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56 CHAPTER 4: Vital Signs, Anthropometric Data, and Pain
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FIG. 4-2Sites of Palpable Arteries. A. The temporal artery is anterior to the ear and overlies the temporal
bone, one of the few normally tortuous arteries. The common carotid is deep in the neck near the anterior border of the
sternocleidomastoid muscle. The bifurcation of this artery is opposite the superior border of the thyroid cartilage. The carotid
sinus is at the bifurcation. B. Elongation or dilation of the ascending aorta and arch makes this vessel accessible
to palpation in the suprasternal notch. With slight shifting to the right or left, the innominate or left carotid arteries may also
be felt in the notch. C. The brachial artery lies deep in the biceps-triceps furrow on the medial side of the arm near the
elbow. It courses toward the midline of the antecubital fossa, where it is usually just medial to the biceps tendon. D. The
radial artery is just medial to the outer border of the radius and lateral to the tendon of the flexor carpi radialis, where the
finger can press it against the bone. The ulnar artery is in a similar position to the ulna, but it is buried deeper, so it often
cannot be felt. E. The abdominal aorta and parts of the iliac arteries can usually be felt as generalized pulsations
through the abdominal wall. The femoral artery is palpable at the inguinal ligament midway between the anterior superior
iliac spine and the pubic tubercle. F. The posterior tibial artery is palpable as it curves forward below and around the
medial malleolus of the tibia. The dorsalis pedis artery is felt usually in the groove between the first two tendons on
the medial side of the dorsum of the foot.
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FIG. 4-3Disturbances of Cardiac Rate and Rhythm II. In all diagrams, the audible heart sounds are the only
physical signs indicating the mechanism. A. Second-degree AV block with a 2:1 ratio. Alternate stimuli from the
atria are blocked in the AV node, so the ventricles beat only half as fast as the atria. The only physical sign is a slow regular
heartbeat with first sounds of equal intensity. B. Complete AV block. The ventricles beat independently of the atria,
usuall y with a rate <50/min accelerating minimally with exertion. A louder-than-common first sound occurs when ventricular
filling is augmented by an atrial contraction occurring by chance at the optimal time; this is called by the French—the “bruit
de canon.” C and D. When ventricular beats are regular with rates between 160 and 220/min, two conditions must be
distinguished. C. Paroxysmal atrial tachycardia. D. Atrial flutter. Vagal st imulation may convert paroxysmal atrial
tachycardia to normal rhythm, but there is no temporary slowing. In contrast, the only response of flutter to vagus stimulus
is slowing for a few beats.
tachycardia with block, idioventricular tachycardia (accelerated ventricular
rhythm and slow or benign VT), and atrial utter (Fig. 4-3D) with 3:1 or 4:1
AV block.
Irregular rhythms without pattern. Consider atrial utter with variable AV
block, atrial brillation, multifocal atrial tachycardia (MAT), and frequent
atrial or ventricular premature beats occurring without a consistent pattern.
These rhythms produce rates of 50–200 bpm. Atrial utter with variable AV
block rarely exceeds 150 bpm and MAT is usually 100–150 bpm.
Regularly irregular rhythms. Consider atrial or ventricular premature beats
occurring at regular intervals (i.e., bigeminal, trigeminal, and quadrigeminal premature beats) or Mobitz I (Wenckebach) AV block producing grouped
beats. An ECG is necessary for denitive diagnosis.
Common dysrhythmias and their physical signs. Only an electrocardio-
gram can diagnose specic rhythms.
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Respiratory (sinus) arrhythmia. Depolarizations originate in the SA node
and conduct normally. The heart rate accelerates near end-inspiration and
decelerates during expiration (Fig. 4-1D). This is less noticeable at slow rates.
This is normal.
Sinus tachycardia.
rate of SA node depolarizations to 100–160 bpm with a regular rhythm; conduction is normal. Vagal stimulation produces smooth deceleration. This is
normal and expected with exercise, anxiety, hyperthyroidism, anemia, fever,
pregnancy, β-adrenergic medications, and deconditioning from any cause.
Absence of tachycardia in these situations requires an explanation. DDX: At
rates >140, sinus tachycardia must be distinguished from atrial utter with
2:1 block. In utter, vagal stimulation slows the rate stepwise; PAT doesn’t
slow but can convert to NSR.
Orthostatic tachycardia. See page 67, Orthostatic Hypotension. A pulse rise
>15 bpm going from supine to sitting or measured 2 minutes after going from
sitting to standing, suggests intravascular volume depletion.
Postural orthostatic tachycardia syndrome (POTS).
It usually affects women 15–50 years of age following a minor illness. Standing
from lying or sitting increases the heart rate to >120 bpm or >30 bpm above
baseline. Tachycardia is often associated with tremor, palpitations, and nausea (signs of autonomic hyperactivity) or light headedness, weakness, and
visual changes (signs presyncope). Sinus bradycardia.
vagal stimulation or a SA node disorder. The rhythm is regular, and conduc-
tion is normal. Rates are rarely <40 bpm. This is expected in well-conditioned
athletes. Severe hypothyroidism and sick sinus syndrome (SSS) are other
causes. DDX: The rate accelerates smoothly with exertion.
Sinus rhythm with second-degree AV block.
block, there is decremental conduction in the AV node so that, after a series of
conducted beats, one beat is dropped. This produces grouped beats with a P
to QRS ratio of n:n–1 (e.g., 3:2, 5:4). In Mobitz II block, SA impulses are regularly blocked in the His bundle or below; complete heart block may occur. The
atrial rate is a multiple of the ventricular rate, 2:1, 3:1, 4:1, or higher, e.g., when
every third atrial impulse is transmitted, it is 3:1 block.
common AV block. The ventricular complexes appear in groups followed by
a pause. The beat-to-beat interval shortens until a beat is dropped producing
a longer pause, then the cycle repeats. The shortening R-R interval is only
apparent on ECG. In Mobitz II block, ventricular systoles occur at regular
intervals with a rate dependent upon the sinus rate and degree of block (Fig.
4-3A). Each beat has the same intensity. In 2:1 block, two A-waves may be
seen in the jugular vein for each ventricular contraction. Although 2:1 block is
relatively common, 3:1 block is rare. DDX: In sinus bradycardia and seconddegree block the rate increases with exertion.
CLINICAL OCCURRENCE: Acute infections (especially rheumatic fever,
Lyme disease, and diphtheria), valvular heart disease, digitalis intoxication,
hyperkalemia, drugs (diltiazem, verapamil, β-blockers), coronary artery
disease.
Exertion and increased sympathetic tone increase the
The cause is unknown.
The slow rate is due to
In Mobitz I (Wenckebach) AV
Mobitz I is the most
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Third-degree (complete) AV block. The atria beat regularly, but there
is no conduction from the atria to the ventricles. Block may occur in the
AV node or ventricular conduction system (His bundle or both bundle
branches). Junctional pacemakers establish an escape rhythm at 25–60
bpm; the higher the pacemaker, the faster the escape rate. Ventricular
contractions are regular. When an atrial systole precedes ventricular con-
traction, the intensity of the heart sounds increases (Fig. 4-3B). When
ventricular contraction and atrial contraction nearly coincide, there is a
booming sound, bruit de canon; it comes infrequently, so listen for >60
seconds. The causes are the same as second-degree AV block with the
addition of degenerative and granulomatous diseases such as sarcoid-
DDX: Exertion does not accelerate the ventricular rate. The varia-
osis.
tion in intensity of the rst sounds is distinctive.
Premature beats.
A depolarization arises from an ectopic focus in the atrium
or ventricle producing a premature beat. An atrial premature beat occurs
before its expected time (Fig. 4-1B) with a shorter compensatory pause than
with ventricular premature beats. If the premature beat occurs shortly after
a normal ventricular systole, ventricular lling is minimal, the heart sounds
are less intense, and the stroke volume may be insufcient to produce a palpable arterial pulse. Very frequent premature beats are a diagnostic problem
(Fig. 4-4A).
Coupled rhythm: bigeminy, trigeminy. One or two normal beats are fol-
lowed regularly by a premature beat arising from reentry or an ectopic
focus in the atrium or ventricle. The ventricular beats are grouped in pairs
(bigeminy) or triplets (trigeminy), the last a premature beat; the compensatory pause after the premature beat separates one group from its successor
(Fig. 4-4C). Bigeminy has a regular rhythm. Since the premature beat may
not be palpable, a regular rhythm at half the true ventricular rate may be
suspected if only the peripheral pulse is examined; heart auscultation reveals
the bigeminy. As with other premature beats, exercise may restore the normal
rhythm. Coupled premature ventricular contractions (PVCs) occur in normal
hearts, all forms of organic heart disease and digitalis intoxication. DDX: A
similar pulse pattern is produced by Mobitz type I second-degree AV block
(Wenckebach) with 3:2 Wenckebach simulating bigeminy and 4:3 simulating
trigeminy.
Grouped beats and dropped beats. The causes include sinus pauses, SA exit
block, second-degree AV block (Mobitz type I or II), or regular premature
atrial beats in a trigeminal or quadrigeminal pattern that are blocked in the
AV node.
A series of two, three, four, or more beats is followed by a pause.
The pattern may recur regularly. The rhythm is unchanged by increases in
the heart rate. Electrocardiography is essential to distinguish between these
rhythms.
Atrial brillation. The risk for atrial brillation increases with increasing
atrial volume. The atria do not contract synchronously. Stimuli arrive randomly at the AV node. Most are blocked but some conduct to the ventricles
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FIG. 4-4Disturbance of Cardiac Rate and Rhythm III. As in previous diagrams, only the audible heart sounds are
physical signs of these disorders. A. Normal rhythm is interspersed with two random premature beats. If
such beats are ver y frequent, the ear may not be able to distinguish t hem from atrial fibrillation. The rhythm seems regular as
the rate reaches ~120 bpm. B. Atrial fibrillation. The ventricular rhythm is grossly irregular and continues to be irregular
as the rate accelerates to >120/min. C. Bigeminy. A normal beat is followed by a premature beat, this pattern repeating
many times. The premature beats tend to extinguish when exercise accelerates the rate to >120/min. D. Dropped beats
in second-degree AV block. Each successive impulse going through the AV node is delayed longer until one fails to
conduct. In contrast to premature beats, exercise tends to increase the number of dropped beats.
at irregular intervals (Fig. 4-4B). The pulse is irregularly irregular without
pattern. Rapid irregular ventricular contractions are difcult to identify by
palpation. At ventricular rate >70 bpm, the rhythm may seem regular with
premature beats. At rates <60 or >120 bpm, the irregularity may be difcult
to detect. Because ventricular contractions occur at all stages of chamber lling, the heart sounds and pulse volume vary in intensity. The pulse volume is
greater after longer R–R intervals. The ventricular rate is accelerated by exertion. Atrial brillation can only be diagnosed by ECG with accurate measuring of the intervals.
DDX: In utter with variable AV block, exercise increases
the rate by large increments.
CLINICAL OCCURRENCE: Organic heart disease (especially mitral and
tricuspid valve disease and congestive heart failure), hyperthyroidism, acute
infections including rheumatic fever, postoperative (especially chest surgery), electrolyte imbalances, hypoxia, and hypercarbia. Lone atrial brillation, occurring without structural or metabolic abnormalities, increases in
frequency with age >70.
Atrial utter. Atrial reentry circuits incite atrial contraction 220–360 times
per minute (Fig. 4-3D). The AV node cannot transmit such rapid stimuli, so
block develops, at 2:1, 3:1, 4:1, or higher; the block may be highly variable.
Digitalis, verapamil, diltiazem, and β-adrenergic blocking drugs increase
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the AV block. Vagal maneuvers may suddenly increase block, the atrial rate
remaining unchanged.
Ventricular contractions are regular with consistent
beat-to-beat intensity of heart sounds. Variable block produces irregular ventricular contractions, mimicking atrial brillation. Flutter is seen with almost
any organic heart disease and is especially common after heart surgery.
DDX:
In sinus tachycardia, vagal stimulation causes smooth slowing; PSVT will not
slow but may convert.
Paroxysmal supraventricular (atrial) tachycardia (PSVT, PAT, SVT).
The
mechanism is most often reentry or reciprocating tachycardia involving the
AV node. True ectopic atrial tachycardia does occur. Attacks last minutes to
days, beginning and ending suddenly. The rhythm is regular at 150–225 bpm.
All beats have the same intensity. PSVT occurs in normal hearts and with AV
bypass pathways (Wolf–Parkinson–White syndrome). DDX: Vagal stimulation and adenosine do not slow the rate. There is either no response or the
attack is abruptly terminated (Fig. 4-3C). Sinus tachycardia slows smoothly;
atrial utter slows with varying AV block.
Ventricular tachycardia (VT). The mechanism is usually reentry trig-
gered by a PVC and sustained by dispersion of conduction and repolarization in damaged ventricular muscle. Urgent treatment is needed
since ventricular brillation (VF) may supervene leading to sudden
death. There is usually complete AV dissociation, the ventricles beating
faster than the atria. The onset and, when self-limited, the ending are
abrupt. The ventricular rate usually is 150–250 bpm, but can be <150
bpm. The rhythm is regular and unaffected by vagal stimulation; it must
be distinguished from atrial utter and PSVT. The variable relationship
of atrial to ventricular systole produces variation in the intensity of the
rst sound. Some sounds are especially loud cannon sounds resulting
from superimposition of atrial systole with ventricular systole. The cannon sounds are absent when the atria are brillating. Only the rst heart
sound may be audible.
CLINICAL OCCURRENCE: Acquired heart diseases: Acute myocardial
ischemia and infarction, coronary artery disease, drugs (digitalis, quinidine,
procaine amide), heart trauma from surgery or catheterization. Congenital
heart diseases: Right ventricular dysplasia, long QT syndrome, hypertrophic
cardiomyopathies and Brugada syndrome.
Ventricular brillation (VF). Chaotic depolarization of ventricular mus-
cle bers does not produce effective ventricular contraction. No ven-
tricular emptying occurs, so there are no heart sounds. The diagnosis
is made by ECG. Unless terminated by prompt electrical debrillation,
death follows rapidly.
Abnormal pulse contour and volume. See Chapter 8, page 334.
Respiratory Rate and Pattern.
Normal respirations. The normal newborn respiratory rate is ~44 breaths
per minute gradually decreasing to 14–18 bpm in adults, women having
slightly higher rates than men. Breathing tends to be faster when it’s being
observed, so count unobtrusively.
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Increased respiratory rate—tachypnea. Increased respiratory rate occurs
with central nervous system (CNS) stimulation and as compensation for
metabolic acidosis. Hypoxia, increased oxygen demand, and increased CO
generation, and increased PaCO
In restrictive lung disease, minute ventilation is maintained by increasing the
respiratory rate to compensate for reduced tidal volume. Tachypnea occurs
with exertion, fear, fever, cardiac insufciency, pain, pulmonary embolism,
pleurisy, anemia, hyperthyroidism, and acute respiratory distress of any
cause. Breathing is faster with respiratory muscle weakness, emphysema,
pneumothorax, and obesity. An arterial blood gas (ABG) distinguishes pathological from compensatory tachypnea.
increase respiratory rate and tidal volume.
2
2
Decreased respiratory rate—bradypnea.
Minute ventilation is preserved
when slowing rates are accompanied by increasing tidal volumes (hyperpnea). Slow rates without increased tidal volume indicate an abnormality
of the medullary respiratory center and result in alveolar hypoventilation. A
slow respiratory rate is not abnormal if gas exchange is preserved. Alveolar
hypoventilation (PaCO
drugs (e.g., opiates, benzodiazepines, barbiturates, alcohol), uremia, or struc-
> 45 mm Hg) is often the result of CNS depressant
2
tural intracranial lesions, especially with increased intracranial pressure.
Deep breathing—hyperpnea (Kussmaul breathing).
increases CO
excretion by increasing alveolar ventilation (hyperventilation),
2
Increasing tidal volume
the appropriate compensatory response to metabolic acidosis. It is also seen
with hypoxia and is a direct toxic effect of salicylates. The key observation is
deep, regular breaths. Triggers are metabolic acidosis (diabetic ketoacidosis,
uremia), and decreased oxygen delivery from severe anemia. Hypernea is not
synonymous with hyperventilation which can only be diagnosed by ABG.
Shallow breathing—hypopnea. Decreased medullary respiratory drive,
respiratory muscle weakness, airway obstruction, and restrictive disease
limit tidal volume. Muscular weakness results from myasthenia gravis,
amyotrophic lateral sclerosis, Guillain–Barré, drugs (e.g., paralyzing agents,
rarely amino-glycosides), and exhaustion from prolonged increased work
of breathing accompanying decreased chest wall and/or lung compliance.
Decreased effective lung volume results from alveolar lling disorders (pulmonary edema, acute lung injury, alveolar hemorrhage, pneumonia, etc.),
severe restrictive lung or chest wall disease, or severe airways obstruction
(asthma, emphysema). Hypopnea associated with obstructive sleep apnea is
particularly common.
Periodic breathing—Cheyne–Stokes respiration. Cyclic hyperventilation fol-
lowed by compensatory apnea is caused by phase delay in the feedback controls
attempting to maintain a constant PaCO
breathing pattern. In each cycle, the rate and amplitude of successive breaths
. This is the most common periodic
2
increase to a maximum, then progressively diminish into the next apneic
period. Pallor may accompany the apnea. The patient is frequently unaware of
the irregular breathing. Patients may be somnolent during the apneic periods
and then arouse and become restless during the hyperpneic phase.
CLINICAL OCCURRENCE: It is seen during sleep in normal children and
the aged. Disorders of Cerebral Circulation: Stroke, atherosclerosis; Heart
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Failure: Low cardiac output of any cause; Increased Intracranial Pressure:
Meningitis, hydrocephalus, brain tumor, subarachnoid hemorrhage, intracerebral hemorrhage; Brain Injury: Stroke, head injury; Drugs: Opiates, barbiturates, alcohol;
High Altitude: During sleep before acclimatization.
Irregular breathing—Biot breathing.
An uncommon variant of Cheyne-
Stokes respiration, periods of apnea alternate irregularly with a series of equal
depth breaths that terminate abruptly. It is most often seen in meningitis.
Irregular breathing—painful respiration.
Painful chest movements inter-
rupt normal breathing. Causes are pleurisy, injured or inamed muscles,
fractured ribs or cartilage, or upper abdominal inammation, e.g., liver and
subdiaphragmatic abscess, acute cholecystitis, and peritonitis.
Irregular breathing—sleep apnea. Obstructive sleep apnea (OSA) results
from extra-thoracic airway obstruction caused by pharyngeal muscle
and/or tongue relaxation. Ineffective inspiratory efforts often terminate
with a loud snort or snore. Central apnea results from decreased or absent
medullary respiratory drive. Hypoxia, acidosis, and cardiac dysrhythmias
accompany the apneic periods. Arousals associated with apneas lasting
>10 seconds lead to deep sleep deprivation and daytime somnolence.
The classic patient is a morbidly obese male with daytime somnolence,
polycythemia, alveolar hypoventilation, and pulmonary hypertension producing right ventricular failure. Early symptoms include early
morning headaches, depression, irritability, and systemic hypertension.
Physical exam ndings predictive of OSA are oropharyngeal narrowing
(Mallampati grade ≥3, Chapter 7, page 231), tonsil size, neck circumference, and BMI.
Irregular breathing—sighing. Occasionally a long, deep sigh interrupts
resting respirations. The patient may sense shortness of breath, but without limitation of aerobic exercise. This is commonly encountered in anxious
individuals.
Blood Pressure (BP) and Pulse Pressure: Every patient’s BP should be
checked at each visit to detect hypertension and establish a benchmark for
future comparisons. At the rst visit, take the BP in both arms and again in
both arms if there are new cardiovascular or neurologic complaints. Elevated
arm pressures in a young person mandates taking pressures in both legs.
Many circumstances temporarily raise BP, for example, anxiety, the whitecoat syndrome, rushing to make the appointment on time, bladder distention, chronic alcoholism, amphetamines, cocaine, recent caffeine intake, and
cigarette smoking. Frequent BP checks are encouraged.
BP measurement. The pressure necessary to occlude an artery, measured in
millimeters of mercury, is assumed to be the intraarterial pressure. The arm
cuff should ≥10 cm wide, the thigh cuff ≥18 cm. Unless a wide cuff is used,
pressures from a thick arm are 10–15 mm Hg higher than the actual pressure.
In some situations, the BP measured by the arm cuff may be higher than
the actual intraaortic pressure; this can lead to further efforts to lower an
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already low BP with tragic consequences. It is important for the clinician
caring for critically ill patients to understand this possibility.
When using a sphygmomanometer, intense peripheral vasoconstriction accompanying hypotensive states, as in shock, can lead to serious
underestimation of intraarterial pressure. With less vasoconstriction the
Korotkoff sounds underestimate the systolic pressure and overestimate
diastolic pressure.
Measuring brachial artery pressure.
rest. If sitting, support the back and feet. Apply the cuff snugly to a bare arm
with the distal cuff margin ≥3 cm above the antecubital fossa, approximately
at heart level. While palpating the brachial artery, inate the cuff to ≥30 mm
Hg above where the pulse disappears. While listening with the bell pressed
lightly over the artery, drop the pressure at ≤2 mm Hg per second. Arterial vibrations, Korotkoff sounds, determine the BP. The pressure at which
sounds rst appear is the systolic pressure. Continuing to deate the cuff,
the sounds become louder, maintain a maximum, then become mufed, and
nally disappear. Note the pressures at mufing and disappearance. Record
the readings, e.g., 130/80/75. The highest value is the systolic pressure, but
it is unclear whether the second or third value is the best estimate of diastolic pressure. The American Heart Association recommends the point of
disappearance for the diastolic pressure. If, as sometimes occurs with., hyperthyroidism and aortic regurgitation, the sounds persist to zero pressure
accept the second value, since zero diastolic pressure is impossible. To check
the auscultation result, and when Korotkoff sounds are imperceptible, palpate the brachial or radial artery recording the pressure at which the pulse
rst appears. A Doppler ultrasound device identies the pulse and systolic
pressure. Sometimes the Korotkoff sounds appear, disappear, then reappear
as the cuff pressure is lowered, producing an auscultatory gap. This is observed in older individuals with hypertension and may indicate increased
arterial stiffness. To avoid a falsely low systolic pressure, inate the cuff to
well above the putative systolic pressure. The pulse pressure is the difference
between systolic and diastolic pressures. The normal mean value is 50 mm
Hg in men and women.
Wrist BP.
be recorded. With the cuff around the forearm, listen over the radial artery.
If it is difcult to get an accurate brachial BP, the wrist BP should
Measure the BP after a 5–10 minutes
Femoral artery BP. With the patient lying prone, wrap a wide cuff around the
thigh, with the lower margin several centimeters above the popliteal fossa.
Inate the cuff and auscultate the popliteal artery. Even compression is difcult on a conical thigh.
Ankle BP. With the patient supine, the cuff just above the malleolus, place
the bell on the posterior tibial artery behind the medial malleolus or over the
dorsalis pedis artery at the ankle’s extensor retinaculum. With unobstructed
arteries, BP by this method is comparable to brachial artery BP.
Detection of variable pulse waves. Differing pulse wave volumes, too subtle
to be detected by palpation, can be observed on the monometer in atrial
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brillation, pulsus paradoxus (tamponade), chronic obstructive pulmonary
disease (COPD), and pulsus alternans.
Normal arterial pressure.
The denitions of normal BP and hyperten-
sion continue to evolve (Table 4-1). There is normally a circadian variation
in the BP, highest midmorning, and falling during the day, reaching a low
point at ~3 . Systolic pressure increases with age and cardiovascular risk
increases with pressures >115/75 and doubles for each additional 20/10
mm Hg. BP is a continuous biologic variable not allowing a clear normalabnormal dichotomy. It should be thought of as one of many risk factors for
cardiovascular disease, especially stroke and heart failure, the importance
of which must be interpreted in the context of the patient’s gender, age, and
other cardiovascular risk factors. Many guidelines are published and continuously revised, each eliciting new controversies. It is generally agreed
that pressures reproducibly >140 systolic and >90 diastolic are undesirable
and treatment should be considered. Also, systolic pressure >180 and diastolic pressure >120 present imminent risk and should be treated. Severe
BP elevation associated with new or progressive end-organ damage is a
true emergency requiring immediate BP control, usually over the course of
minutes to hours. Table 4-1A presents the classication from Joint National
Committee (JNC) which remains a reasonable starting point for discussion
of BP issues with patients. Table 4.1B presents the recent changes to this classication by ACC/AHA (American College of Cardiology and American
Heart Association).
Inequality of arm BPs.
Arm BPs normally differ by <10 mm Hg. Greater in-
equality is frequent and sometimes cannot be explained. Consider subclavian
artery obstruction, thoracic outlet syndrome, and aortic dissection
TABLE 4-1AJNC-7 BP Classification
Classification Systolic Pressure (mm Hg) Diastolic Pressure (mm Hg)
Normal <120 <80
Prehypertension 120–139 80–89
Hypertension
Stage 1 140–159 90–99
Stage 2 >159 >100
TABLE 4-1BACC/AHA BP Classification
BP Category SBP DBP
Normal <120 mmHg and <80 mmHg
Elevated 120–129 mmHg and <80 mmHg
Hypertension
Stage 1 130–139 mmHg or 80–90 mmHg
Stage 2 ≥140 mmHg or ≥90 mmHg
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