1. History, signs and symptoms of Hypertension
Dr. Ali-Akbar Tavassoli

2. Definition and classification of BP levels (mmHg)
BP stage
SBP mmHg
DBP mmHg
Normal
< 120
< 80
Prehypertension
80-89
Stage1 hypertension
90-99
Satge2 hypertension
≥ 160
≥ 100
Isolated Systolic Hypertension
≥ 140
> 90

4. Source of Errors of BP Measurement
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

5. Source of Errors of BP Measurement (cont.)
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

6. 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

7. 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

8. Psudo-hypertension
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

9. Orthostatic Hypotension
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

10. Pulsus Paradoxus Normally SBP decreases in inspiration
if inspiratory decreases > 10mmHg, we call it Pulsus Paradoxus!
Major causes:
Pericardial tamponade
Status asthmaticus and obstructive lung disease

11. Diagnostic evaluation: medical and physical examination
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

12. Physical examinations:
1. Signs suggesting secondary HTN
2. Signs of organ damage
3. Evidence of visceral obesity

13. Risks influencing prognosis in patients with hypertension
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

14. Subclinical target organ damage
Left ventricular hypertrophy
Ultrasound evidence of arterial wall thickening or atherosclerotic plaque
Estimated GFR =< 60 ml/min/1.73 m3
Microalbuminuria

15. Clinical 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

16. Identifiable causes of hypertension
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

17. Drug-induced HTN
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)

18. Associated conditions
Obesity
Excess alcohol intake

19. HTN and tachycardia Hyperthyroidism Pheochromocytoma
Hyperkinetic syndrome
Anxiety

20. HTN and bradycardia B-Blocker Heart block Hypothyroidism
Increased intracranial pressure (Cushing reflex) as ICH, Tumors, Meningitis…

21. HTN with nocturia Renal disease Hyperparathyroidism Hyperaldostronism
Sleep-disordered breathing

22. HTN and postural hypotension
Pheochromocytoma
Renovascular HTN (decreased diastolic pressure)
Drugs (alpha-blocker, antidepressant)
Autonomic failure
Porphyria

23. HTN with café au lait spots
Pheochromocytoma
Renovascular HTN (Fibromascular)
Abdominal Coarcation

24. HTN and palpable abdominal mass
Polycystic kidney disease
Renal tumors
Hydronephrosis
Rarely pheochromocytoma

25. HTN and attacks of Paroxysms
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

26. HTN with hyperglycemia
Diabetes
Pheochromocytoma
Acromegaly
Cushing syndrome

27. HTN and unprovoked hypokalemia
Primary hyperaldostronism
Renovascular HTN
Malignant HTN
Cushing syndrome
Liddle syndrome

28. HTN with hypercalcemia
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

29. Features of clinical clues for secondary HTN
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

30. Age 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)

31. Secondary HTN Coarcation of Aorta
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

32. Sings or symptoms suggesting Renovascular hypertension
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

33. Sings or symptoms suggesting Renovascular hypertension (cont.)
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

35. Post-transplant Hypertension
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)

36. Pheochromocytoma Signs and symptoms “10 H’s”
HTN (>90%)
Hypotension (orthostatic)
HTN crises (50%)
History of labile blood pressure
Headache
Heart consciousness (palpitation)
Heat intolerance
Hyperhydrosis (sweating)
Hypermetabolism
Hyperglycemia

37. Pheochromocytoma HTN+ “10 P’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

38. Conditions that may simulate Pheochromocytoma
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

39. Conditions that may simulate Pheochromocytoma (cont.)
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

40. HTN Cause Endocrinological Menopausal symptoms Thyrotoxicosis
Hypothyroidism
Diabetes Mellitus
Hypoglycemia
Carcinoid
Mastocytosis
Factitious: ingestion of sympathomimetics

41. Primary hyperaldostronism Clinical and lab clues
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)

42. The clinical features of preeclampsia
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

43. scan

44. Differences between preeclampsia and chronic HTN

45. HTN patients require additional diagnostic testing
-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

46. Complications of hypertension
1-Hypertensive
Accelerated-malignant hypertension (grades III and IV retinopathy)
Encephalopathy
Cerebral hemorrhage
LVH
CHF
Renal insufficiency
Aortic dissection
2-Atherosclerotic