypertension

Left ventricular hypertrophy Ultrasound evidence of arterial wall

thickening or atherosclerotic plaque Estimated GFR =< 60 ml/min/1.73 m3

Microalbuminuria

Subclinical target organ damage

Cerebrovascular disease Ischemic stroke Cerebral hemorrhage TIA Heart disease MI or ACS Angina Coronary revascularization CHF Renal disease Diabetic nephropathy Chronic kidney disease Proteniuria>300 mg/24 h Peripheral arterial disease Advanced retinopathy Papiledema

Clinical target organ damage

Sleep apnea Drug induced or related causes (see table 9) Chronic kidney disease Primary aldostronism Renovascular disease Chronic steroid therapy and Cushing’s

syndrome Pheochromocytoma Coarcation of the Aorta Thyroid or parathyroid diseases

Identifiable causes of hypertension

Non-steroidal antiinflammatory drugs; cycloxygenase 2 inhibitors

Cocaine, amphetamines, other illicit drugs Sympathomimmetics (decongestant, anorectics) Oral contraceptives Adrenal steroids Cyclosporine and Tacrolimus Erythropoietin Licorice (including some chewing tobacco) Selected over-the-counter dietary supplements and

medicines (e.g, ephedra, mahung, bitter orange)

Drug-induced HTN

Obesity Excess alcohol intake

Associated conditions

Hyperthyroidism Pheochromocytoma Hyperkinetic syndrome Anxiety

HTN and tachycardia

B-Blocker Heart block Hypothyroidism Increased intracranial pressure (Cushing

reflex) as ICH, Tumors, Meningitis…

HTN and bradycardia

Renal disease Hyperparathyroidism Hyperaldostronism Sleep-disordered breathing

HTN with nocturia

Pheochromocytoma Renovascular HTN (decreased diastolic

pressure) Drugs (alpha-blocker, antidepressant) Autonomic failure Porphyria

HTN and postural hypotension

Pheochromocytoma Renovascular HTN (Fibromascular) Abdominal Coarcation

HTN with café au lait spots

Polycystic kidney disease Renal tumors Hydronephrosis Rarely pheochromocytoma

HTN and palpable abdominal mass

Pheochromocytoma Rebound HTN after abrupt cessation of

clonidine and other antihypertensive drugs Hypertensive crises with MAO inhibitors Acute pulmonary edema Hypoglycemia Anxiety and panic attacks Spinal cord transection (during bladder

distension or muscle spasm) Menopausal symptoms

HTN and attacks of Paroxysms

Diabetes Pheochromocytoma Acromegaly Cushing syndrome

HTN with hyperglycemia

Primary hyperaldostronism Renovascular HTN Malignant HTN Cushing syndrome Liddle syndrome

HTN and unprovoked hypokalemia

Hyperparathyroidism Pheochromocytoma During chronic thiazide therapy in patients

with pre-existing hyperparathyroidism o r vitamin D-treated hypoparathyroidism

MEN and other disease such as sarcoidosis, multiple myeloma

HTN with hypercalcemia

Age on onset: <25 or > 50 Recent HTN with rapid progression Malignant HTN without history of chronic HTN Symptomatic HTN History of hematuria, flank pain, back trauma, surgery and

abdominal radiation Palpable kidney HTN with unprovoked hypokalemia, hypercalcemia,

hyperglycemia, serum cr>1.5, anemia, weight loss Abdominal bruit HTN with pulse pressure or unequal pulses of lower and

upper extremities

Features of clinical clues for secondary HTN

Age is an important factor in hypertensive patients ◦ New born infants (always secondary

hypertension) Renovascular, thrombosis or renalartery stenosis

(RAS) Coarctation of aorta (COA) Congenital renal malformation Broncopulmonary dysplasia

◦ Pre school (almost always secondary) Renal (pronchymal or vascular)

◦ After 10 years Renal disease Essential hyper tension (strongly with family history

and obesity)

Age

Absent or reduced pulses in the lower extremities

Pulsation in neck Palpable pulsations over intercostal arteries

in the posterior thorax Bruits over the intercostal arteries Rib notching on CXR Cold feet Pain in legs with exercise

Secondary HTN Coarcation of Aorta

Age <30 or >50 Young female (fibromuscular) or old men

(atherosclerosis) Sever resistant HTN Abrupt onset of HTN Abdominal continuous or prolonged high-pitched

systolic bruit Symptoms of atherosclerosis elsewhere Orthostatic drop of DBP Recurrent pulmonary edema especially with good left

ventricular function Significant azotemia in response to ACEI

Sings or symptoms suggesting Renovascular hypertension

Small unilateral kidney HTN and unexplained impairment in renal

function Arteritis (Takayasu’s-PAN) Rejected kidney Aortic dissection Retroperitoneal fibrosis Significant kidney ptosis on IVP or orthostatic HTN Lab test: hypokalemia, proteniuria, increased

renin levels Azotemia in the elderly patient with

atherosclerosis elsewhere

Sings or symptoms suggesting Renovascular hypertension (cont.)

Very Frequent Causes:

◦ Retained native kidney◦ Recurrent disease in allograft◦ Acute or chronic rejection◦ Donor factor◦ Transplant renal artery stenosis◦ Immunosuppressive drugs (steroid, cyclosporine,

etc)

Post-transplant Hypertension

HTN (>90%) Hypotension (orthostatic) HTN crises (50%) History of labile blood pressure Headache Heart consciousness (palpitation) Heat intolerance Hyperhydrosis (sweating) Hypermetabolism Hyperglycemia

Pheochromocytoma Signs and symptoms “10 H’s”

Pain Paroxysm (50%) Postural hypotension Pallor Polar (coldness) Perspiration Pressor response to antihypertensive agents (alpha-

blockers, vasodilators, TCA or during induction of anesthesia)

Pupils dilatation Psychological disorders*symptoms and signs may occur without HTN crises

Pheochromocytoma HTN+ “10 P’s”

Hyperdynamic labile HTN Paroxysmal tachycardia Angina, Coronary insufficiency Acute pulmonary edema Ecclampsia HTN crises during or after surgery HTN crises with MAO inhibitors Rebound HTN after abrupt cessation of

clonidine or other antihypertensives

Conditions that may simulate Pheochromocytoma

Psychoneurological Anxiety with hyperventialtion Panic attacks Migraine and cluster headaches Brain tumor Basilar artery aneurysm Stroke Diencephalic seizure Porphyria Lead poisoning Familial dysautonomia Acrodynia Autonomic hyperreflexia as with quardiplegia Baroreflex failure Fatal familial insomnia

Conditions that may simulate Pheochromocytoma (cont.)

Endocrinological

◦ Menopausal symptoms◦ Thyrotoxicosis◦ Hypothyroidism◦ Diabetes Mellitus◦ Hypoglycemia◦ Carcinoid◦ Mastocytosis◦ Factitious: ingestion of sympathomimetics

HTN Cause

HTN Bilateral headache Proximal muscle weakness of extremities and paresthesia Lack of edema Nocturia and polyuria Unprovoked hypokalemia (<3.5 meq/L) Failure to normalized serum K values within 4 weeks off

diuretics Sever hypokalemia after initiation of diuretic therapy Difficulty maintaining normal serum K values despite

concomitant use of oral K or K-sparing agents with conventional dose of diuretics

24-h urinary K (>30 meq/L) despite low serum K (<3meq/L)

Primary hyperaldostronismClinical and lab clues

HTN Epigastric/right upper quadrant pain Fetal growth restriction Convulsion Headache Coma ICH Visual disturbance Pulmonary edema Bleeding from venipuncture sites Proteinuria ARF Placental abruption Hyperreflexia Edema Clonus

The clinical features of preeclampsia

scan

Differences between preeclampsia and chronic HTN

-Age, history, examination, severity of HTN, or initial laboratory findings suggest secondary HTN

Resistant HTN on maximal dosage of at least 3 appropriate anti-hypertensive drugs

Previous good BP control with acute unexplained exacerbation

HTN associated with grade 3 or 4 retinopathy New-onset HTN after age 60 Suspected new or worsening target organ

damage

HTN patients require additional diagnostic testing

1-Hypertensive Accelerated-malignant hypertension

(grades III and IV retinopathy) Encephalopathy Cerebral hemorrhage LVH CHF Renal insufficiency Aortic dissection 2-Atherosclerotic

Complications of hypertension