1. HYPERTENSION __Ch. 11 VASCULAR DISEASES __Ch. 12
LESSON 3
HYPERTENSION __Ch. 11
VASCULAR DISEASES __Ch. 12

2. HYPERTENSION

3. Demography of htn 50 million have the disease 70% aware of it
Only 50% get treated
Only 25% have controlled bp
More common in Afro Americans
Major cause for end stage renal disease and
heart failure

4. Assessment and Diagnosis of HTN

5. Assessment and Diagnosis of HTN

6. Physical exam should include:
Vital Stat: height, weight, and waist circumference
funduscopic exam (retinopathy); carotid auscultation (bruit)
jugular venous pulsation
thyroid gland (enlargement)
cardiac auscultation
chest auscultation abdominal exam (bruits, masses, pulsations)
exam of lower extremities
routine labs include urinalysis, complete blood count, electrolytes (potassium, calcium), creatinine, glucose, fasting lipids, and 12-lead electrocardiogram
(left ventricular heave, S3 or S4, murmurs, clicks)/(rales, evidence of chronic obstructive pulmonary disease)/ (diminished arterial pulsations, bruits, edema); and neurologic exam (focal findings)/

7. secondary causes of hypertension- suggestive (clues in parentheses) of:
(1) Pheochromocytoma
(labile or paroxysmal hypertension accompanied by sweats, headaches, and palpitations)
(2) Renovascular disease
(abdominal bruits)
(3) APKD-autosomal dominant polycystic kidney disease (abdominal or flank masses)
(4) Cushing's syndrome
(truncal obesity with purple striae)
(5) Primary hyperaldosteronism (hypokalemia)
(6) Hyperparathyroidism (hypercalcemia)
(7) Renal parenchymal disease (elevated serum creatinine, abnormal urinalysis),
(8) Poor response to drug therapy,
(9) SBP > 180 or DBP > 110 mm Hg, or
(10) sudden onset of hypertension.
Cushings = bull neck, round red flushed face, trunk obesity, stretchmarks. People on sterioids also get htn.
Hyperaldosteronism related to salt and fluid.

8. JNC VII 2003 recommendations
Normal: recheck in 2 years (see Comments)
1. Prehypertension: SBP 120–139 or DBP 80–89
Prehypertension:
recheck in 1 year
2. Stage 1 hypertension: SBP 140–159 or DBP 90–99
Stage 1 hypertension:
confirm within 2 months
2 separate office visits)
Stage 2 hypertension: evaluate or refer to source of care within 1 month (evaluate and treat immediately if BP > 180/110)
4. Perform physical exam and routine labs.a
3. Stage 2 hypertension: SBP >160 or DBP>100 (based on average of 2 measurements on different days)
5. Pursue secondary causes of hypertension.b
6. Treatment goals are for BP < 140/90, unless diabetes or renal disease present (< 130/80).
7. Ambulatory BP monitoring is a better (and independent) predictor of cardiovascular outcomes compared with office visit monitoring; and covered by Medicare when evaluating white-coat hypertension.
Be familiar with this. Check every person every 2 yrs. If prehypertensive, 1ce per year and change their lifestyle!

9. Prehypertension
gray area of 120–139/80–89 mm Hg
a trend away from defining hypertension as a simple numerical threshold
antihypertensive medications be offered to persons with prehypertension with compelling indications

10. Lifestyle Modifications for Primary Prevention of Hypertension
Recommendation
Approximate SBP Reduction (Range)
Weight reduction
Maintain normal body weight (BMI 18.5–24.9 kg/m2).  
5–20 mm Hg per 10 kg weight loss
Adopt DASH eating plan
Consume diet rich in fruits, vegetables, and low fat dairy products with a reduced content of saturated and total fat.
8–14 mm Hg
Dietary sodium reduction
Reduce dietary sodium intake to no more than 100 mmol/day (2.4 g sodium or 6 g sodium chloride).
2–8 mm Hg
Physical activity
Engage in regular aerobic physical activity such as brisk walking (at least 30 min/day, most days of the week).
4–9 mm Hg
Moderation of alcohol consumption
Limit consumption to no more than 2 drinks (1 oz or 30 mL ethanol; eg, 24 oz beer, 10 oz wine, or 3 oz 80-proof whiskey) per day in most men and to no more than 1 drink per day in women and lighter-weight persons.
2–4 mm Hg

11. ? DASH: Dietary Approaches to Stop Hypertension
Type of food
Number of servings for Calorie diets
Servings on a 2000 Calorie diet
Grains and grain products (include at least 3 whole grain foods each day)
6 - 12
7 - 8
Fruits
4 - 6
4 - 5
Vegetables
Low fat or non fat dairy foods
2 - 4
2 - 3
Lean meats, fish, poultry
2 or less
Nuts, seeds, and legumes
3 - 6 per week
4 - 5 per week
Fats and sweets
limited

12. LOW RISK CANDIDATES Modification Recommendation
Approximate Systolic BP Reduction, Range
Weight reduction
Maintain normal body weight (BMI, 18.5–24.9)
5–20 mm Hg/10-kg weight loss
Adopt DASH eating plan
Consume a diet rich in fruits, vegetables, and low-fat dairy products with a reduced content of saturated fat and total fat
8–14 mm Hg
Dietary sodium reduction
Reduce dietary sodium intake to no more than 100 mEq/L (2.4 g sodium or 6 g sodium chloride)
2–8 mm Hg
Physical activity
Engage in regular aerobic physical activity such as brisk walking (at least 30 minutes per day, most days of the week)
4–9 mm Hg
Moderation of alcohol consumption
Limit consumption to no more than two drinks per day (1 oz or 30 mL ethanol [eg, 24 oz beer, 10 oz wine, or 3 oz 80-proof whiskey]) in most men and no more than one drink per day in women and lighter-weight persons
2–4 mm Hg

13. COMPELLING CONDITIONS
RECOMMENDED DRUGS
HIGH RISK CONDITIONS
DIURETIC
β BLOCKER
ACEi
ARB
CCB
ALDOSTERONE
ANTAGONIST
HEART FAILURE $
POST MYOCARDIAL INFARCTION
HIGH CAD RISK
DIABETES MELLITUS
CRHONIC KIDDNEY DISEASE
REURRENT STROKE PREVENTION

14. PRIMARY HYPERTENSION NO IDENTIFIABLE CAUSE (95%)
30% OF BLACKS/20% OF WHITES
25-55 YEAR AGE GROUP
MULTIFACTORIAL

15. PRIMARY HYPERTENSION: CAUSES
GENETIC
OBESITY
SALT INTAKE
SYMPATHETIC SYSTEM OVERACTIVITY
ABNORMAL CVS DEVELOPMENT
RENIN-ANGIOTENSIN ACTIVITY
ALCOHOL/CIGARETTE/POLYCYTHEMIA

16. Associated causes of hypertension
  Sleep apnea
Drug-induced or drug-related
Chronic kidney disease
Primary aldosteronism
Renovascular disease
Long-term corticosteroid therapy and
Cushing's syndrome
Pheochromocytoma
Coarctation of the aorta
Thyroid or parathyroid disease

17. RENAL ARTERY STENOSIS 1-2% OF HTN PATIENTS YOUNGER(<20 YRS AGE)
FIBROMUSCULAR HYPERLASIA (f<50)
LEADS TO EXCESSIVE RENIN RELEASE

18. RENAL ARTERY STENOSIS SUSPECT WHEN: HTN ONSET <20 YRS AGE OR
OCCURS AFTER 50
DRUG RESITANT HTN
PRESENCE OF EPIGASTRIC OR
RENAL BRUITS
PRESENCE OF SIGNIFICANT PERIPHERAL VASCULAR DISEASE
RENAL FUNCTION DETERIORATES AFTER ACEi administration

19. RENAL ARTERY STENOSIS Tests- Radioisotope renography duplex us
MRA/CT ANGIO
RENAL ARTERIOGRAPHY
TREATMENT- vascular reconstruction

20. Primary hyperaldosteronism
Due to excessive aldosterone secretion
Test-
check plasma aldosterone levels
Plasma rennin levels
Calculate aldosteone/rennin ratio (nomral <25)
Cause- Adrenal Adenoma- requires ct/mri scan

21. Glucocorticoid excess HTN (75-85%) of cases
CUSHING’S SYNDROME
Glucocorticoid excess
HTN (75-85%) of cases
Increased Rennin-Angiotensin activity

22. Pheochromocytoma 0.1% of all htn patients 2/1ooo,ooo incidence
Hypertensive crisis (BP 300>)
Associated with Café au Lait spots and neurofibromatosis

23. Other causes for secondary HTN
Estrogen
Acromegaly
Hyperthyroidism
hypothyroidism
DRUGS: cyclosporine and NSAIDs

24. Complications of HTN
excess morbidity and mortality related to hypertension
risk doubles for each 6 mm Hg increase in diastolic blood

25. Complications of HTN Cardiac Complications –
Left Ventricular Hypertrophy congestive heart failure
ventricular arrhythmias
myocardial ischemia and
sudden death.

26. Complications of HTN
Cerebrovascular Disease and Dementia - hemorrhagic and ischemic stroke
higher incidence of subsequent dementia of both vascular and Alzheimer types
markedly reduced by antihypertensive therapy

27. Complications of HTN Hypertensive Renal Disease – renal insufficiency
hypertensive nephropathy
more common in blacks
associated with Diabetes Mellitus
Benefits with ACEi therapy

28. Increased Atherosclerosis
Complications of HTN
Aortic dissection
Increased Atherosclerosis

29. SYMPTOMS OF HTN mainly referable to involvement of the target organs:
Heart
Brain
Kidneys
Eyes and
Peripheral arteries.

30. Symptoms of HTN Mainly asymptomatic
Early morning suboccipital pulsating HA
Hypertensive Encephalopathy: Somnolence/confusion/Visual/
Nausea/Vomiting
(Diastolic BP >130)

31. Signs of HTN Heart: Left ventricular enlargement/Hypertrophy
LAB workup: CBC/Urinalysis/FBS/LIPIDS/
Serum Uric Acid /Electrolytes/Creatinine/
BUN
ECG/CXR

32. Basic Testing in the Hypertensive Patient
   Primary work-up (all patients)
Urinalysis and sediment review (identifies possible renal disease or end-organ dysfunction)
Basic chemistry including potassium, fasting glucose, blood urea nitrogen, and creatinine (evaluates for renal disease; low or low-normal potassium may be seen in hyperaldosteronism; fasting glucose can assess for diabetes)
Complete blood cell count (evaluates for polycythemia, which can cause secondary hypertension)
Lipid panel (risk stratification for patients with dyslipidemia)
Electrocardiogram (risk stratification in patients with coronary artery disease; evaluate for left ventricular hypertrophy

33. Goals of the Initial Evaluation
Establish the diagnosis.
Staging the disease. If present, hypertension is staged using the criteria outlined in the JNC 7 consensus statement. This guides immediate management.
Rule out secondary hypertension.
Identify end-organ effects. The initial history, physical examination, and laboratory work-up should include investigations that will identify common end-organ damage
Identify the presence or absence of other major cardiovascular risk factors, in particular those that are modifiable with intervention.

34. ECG: LV Strain Pattern Suggests Advanced disease Poor prognosis
Other Investigations:
Renal US/CT/MRI scans

35. Management Algorithm

36. NON PHARMACOLOGIC THERAPY
CHANGE LIFESTYLE: DASH DIET
Weight reduction
Reduced alcohol consumption
Reduced salt intake
Gradually increasing activity levels

37. Goals of Treatment diabetic patients, CKD, should be lower
(< 130/80 mm Hg)
Others (<140/90)
long-term adverse consequences of drug therapy – β blockers, Thiazides
statins can significantly improve outcomes in DM/Post MI (total and LDL cholesterol levels of
< 194 mg/dL and < 116 mg/dL )

38. Current Antihypertensive Agents
Diuretics –
HCTZ (Esidrix®, Hydro-Diuril®)
LOOP DIURETICS - Ethacrynic acid (Edecrin®) Furosemide (Lasix®)
ALDOSTERONE RECEPTOR BLOCKERS  - Amiloride (Midamor®)
Spironolactone (Aldactone®)
alone -control blood pressure in 50%

39. Side effects of diuretics
Hypo-K+, Hypo-Mg2+, Hypo-Ca2+, Hypo-Na+,
Hyper-uric acid (gout),  Hyper-glucose,
Increase LDL cholesterol, Increase triglycerides; rash, erectile dysfunction.

40. Adrenergic Blocking Agents
Beta blockers
decrease the heart rate and cardiac output
Acebutolol(Sectral®)
Atenolol(Tenormin®)
Metoprolol(Lopressor®)
Pindolol (Visken®)
Propranolol (Inderal®)

41. Side effects of Beta Blockers
exacerbating bronchospasm
bradycardia or AV block
precipitating or worsening l vf
nasal congestion
Raynaud's phenomenon
nightmares
Increase TGL Decrease HDL

42. ACE Inhibitors initial medication Benazepril (Lotensin®)
Captopril (Capoten®)
Enalapril (Vasotec®)

43. RAAS System

44. Side Effects Of ACEi Cough hypotension dizziness renal dysfunction
hyperkalemia
angioedema
taste alteration and
rash
Contraindicated in pregnancy
Acute Renal Failure

45. Angiotensin Receptor Blockers: ARBs
Candesartan (Atacand®)
Eprosartan (Teveten®)
Irbesartan (Avapro®)
Losartan (Cozaar®)
do not cause cough

46. The ABCD rule B* and D* may induce more new-onset diabetes
A= ACEi or ARBs
*B=β Blockers
C= CCBs
*D= Diuretic (thiazide)

47. BHS Guidelines Young Elderly (low renin) A B C D A ACE Inhibitor
B Beta Blocker
C Calcium Channel Blocker
D Diuretic

48. Afro-Americans and HTN
more likely to become hypertensive and
more susceptible to the cardiovascular complications
Respond differently to drugs –ACEi and ARBs are less effective

49. Follow up of HTN patients
Achieve good control
Need less frequent visits
Yearly monitoring of blood lipids and
an ECG should be repeated at 2- 4 years

50. HTN Crisis (>220/130)
requires prompt recognition and aggressive management
blood pressure must be reduced within a few hours
hypertensive encephalopathy
(headache, irritability, confusion, and
altered mental status due to cerebrovascular spasm)

51. HTN Crisis
hypertensive nephropathy (hematuria, proteinuria, and progressive renal dysfunction )
intracranial hemorrhage, aortic dissection, preeclampsia-eclampsia, pulmonary edema, unstable angina, or myocardial infarction

52. initial goal in hypertensive emergencies
reduce the pressure by no more than 25% (1 or 2 hours )
then toward a level of
160/100 mm Hg within 2–6 hours
Excessive reductions may precipitate coronary, cerebral, or renal ischemia

53. α – Alpha ADRENOCEPTOR BLOCKERS
Prazosin (Minipress®)
Terazosin (Hytrin®)
Doxazosin (Cardura®)
relax arterial smooth muscle, and reduce blood pressure
no adverse effect on serum lipid levels
they increase HDL cholesterol
reduce total cholesterol

54. Pulmonary Heart Disease (Cor Pulmonale)
Symptoms and signs of chronic bronchitis and pulmonary emphysema.
Elevated jugular venous pressure, parasternal lift, edema, hepatomegaly, ascites.
RV hypertrophy and eventual failure

55. Findings in Cor Pulmonale
chronic productive
cough
exertional dyspnea
wheezing respirations
easy fatigability, and weakness
oxygen saturation is often below 85%

56. Cor Pulmonale Oxygen salt and fluid restriction and diuretics
the average life expectancy is 2–5 years when CHF appears

57. Aneurysms of the Abdominal Aorta
asymptomatic, detected during a routine physical examination or a diagnostic study.
Severe back or abdominal pain, a pulsatile mass, and hypotension indicate rupture
90% of abdominal aneurysms originate below the renal arteries

58. Aneurysms of the Abdominal Aorta
90% of abdominal aneurysms originate below the renal arteries
5–8% of men over the age of 65 years
detection of a prominent aortic pulsation

59. Hypotension & Shock

60. Features Hypotension, tachycardia, oliguria, altered mental status.
Peripheral hypoperfusion and
hypoxia.

61. physiologic response to Shock
Sympathetic response
Release of Norepinephrine
Renin
ADH
Glucagon
Cortisol
Growth Hormone

62. Causes Hypovolemic Cardiogenic Obstructive- Pneumothorax/
Pulmonary embolism
Distributive- pancreatitis
Septic shock

63. Features of Septic Shock
fever
chills
hypotension
Hyperglycemia and
altered mental status
due to gram-negative bacteremia: (E coli, Klebsiella, Proteus, and Pseudomonas)

64. Hypotension systolic blood pressure of 90 mm Hg or less
A drop in systolic pressure of more than 10–20 mm Hg and
an increase in pulse of more than 15 with positional change

65. Treatment General Measures
Basic life support-(BLS) airway/oxygen/cpr
Advanced Cardiac Life Support – (ACLS)

66. Orthostatic Hypotension
Vasomotor Syncope
Elderly
Diabetics
greater than normal decline
(20 mm Hg) in blood pressure immediately upon arising from the supine to the standing position

67. VASCULAR DISORDERS

68. Aneurysms of Abdominal Aorta AAA
Most aortic aneurysms are asymptomatic, detected during a routine physical examination or a diagnostic study.
Severe back or abdominal pain, a pulsatile mass, and hypotension indicate rupture.
Concomitant atherosclerotic occlusive disease of the lower extremities is present in 25% of patients.

69. AAA 90% below the level of renal arteries
Normal aortic diameter 2cms. >3 cms is aneurysm
1951 from 8.7 per 100,000
per 100,000
Prevalence 5-8% M > 65
US screen
Associated with popliteal artery aneurysms

70. AAA Rupture Signs! A RED FLAG needs referral to ER
Severe back/ abdo/flank pain
Hypotension
90% fatal unless repaired surgically

71. AAA Therapy Beta blockers Surgical excision and graft Rupture risk-
2% (4-5.5cm)/ 7%
(6-6.9cma0/ 25% (>7cm)
Five-year survival after surgical repair is 60–80%

72. Peripheral Artery Aneurysms (Popliteal & Femoral)
Associated AAA
Popliteal most common peripheral
artery aneurysm
Arterial thrombus rather than rupture –
needs amputation (30%)
US diagnostic
Surgery

73. Lower Extremity Occlusive Disease:
8-12 million affected
Independent risk factor for CAD
‘Intermittent claudication’
M,F (40-55)
Atherosclerosis, diabetes, HTN
erectile dysfunction,
claudication,
rest pain, and
gangrene
Triad of bilateral hip and buttock claudication, erectile dysfunction, and absent femoral pulses is known as Leriche's syndrome.

74. Tests Absent/ diminshed peripheral pulses
ankle–brachial index (ABI) - A normal ratio of ankle to brachial systolic blood pressures is 1.0; less than 0.8 is consistent with claudication.
Rest pain and nonhealing ulcers
Lipid-lowering medications have been shown to produce a 40% risk reduction for new-onset claudication or worsening of claudication.
phosphodiesterase inhibitor, cilostazol (100 mg orally twice daily)
Carnitine
Ginkgo biloba

75. Acute Limb Ischemia embolic, thrombotic, or traumatic.
six Ps: pain, pallor, pulselessness,
paresthesias, poikilothermia,
and paralysis.
Embolic- 90% cardiac
Heparin and embolectomy
EMERGENCY!
Critical time <6hrs

76. Thromboangiitis Obliterans (Buerger's Disease)
Cause unknown
M <40, smokers, European/Asiatic
Claudication/ Rest pain
Necrosis/ ulceration
Foot arch pain, rest pain, calf pain
Proximal pulses present / distal pulses absent
DD: ?SLE/ clotting disorders/ ergot ingestion, cannabis arteritis
STOP SMOKING

77. Vasculitis
fever, malaise, weight loss, elevated white blood cell count and sedimentation rate, arthralgias, conjunctivitis, or erythema nodosum.
Drugs- amphetamines, cocaine, hydralazine, procainamide
Infections-hepatitis B, gonococcus, streptococcus

78. Raynaud's Disease & Raynaud's Phenomenon
idiopathic, it is called Raynaud's disease.
precipitating systemic or regional disorder (autoimmune diseases, myeloproliferative disorders, multiple myeloma, cryoglobulinemia, myxedema, macroglobulinemia, or arterial occlusive disease), it is called Raynaud's phenomenon
? up-regulation of vascular smooth muscle 2-adrenergic receptors.
Episodic bilateral digital pallor, cyanosis, and rubor.
Precipitated by cold or emotional stress; relieved by warmth.
Seventy to 80 percent of patients are women.
digital color change (white-blue-red) with exposure to cold environment or emotional stress.

79. Raynaud's disease appears first between ages 15 and 45, almost always in women.
A patient with suggestive symptoms that persist for over 3 years without evidence of an associated disease is given the diagnosis of Raynaud's disease.

81. Varicose Veins
Dilated, tortuous superficial veins in the lower extremities.
Associated with fatigue, aching discomfort, bleeding, or localized pain.
Edema, pigmentation, and ulceration suggest concomitant venous stasis disease.
Increased frequency after pregnancy.
? varicoceles, esophageal varices, and hemorrhoids
Seen in 15% long saphenous veins
Factors: F, pregnancy, family history, prolonged standing, and history of phlebitis
Inherited vein wall or valvular defect

82. Varicose Veins
Dull, aching heaviness or a feeling of fatigue brought on by periods of standing is the most common complaint.
Itching from an associated eczematoid dermatitis may occur above the ankle.
Complications of varicose veins include secondary ulceration, bleeding, chronic stasis dermatitis, superficial venous thrombosis, and thrombophlebitis.

83. Varicose Veins Therapy- Non surgical- compression stockings
Leg elevations/exercises/ Ace wraps
Surgery- ligations
10% recur
endovenous laser ablation (EVLA)
ultrasound guided sclerotherapy (UGS)
varicose vein surgery
EVLA uses a laser fiber inside the vein to permanently seal the abnormal varicose vein.

84. DVT
Pain in the calf or thigh, often associated with edema. Fifty percent of patients are asymptomatic.
History of congestive heart failure, recent surgery, trauma, neoplasia, oral contraceptive use, or prolonged inactivity.
Physical signs unreliable.
Duplex ultrasound is diagnostic.
800,000 new patients/year
stasis, vascular injury, and hypercoagulability

85. DVT 65% recover 35% develop post dvt venous insufficiency
80% DVT in calf
Related to surgery 3% show symptoms/ 30% show no signs/symptoms
Contributing factors: Prolonged bed rest or immobility caused by cardiac failure, stroke, ventilatory support, pelvic bone or limb fracture, paralysis, extended air travel, or a lengthy operative procedure

86. DVT Other risk factors- advanced age type A blood group Obesity
previous thrombosis
multiparity
use of oral contraceptives
inflammatory bowel disease and
lupus erythematosus
50% asymptomatic
Uncommon causes-
malignancy
nephrotic syndrome
inherited deficiency disorders-
protein C or S or antithrombin III,
homocystinuria,
factor V Leiden mutation, or
paroxysmal nocturnal hemoglobinuria

87. Diagnostic tests necessary – Duplex Doppler US Venograms rarely used
D-dimer test
Complications of DVT include pulmonary embolism
Therapy- Heparin and warfarin
For the first episode of uncomplicated DVT is 3–6 months of warfarin to maintain a goal INR of 2.0–3.0. After a second episode, warfarin is continued indefinitely.
Recent evidence suggests that a negative D-dimer test in a patient in whom DVT is suspected is sufficient to omit ultrasound testing.

88. Chronic venous insufficiency
History of phlebitis or leg injury.
Ankle edema is the earliest sign.
Late signs are stasis pigmentation, dermatitis, subcutaneous induration, varicosities, and ulceration.
incurable but manageable problem.

89. Lymphangitis & Lymphadenitis
Red streak extending from an infected area toward enlarged, tender regional lymph nodes.
Chills, fever, and malaise may be present.
Streptococcal or staphylococcal infections
Superficial scratch with cellulitis, an insect bite, or an established abscess.
Red streak extending toward tender, enlarged regional lymph nodes is diagnostic.
WBC elevated
DD Cat scratch disease (Bartonellosis)
IV antibiotics otherwise septicemia can happen

90. Lymphedema Painless edema of upper or lower extremities.
Involves the dorsal surfaces of the hands and fingers or the feet and toes.
Developmental or acquired, unilateral or bilateral.
Edema is pitting initially and becomes brawny and nonpitting with time.
Ulceration, varicosities, and stasis pigmentation do not occur. There may be episodes of lymphangitis and cellulitis.

91. Lymphedema causes Congenital Familial Unilateral (F:M 3.5:1)
Secondary- Obstruction lymphatics/ Lymphnode resection/ Radiation/ Lymphomas/
No cure
External compression, leg elevation, massage