Transcript LESSON 3 - CatsTCMNotes

LESSON 3
HYPERTENSION __Ch. 11
VASCULAR DISEASES __Ch. 12
HYPERTENSION
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
3
Assessment and Diagnosis of HTN
4
Assessment and Diagnosis of HTN
5
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
6
secondary causes of hypertensionsuggestive (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,
urinalysis),
abnormal
(8) Poor response to drug therapy,
(9) SBP > 180 or DBP > 110 mm Hg, or
(10) sudden onset of hypertension.
7
JNC VII 2003 recommendations
Normal: recheck in 2 years (see
Comments)
1. Prehypertension: SBP 120–139 or DBP 80–89
Prehypertension:
2. Stage 1 hypertension: SBP 140–159 or DBP 90–99
recheck in 1 year
Stage 1 hypertension:
2 separate office visits)
confirm within 2 months
Stage 2 hypertension: evaluate
4. Perform physical exam and routine labs.a
or refer to source of care within 1
month (evaluate and treat
immediately if BP > 180/110)
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 white8
coat hypertension.
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
9
Lifestyle Modifications for
Primary Prevention of Hypertension
Modification
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 2–4 mm Hg
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.
10
? DASH:
Dietary Approaches to Stop Hypertension
Type of food
Number of servings
for 1600 - 3100
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
4-6
4-5
2-4
2-3
1.5 - 2.5
2 or less
3 - 6 per week
4 - 5 per week
2-4
limited
Low fat or non fat dairy foods
Lean meats, fish, poultry
Nuts, seeds, and legumes
Fats and sweets
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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 lowfat 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
2–4 mm Hg
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 lighterweight persons
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COMPELLING CONDITIONS
RECOMMENDED DRUGS
HIGH RISK
CONDITIONS
HEART FAILURE
DIURETIC
β BLOCKER
ACEi
ARB
ALDOSTERONE
ANTAGONIST
$
POST
MYOCARDIAL
INFARCTION
$
$
$
$
$
$
$
$
DIABETES
MELLITUS
$
$
$
$
$
$
CRHONIC KIDDNEY
DISEASE
$
$
$
HIGH CAD RISK
REURRENT
STROKE
PREVENTION
CCB
$
$
$
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PRIMARY HYPERTENSION
NO IDENTIFIABLE CAUSE (95%)
30% OF BLACKS/20% OF WHITES
25-55 YEAR AGE GROUP
MULTIFACTORIAL
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PRIMARY HYPERTENSION: CAUSES
GENETIC
OBESITY
SALT INTAKE
SYMPATHETIC SYSTEM OVERACTIVITY
ABNORMAL CVS DEVELOPMENT
RENIN-ANGIOTENSIN ACTIVITY
ALCOHOL/CIGARETTE/POLYCYTHEMIA
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Associated causes of hypertension
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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
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RENAL ARTERY STENOSIS
1-2% OF HTN PATIENTS
YOUNGER(<20 YRS AGE)
FIBROMUSCULAR HYPERLASIA (f<50)
LEADS TO EXCESSIVE RENIN RELEASE
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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
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RENAL ARTERY STENOSIS
TestsRadioisotope renography
duplex us
MRA/CT ANGIO
RENAL ARTERIOGRAPHY
TREATMENT- vascular reconstruction
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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
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CUSHING’S SYNDROME
Glucocorticoid excess
HTN (75-85%) of cases
Increased Rennin-Angiotensin
activity
21
Pheochromocytoma
0.1% of all htn patients
2/1ooo,ooo incidence
Hypertensive crisis (BP 300>)
Associated with Café au Lait spots
and neurofibromatosis
22
Other causes for secondary HTN
Estrogen
Acromegaly
Hyperthyroidism
hypothyroidism
DRUGS: cyclosporine and NSAIDs
23
Complications of HTN
excess morbidity and mortality related to
hypertension
risk doubles for each 6 mm Hg increase in diastolic
blood
24
Complications of HTN
Cardiac Complications –
Left Ventricular Hypertrophy congestive
heart failure
ventricular arrhythmias
myocardial ischemia and
sudden death.
25
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
26
Complications of HTN
Hypertensive Renal Disease –
renal insufficiency
hypertensive nephropathy
more common in blacks
associated with Diabetes Mellitus
Benefits with ACEi therapy
27
Complications of HTN
Aortic dissection
Increased Atherosclerosis
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SYMPTOMS OF HTN
mainly referable to involvement of the target organs:
Heart
Brain
Kidneys
Eyes and
Peripheral arteries.
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Symptoms of HTN
Mainly asymptomatic
Early morning suboccipital pulsating HA
Hypertensive Encephalopathy:
Somnolence/confusion/Visual/
Nausea/Vomiting
(Diastolic BP >130)
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Signs of HTN
Heart: Left ventricular enlargement/Hypertrophy
LAB workup: CBC/Urinalysis/FBS/LIPIDS/
Serum Uric Acid /Electrolytes/Creatinine/
BUN
ECG/CXR
31
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
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Goals of the Initial Evaluation
1.Establish the diagnosis.
2.Staging the disease. If present, hypertension is staged using
the criteria outlined in the JNC 7 consensus statement. This guides
immediate management.
3.Rule out secondary hypertension.
4.Identify end-organ effects. The initial history, physical
examination, and laboratory work-up should include investigations that
will identify common end-organ damage
5.Identify the presence or absence of other major cardiovascular
risk factors, in particular those that are modifiable with intervention.
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ECG: LV Strain Pattern
Suggests Advanced disease
Poor prognosis
Other Investigations:
Renal US/CT/MRI
scans
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Management Algorithm
35
NON PHARMACOLOGIC THERAPY
CHANGE LIFESTYLE: DASH DIET
Weight reduction
Reduced alcohol consumption
Reduced salt intake
Gradually increasing activity levels
36
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 )
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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%
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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.
39
Adrenergic Blocking Agents
Beta blockers
decrease the heart rate and cardiac output
Acebutolol(Sectral®)
Atenolol(Tenormin®)
Metoprolol(Lopressor®)
Pindolol (Visken®)
Propranolol (Inderal®)
40
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
41
ACE Inhibitors
initial medication
Benazepril (Lotensin®)
Captopril (Capoten®)
Enalapril (Vasotec®)
42
RAAS System
43
Side Effects Of ACEi
Cough
hypotension
dizziness
renal dysfunction
hyperkalemia
angioedema
taste alteration and
rash
Contraindicated in pregnancy
Acute Renal Failure
44
Angiotensin Receptor Blockers:
ARBs
Candesartan (Atacand®)
Eprosartan (Teveten®)
Irbesartan (Avapro®)
Losartan (Cozaar®)
do not cause cough
45
The ABCD
rule
B* and D* may induce more new-onset diabetes
A= ACEi or ARBs
*B=β Blockers
C= CCBs
*D= Diuretic (thiazide)
46
BHS Guidelines
Young
A
A
B
C
D
Elderly
B
C
ACE Inhibitor
Beta Blocker
Calcium Channel Blocker
Diuretic
(low renin)
D
47
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
48
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
49
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)
50
HTN Crisis
hypertensive nephropathy (hematuria, proteinuria,
and progressive renal dysfunction )
intracranial hemorrhage, aortic dissection,
preeclampsia-eclampsia, pulmonary edema, unstable
angina, or myocardial infarction
51
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
52
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
53
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
54
Findings in
Cor Pulmonale
chronic productive
cough
exertional dyspnea
wheezing respirations
easy fatigability, and weakness
oxygen saturation is often
below 85%
55
Cor Pulmonale
Oxygen
salt and fluid restriction and
diuretics
the average life expectancy is 2–5 years when CHF
appears
56
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
57
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
58
Hypotension & Shock
Features
Hypotension,
tachycardia,
oliguria,
altered mental status.
Peripheral hypoperfusion and
 hypoxia.
60
physiologic response to Shock
Sympathetic response
Release of Norepinephrine
Renin
ADH
Glucagon
Cortisol
Growth Hormone
61
Causes
Hypovolemic
Cardiogenic
Obstructive- Pneumothorax/
Pulmonary embolism
Distributive- pancreatitis
Septic shock
62
Features of Septic Shock
fever
chills
hypotension
Hyperglycemia and
 altered mental status
due to gram-negative bacteremia: (E coli, Klebsiella,
Proteus, and Pseudomonas)
63
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
64
Treatment General Measures
Basic life support-(BLS) airway/oxygen/cpr
Advanced Cardiac Life Support – (ACLS)
65
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
66
VASCULAR DISORDERS
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.
68
AAA
90% below the level of renal arteries
Normal aortic diameter 2cms. >3 cms is aneurysm
1951 from 8.7 per 100,000
1980 36.5 per 100,000
Prevalence 5-8% M > 65
US screen
Associated with popliteal artery aneurysms
69
AAA Rupture Signs!
A RED FLAG needs referral to ER
Severe back/ abdo/flank pain
Hypotension
90% fatal unless repaired surgically
70
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%
71
Peripheral Artery Aneurysms
(Popliteal & Femoral)
M >50
Associated AAA
Popliteal most common peripheral
artery aneurysm
Arterial thrombus rather than rupture –
needs amputation (30%)
US diagnostic
Surgery
72
Lower Extremity Occlusive
Disease:
8-12 million affected
Independent risk factor for CAD
‘Intermittent claudication’
M,F (40-55)
Atherosclerosis, diabetes, HTN
Triad of bilateral hip and
erectile dysfunction,
buttock claudication, erectile
claudication,
dysfunction, and absent
rest pain, and
femoral pulses is known as
gangrene
Leriche's syndrome.
73
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
74
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
75
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
76
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
77
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
receptors.
2-adrenergic
78
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.
79
80
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
81
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.
82
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
83
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
84
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
85
DVT
Other risk factorsadvanced age
Uncommon causestype A blood group
malignancy
Obesity
nephrotic syndrome
previous thrombosis
inherited deficiency disordersmultiparity
protein C or S or antithrombin III,
use of oral contraceptives
homocystinuria,
inflammatory bowel disease and
factor V Leiden mutation, or
 lupus erythematosus
 paroxysmal nocturnal
50% asymptomatic
hemoglobinuria
86
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.
87
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.
88
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
89
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.
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Lymphedema causes
Congenital
Familial
Unilateral (F:M 3.5:1)
Secondary- Obstruction lymphatics/ Lymphnode
resection/ Radiation/ Lymphomas/
No cure
External compression, leg elevation, massage
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