1. vital signs lesson plan

Name of the institution : Narayana college of nursing
Programme : B Sc Nursing
Subject : Anatomy
Unit : II
Topic : structure of heart
Group : I st year B Sc Nursing Students
Date :
Duration : 45 mts
Venue :
Total no of students : 40 students
Time :
Method of teachimg : Lecture cum discussion ; BRICS2
AV aids :
Previous knowledge of the student
Name of the student teacher :
Name of the Evaluator :

GENERAL OBJECTIVE
The students will be able to gain in-depth knowledge regarding vital signs and to develop the desirable attitude and
acquire skills to practice at different health care settings.
SPECIFIC OBJECTIVES
At the end of the class, the student will be able to,
 Define vital signs
 Enlist the guidelines for measuring the vital signs
 Define temperature
 Explain alterations in temperature
 Define pulse
 Enlist various sites of assessment of pulse
 Define respiratory rate
 Brief out the method of assessing the respiratory rate
 Define blood pressure
 Explain method of assessing the blood pressure.

Sl.no Time Specific
Objectives
CONTENT Teachers
Activity
Learners
Activity
AV
Aids
Evalu-
ation
Vital
signs BRINGING BACK TO THE STUDY
INTRODUCTION
c
BLOCK BASED LEARNING
Block based learning is a dedicated learning of one subject at a
time; focuses on more immersed learning. For ex. teaching learning
activity is prepared for one topic in one unit.
Programme: B.Sc(N)
Subject: fundamentals of nursing
Unit- II

VITAL SIGNS
vital signs are Indications that a person is still alive. Vital signs
include breathing, sounds of the heart beat, a pulse that can be felt, a
reduction in the size of the pupils in response to bright light,
movement in response to a painful stimulus and signs of electrical
activity in the brain on the electroencephalogram.
Basic indicators of body function, usually meaning heartbeats per
minute, breaths per minute, blood pressure, body temperature, and
weight.
There are no clear evidence-based guidelines for how often vital
signs should be assessed (Kowalak, 2015). In medical-surgical
settings, vital signs are generally assessed every 4-8 hours. Some
patient care units may decide, based on patient acuity or population,
that vital signs should be assessed more frequently.
The following should be considered when deciding on the
frequency of vital sign assessment:
The patient’s diagnosis and comorbidities
The patient’s level of acuity and risk for complications
Treatments and medications that the patient is receiving
Trends in the patient’s vital signs
Provider orders
Agency policy

In addition to assessing vital signs per unit policy, they should
also be evaluated at the following times:
 Admission, transfer or discharge
 At the time of any change in condition
 Before and after a surgical or diagnostic procedure
 Before administering medications, which may affect cardiac
or respiratory function (Taylor, Lillis & Lynn, 2016).
Many facilities also use other strategies in addition to vital signs for
evaluating a patient’s stability and acuity. For example, the
Modified Early Warning System (MEWS) includes temperature,
heart rate, respiratory rate, blood pressure and level of consciousness
and can be used to detect early signs of decompensation (Mathukia,
WuQiang, Biege & Krishnamurthy, 2014).
Post-operative Vital Signs:
There is also little evidence-based information to provide guidance
on how often vital signs should be evaluated in the postoperative
patient. The American Society of PeriAnesthesia Nursing (ASPAN)
recommends 15 minute vital monitoring and documentation in the
first hour of the postanesthesia recovery period (ASPAN, 2016).
Although unit policies vary, postoperative vital signs (temperature,

heart rate, respiratory rate, blood pressure, pain and pulse oximetry)
on a medical-surgical unit are generally recommended:
 Every 15 minutes x 4
 Every 30 minutes x 2
 Every hour x 24 hours, and then every 4 hours (if stable) (Menez,
2016)

TEMPERATURE
1. Body temperature is the degree of hotness or coldness of a body
or environment. It is the somatic sensation of heat or cold. It is
the degree of or intensity of heat of a body in relation to external
environment. The body temperature is the difference between
the amount of heat produced by body processes & the amount of
heat lost to the external environment. Temperature Regulation
2. Body Temperature = Thermogenesis–Heat Loss
3. TYPES OF TEMPERATURE:
Core temperature- it is the temperature of internal body
tissues below the skin & subcutaneous tissues.
The sites of measurement are rectum, tympanic membrane,
esophagus, pulmonary artery & urinary bladder.
Surface body temperature- it refers to the body temperature
of external body tissues at the surface that is of the skin &
subcutaneous tissues.
SITES
PHYSIOLOGY OF THERMOREGULATION-
It is precisely regulated by physiological & behavioral
mechanisms in number of ways:-
 Neural control
 Vascular control
 Skin in temperature regulation
 Behavioral control
FACTORS AFFECTING BODYTEMPERATURE

 AGE
 EXERCISE
 HORMONAL LEVEL
 STRESS CIRCARDIAN RHYTHM
 ENVIRONMENT
FEVER : Fever is an elevation of body temperature that
exceeds normally daily variation and occurs in conjunction
with an increase in the hypothalamic set point for e.g. 37⁰ C-
39⁰ C.
CAUSES OF FEVER :
 Hot environment.
 Excessive exercise.
 Neurogenic factors like injury to
hypothalamus.
 Dehydration after excessive dieresis.
 As an undesired side effect of a
therapeutic drug.
 Chemical substances e.g. caffeine and
cocaine directly injected into the
bloodstream.
 Infectious disease and inflammation.
 Severe hemorrhage.
CLASSIFICATION OR PATTERNS OF FEVER:
1. Intermittent fever: Temperature returns to acceptable value at
least once in 24 hours. The temperature curve returns to normal
during the day and reaches its peak in the evening. E.g.- in

septicemia.
2. Remittent fever: fever spikes & falls without a return to the
normal temperature levels. The temperature fluctuates but does not
return to normal. E.g.- TB, viral diseases, bacterial infections
3.Sustained fever: the temperature remains continuously elevated
above 38 degree Celsius & demonstrates little fluctuation.
4. Relapsing fever: periods of febrile periods interspersed with
acceptable temperature values i.e. periods of fever are interspersed
with periods of normal temperature.
CHRONOLOGY OF EVENTS REQUIRED FOR INDUCTION
OF FEVER GRADES OF FEVER:
1) low grade fever: 37.1-38.2C(98.8-100.6F)
2) high grade fever: 38.2-40.5C(100.6-104.9F)
3) hyperpyrexia: >40.5C(104.9F)
SIGNS & SYMPTOMS OF FEVER:
Symptoms- Flushed face
hot dry skin
anorexia
headache
nausea and sometimes vomiting
constipation and sometimes diarrhea
bodyaches
scant highly colored urine.
Clinical signs-
 Increased heart rate, respiratory rate and depth
 shivering; pale cold skin
 cyanotic nail beds

HYPERTHERMIA: It is elevated body temperature due to
failed thermoregulation that occurs when a body produces or
absorbs more heat than it dissipates. Temperature ranges -
>37.5- 38.3degree Celsius (99.5- 100.9 degree Fahrenheit).
CAUSES OF HYPERTHERMIASYNDROMES:
Heat stroke: prolonged exposure to sun or high
environmental temperatures. These condition causes heat
stroke – a dangerous heat emergency with a high mortality
rate.
Drug induced hyperthermia: due to increased use of
psychotropic drugs e.g. Monoamine oxidizes inhibitors,
tricycle antidepressants, amphetamines, phencyclidine, lys
ergic acid diethylamide or cocaine, selective serotonin uptake
inhibitors(SSRIs), MAO‘s( Serotonin Syndrome), use of
narcoleptic agents like antipsychotic phenothiazine's,
haloperidol ( NMS),
Endocrinopathy: thyrotoxicosis and pheochromocytoma can
lead to increased thermogenesis
Central nervous system damage: cerebral hemorrhage,
status epileptics, hypothalamic injury can cause hyperthermia
DIAGNOSTIC FINDINGS:
o History taking
o Physical examination
o Laboratory tests: i. Clinical pathology ii.

Chemistry iii. Microbiology iv. Radiology
MEDICAL MANAGEMENT:
Acetaminophen: adult: 325-650 mg PO q 4-6 hrs.
o Children: 10-15mg/kg body
weight q4-6 hrs.
Ibuprofen (NSAID) - adult-200-400mg PO q6hrs;
o children: 5mg/kg body wt for
temp. <102.5F;
 10 mg/kg body
wt. for temp
102.5F
Aspirin: adult 325-650 mg PO q6hrs;
 children 10-20 mg q 6hrs.
Gluco corticosteroid: potent antipyretic inhibit PGE2
synthesis.
Mepridine, morphine sulphate, chlorpromazine used in
severe hyperthermia patient’s.
NURSING MANAGEMENT OF FEVER AND
HYPERTHERMIA: ASSESSMENT
 Monitor vital signs.
 Assess skin color and temperature.
 Monitor white blood cell count

 hematocrit value
 pertinent laboratory reports for indication of infection or
dehydration.
NURSING DIAGNOSIS:
1) During chill phase:
 Risk for altered body temperature as evidenced
by shivering and feeling cold
2) During fever phase:
 Hyperthermia as evidenced body temperature
>38.5C, irritability, increased respiratory rate and
dry skin
 impaired comfort as evidenced by restlessness
 imbalanced nutrition related to fever as
evidenced by anorexia and lack of food intake
5) During Flush phase-
 Altered fluid & electrolyte balance related to
excessive sweating
NURSING MANAGEMENT OF FEVER AND
HYPERTHERMIA:
 Provide adequate nutrition and fluids to meet the increased
metabolic demands and prevent dehydration.
 Reduce physical activity to limit heat production especially
during the flush stage.
 Provide a tepid sponge bath to increase heat loss through
conduction.

 Provide dry clothing and bed linens.
 Remove excess blankets when the client feels warm, but
provide extra warmth when the client feels chilled.
 Measure intake and output.
 Administer antibiotics as ordered.
 Provide oral hygiene to keep the mucous membranes moist.
FEVER OF UNKNOWN ORIGIN
Fever of Unknown Origin(FUO) was defined by Peterson &
Benson in 1961 as having following features-
 temperature of > 38.3 degree Celsius (>101 degree
Fahrenheit) in several occasions.
 A duration of fever of > 3 weeks.
Failure to reach a diagnosis despite one week of
inpatient investigation.
CLASSIFICATION OF FUO: Derrick and Street have
purposed a new system for classification of FUO
Classic FUO: E.g. infections, malignancy, inflammatory
diseases, drug fever.
Nosocomial FUO: a temperature of >= 38.3 C (>=101 F)
develops on several occasions in a hospitalized patients who are
receiving acute care and in whom infection was not present at time
of admission. For e.g. septic thrombophlebitis, sinusitis, drug fever.
Neutropenic FUO: a temperature of >= 38.3 C (>=101 F)
develops on several occasions in a patient whose neutrophil

count is < 500/micro liter.
CAUSES OF FUO:
 Infections
 Neoplasm’s
 Collagen vascular/ Hypersensitivity diseases
 Miscellaneous conditions
 Inherited and metabolic diseases
 Thermoregulatory Disorders
DIAGNOSIS OF FUO:
 History
 Physical examination
 Blood investigations-tumor markers, PPD for TB,
serological studies, peripheral smears, multiple samples for
culture and sensitivity
 X-Ray studies
 Bone marrow biopsy, Liver biopsy
 CT scan, MRI, ultrasonography.
TREATMENT:
 Continuous observation and examination.
 Do not start with immediate Antibiotic Therapy as it
can delineate the cause of FUO.
 The debilitating symptoms are treated by NSAIDS and
glucocorticoids.
 If neutropenia and vital sign instability are present then

empirical therapy with fluroquinolone and piperacillin is given.
 When no underlying source of infection is found even
after 6 months the prognosis is generally good.
HYPOTHERMIA:
Hypothermia is a state in which the core body
temperature is lower than 35 degree Celsius and 95 degree
Fahrenheit. At this temperature many of the compensatory
mechanism to conserve heat begin to fall.
HYPOTHERMIA:
• Normal Range: – 96-100º F
• Mild Hypothermia: – 90-95º F
• SevereHypothermia – < 90º F
CAUSES:
o Exposure to cold environment in winter months and
colder climates.
o Occupational exposure or hobbies that entail
extensive exposure to cold for e.g. hunters, skiers,
sailors and climbers.
o Endocrine dysfunction: hypothyroidism, adrenal
insufficiency , hypoglycemia
o Medications like ethanol, phenothiazines,
barbiturates, benzodia zepines, cyclic
antidepressants, anesthetics.
o Neurologic injury from trauma, Cerebral vascular

accident, Subarachnoid hemorrhage. Sepsis
RISK FACTORS FOR HYPOTHERMIA:
 Age extremes: elderly, neonates.
 Outdoor exposure: occupational, sports- related, inadequate
clothing.
 Drugs and intoxicants: ethanol, phenothiazine's, barbiturates,
anesthetics, neuromuscular blockers and others.
 Endocrine related: hypoglycemia, hypothyroidism, adrenal
insufficiency, and hypopituitarism.
 Neurologic related: stroke, hypothalamic disorders,
Parkinson‘s disease, spinal cord injury.
 Multisystem: malnutrition, sepsis, shock, hepatic or renal
failure.
 Burns and exfoliative dermatologic disorders.
 Immobility or debilitation.
SIGNS AND SYMPTOMS
• MILD Hypothermia: – Lethargy – Shivering – Lack of
Coordination – Pale, cold, dry skin – Early rise in heart rate, and
respiratory rates.
• SEVERE Hypothermia: –No shivering –Heart rhythm
problems –Cardiac arrest –Loss of voluntary muscle control –
Low blood pressure –Undetectable pulse and respirations
DIAGNOSIS:  Measuring the core temperature at two sites-

rectum & esophagus with the help of rectal probe & esophageal
probe.
MANAGEMENT: continuous monitoring
 Rewarding
 supportive care.
REWARMING:
PASSIVE: involves the use of blankets to cover
bodyand head to trap heat being lost.
ACTIVE: the application of outside heat to raise
body temperature External – heat blanket/forced hot air system
Internal – introduction of warm fluids into the body Warm IVF,
bodycavity lavage, extracorporeal
• Active Rewarming of MILD Hypothermia: – Active external
methods: • Warm blankets • Heat packs • Warm water immersion
(with caution) – Active internal methods: • Warmed IV fluids
• Active Rewarming of SEVERE Hypothermia: –Active external
methods: • Warm blankets • Heat packs • Warm water immersion
(with caution) –Active internal methods: • Warmed IV fluids •
Warmed, humidified oxygen
NURSING MANAGEMENT OF HYPOTHERMIA:
 Provide extra covering and monitor temperature.
 Cover head properly.
 Use heat retaining blankets.

 Keep patient‘s linen dry.
 Control environmental temperature.
 Provide extra heat source (heat lamp, radiant warmer,
pads, and blankets).
 Carefully assess for hyperthermia or burn.
 Regulate heat sourceaccording to physical response.
FROST BITE: Frost bite is the condition in which the tissue
temperature drops below 0 degree Celsius. It results in cellular and
vascular damage. Body parts more frequently affected by frostbite
include the digits of feet and hands, tip of nose, and earlobes.
PREDISPOSINGFACTORS:
 Contact with thermal conductors such as metal or
volatile solutions
 immobility
 careless application of cold packs
 vaso constrictive medications
CLASSIFICATION OF FROST BITE:
o First degree frost bite: causes only anesthesia and
erythematic.
o Second degree frost bite: appearance of superficial
vesiculation surrounded by edema leads to very cold
extremities.
o Third degree frost bite: hemorrhagic vesicles due to
serious microvasculature injury which further leads to
cyanosis. Fourth degree frost bite: damage in sub

cuticular, muscular and osseous tissue.
SYMPTOMS:
a. The injured area is white or mottled blue white, waxy
and firm to the touch.
b. There is tingling and redness followed by pallor and
numbness of the affected area.
c. There are three degrees: transitory hyperemia
following numbness, formation of vesicles and
gangrene.
d. The affected area is insensitive to touch.
MANAGEMENT OF FROST BITE:
Before thawing: remove client from cold environment, stabilize
core temperature, treat hypothermia, protect the frozen part and do
not apply friction or massage.
During thawing: provide parental analgesia e.g. keratolac &
Provide ibuprofen 40 mg PO. Immerse part in 37-40 C circulating
water containing an antiseptic soap for 10-45 minutes. Encourage
patient to gently move the part.
After thawing:
i) gently dry and elevate it.
ii) Apply pledges between toes; if macerated.
iii) If clear vesicles are intact aspirate the fluid or the

fluid will reabsorb in days; if broken then debride
and dress with antibiotic.
iv) Continue analgesics Ibuprofen 400mg 8-12 hourly.
Provide tetanus prophylaxis and hydrotherapy at
37C.
v) The patient should be stimulated with orally
administered hot fluids such as tea and coffee.
vi) The patient should not be allowed to smoke.
vii) Artificial respiration should be administered if the
patient is unconscious.
Measuring body temperature:
1. Oral temperature :
 Wait at least fifteen minutes after the resident has
eaten, smoked, or had a drink.
 If using a glass thermometer, hold the end and shake
the thermometer by snapping your wrist downward
several times, shaking the mercury to the bottom of
the glass.
 If you are using an electronic thermometer, check to
be sure it is working.
 Use equipment designed for oral use, not rectal.
 Place a disposable cover on the thermometer, or
follow your facility’s policy for disinfecting
thermometers before reusing them.
 Never wash a glass thermometer in hot water.
 Be sure the thermometer is not broken, chipped, or

cracked.
 Ask the resident to wet his lips, and then insert the tip
of the thermometer under the resident’s tongue and
slightly to the side.
 You may have to push a button on an electronic
thermometer to activate it.
 Ask the resident to close his lips over the
thermometer. A glass thermometer should stay in
place for at least three minutes.
 An electronic thermometer should stay in place until
it beeps.
 When finished, remove the thermometer from the
resident’s mouth and disposeof the cover.
 Hold a glass thermometer horizontally at eye level,
turning it until you can see a solid line of mercury.
 The point at which the line stops is the temperature
reading.
 Electronic thermometers will tell you the temperature
with a digital reading.
 Document the reading.
 Disinfect and store the thermometer according to
policy.
Axillary temperature:
Under the arm, Hold the thermometer in the center of the
resident’s armpit for at least nine minutes, or until it beeps.
Rectaltemperature :

 Assist the resident to lie on her side with her upper leg
pulled up toward her chest as much as possible.
 Lubricate the covered rectal thermometer or rectal
electronic probe and gently insert it no further than one
inch into the resident’s rectum.
 Keep the resident covered during this procedure to
protect privacy.
 Hold in place for at least 3 minutes, while supporting the
resident to prevent any movement that could cause
injury.
 Be careful to avoid trauma to the rectum.
 Use gloves and Standard Precautions.
Respiratoryrate
The function of the respiratory system is to supply adequate oxygen
to the tissues and to remove the waste product carbon dioxide. This
is achieved with the inspiration and expiration of air. With each

breath there is a pause after expiration.
Normal/idealvalues
The rate of respiration will vary with age and gender. A respiratory
rate of 12-18 breaths per minute in a healthy adult is considered
normal (Blows, 2001).
Tachypnoea:the rate is regular but over 20 breaths per minute.
Bradypnoea: the rate is regular but less than 12 breaths per minute.
Apnoea: there is an absence of respiration for several seconds - this
can lead to respiratory arrest.
Dyspnoea: difficulty in breathing, the patient gasps for air.
Cheyne-Stokes: respiration the breathing is shallow, very slow and
laboured with periods of apnoea. This type of breathing is often seen
in the dying patient.
Hyperventilation: patients may breathe rapidly due to a physical or
psychological cause, for example if they are in pain or panicking.
Hyperventilation reduces the carbon dioxide levels in the blood,
causing tingling and numbness in the hands; this may cause further
distress. In adults, more than 20 breaths a minute is considered
moderate, more than 30 breaths is severe (Mallett and Dougherty,
2004).
Recording respirations
Respirations are recorded for a number of reasons:

 To acquire a baseline;
 To monitor a patient with breathing problems;
 To aid in the diagnosis of disease;
 To evaluate the response to medication that affects the respiratory
system.
When measuring and recording respirations the rate, depth and
pattern of breathing should be recorded.
 The depth (volume) of the breath is known as the tidal
volume, this should be around 500ml (Blows, 2001).
 The rate should be regular with equal pause between each
breath.
 The rate can be irregular with disease of the respiratory
system.
 Any irregularities should be noted and reported to the medical
team.
 When observing the respiratory rate, it is important to note the
colour of the patient’s lips.

 They may be cyanosed (blue) or discoloured if the patient has
respiratory problems.
 Cyanosis can also be observed in the nail bed, tip of the nose
and ear lobes (Woodrow, 2005).
 The patient’s oxygen saturation (SaO2) may be recorded using
a pulse oximeter.
 This will provide an accurate reading of oxygenation in the
red blood cells. Using a pulse oximeter may require the
patient to have less arterial blood gases performed, by
providing the medical team with a guide to the patients
oxygenation level.
Observe the breathing: is the patient mouth breathing, pursing the
lips on expiration, using the abdominal muscles or flaring the
nostrils?
Nostril flaring in children and babies is indicative of acute
respiratory distress (Field, 2000).
The respiratory rate is recorded along with other vital observation:
pulse, blood pressure and temperature.
Procedure:

 Explain to the patient what you are about to do - even if the
patient is unconscious;
 Ensure the patient is comfortable;
 Make sure the patient is as relaxed as possible;
 Observe if the patient is distressed in any way;
 It is best to monitor and record the respirations immediately after
taking the pulse; this will aid in a more accurate recording, as the
patient will not be aware that you are observing respirations.
Awareness that respirations are being recorded can make people
alter their breathing;
 Observe the rise and fall of the chest (inspiration and expiration) -
this counts as one breath;
 The respirations should be counted for a full minute in order to
have an accurate recording;
 Note the pattern of breathing and the depth of the breaths;
 Document your findings on the patients observation chart, note
any changes and report to the medical team;
 Before leaving, ensure the patient is comfortable.
When and how often should the respirations be recorded?
The patient’s condition will dictate the frequency of recording.
Respirations should always be recorded when a patient is first

admitted into hospital, to acquire a baseline record.
Safety measures:
 Wash hands thoroughly between patients - to eliminate the risk of
cross infection;
 Record respirations for a full minute to monitor the respiration
pattern and to ensure accuracy of the observation;
 If a patient has been prescribed oxygen, ensure the oxygen mask
or nasal cannulae is correctly placed prior to recording
respirations, and also check that the oxygen flow rate is set as
prescribed and recorded on the observation chart.
PULSERATE
The momentary stretching and relaxing of the arteries occurs with
each heartbeat - this is what is felt as the pulse, and should have
regular and consistent rhythm.

The pulse starts in the aorta (for the systemic system) and
spreads as a “pulse wave”, which travels through all the
arteries.
The farther away from the heart the artery is located, the
fainter the pulse, because the energy of the pulse becomes
dissipated as it moves through the arteries.
By the time blood reaches the capillaries, there is no longer a
pulse, and pulses cannot be felt in the veins that return blood
to the heart.
Assessing the pulses: what to look for
 A normal adult pulse will beat regularly between 60 and 100
times each minute at rest; in babies and children they are
much faster.
 Pulses are usually easily palpable; patients with a weak or
unstable pulse should be assessed further; weak pulses
indicate reduced cardiac output and can progress to
deterioration, for example fainting, or perhaps a more serious
problem.

 The rhythm of the pulses should be regular and consistent;
unstable or irregular pulses indicate irregular contractions of
the heart and should be referred to a senior clinician. A
strong, bounding pulse indicates high blood pressure.
 It is important that any deviations from the norm can be easily
explained.
 As mentioned, pain, stress or exertion will increase the pulse
rate, but it should return to normal when the underlying
trigger is abated.
 A slower-than-normal pulse can result from some
medications, for example digoxin and beta-blockers, and may
also be present in people who are accustomed to strenuous
activity.
 In the case of very fit people, a slower pulse results from their
heart capacity being enlarged, and therefore needing to beat
fewer times to circulate the blood adequately.
Required competencies and documentation
Nurses must be able to:
Identify key anatomical sites – this makes it easier to access sites

and maximises the potential for a safe assessment
Obtain informed consent
Ensure the patient is relaxed and the relative position of the chosen
site is equal to, or lower than, the level of the heart
When assessing a patient’s pulse, the following must always be
documented:
Time
Pulse rate
Pulse quality
Main pulses
There are many pulses in the bodybut the main ones are:
 Carotid
 Brachial
 Radial
 Femoral
 Posterior tibial
 Dorsal pedal
When assessing any pulse, the site being assessed should ideally be
level with, or below, the level of the heart. If the site is above the

heart, blood is travelling upwards and so the pulse might be less
easy to palpate. Some people have stronger palpable pulses on one
side than the other so if you experience difficulty feeling a pulse, try
the oppositeside.
Pulse assessments must always be accurately documented, and any
deviations from the norm reported. Providing they are conscious and
competent, a patient’s consent must be gained before a pulse
assessment is undertaken.
Carotid pulse
 The landmark for this pulse is the anterior triangle. This is
formed by the mandible, trachea and muscle.
 The carotid pulse is located in front of the
sternocleidomastoid and is sometimes deeper than anticipated.
 When locating this pulse, the patient’s head should be in a
comfortable position that requires no hyperextension.
 It is important to assess this pulse on one side only and move
the fingertips progressively towards the anticipated site of
palpation.

 Caution must be exercised when assessing the carotid pulse
due to the proximity of the carotid sinus - stimulation of the
carotid sinus can result in a reduced pulse rate, which will be
undesirable for a patient with bradycardia, for example.
Brachial pulse
This pulse is commonly used when manually assessing blood
pressure. The main site is at the brachial plexus, in line with the
biceps tendon. The patient’s arm should be extended, with the palm
facing upwards. Find the medial aspect of the volar forearm, close to
the elbow joint and ulnar styloid.
Radialpulse
 To find the radial pulse, trace the thumb to its base and to
where the radial bone begins at the wrist.
 On the volar/palmar aspect is the radial styloid - the thickened
bone at the distal end of the radius.
 Applying excess or insufficient pressure will make it difficult
to feel the pulse; the ideal pressure is equal to the weight of
the hand and wrist, which will happen automatically when the
correct position is adopted and the pulse felt for.

 To achieve the correct position, place two fingertips directly
alongside the radial styloid, just to the inside.
 Turn the patient’s hand over to allow it to hang from your
fingertips. Ensure the patient’s arm is relaxed, so you are
supporting the weight of hand and wrist on your fingertips.
 If the patient has cold hands a radial pulse may be difficult to
palpate because of reduced peripheral circulation. Similarly, if
blood pressure is very low, the peripheral circulation will be
compromised.
Femoral pulse
The femoral artery lies midway between the pubic symphysis and
the anterior superior iliac spine . Maximal pulsation of the femoral
artery occurs immediately below the level of the inguinal ligament.
Use the pads of your fingertips to press on this area. If there is a lot
of subcutaneous fat you will need to press more firmly, however
take care not to compress the artery too much or the pulse will not
be felt.
Posterior tibial pulse
Locate the inner ankle (medial malleolus) and feel 2-3cm behind

and below it. The posterior tibial pulse is deeper than the dorsal
pedal pulse and requires more concentration to locate and assess.
Dorsal pedal pulse
To find the dorsal pedal pulse, trace a line between the medial and
lateral malleoli towards the first toe. The pulse is located between
the malleoli and can be found about a third of the distance from
there
Measuring pulse and respirations
 Place the resident’s hand in a resting position on a surface,
palm up.
 Feel along the inside of the wrist with your fingertips,
locating the pulse below the resident’s thumb and just below
the bend of the wrist.
 Do not use your thumb, as it has a strong pulse of its own.
 Look at your watch and find a starting point. Count the beats
you feel for thirty seconds, and then multiply that number by
two.
 If the pulse is irregular, count for a full minute and don’t
multiply.
 When you have finished counting the pulse, stay in the same
position and watch the resident’s chest.
 It is best if the resident is not aware that you are counting his

breathing, because he may alter his breathing rate if he is
conscious of being watched.
 Look at your watch and find a starting point. Count each time
the resident’s chest rises and falls as one single respiration.
 Count respirations for thirty seconds and multiply by two.
 If breathing is irregular, count for a full minute and don’t
multiply.
 Document both the pulse and the respirations; writing down
the number of heartbeats and the number of breaths you
counted per minute.
 Notify your supervisor of irregularities or measurements
outside the normal range.
BLOOD PRESSURE
Definition:

Blood pressure (BP) is the pressure of circulating blood on
the walls of blood vessels. Most of this pressure is due to work done
by the heart by pumping blood through the circulatory system.
Used without further specification, "blood pressure" usually refers to
the pressure in large arteries of the systemic circulation.
Blood pressure is usually expressed in terms of the systolic pressure
(maximum during one heartbeat) over diastolic pressure (minimum
in between two heartbeats) and is measured in millimeters of
mercury (mmHg), above the surrounding atmospheric pressure.
Normal resting blood pressure in an adult is approximately 120
millimetres of mercury (16 kPa) systolic, and 80 millimetres of
mercury (11 kPa) diastolic, abbreviated "120/80 mmHg".
Globally, the average blood pressure, age standardized, has
remained about the same since 1975 to the present, at approx.
127/79 mmHg in men and 122/77 mmHg in women.
Traditionally, blood pressure was measured non-invasively using
ausculation with a mercury-tube sphygmomanometer.
Ausculation is still generally considered to be the gold standard of
accuracy for non-invasive blood pressure readings in clinic.

However, semi-automated methods have become common, largely
due to concerns about potential mercury toxicity, although cost, ease
of use and applicability to ambulatory blood pressure or home blood
pressure measurements have also influenced this trend.
Early automated alternatives to mercury-tube sphygmomanometers
were often seriously inaccurate, but modern devices validated to
international standards achieve an average difference between two
standardized reading methods of 5 mm Hg or less and a standard
deviation of less than 8 mm Hg.
Most of these semi-automated methods measure blood pressure
using oscillometry.
Blood pressure is influenced by cardiac output, total peripheral
resistance and arterial stiffness and varies depending on situation,
emotional state, activity, and relative health/disease states. In the
short term, blood pressure is regulated by baroreceptors which act
via the brain to influence the nervous and the endocrine systems.
Blood pressure that is too low is called hypotension, and pressure
that is consistently high is hypertension. Both have many causes and
may be of sudden onset or of long duration. Long-term hypertension
is a risk factor for many diseases, including heart disease, stroke and
kidney failure. Long-term hypertension is more common than long-

term hypotension, which is usually only diagnosed when it causes
symptoms.
Classification, normaland abnormal values
Systemic arterial pressure
The Task Force for the management of arterial hypertension of the European
Society of Cardiology (ESC) and the European Society of Hypertension (ESH)
classification of office blood pressure (BP)a and definitions of hypertension
gradeb. The same classification is used for all ages from 16 years. a BP category
is defined according to seated clinic BP and by the highest level of BP, whether
systolic or diastolic. b Isolated systolic hypertension is graded 1, 2, or 3
according to systolic BP values in the rangesindicated.
Category systolic BP, mmHg diastolic BP, mmHg
Optimal < 120 < 80
Normal 120–129 80–84
High normal 130–139 85–89
Grade 1 hypertension 140–159 90–99

Grade 2 hypertension 160–179 100–109
Grade 3 hypertension ≥ 180 ≥ 110
Isolatedsystolic hypertensionb
≥ 140 < 90
The risk of cardiovascular disease increases progressively above
115/75 mmHg, below this level there is limited evidence.
Observational studies demonstrate that people who maintain arterial
pressures at the low end of these pressure ranges have much better
long-term cardiovascular health. There is an ongoing medical debate
over what is the optimal level of blood pressure to target when using
drugs to lower blood pressure with hypertension, particularly in
older people.
The table shows the most recent classification (2018) of office (or
clinic) blood pressure by The Task Force for the management of
arterial hypertension of the European Society of Cardiology (ESC)
and the European Society of Hypertension (ESH).

A digital sphygmomanometer used for measuring blood pressure
Various other factors, such as age and sex, also influence a person's
blood pressure. Differences between left and right arm blood
pressure measurements tend to be small. However, occasionally
there is a consistent difference greater than 10 mmHg which may
need further investigation, e.g. for peripheral arterial disease or
obstructive arterial disease.
There is no accepted diagnostic standard for hypotension, although
pressures less than 90/60 are commonly regarded as hypotensive. In
practice blood pressure is considered too low only if symptoms are
present.
Systemic arterial pressure and age
Fetal blood pressure
In pregnancy, it is the fetal heart and not the mother's heart that

builds up the fetal blood pressure to drive blood through the fetal
circulation. The blood pressure in the fetal aorta is approximately
30 mmHg at 20 weeks of gestation, and increases to approximately
45 mmHg at 40 weeks of gestation.
The average blood pressure for full-term infants:
Systolic 65–95 mmHg
 Diastolic 30–60 mmHg
Childhood
Reference ranges for blood pressure (BP) in children
Stage
Approximate
age
Systolic BP,
mmHg
Diastolic BP,
mmHg
Infants 0 to 12 months 75–100 50–70
Toddlers and
preschoolers
1 to 5 years 80–110 50–80
Schoolage 6 to 12 years 85–120 50–80
Adolescents 13 to 18 years 95–140 60–90

In children, the normal ranges for blood pressure are lower than for
adults and depend on height. Reference blood pressure values have
been developed for children in different countries, based on the
distribution of blood pressure in children of these countries.
Aging adults
In adults in most societies, systolic blood pressure tends to
rise from early adulthood onward, up to at least age 70.
diastolic pressure tends to begin to rise at the same time but to
start to fall earlier in mid-life, approximately age 55.
Mean blood pressure rises from early adulthood, plateauing in
mid-life, while pulse pressure rises quite markedly after the
age of 40.
Consequently, in many older people, systolic blood pressure
often exceeds the normal adult range, if the diastolic pressure
is in the normal range this is termed isolated systolic
hypertension.
The rise in pulse pressure with age is attributed to increased
stiffness of the arteries.
An age-related rise in blood pressure is not considered healthy
and is not observed in some isolated unacculturated
communities.

Regulationof blood pressure
The endogenous, homeostatic regulation of arterial pressure is not
completely understood, but the following mechanisms of regulating
arterial pressurehave been well-characterized:
 Baroreceptor reflex: Baroreceptors in the high pressure
receptor zones detect changes in arterial pressure. These
baroreceptors send signals ultimately to the medulla of the
brain stem, specifically to the rostral ventrolateral medulla
(RVLM). The medulla, by way of the autonomic nervous
system, adjusts the mean arterial pressure by altering both the
force and speed of the heart's contractions, as well as the
systemic vascular resistance. The most important arterial
baroreceptors are located in the left and right carotid sinuses
and in the aortic arch.[70]
 Renin–angiotensin system (RAS): This system is generally
known for its long-term adjustment of arterial pressure. This
system allows the kidney to compensate for loss in blood
volume or drops in arterial pressure by activating an
endogenous vasoconstrictor known as angiotensin II.
 Aldosterone release: This steroid hormone is released from
the adrenal cortex in response to angiotensin II or high serum
potassium levels. Aldosterone stimulates sodium retention
and potassium excretion by the kidneys. Since sodium is the
main ion that determines the amount of fluid in the blood
vessels by osmosis, aldosterone will increase fluid retention,

and indirectly, arterial pressure.
 Baroreceptors in low pressure receptor zones (mainly in the
venae cavae and the pulmonary veins, and in the atria) result
in feedback by regulating the secretion of antidiuretic
hormone (ADH/Vasopressin), renin and aldosterone. The
resultant increase in blood volume results in an increased
cardiac output by the Frank–Starling law of the heart, in turn
increasing arterial blood pressure.
These different mechanisms are not necessarily independent of each
other, as indicated by the link between the RAS and aldosterone
release. When blood pressure falls many physiological cascades
commence in order to return the blood pressure to a more
appropriate level.
1. The blood pressure fall is detected by a decrease in blood
flow and thus a decrease in glomerular filtration rate (GFR).
2. Decrease in GFR is sensed as a decrease in Na+ levels by the
macula densa.
3. The macula densa causes an increase in Na+ reabsorption,
which causes water to follow in via osmosis and leads to an
ultimate increase in plasma volume. Further, the macula densa
releases adenosine which causes constriction of the afferent
arterioles.
4. At the same time, the juxtaglomerular cells sense the decrease
in blood pressure and release renin.
5. Renin converts angiotensinogen (inactive form) to angiotensin

I (active form).
6. Angiotensin I flows in the bloodstream until it reaches the
capillaries of the lungs where angiotensin converting enzyme
(ACE) acts on it to convert it into angiotensin II.
7. Angiotensin II is a vasoconstrictor which will increase blood
flow to the heart and subsequently the preload, ultimately
increasing the cardiac output.
8. Angiotensin II also causes an increase in the release of
aldosterone from the adrenal glands.
9. Aldosterone further increases the Na+ and H2O reabsorption
in the distal convoluted tubule of the nephron.
Currently, the RAS is targeted pharmacologically by ACE inhibitors
and angiotensin II receptor antagonists, also known as angiotensin
receptor blockers (ARBs). The aldosterone system is directly
targeted by spironolactone, an aldosterone antagonist. The fluid
retention may be targeted by diuretics; the antihypertensive effect of
diuretics is due to its effect on blood volume. Generally, the
baroreceptor reflex is not targeted in hypertension because if
blocked, individuals may suffer from orthostatic hypotension and
fainting.
Measurement

Taking blood pressure with a sphygmomanometer
 Arterial pressure is most commonly measured via a
sphygmomanometer, which uses the height of a column of
mercury, or an aneroid gauge, to reflect the blood pressure by
auscultation.
 The most common automated blood pressure measurement
technique is based on the oscillometric method.
 Fully automated oscillometric measurement has been
available since 1981.
 This principle has recently been used to measure blood
pressure with a smartphone.
 Measuring pressure invasively, by penetrating the arterial wall
to take the measurement, is much less common and usually
restricted to a hospital setting.
 Novel methods to measure blood pressure without penetrating
the arterial wall, and without applying any pressure on
patient's bodyare currently being explored.

 So-called cuffless measurements, these methods open the
door to more comfortable and acceptable blood pressure
monitors.
 See by instance, a cuffless blood pressure monitor at the wrist
that uses only optical sensors
Measuring blood pressure
1.The resident should be relaxed and comfortable, either
sitting or lying down.
2. Be sure there is no tight clothing restricting circulation on
the arm.
3. The arm should be bare. Loose sleeves can be pushed up.
4. Rest the resident’s arm on a surface such as a table or
chair arm, with the palm up and the arm out straight.
5. The resident should not hold his arm up, as using muscles
could raise the pressure.
6. Use a blood pressure cuff that is the right size for the
resident.
7. The cuff should fit easily around the arm and overlap,
but not be so large that it overlaps itself too far.
8. A cuff that is the wrong size will give an incorrect
reading.
9. Wrap the fully deflated cuff snugly (not too tight) around
the resident’s arm about an inch above the bend in the
elbow.
10.The cuff contains a sensor, usually marked with an arrow,
which should be placed over the brachial artery.

11.The brachial artery runs along the inside of the arm, on
the side next to the body.
12.Place the gauge where you can easily see it. Put your
stethoscopeearpieces in your ears.
13.Close the valve on the sphygmomanometer bulb. This
usually means turning the valve clockwise.
14.Find the brachial pulse by placing your fingers just above
the bend in the elbow along the side of the arm closest to
the body.
15.Keeping your fingers on the brachial artery, inflate the
cuff until you can no longer feel the pulse, and then
continue inflating for an additional 30 mm on the gauge.
16.Usually you will inflate the cuff until the gauge reads
between 170 and 200.
17. Place the flat disk part of your stethoscope (the
diaphragm) on the brachial artery just below the cuff and
just above the bend in the elbow.
18.Open the valve on the bulb slowly and steadily, turning it
counter-clockwise.
19.The cuff will begin to deflate.
20.Listen closely to the sounds coming through the
stethoscope. At the first pulse sound you hear, note the
gauge reading.
21. This is the systolic pressure reading.
22.Note the gauge reading again when the pulse sound
disappears. This is the diastolic pressure.
23.Deflate the cuff and remove it.

24.Record the blood pressure according to your facility’s
policy.
REFLECTIVE LEARNING:
1. Define vital signs
2. What are the types of temperature.
3. Enumerate sites of pulse assessment.
4. List out the variations of respiratory rate.
KEYS:
1.vital signs are the indication of living
2. hyper thermia, hypothermia, frost bite
3. carotid, brachial, radial, femoral, posterior tibial, Dorsal pedal
4. tachypnea, bradypnea
RESEARCHBASED LEARNING:
Vitalsignsmonitoring and nurse–patient interaction: A
qualitativeobservationalstudyof hospitalpractice
Author links open overlay panelM.Cardona-
Morrella
M.Prgometb
R.Lakeb
M.Nicholsonc
R.Harrisond
J.Longb
J.Westbrookb
J.Braithw aiteb
K.Hillmanac
Show more
Background
High profile safety failures have demonstrated that recognising early warning
signs of clinical and physiological deterioration can prevent or reduce harm

resulting from serious adverse events. Early warning scoring systems are now
routinely used in many places to detect and escalate deteriorating patients.
Timely and accurate vital signs monitoring are critical for ensuring patient
safety through providing data for early warning scoring systems, but little is
known about current monitoring practices.
Objective
To establish a profile of nurses’ vital signs monitoring practices, related
dialogue, and adherence to health service protocol in New South Wales,
Australia.
Methods
Direct observations of nurses’ working practices were conducted in two wards.
The observations focused on times of the day when vital signs were generally
measured. Patient interactions were recorded if occurring any time during the
observation periods. Participants (n = 42) included nursing staff on one chronic
disease medical and one acute surgical ward in a large urban teaching hospital
in New South Wales.
Results
We observed 441 patient interactions. Measurement of vital signs occurred in
52% of interactions. The minimum five vital signs measures required by New
South Wales Health policy were taken in only 6–21% of instances of vital signs
monitoring. Vital signs were documented immediately on 93% of vitals-taking
occasions and documented according to the policy in the patient's chart on 89%
of these occasions. Nurse–patient interactions were initiated for the purpose of
taking vital signs in 49% of interactions, with nurse–patient discourse observed
during 88% of all interactions. Nurse–patient dialogue led to additional care

being provided to patients in 12% of interactions.
Conclusion
The selection of appropriate vital signs measured and responses to these appears
to rely on nurses’ clinical judgement or time availability rather than on policy-
mandated frequency. The prevalence of incomplete sets of vital signs may limit
identification of deteriorating patients. The findings from this study present an
important baseline profile against which to evaluate the impact of introducing
continuous monitoring approaches on current hospital practice.
INTERACTIVE LEARNING:
Total batch devided into 4 groups and discussed regarding vital signs.
INTERNET BASED LEARNING
http://www.ncbi.nlm.nih.gov
http://medicalfacts.com
http://researchgate.in
encyclopedia
CONTEXTUAL LEARNING:
ASSIGNMENT: (10 M)
Write an assignment on vital signs
CAPSTONE PROJECT:
Students write the words regarding vital signs in 200 words.

SUPERVISED LEARNING:
Students divided into 5 groups 1st ( defenition, guidelines ) 2nd (temperature ,
physiology, types management) 3rd (respiratory rate, method of assessment,
variations) 4th (pulse rate, method of assessment, various sites of assessment) 5
th (blood pressure, types, method of assessment) made them to discuss and read.
SUMMATIVE LEARNING:
Vital signs are the indicators living of a human being. It includes temperature,
pulse, respiratory rate, pulse rate, blood pressure. All are the representatives of
the physiological changes of the human body
CONCLUSION:
Today we have discussed regarding vital signs, guidelines for measuring the
vital signs, discussed in detail about temperature, respiratory rate, blood
pressure, pulse rate its physiology and abnormalities its management..procedure
for measuring the vital signs.
BIBLIOGRAPHY
TEACHERS REFERENCE
 A K Kurana’s, “ fundamentals of nursing ”, 2003, by new age
international limited, Bangalore. PP 205-242
 KOZIER’s text book of fundamentals of nursing , 2014, by jaypee
publications page no 568-575
 Brunner and Suddharth’s “textbook of medical surgical nursing”, 11th
edition, volume 2, 2006 by Lippincott William Wilkins publications. PP

2054-2059
 Joyce M Black’s “Medical surgical nursing”, 7thedition, volume 1, 2000,
by elesevier publications. PP 1943-1948
 Lewis, Heitkemper’s “medical surgical nursing”, 6th edition,2006,by
mosby’s publications. PP 456-461
 Phipps “medical surgical nursing” 8th edition, 2007 by mosby elesevier
publications. PP 1818-1823,1797-1800
 Renu Jogi’s “Basic ophthalmology”,3rd edition, 2003 by jaypee
publications, New delhi. PP 246-279
 Tortora , Grabowski’s “Anatomy and physiology” , 10th edition 2003 by
wiley & sons,inc, USA, PP 824-825

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