Vital sign measurement
Clinical vital signs (BP, pulse, RR, temp)
I Ex
Pulse
The arterial pulse is generated by left ventricular systolic contraction ejecting blood into the aorta. The
pulse wave travels along the arteries at a rate dependent upon the force of ejection and the elastic
properties of the arterial wall. The regularity of the pulse wave is determined by the rhythm of cardiac
electrical depolarization and muscular contraction.
Examination of the Pulse
Palpation of the arterial pulse
The pulse may be palpated in any of the accessible arteries: External carotid, brachial, radial or ulnar
arteries; femoral posterior tibial and doraslis pedis arteries.
Arterial signs of cardiac action
The contour of the arterial pulse wave is affected by the contractility of the left ventricle, the
distensibility of the aorta, the size of the aortic valve orifice and the LV outflow tract. The carotid pulse
most accurately reflects the contour of the aortic pulse wave. Alterations of the normal pulse contour
and volume are diagnostically significant.
 Normal Arterial Pulse
The palpable primary wave starts with a swift upstroke to the peak systolic pressure, followed by a
more gradual decline. A second, and normally smaller, upstroke, the dicrotic wave, occurs at
approximately the end of ventricular systole, but is not usually palpable. It is caused by the blood
column; rebounding off the closed aortic valve.

Twice Peaking (Dicrotic) Pulses
There are two types of twice peaking arterial pulses:
1.
Pulsus bisferiens with two palpable waves during systole: severe aortic regurgitation
especially when associated with moderate aortic stenosis, hypertrophic subaortic stenosis, and
hyperkinetic circulatory states such as hyperthyroidism
2.
Dicrotic pulse, which has one wave palpable in systole and a second in diastole: very low
cardiac output as with dilated cardiomyopathy or cardiac tamponade, especially in patients
with normal aortic compliance.

Bounding or Collapsing Pulse (Corrigan Pulse, Water-Hammer Pulse)
A large stroke volume and/or vigorous LV contraction generates a rapid upstroke of the pulse
wave followed by a rapid runoff of blood from the aorta. With high pulse pressure, the upstroke may be
very sharp, while the downward slope is precipitous. It may be accompanied by the pistol-shot sound.
This is encountered in hyperthyroidism, anxiety, aortic regurgitation, patent ductus arteriosus, and
arteriovenous fistula.
Plateau Pulse (Pulsus Tardus)
The upstroke is gradual and the peak delayed toward late systole seen in sever aortic stenosis.

Pulse volume
Absent Pulses:
Takayasu aortitis
Pulsus alternans
Well heard as alternating heart sounds when reducing BP cuff pressure suggestive of LV
dysfunction.
Pulsus Bigeminy
Felt as double beats should be confirmed as bigeminy with ECG.
Pulsus Paradoxus
Inspiration decreases intrathoracic pressure, normally increasing blood flow into the chest and
right ventricle. Despite the increased right ventricular stroke volume, inspiratory dilation of the
pulmonary vasculature decreases LV filling resulting in decreased LV stroke volume and systolic blood
pressure. In pericardial tamponade total heart volume is limited, and further reduced during inspiration,
so that LV filling, LV stroke volume and systolic blood pressure all fall dramatically with inspiration.
Labored breathing associated with exacerbations of obstructive airway disease also produce a
paradoxical pulse. Under normal resting conditions, there is an inspiratory fall of less than 10 mm Hg
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in the arterial systolic pressure and an accompanying inspiratory fall in venous pressure. A paradoxical
pulse exists when inspiration creates more than a 10 mm Hg drop in systolic arterial pressure. The
exaggerated waxing and waning in the pulse volume may be detected by palpation; more often, it can
only be detected by use of the sphygmomanometer. DDX: Similar findings can be seen with an
irregular rhythm or AV asynchrony. CLINICAL OCCURRENCE: Pericardial tamponade, pulmonary
emphysema, severe asthma.
Inequality of Pulses
Disparity between the right and left arterial pulse volumes are detected by simultaneous
palpation. If possible, confirm the finding by taking the blood pressure at both sites. Arterial pressure
differences between the two arms must be considered with circumspection: pressures not measured
precisely simultaneously are >10 mm Hg different in up to 20% of normal individuals, whereas, when
measured simultaneously by cuff, 5% or less show the same difference. Nonsimultaneously measured
systolic pressure differences of >10 mm Hg occur in almost 30% of hypertensive patients. DDX:
Asymmetry suggests atherosclerosis, dissecting aneurysm or another arterial disease.
Variations in Ventricular Rate and Rhythm
Regular rhythms with rates greater than 120 bpm
Rhythms include sinus tachycardia, atrial flutter with 2:1 AV block, paroxysmal
supraventricular tachycardia, and ventricular tachycardia. The response to vagus stimulation may give
an indication of which rhythm is present. In flutter, the rate slows stepwise. Paroxysmal atrial
tachycardia does not slow, but may convert to normal rhythm and rate. Sinus rhythm may gradually
slow and ventricular tachycardia does not change.
Regular rhythms with rates of 60 to 120 bpm
These include sinus rhythm, accelerated junctional rhythm (also known as nonparoxysmal
junctional tachycardia), atrial tachycardia with block, idioventricular tachycardia (also known as
accelerated ventricular rhythm and slow or benign ventricular tachycardia), and atrial flutter with 3:1 or
4:1 AV block.
Rhythms that are irregular in no repetitive manner
Atrial flutter with variable AV block, atrial fibrillation, multifocal atrial tachycardia, and
frequent atrial or ventricular premature beats that occur with no consistent pattern all need to be
considered.
Irregular rhythms with "reproducible irregularity"
This pattern suggests either 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. It is necessary to obtain an ECG to reach a definitive diagnosis.
Blood Pressure and Pulse Pressure
The intraarterial BP can be measured directly, but this is only done in intensive care units. Clinically,
the indirect method is used, in which external pressure is applied to the overlying tissues and the
pressure (measured in millimeters of mercury) necessary to occlude the artery is assumed equal to the
intraarterial pressure. The arm cuff should be at least 10 cm wide; for the thigh, a width of 18 cm is
preferable. The tension to compress the overlying tissues is usually regarded as negligible, but a thick
arm will yield readings 10 to 15 mm Hg higher than the actual pressure unless a wide cuff is used.
Finding that the radial artery remains palpable after the BP cuff is inflated above systolic pressure (the
Osler maneuver) demonstrates the calcified arteries that may produce this condition.
Other sites for BP measurement:
Wrist BP
It is often difficult to get an accurate BP in a short fat arm in which case the BP should be checked at
the wrist. The cuff is wrapped around the forearm and the stethoscope bell is placed over the radial
artery.
Femoral artery BP
When taking the arterial pressure in the femoral artery, have the patient lie prone on a table or bed.
Wrap a wide cuff (18 cm or more) around the thigh so that the lower margin of the cuff is several
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centimeters proximal to the popliteal fossa. Inflate the cuff and auscultate the popliteal artery. It is
often difficult to get even compression with the cuff on a conical thigh.
Ankle BP
This may is more convenient than the femoral BP. With the patient supine, apply the cuff just above
the malleolus. Place the chest piece of the stethoscope distal to the cuff and behind the medial
malleolus on the posterior tibial artery or on the dorsal extensor retinaculum of the ankle over the
dorsalis pedis artery. In patients with unobstructed arteries BP by this method is comparable to brachial
artery BP.
Inequality of BP in Arms
BPs normally differ by < 10 mm Hg between the arms; the right arm is usually greater than
the left. Inequality is frequent and sometimes cannot be explained. Conditions to be considered are
obstruction in the subclavian artery, thoracic outlet syndrome and aortic dissection.
JNC-7 BP Classification
Classification
Systolic Pressure mm Hg Diastolic Pressure mm Hg
Normal
<120
Prehypertension 120–139
<80
80–89
Hypertension
Stage 1
140–159
90–99
Stage 2
>159
>100
High Blood Pressure
Most hypertension is of unknown cause and is termed "essential hypertension." The primary lesion is
suspected to be in the kidney. Increased diastolic pressure results from increased peripheral resistance,
either by vasoconstriction or intimal thickening. Increased systolic pressure can result from increased
stroke volume or decreased compliance of the aorta (in which case the pulse pressure is widened) and
with increased diastolic pressure (with a normal or increased pulse pressure). The systolic pressure may
be elevated with a normal diastolic pressure: isolated systolic hypertension. More commonly, both the
systolic and diastolic pressures are elevated. If only the diastolic pressure is elevated, the pulse pressure
is narrowed and one should suspect impaired cardiac output. The diastolic pressure represents the
minimal continuous load to which the vascular tree is subjected and makes the greatest contribution to
the mean arterial pressure. Both isolated systolic and systolic combined with diastolic hypertension are
strongly correlated with stroke, heart failure, left ventricular hypertrophy, and chronic kidney failure. In
patients older than 50 years of age, elevated systolic BP is more important than diastolic BP as a risk
factor for cardiovascular disease.
Systolic hypertension is seen with increased cardiac output (hyperthyroidism, anemia, arteriovenous
fistulas, aortic regurgitation, anxiety), a rigid aorta as a result of atherosclerosis, and is particularly
common in the older adults.
Causes of Secondary Hypertension:
Congenital
 coarctation of the aorta,
 congenital adrenal hyperplasia (early or late onset),
 polycystic kidney disease
Endocrine
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pheochromocytoma,
aldosteronoma,
adrenal hyperplasia,
hypercortisolism (Cushing disease and syndrome),
hyperthyroidism/ hypothyroidism,
hyperparathyroidism,
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 acromegaly
Inflammatory/Immune
 atherosclerosis,
 vasculitis
Metabolic/Toxic
 renal insufficiency,
 medications (NSAIDs estrogens, oral contraceptives, cyclosporine),
 drug abuse (cocaine, amphetamines, etc.),
 porphyria,
 lead poisoning,
 hypercalcemia
Mechanical/Trauma
 obstructive sleep apnea
Neoplastic
 adrenal adenoma,
 pheochromocytoma,
 pituitary adenoma,
 brain tumors
Neurologic
 stroke,
 diencephalic syndrome,
 increased intracranial pressure,
 acute spinal cord injury
Vascular
 renal artery stenosis (atherosclerosis, fibromuscular dysplasia)
Low BP
Hypotension results from a loss of blood volume, loss of vascular tone, or decreased cardiac output.
Both the systolic and diastolic pressures are diminished below the patient's normal: note that values
within the normal range are hypotensive for the patient who has previously had sustained hypertension.
Signs of hypoperfusion (cool skin, decreased urine output, decreased mental alertness) and
compensatory cardiovascular responses (peripheral vasoconstriction, tachycardia) indicate that low BP
is pathologic.
Causes for hypotension:
Loss of Blood Volume
 bleeding,
 capillary leak syndrome (anaphylaxis, sepsis, idiopathic),
 third-spacing (ascites, burns, secretory diarrheas),
 polyuria (diabetes mellitus, diabetes insipidus, diuretics),
 inadequate fluid intake,
 excessive sweating (heat prostration and heat stroke),
 adrenal insufficiency
Loss of Vascular Tone
 sepsis,
 drugs (vasodilators, tricyclic antidepressants, ganglionic blockers),
 fever,
 autonomic insufficiency (multisystem atrophy),
 acute spinal cord injury (spinal shock),
 arteriovenous malformations
Decreased Cardiac Output
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acute myocardial infarction,
ischemic cardiomyopathy,
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idiopathic dilated cardiomyopathy,
aortic stenosis,
pulmonary embolism,
pericardial tamponade and
severe mitral insufficiency.
Orthostatic (Postural) Hypotension
The patient is hypovolemic, sympathetic drive to the heart and blood vessels is diminished, or venous
return to the heart is deficient. The BP is normal in the recumbent position, but when the patient stands
there is a fall, within 3 minutes, of 20 mm Hg in the systolic or 10 mm Hg in the diastolic BP and/or
the heart rate rises by >15 bpm. This is an early sign of intravascular volume loss.
When the drop in BP is not accompanied by a rise in pulse rate, autonomic insufficiency is suggested.
Patients with chronic orthostatic hypotension frequently have postprandial hypotension and reversal of
the normal circadian BP pattern (i.e., higher BP at night than during the day).
Causes of Orthostatic Hypotension:
Loss of Blood Volume
Loss of Vascular Tone
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deconditioning after long illnesses,
autonomic insufficiency (multisystem atrophy),
peripheral neuropathies (diabetes, tabes dorsalis, alcoholism),
drugs (vasodilators, tricyclic antidepressants, ganglionic blockers)
Impaired Venous Return
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ascites,
pregnancy,
venous insufficiency,
inferior vena cava obstruction or
hemangiomas of the legs.
Pulse Pressure
Widened Pulse Pressure
Pulse pressure increases when the peak systolic pressure is increased (increased stroke volume,
increased rate of ventricular contraction, decreased aortic elasticity) and/or there is a decreased
diastolic pressure (decreased peripheral resistance, arteriovenous shunts, aortic insufficiency). A pulse
pressure of 65 mm Hg is abnormal. With a large stroke volume, the pulse is often described as
bounding or, in the case of aortic regurgitation, collapsing. The head may bob with each heart beat.
Thrills may be palpable and murmurs audible over AV shunts, either congenital/traumatic, or
iatrogenic. With decreased peripheral resistance from vasodilation, the skin is usually warm and
flushed. Widened pulse pressure is associated with increased cardiovascular morbidity and mortality.
Causes of widened pulse pressure:
Increased Systolic Pressure
 systolic hypertension,
 atherosclerosis,
 increased stroke volume (aortic regurgitation, hyperthyroidism, anxiety, bradycardia, heart
block, post-PVC, after a long pause in atrial fibrillation, pregnancy, fever, systemic
arteriovenous fistulas)
Increased Diastolic Runoff
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aortic regurgitation,
sepsis,
vasodilators,
patent ductus arteriosus,
hyperthyroidism,
arteriovenous fistulas,
beriberi.
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Narrowed Pulse Pressure
Pulse pressure narrows with decreased stroke volume and decreased rate of ventricular ejection. Pulse
pressures less than 30 mm Hg may occur with tachycardia and many other conditions associated with a
low stroke volume.
Causes of Narrowed Pulse Pressure:
Decreased Stroke Volume
 severe aortic stenosis,
 dilated cardiomyopathy,
 restrictive heart disease,
 constrictive pericarditis,
 pericardial tamponade,
 intravascular volume depletion,
 venous vasodilatation
Decreased Rate of Ventricular Contraction
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ischemic and dilated cardiomyopathy,
aortic stenosis,
myocarditis
Respiratory Rate and Pattern
Respiratory Rate
Normal respirations
In the newborn, the normal respiratory rate is approximately 44 cycles per minute; it decreases
gradually the rate until maturity when the rate in adults is between 14 and 18 cycles per minute.
Women have slightly higher rates than men. Since people tend to breathe faster when their breathing is
being observed, the respiratory rate should be counted unobtrusively, such as pretending to count the
pulse.
Tachypnea
Increased respiratory rate occurs with central nervous system (CNS) stimulation and as compensation
for increasing PaCO2, decreases in tidal volume or metabolic acidosis. Hypoxia, increased oxygen
demands, and increased CO2 generation each lead to an increase in respiratory rate and tidal volume.
Minute ventilation is maintained in restrictive disease of the lung or chest wall by increasing the
respiratory rate to compensate for the reduced tidal volume.
Tachypnea occurs with exertion, fear, fever, cardiac insufficiency, pain, pulmonary embolism, acute
respiratory distress from infections, pleurisy, anemia, and hyperthyroidism. Breathing is faster when
restricted by weakness of the respiratory muscles, emphysema, pneumothorax, or obesity. An arterial
blood gas is required to distinguish pathological from compensatory tachypnea: a primary respiratory
alkalosis indicates a pathological state.
Bradypnea
Minute ventilation is preserved when slow rates are accompanied by an increased tidal volume
(hyperpnea). Slow rates without an increase in tidal volume produce alveolar hypoventilation
indicating an abnormality of the medullary respiratory center. A slower than usual respiratory rate is
not abnormal if gas exchange is preserved as demonstrated by arterial blood gas determination. When
alveolar hypoventilation occurs (PaCO2 > 45 mm Hg), metabolic encephalopathy as a result of CNSdepressant drugs (e.g., opiates, benzodiazepines, barbiturates, alcohol) or uremia, or structural
intracranial lesions (especially conditions with increased intracranial pressure) are most likely.
Respiratory Pattern
Deep Breathing—Hyperpnea (Kussmaul Breathing)
An increased tidal volume produces increased alveolar ventilation, which increases excretion of CO2.
This is an appropriate compensatory response to metabolic acidosis of any cause and is a direct toxic
effect of salicylates. It is also seen with hypoxia. The term Kussmaul breathing is applied to deep,
regular respirations, whether the rate be normal, slow, or fast. Common examples of precipitating
metabolic acidoses are diabetic ketoacidosis and uremia. Hypoxemia (e.g., pneumonia, pulmonary
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embolism) and decreased oxygen delivery as a result of severe anemia or hemorrhage also lead to
hyperpnea.
Shallow Breathing—Hypopnea
Decreased depth of breathing results from decreased medullary respiratory center drive, weakness of
the respiratory muscles, or loss of alveolar volume from any cause. Depression of the medullary
respiratory center occurs as in bradypnea. Muscular weakness can result from myasthenia gravis,
amyotrophic lateral sclerosis, Guillain-Barré syndrome, drugs (e.g., paralyzing agents, rarely
aminoglycosides) and exhaustion when the work of breathing is increased due to decreased chest wall
and/or lung compliance as in severe asthma. Decreased lung volumes can result from alveolar filling
disorders (congestive heart failure with pulmonary edema, acute lung injury, alveolar hemorrhage,
pneumonia, etc.), severe restrictive disease of the lung or chest wall or severe airways obstruction
(asthma, emphysema).
Periodic Breathing—Cheyne-Stokes Respiration
The pattern results from cyclic hyperventilation followed by compensatory apnea caused by phase
delay in the feedback controls trying to maintain a constant PCO2. This is the most common periodic
breathing pattern. Respirations are interrupted by periods of apnea. In each cycle, the rate and
amplitude of successive breaths 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.
Causes of Cheynes-Stokes Respiration:
Normal
 Children and aged
Disorders of the Cerebral Circulation
 stroke, atherosclerosis
Heart Failure
 low cardiac output of any cause
Increased Intracranial Pressure
 meningitis,
 hydrocephalus,
 brain tumor,
 subarachnoid hemorrhage,
 intracerebral hemorrhage
Brain Injury
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Drugs
stroke,
head injury
 opiates,
 barbiturates,
 alcohol
High Altitude
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during sleep, before acclimatization
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