HTA Flashcards
BLOOD PRESSURE (BP)
The force exerted by the blood against any unit area of the vessel wall
• Standard Units of Pressure: millimeters of mercury (mm Hg)
→ because the mercury manometer has been used since antiquity as the standard reference for measuring pressure
BP in the arterial system it is Labile & Varies
1.During the cardiac cycle
‒ Peak (↑) in systole (SBP) and
‒ Fall (↓) to its lowest trough in diastole (DBP)
→ levels that may be measured with the blood pressure cuff, or sphygmomanometer
- With respiration (SBP fall during inspiration)
- Standing SBP should not drop more than 10 mm Hg, and diastolic pressure should remain unchanged or rise slightly, after resting supine
PULSE PRESSURE
=The difference between SBP and DBP
FACTORS THAT MAY ALTER SYSTOLIC PRESSURE,
DIASTOLIC PRESSURE, OR BOTH
- Left ventricular stroke volume
- Ejection velocity
- Distensibility of the aorta and the large arteries
- Peripheral vascular resistance, particularly at the arteriolar level
- Volume of blood in the arterial system
Blood pressure levels vary over 24-hour period with:
Physical activity Emotional state Other conditions: pain Environmental factors: noise, temperature Diet: salt Tobacco Drugs
HOW IS BLOOD PRESSURE REGULATED?
Hemodynamic Factors
BP = CO (Cardiac Output) x TPR (Total Peripheral Resistance)
CO = SV (Stroke Volume) x HR (Heart Rate):
SV is determined by:
(1) Cardiac Contractility
(2) the Preload (The venous return to the heart)
(3) the Afterload (The resistance the LV must overcome to eject blood into aorta)
BP directly regulated by 4 systems
- the Heart, which supplies the Pumping pressure
- the blood vessel Tone, which largely determines systemic Resistance
- the Kidney, which regulates Intravascular Volume
- Hormones, which modulate the functions of the other 3 systems
Regulation of systemic blood pressure
SLIDE 3
How BP levels increases CVD risk
In people between 40–70 yo HTN double the risk of CVD with 20 mm
SBP or with 10 mm
DBP
Hypertension-Epidemiology
Prevalence
> 1 in 5 Women & 1 in 4 Men have HTN (reported by WHO)
> 150 million Europe (central and eastern)
121.5 mil. adults ≥ 20 y USA (63.1 M; 58.4 F)
~ 1,13 billion global prevalence estimated - 2015
Increases with ageing > 60% older >60 y
1,5 bill pts. estimated → 2025
What is hypertension ?
A major public health problem
A major modifiable risk factor for
- Stroke,
- Myocardial infarction,
- Vascular disease, and
- Chronic kidney disease
the major Preventable cause of - Cardiovascular disease (CVD) and
- All-cause death
HYPERTENSION DEFINITION
Difficult issue because:
- in the overall population BP has a typical bell-shaped curve distribution
- the distinction between Normotension and Hypertension, based on cut-off BP values is Arbitrary (Sir George Pickering)
- The relationship between BP value and related Events (CV and renal)
is Continuous and Progressive without a definite threshold
HYPERTENSION DEFINITION
The most used definitions
- The value from which the long-term risk doubles
- As stated by Rose (1980): “The operational definition of hypertension is the level at which the benefits… of action exceed those of inaction
HYPERTENSION DEFINITION IS ___ BUT
(1)Conventional,
Modifiable and
Perfectible
(2) BUT
“physicians feel more secure when dealing with precise criteria, even if the criteria are basically arbitrary”
medical practice needs a Delimitation Criteria for
1. Diagnosis and
2. Therapeutic approach
CURRENT HTN DEFINITION: 03/2021
based on an average of ≥ 2 careful readings obtained on ≥ 2 occasions
ESC & WHO Definition Hypertension is defined as OFFICE SBP values ≥ 140 mmHg and / or DBP (diastolic BP ) values ≥ 90 mmHg
Based on evidence from multiple
RCTS that treatment of patients with these BP values is
beneficial
The same classification is used in younger, middleaged, and older people, whereas BP centiles are used in children and teenagers, in whom data from interventional trials are not available.
- 2017 ACC/AHA Definition (US) BP categories are:
Normal: Less than 120/80 mm Hg;
Elevated: Systolic between 120-129 and diastolic less than 80;
Stage 1: Systolic between 130-139 or diastolic between 80-89;
Stage 2: Systolic at least 140 or diastolic at least 90 mm Hg
Criteria for Hypertension Based on Office-, Ambulatory (ABPM)-, and Home Blood Pressure (HBPM) Measurement
SBP/DBP, mm Hg
Office BP ≥140 and/or ≥90
ABPM
24-h average ≥130 and/or ≥80
Day time (or awake) average ≥135 and/or ≥85
Night time (or asleep) average ≥120 and/or ≥70
HBPM ≥135 and/or ≥85
HTN Classification__1.
According to presumptive etiology
Primary hypertension: 90 to 95% of HTN patients
= Idiopathic: Presumed Environmental and genetic/epigenetic causes
(! NB the term essential hypertension replaced now by primary
Secondary hypertension (or Identifiable causes HTN): 5- 10%
HTN Classification __1
According to hemodynamic subtypes
Systolic hypertension in teenagers and young adults
Diastolic hypertension in middle age
Isolated systolic HTN in older adults
HTN classification__2.
Classification of Office blood pressurea and
definitions of hypertension gradeb
Category Systolic(mmHg) Diastolic(mmHg)
Optimal <120 and <80
Normal 120–129 and/or 80–84
High normal 130–139 and/or 85–89
Grade 1 hypertension 140–159 and/or 90–99
Grade 2 hypertension 160–179 and/or 100–109
Grade 3 hypertension ≥ 180 and/or ≥ 110
Isolated systolic hypertension(b) ≥ 140 and < 90
HTN: other classification__3.
According to circumstances
‒ White coat hypertension
‒ Masked hypertension
According to circadian pattern
‒ Dipper (BP decreased at night)
‒ Non-dipper (average night= average day)*
‒ Reverse dipper (BP increases during night time)*
* ↑ mortality, ↑ morbidity risk
CONSEQUENCES OF HYPERTENSION
Subclinical Hypertension Mediated Organ Damage
LVH Electrocardiographic (Sokolow -Lyon >38 mm; Cornell >2440 mm*ms) or
LVH Echocardiographic (LVMI: Men 125 g/m2, Women ≥ 110 g/m2)
Carotid wall thickening (IMT > 0.9 mm) or plaque
Carotid-femoral pulse wave velocity >12 m/s
Ankle/brachial BP index <0.9
Slight increase in plasma creatinine
M: 115–133 mmol/l (1.3–1.5 mg/dl); W: 107–124 mmol/l (1.2–1.4 mg/dl)
Low estimated glomerular filtration rate (<60 ml/min/1.73 m2- MDRD) or creatinine clearance (<60 ml/min-Cockroft Gault formula)
Microalbuminuria 30–300 mg/24 h or albumin-creatinine ratio: ≥22 (M); or ≥31 (W) mg/g creatinine
CONSEQUENCES OF HYPERTENSION
Clinical Hypertension Mediated Organ Damage 1,2
- Cerebrovascular disease
- Ischemic stroke
- Cerebral hemorrhage
- Transient ischemic attack
- Lacunar syndrome
- Cognitive impairment - Heart disease
- LVH- left ventricular hypertrophy
- Hypertensive heart disease
- Ischemic heart disease (Angina,
- Myocardial infarction, Acute coronary syndr.; Coronary revascularization)
- Atrial fibrillation
- LV Diastolic and systolic dysfunction; Heart failure
CONSEQUENCES OF HYPERTENSION
Clinical Hypertension Mediated Organ Damage 3,4,5
- Renal disease
- Proteinuria (>300 mg/24 hr)
- Hypertensive nephropathy
(Nephrosclerosis)
- Chronic kidney disease - Vascular complications
- Peripheral arterial disease &
- Intermittent claudication
- Aortic Aneurism & Ao dissection - Eye
- Arterial narrowing
- Advanced retinopathy
- Hemorrhages or exudates
- Papilledema
Pathogenesis of the major consequences of HTN
slide 13
Diagnostic evaluation
Aims
(1) Establishing BP levels: BP measurement
(2) Identifying secondary causes of hypertension
(3) Evaluating the overall cv risk by searching for
Other associated risk factors
HTN mediated organ damage (HMOD)
Concomitant diseases or accompanying clinical conditions
(4) Identify reversible exacerbating factors
(5) Document progression
The diagnostic procedures:
1. Anamnesis
2. Medical history
3. Physical examination in the setting of HTN, but not only
4. Laboratory and instrumental investigations
(1) BP measurement
4 approaches to BP measurement
- Conventional office BP
- Automated office BP
- Home monitoring
- Ambulatory BP monitoring
All cases
BP should be measured with appropriate technique
Using validated & periodically calibrated devices
Home readings taken under varying circumstances AND 24-hr ambulatory
recordings may be Preferable and more accurate in Predicting subsequent
cardiovascular disease
BP measurement: Conditions for the Patient
POSTURE
Sitting pressures are usually adequate for routine follow-up.
Patient should sit quietly with back supported for 5 min and arm supported at level of heart
Measure BP 1 min & 3 min after standing from a seated position in all patients at the first measurement to exclude orthostatic hypotension.
For patients > 65 yr, Diabetic, or receiving Antihypertensive Therapy, check for postural changes (Lying and standing BP) in subsequent visits.
BP measurement: Conditions for the Patient
Circumstances
Quiet, warm setting
The patient should avoid caffeine, exercise, and smoking for at least 30 minutes before measure
No exogenous adrenergic stimulants (e.g., phenylephrine in nasal decongestants or eye drops for pupillary dilation)
Neither the patient nor the observer should talk during the rest period or during the measurement
Remove clothing covering the location of cuff placement
The patient should not be holding his/her arm because isometric exercise will affect the BP levels.
BP measurement: Equipment
Cuff size:
Use a standard bladder cuff (12–13 cm wide and 35 cm long) for most patients, but have larger and smaller cuffs available for larger (arm circumference >32 cm) and thinner arms, respectively
The cuff should be positioned at the level of the heart, with the back and
arm supported to avoid muscle contraction and isometric exercise- dependant increases in BP
The bladder should encircle and cover 2/3 of the length of the arm; if bladder is too small, false high readings may result
Manometer: Auscultatory or Oscillometric Mercury Sphygmomanometers Aneroid Sphygmomanometers Electronic Oscillometric Sphygmomanometers Should be calibrated periodically
For infants, use ultrasound equipment, e.g., the Doppler method
BP measurement: Technique
- BP cuff should be placed on bare skin
* Shirtsleeves should not be rolled up because this may create a tourniquet effect.
BP measurement: Technique
Cuff Placement and Stethoscope
• The observer must first palpate the brachial artery in the ante-cubital fossa and place the center of the bladder length of the cuff (commonly marked on the cuff by the manufacturer) so that it is over the arterial
pulsation of the patient’s bare upper arm
• The lower end of the cuff should be 2 to 3 cm above the antecubital fossa
BP measurement: Performance
1) Inflate the bladder quickly to a pressure 20 mm Hg Above the Systolic,
→ as recognized by disappearance of the radial pulse
2) Deflate the bladder 2-3 mm Hg every second
3) Record the Korotkoff phase I (appearance) & Korotkoff phase V (disappearance) except in little children, in whom use of phase IV (muffling) may be preferable
Korotkoff Phase
If Korotkoff sounds are weak, have the patient raise the arm and open and close the hand 5-10 times, after which the bladder should be inflated quickly
Record heart rate and use pulse palpation to exclude arrhythmia.
Additional measurements may have to be performed in patients with unstable BP values due to arrhythmias, such as in patents with AF, in whom manual auscultatory methods should be used as most automated devices have not been validated for BP
measurement in patients with AF (atrial fibrilation)
BP measurement: Technique
Number of readings
Average readings
Number of readings
On each occasion,
3 BP measurements should be recorded, 1–2 min apart,
+ additional measurements only if the first 2 readings differ by >10 mmHg
BP is recorded as the average of the last two BP readings
Average readings:
Use an average of ≥2 readings obtained on ≥2 occasions
BP measurement : For Diagnosis
Whenever possible, the diagnosis should not be made on a single office visit.
Usually 2–3 office visits at 1–4-week intervals (depending on the BP level) are
required to confirm the diagnosis of hypertension.
The diagnosis might be made on a single visit, if BP is ≥180/110 mm Hg and there is evidence of cardiovascular disease (CVD)
Orthostatic hypotension is defined as a reduction in SBP of ≥ 20 mmHg or in DBP of ≥ 10 mmHg within 3 min of standing
If possible and available, the diagnosis of HTN should be confirmed by out-of-
office BP measurement (ISH 2020)
Initially
Take pressure in both arms;
→ if pressure differs, use arm with higher pressure, for further readings
If arm pressure is elevated,
→ take pressure in one leg, particularly in pats. younger than 30 y
BP measurement: Recordings
- Note the Pressure, patient Position, which Arm, and cuff Size (e.g., 140/90, seated, right arm, large adult cuff)
- Note the time that the most recent BP medication was taken before measurements.
Interpretation
- Blood pressure of 2–3 office visits ≥140/90 mm Hg indicates hypertension
Provide patients their SBP/DBP readings both verbally and in writing.
Checklist for Accurate Measurement of BP
Key Steps for Proper BP Measurements
Step 1: Properly prepare the patient.
Step 2: Use proper technique for BP measurements.
Step 3: Take the proper measurements needed for diagnosis and
treatment of elevated BP/hypertension.
Step 4: Properly document accurate BP readings.
Step 5: Average the readings.
Step 6: Provide BP readings to patient.
BP Measurement Definitions
BP Measurement Definition
SBP : First Korotkoff sound*
DBP : Fifth Korotkoff sound*
Pulse pressure : SBP minus (-) DBP
Mean arterial pressure : DBP plus (+) 1/3 pulse pressure†
Mid-BP : Sum of SBP and DBP, divided by 2
†Calculation assumes normal heart rate .
BP indicates blood pressure; DBP, diastolic blood pressure; and SBP, systolic blood pressure.
Selection Criteria for BP Cuff Size for Measurement of
BP in Adults
Arm Circumference Usual Cuff Size
22–26 cm Small adult
27–34 cm Adult
35–44 cm Large adult
45–52 cm Adult thigh
(2) Identifying secondary causes of
hypertension : 1+2+3
1. Renal causes (2.5-6%) [parenchymal &vascular diseases] - Chronic kidney disease - Polycystic kidney disease - Urinary tract obstruction - Renin-producing tumor - Renovascular: Stenoses (Atherosclerotic, Fibromuscular Dysplasia), Embolism, - Vasculitis 2. Vascular causes - Coarctation of aorta - Vasculitis - Collagen vascular disease
- Hormonal causes
- Primary hyperaldosteronism
- Cushing syndrome
- Pheochromocytoma
(2) Identifying secondary causes of
hypertension : 4+5+6
- Neurogenic causes
- Brain tumor
- Autonomic dysfunction
- Sleep apnea
- Intracranial hypertension - Drugs and toxins
- Alcohol, cocaine, NSAIDS,
- Erythropoietin, Adrenergic medications
- Decongestants containing ephedrine Herbal remedies containing licorice or ephedrine, nicotine - Other causes
- Hyper and hypothyroidism
- Hypercalcemia, Hyperparathyroidism
- Obstructive sleep apnea
- Pregnancy-induced hypertension
- Acute stress: massive burns, trauma, surgery
(3) Evaluating the overall (total) cv risk
What is Risk ?
• A cumulative probability of an event, usually expressed as percentage
Example: 5 CV events in 100 pts = 5 % risk
This is called an Absolute risk & Refers to a specific time period (10 yr)
Relative risk (RR) is a ratio of risks
Example: 12% risk in hypertensives, 4% risk in normotensives→ RR = 0.12 / 0.04 = 3
“hypertensives have 3 times the risk of normotensives”
Lifetime risk is the Absolute Risk of a person for an event during his/her whole remaining life
From individual point of view it is probably the most
accurate expression of Risk & of Intervention Benefit
(3) Evaluating the overall cv risk
by searching for
Other risk factors & total risk
Hypertension Mediated Organ Damage
Concomitant diseases or accompanying clinical conditions
ATS / CVD risk factors
MAJOR OTHERS
MODIFIABLE
1. Dyslipidemia ─ Obesity
─ LDL‐C (CT) ─ Insulin resistance
─ HDL ─ Sedentarism
─ TG ─ Possible/proposed risk factors for ATS
• Inflammation (hsPCR,fibrinogen, IL‐6,
2. Hypertension • ↑ Thrombogenic status
3. Diabetes • Homocysteine
4. Smoking • Lipoprotein (a)
─Nontraditional risk Factors
NON MODIFIABLE Rheumatoid arthritis
5. Male Sex ─ Family hyst. of of premature ATS/cvd
─ Age (yr)—men >55; women >65 yr
─ Poverty, low education
• Total CV Risk
Most patients have MULTIPLE CV risk factors
OF ALL HYPERTENSIVES
65% have dyslipidaemia
16% have T2 diabetes
45% are obese/overweight
OF ALL DYSLIPIDAEMICS
48% have HTN
14% have T2 diabetes
35% are obese/overweight
OF ALL T2 DIABETICS
60% have HTN
60% have dyslipidaemia
90% are obese/overweight
We need Total Risk Assessment Tools in Clinical Practice
And we as have Instruments: Several algorithms and charts
- Framingham (US)
- SCORE charts (ESC countries)
- UKPDS Risk Engine for T2DM, PROCAM, etc
Framingham vs SCORE
Framingham
- Based on 5000 Americans
- Predicts coronary event
- Includes nonfatal events
- Cannot be adjusted for national variations
SCORE -Based on > 200.000 Europeans -Predicts CVD -Restricted to fata events -Can be customized using national mortality statistics
Cardiovascular risk categories
- High-risk
People with:
- Markedly elevated single risk factors, in particular TC
>8 mmol/L
(>310 mg/dL), LDL-C >4.9 mmol/L (>190 mg/dL), or BP ≥180 / 110 mmHg.
- Patients with FH without other major risk factors.
- Patients with DM without target organ damage, a with DM duration ≥10 years or another additional risk factor.
- Moderate CKD (eGFR 30-59 mL/min/1.73 m2).
- A calculated SCORE ≥ 5% and <10% for 10-year risk of fatal CVD. - Moderate-risk
- Young patients (T1DM < 35 years; T2DM <50 years) with DM duration <10 yrs, without other risk factors.
- Calculated SCORE ≥ 1 % and < 5% for 10-year risk of fatal CVD. - Low-risk
- Calculated SCORE <1% for 10-year risk of fatal CVD.
Cardiovascular risk categories
- Very-high risk
People with any of the following:
- Documented ASCVD, either Clinical or unequivocal on Imaging.
- Documented ASCVD includes previous ACS (MI or unstable angina), stable angina, coronary revascularization (PCI, CABG, and other arterial
revascularization procedures), stroke and TIA, and peripheral arterial disease.
- Unequivocally documented ASCVD on imaging includes those findings that are known to be predictive of clinical events, such as significant plaque on coronary angiography or CT scan (multivessel coronary disease with two major epicardial arteries having >50% stenosis), or on carotid ultrasound.
- DM with target organ damage, a OR at least 3 major risk factors, OR early onset of T1DM of long duration (>20 years).
- Severe CKD (eGFR <30 mL/min/1.73 m2).
- A calculated SCORE ≥ 10% for 10-year risk of fatal CVD.
- FH with ASCVD OR with another major risk factor.
Anamnesis
Screening of Secondary Causes
History, Symptoms & Physical finding
‒ History of known renal disease, abdominal masses, anemia, and Urochrome pigmentation.
‒ History of sweating, labile hypertension, and palpitations (suggests the diagnosis of pheochromocytoma)
‒ History of cold or heat tolerance, sweating, lack of energy, and bradycardia or tachycardia (may indicate hypothyroidism or hyperthyroidism)
‒ History of obstructive sleep apnea
‒ History of weakness (suggests hyperaldosteronism)
‒ Kidney stones (raise the possibility of hyperparathyroidism)
ANAMNESIS
Evaluate the Presence of other Risk Factors
1.Hypertension: component of metabolic syndrome (MS)
2. Smoking (cigarettes, chewing tobacco)
3. Hypercholesterolemia or low HDL cholesterol as component of MS
4. Diabetes mellitus: component of Metabolic Syndrome (MS)
5. Obesity (BMI ≥30 kg/m2): component of MS
Age >55 y for Men OR > than 65 y for Women: Begins the Increased risk
(!Caveat: ATPIII used earlier age cut points to suggest the need for earlier action)
6. Estimated GFR < 60 mL/min
7. Microalbuminuria
8. Family history of premature cardiovascular disease (men < 55 y; women < 65 y)
9. Lack of exercise
ANAMNESIS
History taking
- Hypertension
- Premature CVD or death
- Familial diseases: pheochromocytoma, renal disease, diabetes, gout
Working and living condition assessment
Eg.: inactivity
Anamnesis
Duration of the hypertension
Prior treatment of the hypertension
Intake of agents that may interfere
Duration of the hypertension
- Last known normal BP
- Baseline values for judging biochemical effects of therapy
- Course of the BP
Prior treatment of the hypertension
Drugs: types, doses, side effects
Intake of agents that may interfere Drugs including over-the-counter medications - Nonsteroidal anti-inflammatory drugs - Corticosteroids - Oral contraceptives - Adrenergic medications - Excessive sodium intake
Alcohol (>2 drinks/day)
Herbal remedies containing licorice or ephedrine
The use of illicit drugs, such as cocaine
ANAMNESIS
Concomitant diseases
Pregnancy-induced hypertension
Dietary history
Weight change Fresh vs. processed foods Sodium intake Saturated fats Source of food preparation Adequate dietary intake of potassium, calcium, and magnesium
ANAMNESIS
Sexual function
Features of obstructive sleep apnea
Early morning headaches
Daytime somnolence
Loud snoring
Erratic sleep
Anamnesis
Symptoms: Hypertension is the “silent killer”
“an Asymptomatic chronic disorder that, undetected and untreated, silently damages the blood vessels, heart, brain, and kidneys.”
Ask for Symptoms of target organ damage
- Heart : Chest pain, Dyspnea
- Brain : Headaches, Dizziness
- Chronic kidney disease : Claudication, cold extremities
- Peripheral arterial disease : Transient weakness or blindness
- Retinopathy : Loss of visual acuity
SYMPTOMS of HYPERTENSIVE CRISIS* are not specific:
Symptoms are secondary to:
Acute end-organ damage
Neurologic: hypertensive encephalopathy, cerebral vascular accident/cerebral
infarction, subarachnoid hemorrhage, intracranial hemorrhage
Cardiovascular: myocardial ischemia/infarction, acute left ventricular
dysfunction, acute pulmonary edema, aortic dissection, unstable angina
Other: acute renal failure/insufficiency, papilledema / retinopathy, eclampsia,
microangiopathic hemolytic anemia
Headaches
Subconjunctival hemorrhage
Epistaxis (Nosebleeds)
Facial flushing
Chest pain
Visual changes, phosphenes
Tinnitus
Hematuria
Hypertensive Encephalopathy= Papilledema with the following: Headache, Blurred
vision, Confusion, Somnolence, → Coma
Dizziness (generally it is a side effect of some BP medications)
Symptoms
examples:
- Require hospitalization and parenteral drug therapy
*Terms Definition Hypertensive crises (HTN emergencies)
a heterogeneous group of hypertensive disorders
Charact. by severe HTN + acute TOD (brain, heart, kidney, retina, or blood vessels
BP ≥ 220/130 mm Hg (except women with preeclampsia without preexisting HTN)
* AHA 2018: Systolic over 180 and/or diastolic over 120
require immediate reduction of BP with IV medication
.
Hypertensive urgency
• severe uncontrolled HTN without evidence of acute TOD
• In the absence of Symptoms and Acute Target-organ damage, a patient with a BP of
220/130 mm Hg should be treated with a short-acting oral medication.
Severe hypertension
defined as a BP of 180/110 - 220/130 mm Hg without symptoms or acute target-
organ damage, almost always occurs in patients with chronic hypertension who depleted or discontinued their BP medication.
Long-acting oral medication can simply be restarted
Physical examination
- Normal or
- Abnormalities Secondary to Risk factors OR HMOD
Start with BP measurement
Both Arms
Arm & Leg systolic BP measurements: difference >20 mmHg
suggests Aortic Coarctation
Check for Orthostatic Hypotension
Assess for Obesity & Metabolic Syndrome
Weight, Height, BMI
Waist Circumference
Physical examination Skin Subcutaneous tissue Head & Eyes Neck Thorax
Skin Signs of Cushing's Disease: Striae, Acne Vulgaris, Hirsutism Subcutaneous tissue: edema due to Heart failure Renal diseases
Head & Eyes
Moon facies suggests Cushing’s syndrome
Examination of optic fundi for evidence of HMOD such as papilledema
Neck
Auscultation of the suprasternal notch to determine if a bruit suggestive of coarctation is present
Palpation of thyroid gland
Carotid Bruits (HMOD-carotid atherosclerosis)
Neck vein exam (JVD in HF)
Thorax
Respiratory
Auscultation: congestion rales (if Heart Failure+)
Physical examination
Cardiovascular Normal or modified depending on the target organ damage
Inspection: JVD if HF occur as a consequence of longstanding, untreated HTN
Palpation: strong ± displaced apical impulse (if cardiomegaly)
Percution: ±cardiomegaly (if LVH ± dilation) PMI displaced down to the left
Auscultation:
‒ Accentuated S2 Heart Sound in AoValve position
‒ S4 Gallop rhythm (decreased LV compliance, diastolic dysfunction)
‒ S3 Gallop rhythm (LV systolic disfunction)
‒ Tachycardia (compensatory if HF, in pheocromocytoma)
‒ Rhythm disturbances: eg. Irregular heart sounds (if Atrial fibrillation)
‒ Murmurs: eg.: Aortic Insufficiency murmur (if Ao anevrism/ Ao valve disease)
Asses together with:
Abnormal EKG or Echocardiogram findings;
Ask for Prior Angiography results
Physical examination Pulses Lower extremity Abdomen Neurologic
Pulses
- Asses Pulse Symmetry
- A radial femoral delay → (Aortic coarctation)
- Peripheral Vascular Disease
- Femoral bruits
- Femoral pulses: Delayed or absent in Aortic Coarctation
Lower extremity:
- Hair Loss in men if ischemic Skin lesions secondary to PVD
- Leg edema if HF occur
Abdomen
> Auscultation
- Abdominal bruit (suggest renal artery stenosis)
> Palpation
- Masses, Enlarged/ tender kidneys, Distended urinary bladder,
- Abnormal aortic pulsations: Aortic Aneurysm
Congestive hepatomegaly if HF present
Neurologic Stroke sequelae (Focal neurologic deficits)
Summary: What is hypertension ?
A number outside the normal range (Arbitrary value)
A risk factor for target organ damage (myocardium, arteries,
brain, kidney, eye)
A sign of a disease (glomerulonephritis, vasculitis,
pheochromocytoma)
An homeostasis parameter
(depends on other parameters, influences other parameters)
Expression of An altered cellular function
CO ← myocardial cell
TPR ← endothelium, vascular smooth muscle
→ A complex syndrome overall
Benefit of BP reduction in HTN patients
Benefits with antihypertensive therapy:
35-40% Average Reduction in Stroke incidence
20-25% Average Reduction in Myocardial infarction
>50% Average Reduction in Heart failure
“In stage 1 HTN (GRD 1 ESC) and additional CVD risk factors, achieving a sustained 12 mmHg reduction in SBP over 10 years will prevent 1 death for every 11 patients treated.”
