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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