AMBO UNIVERSITY

Monitoring

Prepared by: Zenebe B(MSc in Anesthesia )

 Introduction

 Patient monitoring has been a key aspect of

anesthesia since its beginnings as a medical specialty

 Because anesthesia affects all organs, monitoring the

anesthetized patient is required
 
 Appropriate monitoring facilitates timely therapeutic
intervention to prevent undesirable outcome

 
 Monitoring:

Definition

• The word monitor originated from the Latin

word monere, meaning “to warn.”

• Is the process by which an anesthetist obtains

information about the course of the anesthetic,
and interprets and responds to that information,
while continually re-evaluating the situation.
 
 Definition cont’d
• Monitoring is data collection

• Data may be collected manually, by the

senses, or automatically and must be
processed.
• Monitoring modalities arbitrarily categorized
into invasive or noninvasive monitor
 
 Monitoring in the Past

 Visual monitoring of
respiration and overall
clinical appearance
 Finger on pulse
 Blood pressure
(sometimes)
Monitoring in the Past

Finger on the pulse

Standards of monitoring
 ASA Monitoring Guidelines
• STANDARD I
Qualified anesthesia personnel shall be present
in the room throughout the conduct of all
general anesthetics, regional anesthetics and
monitored anesthesia care.
 ASA Monitoring Guidelines
• STANDARD II
During all anesthetics, the patient’s
oxygenation, ventilation, circulation and
temperature shall be continually evaluated.
 Oxygenation
 
• Inspired gas:- Oxygen analyzer with low
oxygen concentration limit alarm in use

• Blood oxygenation can be assessed by pulse

oximetry, color of blood
 Ventilation
 

• Chest excursion, observation of the reservoir

bag auscultation of breath sound

• Correct positioning of a tube in the trachea

must be verified by end-tidal CO2 analysis
• Audible signal when there is disconnection
of connections of breathing system during
mechanical ventilation
 Circulation
 
• Every patient receiving anesthesia shall have
ECG

• Every patient receiving anesthesia shall have

arterial blood pressure and heart rate
determined and evaluated at least every 5
minutes.
 
 Cont’d
• In addition to the above pulse palpation,
auscultation of heart sounds, intra-arterial
pressure, ultrasonic peripheral pulse
monitoring, or pulse oximetry.
 
 Body temperature
 

• There shall be readily available a means to

continuously measure the patient's
temperature.
• When change in body temperature are
intended, anticipated, or suspected, the
temperature shall be measured.
 
Minimum standard of patient monitoring

• Blood Pressure BP
• Electrocardiogram ECG
• Pulse Oximetry:
• Capnography and EtCO2
• Temperature
Anesthesia record sheet
 Anesthesia record
• Although anesthetics had been given since
1846 and many important clinical observations
had been made, the first formal records of
anesthetic administration were
not kept until 1895
• Dr. Harvey Cushing and Dr. Amory Codman,
medical students at the Massachusetts
general Hospital, conceived of "Ether Charts"  
 Harvey Cushing
Not just a famous neurosurgeon …
but the father of anesthesia monitoring

• Invented and popularized the

anesthetic chart
• Recorded both BP and HR
• Emphasized the relationship between
vital signs and neurosurgical events
( increased intracranial pressure leads
to hypertension and bradycardia )
 Cont’d
• There charts were simple, with a few comments
about the patient and the procedure, the
amount of ether administered and the
recording of pulse, respiration, and eventually
temperature *.
 
• They appeared unafraid to record the varied
swings of the few physiologic variables they
noted
 Cont’d
• The interval of record was 5 minutes

• Subsequently, in 1902, Cushing introduced

Riva-Rocci method for measuring blood
pressure, and these data were added to the
record
 
 Purpose of Anesthesia Record

• Anesthesia records are of undeniable value to

patient, anesthetist, surgeon, and nursing
staff.

• Has clinical and non clinical use

 1. Clinical use
Demographic and administrative data
-Patient name, hospital number, age, sex,
the date and time of the procedure, and
the names of the members of anaesthesia
and surgical teams must be recorded.
- The type of surgery (whether it is
Emergency or elective procedure), and
the technique of anaesthesia used
should be recorded.
 Cont’d

Physical status and Hx

• Time of meal (NPO), laboratory results,
weight, temp, pre-medication, ASA
(American society of Anaesthesiologists---
an assessment of the pt's pre-operative
condition/physical status).
• History and P/E of any major organ
system diseases or abnormality, drug Hx,
allergies, smoking and alcohol habits must
be recorded.
 Cont’d
ASA Classification
• ASA class I- A normally health pt.
• ASA class II- A pt with mild systemic disease.
• ASA class III- A Pt with severe systemic disease that is
not incapacitating to life .
 Cont’d
 ASA class IV- A pt with an incapacitating systemic
disease that is a constant threat to life.
 ASA class V- Moribund patient who has little chance
of survival but is submitted to surgery as a last resort
(resuscitative effort)
 ASA class VI- patient with brainstem death coming
for organ donation
 E- Any patient in whom an emergency operation is
required. Can be added to all ASA classes
 ASA PS Classification Definition Adult Examples, Including, but not Limited to: Pediatric Examples, Including but not Limited to: Obstetric Examples, Including but not Limited to:

ASA I A normal healthy patient Healthy, non-smoking, no or minimal alcohol Healthy (no acute or chronic disease), normal BMI  
use percentile for age
ASA II A patient with mild systemic Mild diseases only without substantive Asymptomatic congenital cardiac disease, well Normal pregnancy*,
disease functional limitations. Current smoker, social controlled dysrhythmias, asthma without well controlled
alcohol drinker, pregnancy, obesity exacerbation, well controlled epilepsy, non-insulin gestational HTN,
(30<BMI<40), well-controlled DM/HTN, mild dependent diabetes mellitus, abnormal BMI controlled
lung disease percentile for age, mild/moderate OSA, oncologic preeclampsia
state in remission, autism with mild limitations without severe
features, diet-
controlled
gestational DM.
ASA III A patient with severe systemic Substantive functional limitations; One or more Uncorrected stable congenital cardiac Preeclampsia with
disease moderate to severe diseases. Poorly controlled abnormality, asthma with exacerbation, poorly severe features,
DM or HTN, COPD, morbid obesity (BMI ≥40), controlled epilepsy, insulin dependent diabetes gestational DM with
active hepatitis, alcohol dependence or abuse, mellitus, morbid obesity, malnutrition, severe complications or
implanted pacemaker, moderate reduction of OSA, oncologic state, renal failure, muscular high insulin
ejection fraction, ESRD undergoing regularly dystrophy, cystic fibrosis, history of organ requirements, a
scheduled dialysis, history (>3 months) of MI, transplantation, brain/spinal cord malformation, thrombophilic
CVA, TIA, or CAD/stents. symptomatic hydrocephalus, premature infant disease requiring
PCA <60 weeks, autism with severe limitations, anticoagulation.
metabolic disease, difficult airway, long term
parenteral nutrition. Full term infants <6 weeks of
age.
ASA IV A patient with severe systemic Recent (<3 months) MI, CVA, TIA or Symptomatic congenital cardiac abnormality, Preeclampsia with
disease that is a constant threat CAD/stents, ongoing cardiac ischemia or severe congestive heart failure, active sequelae of severe features
to life valve dysfunction, severe reduction of ejection prematurity, acute hypoxic-ischemic complicated by
fraction, shock, sepsis, DIC, ARD or ESRD not encephalopathy, shock, sepsis, disseminated HELLP or other
undergoing regularly scheduled dialysis intravascular coagulation, automatic implantable adverse event,
cardioverter-defibrillator, ventilator dependence, peripartum
endocrinopathy, severe trauma, severe respiratory cardiomyopathy with
distress, advanced oncologic state. EF <40,
uncorrected/decomp
ensated heart
disease, acquired or
congenital.
ASA V A moribund patient who is not Ruptured abdominal/thoracic aneurysm, Massive trauma, intracranial hemorrhage with Uterine rupture.
expected to survive without the massive trauma, intracranial bleed with mass mass effect, patient requiring ECMO, respiratory
operation effect, ischemic bowel in the face of significant failure or arrest, malignant hypertension,
cardiac pathology or multiple organ/system decompensated congestive heart failure, hepatic
dysfunction encephalopathy, ischemic bowel or multiple
organ/system dysfunction.
ASA VI A declared brain-dead patient    
whose organs are being
removed for donor purposes
 Cont’d
– Graphic records

• Traditional vital signs of circulation,

respiration and measurements of O2 and
Co2 concentration or tension in the
respiratory gases or in the blood are
plotted on the graphic record.
 Cont’d
• Trend
• Trend plots allow for extrapolation
however, there could be unexpected
values and trends with in seconds for
instance during intubations heart rate
and pa Co2 may double within 15
seconds
 Cont’d
• Sampling rate
• The rate at which variable, should be recorded
must be adjusted to the individual variable and to
the clinical circumstances.
• For uneventful, routine cases, an entry every 5
minutes is usual and apparently sufficient.
• In critical emergencies or in pts with unstable
hemodynamics continuous monitoring of the
variables is important.
 Cont’d
– Crutch to memory
• It is necessary to recall time and amount of
the last dose of drugs, tourniquet applied
time, amount of fluid lost and administered
etc.
 Cont’d
Response to perturbations
• It is important to know how a pt responds to a
drug or a procedure, if the same drug is to be
administered or the same procedure is to be
repeated hours, days, or even years later.
 2. Non-clinical use
• Great weight is given to the anaesthesia
record as a legal document when a claim is
made against a member of anaesthesia team
medical team or against a hospital.
• The anaesthetic record serves as a source of
information for billing, research program and
of statistics of anaesthetics administered and
techniques employed.
 Cont’d
Analysis of the anaesthetic record
• The anaesthetic record should include all
employed, all event including procedures such
as, laryngoscopy, position, tourniquet etc.,
drugs that are given, fluid therapy, transfusion,
in their respective time of application
 Scope of the anaesthetic record.

The basic requirements of a chart are that it

should provide a space to record the
followings:
• Name, address, telephone number
Hospital number, date of admission, and age
are usually stamped on the chart in
addressograph plate
 
 Cont’d
• Height and weight
•  Recent meal
• Premedication
• Information of vital importance
- Diseases e.g. myasthenia gravis
- Allergy
- Previous untoward anesthetic experience
- Drug History
- Regional Anesthesia
 cont’d
• Problems during induction of general
anesthesia
• Agents:- Anesthetics, analgesics, and adjuvant
• The technique by which inhalation anesthetic
administered is written directly below the
agent (Closed, Semi-closed)
 Cont’d
• Position of patient
• Fluid therapy
• Blood transfusion
• Urine volume & color
• Blood lost
• Details of apparatus employed
• Monitors employed
 
 Cont’d
• Postoperative Notes

• Postoperative instruction include intervals of

measurement of different variable BP , Pulse,
Diuresis, Drains, Position ,Especial,
Temperature
 
 Cont’d
• Peripheral pulse
• Peripheral perfusion
• Arterial pressure
• Central venous pressure
• Urine production
 Peripheral Pulse
 
Monitoring pulse rate is more important than
monitoring heart rate, in terms of perioperative
hemodynamic assessment

 By definition, the distinction centers on whether a

given electrical depolarization and systolic
contraction of the heart
(heart rate) generates a palpable peripheral
pulsation (pulse rate)
 
 Cont’d
• The pulse deficit describes the extent to which
the pulse rate is less than the heart rate

• This is typically seen in a patient with atrial

fibrillation, in which short R-R interval
compromise cardiac filling during diastole,
resulting in reduced stroke volume and
imperceptible arterial pulse
 Cont’d

• The most extreme example of pulse deficit is

electrical mechanical dissociation or pulse
less electrical activity seen in patients with
cardiac tamponade, extreme hypovolemia,
and other conditions in which cardiac
contraction does not generate a palpable
peripheral pulse
 cont’d
• Most monitors report heart rate and pulse
rate separately

• The former is measured from the ECG trace,

and the latter is determined by a pulse
oximeter
 Peripheral perfusion
 

• This is assessed most usefully by observation

of the patient's extremities
• warm, pink, and dry skin indicates adequate
perfusion

• This is particularly true in children, in whom

cold peripheries usually indicate a degree of
hypovolaemia
 Cont’d
• The core-peripheral temperature gradient is a
useful index of adequacy of peripheral
perfusion.
• One temperature probe is placed centrally (e.g.
in the nasophrynx) and the other peripherally
(e.g. on the great toe)

• The temperature gradient increases with

vasoconstriction and low cardiac out put
 Blood pressure
measurement
• Non-invasive blood pressure
• Invasive blood pressure
 ARTERIAL BLOOD PRESSURE
• The rhythmic contraction of the left ventricle,
ejecting blood into the vascular system, results
in pulsatile arterial pressures.

• The peak pressure generated during systolic

contraction approximates SBP and the lowest
arterial pressure during diastolic relaxation is
DBP
 Cont…
• Pulse pressure is the difference between the
systolic and diastolic pressures.
• The time-weighted average of arterial
pressures during a pulse cycle is the mean
arterial pressure (MAP).
• MAP can be estimated by application of the
following formula:
MAP (SBP) + 2(DBP)/3
 Factor affect correct reading
• Arterial blood pressure is greatly affected by
where the pressure is measured.
• As a pulse moves peripherally through the
arterial tree, wave reflection distorts the
pressure waveform, leading to an
exaggeration of systolic and pulse pressures
• The level of the sampling site relative to the
heart affects
Cont…
 Cont…
• The accuracy of any
method of blood
pressure measurement
that involves a blood
pressure cuff depends
on proper cuff size .
 Common sources of errors

 - Too small cuff will result in high blood pressure

reading.
- A loosely applied cuff will also produce a
reading higher than it should be.
- Falsely low estimates result when cuffs are
too large, when the extremity is above heart level
or if the cuff is deflated too rapidly
Continue
 Others
• Room Temperature
• Alcohol / Caffeine
• Smoking
• Full Bladder
• Talking
• Muscle Tension
• Posture
• Rest Period
 Noninvasive Arterial Blood
Pressure Monitoring
• The most commonly used by anesthetist.
• The techniques and frequency of pressure
determination depend on the patient’s
condition and the type of surgical procedure.
• A blood pressure measurement every 3–5 min
is adequate in most cases.
• Techniques that rely on a blood pressure cuff
are best avoided in extremities with vascular
abnormalities
 Techniques & Complications

A. Palpation
B. Doppler Probe
• When a Doppler probe is substituted for the
• anesthesiologist’s finger, arterial blood
pressure measurement becomes sensitive
enough to be useful in obese patients,
pediatric patients, and patients in shock
 Conti…
Aneroid gauge

Brachial artery

Radial artery

Doppler probe

Doppler
 Cont…
C. Auscultation
• Hypotension, hypertension, cautery may
affect reading
D. Oscillometry
• Because some oscillations are present above
and below arterial blood pressure, a mercury
or aneroid manometer provides an inaccurate
and unreliable measurement
 Cont.…
• Machines that require identical consecutive
pulse waves for measurement confirmation.
• So may be unreliable during arrhythmias (eg,
atrial fibrillation).
• Nonetheless, the speed, accuracy, and
versatility of oscillometric devices have greatly
improved,
Cont…
 2. Invasive Arterial Blood
Pressure Monitoring

Indications
• Major surgical procedures involving large fluid loss
• Surgery of the aorta
• Patients with recent myocardial infarctions, unstable
angina, or severe coronary artery disease
• Patients with decreased left ventricular function
(congestive heart failure)
 Cont…
• Deliberate hypotension or deliberate hypothermia
• Massive trauma cases
• Patients with right-sided heart failure, chronic
obstructive
• pulmonary disease, pulmonary hypertension, or
pulmonary embolism
• Patients with electrolyte or metabolic disturbances
• Inability to measure BP noninvasively
 Contraindications

• If possible, catheterization should be avoided

in smaller end arteries with inadequate
collateral blood flow
• in extremities where there is a suspicion of
preexisting vascular insufficiency
COMPONENTS OF AN IBP MEASURING
SYSTEM
 Artery for Cannulation

1. The radial artery

2. The Ulnar artery.
3. The brachial artery .
4. The femoral artery
5. The axillary artery.
 Complications
• Hematoma, bleeding , vasospasm, arterial
thrombosis, embolization of air bubbles or
thrombi, necrosis of skin.
• Nerve damage, infection, necrosis of
extremities or digits, and unintentional
intraarterial drug injection.
 Factors associated
• Prolonged cannulation
• Hyperlipidemia,
• Repeated insertion attempts,
• The use of larger catheters in smaller vessels,
and
• The use of vasopressors.
 The risks are minimized
• When the ratio of catheter to artery size is small,
• Saline is continuously infused through the
catheter at a rate of 2–3 mL/hr,
• Flushing of the catheter is limited, and
• Meticulous attention is paid to aseptic
technique.
• Placing a pulse oximeter on an ipsilateral finger
 Properties
• Natural frequency: determines how rapidly the
system oscillates after a stimulus

• Damping coefficient: reflects frictional forces

acting on the system
 The natural frequency
The natural frequency of a system may be
increased by:
• Reducing the length of the cannula or tubing
• Reducing the compliance of the cannula or
diaphragm
• Reducing the density of the fluid used in the
tubing
• Increasing the diameter of the cannula or tubing
 Damping
• Anything that reduces energy in an oscillating
system will reduce the amplitude of the
oscillations
Factors that cause overdamping include:
• Friction in the fluid pathway
• Three way taps
• Bubbles and clots
• Vasospasm
• Narrow, long or compliant tubing
• Kinks in the cannula or tubing
 Cont…
Under daming PB Over damding PB
 Clinical considerations

• It is considered the optimal blood pressure

monitoring technique.
• False readings can lead to inappropriate
therapeutic interventions.
• For accurate measurement of pressure, the
catheter– tubing–transducer system must be
capable of responding adequately to the
highest frequency of the arterial.
 Cont…
• The addition of tubing, stopcocks, and air in the
line all decrease the frequency of the system lead
to overdaming and underestimating the systolic
pressure.
• Catheter–tubing–transducer systems must also
prevent hyper resonance, an artifact caused by
reverberation of pressure waves within the
system.
• A damping coefficient (β) of 0.6–0.7 is optimal
 Cont…
• System dynamics are improved by minimizing tubing
length, eliminating unnecessary stopcocks, removing
air bubbles, and using low-compliance tubing.
• Smaller diameter catheters lower natural frequency,
they improve under dampened systems and are less
in vascular complications.

• If a large catheter totally occludes an artery, reflected

waves can distort pressure measurements.
 Arterial line accuracy
• Patency of the line
• Levelling the transducer
• Zeroing the transducer
• Square wave testing
• Transducer accuracy depends on correct
calibration ,zeroing procedures and position

CVS Monitoring by Timsel and Ayele

 Cont…

CVS Monitoring by Timsel and Ayele

 Cont..

CVS Monitoring by Timsel and Ayele

Components of arterial waveform
 Waveform alteration

Pulsus paradoxus- Large

decrease in SBP and pulse
waveform during inspiration.
Tamponade, severe lung
disease, advanced CHF
 Cont…
Aortic insufficiency

• Also called aurtic

regurgitation
• Have wide pulse pressure
• Ventricle get much during
diastole
• Higher Peak systolic
pressure during the next p
• Atrial Fibrillation- Irregular.
Shorter diastolic filling time.
Decreasing systolic peak
amplitude during
premature ventricular
complexes.
CENTRAL VENOUS CATHETERIZATION
 Indications

 For monitoring central venous pressure (CVP),

 Administration of fluid to treat hypovolemia
and shock,
 infusion of drugs and total parenteral
nutrition,
 aspiration of air emboli, gaining venous access
in patients with poor peripheral veins.
 continuous monitoring of central venous
oxygen saturation.
 Contraindications
• Relative contraindications include tumors, clots
• Tricuspid valve vegetation's.
• In patients who are receiving anticoagulants
• The presence of other central catheters or
pacemaker.
 Techniques & Complications
• Central venous cannulation involves introducing a
catheter into a central vein within the thorax.

• Generally, the optimal location of the catheter tip is

just superior to or at the junction of the superior
vena cava and the right atrium.
• When the catheter tip is located within the thorax,
inspiration will increase or decrease CVP,
 Cont…
• All cannulation sites have an increased risk of line-
related infections.
• The subclavian vein is associated with a greater risk of
pneumothorax during insertion, but a reduced risk of
other complications.
• The right internal jugular vein provides a combination
of accessibility and safety
• Left -sided internal jugular vein catheterization has an
increased risk of pleural effusion
 Techniques of cannulation
1. A catheter over a needle (similar to
peripheral catheterization),
2. A catheter through a needle (requiring a
large-bore needle stick), and
3. A catheter over a guide wire (Seldinger’s
technique;
• The majority of central lines are placed using
Seldinger’s technique.
CVS Monitoring by Timsel and Ayele
 Cont…
• The patient is placed in the Trendelenburg
position to decrease the risk of air embolism
and to distend the internal jugular (or
subclavian) vein.
• Venous catheterization requires full aseptic
technique
 Cont…
• .The two heads of the sternocleidomastoid muscle
and the clavicle form the three sides of a triangle
• A 25-gauge needle is used to infiltrate the apex of
the triangle with local anesthetic.
• The internal jugular vein can be located using
ultrasound which strongly recommended and
blindly
• Aspiration of venous blood confirms the vein’s
location
 Clinical Considerations

• Normal cardiac function requires adequate

ventricular filling by venous blood.
• CVP approximates right atrial pressure.
Ventricular volumes are related to pressures
through compliance.
• Highly compliant ventricles accommodate
volume with minimal changes in pressure.
Noncompliant systems have larger swings in
pressure with less volume changes.
 Cont..
• Consequently, an individual CVP measurement
will reveal only limited information about
ventricular volumes and filling.
• Although a very low CVP may indicate a
volume-depleted patient, a moderate to high
pressure reading may reflect either volume
overload or poor ventricular compliance
 Cont…
• Changes associated with volume loading
coupled with other measures of hemodynamic
performance (eg, blood pressure, HR, urine
output) may be a better indicator of the
patient’s volume responsiveness.
• CVP measurements should always be
considered within the context of the patient’s
overall clinical perspective
Central venous waveform
 cont…
a wave:
a is for atrium… this is the right atrial contraction.
• It correlates with the P wave on the ECG.
• It disappears with atrial fibrillation
C wave
• c is for cusp… this is the cusp of the tricuspid
valve, protruding backwards through the atrium,
as the right ventricle begins to contract.
• It correlates with the end of the QRS complex on
the ECG
 Cont…
x descent: This is the movement of the right ventricle,
which descends as it contracts
• At this stage, there is also atrial diastolic relaxation,
which further decreases the right atrial pressure.
v wave: As blood fills the right atrium, it hits the
tricuspid
valve and this is the back-pressure wave
• It also gives an impression of tricuspid competence.
y descent: This is a pressure decrease caused by the
tricuspid valve opening in early ventricular diastole.
Cont…
 The 5 Most Common Central Venous
Catheter Complications
1. Damage to Central Veins
2. Pulmonary Complications
3. Cardiac Complications
4. Device Dysfunction
5. Infection
Introduction to ECGs
 Electrocardiography

– Continuous trace of electrical activity of whole

heart Provides continuous information about
heart rate, presence of arrhythmias, ischaemia
and conduction defects.
It is important to keep in mind that the ECG shows
only electrical activity; it tells us nothing about
how well the heart is working mechanically.

e.g. “Pulseless electrical activity” (PEA); ECG may look

normal, but NO cardiac output
 USES OF ECG

• ECG is useful in determining and diagnosing the following:

Heart rate
Anatomical orientation of the heart
Rhythm and conduction disturbance

Poor blood flow to heart muscle (ischemia)

Coronary artery disease

Hypertrophy of heart chambers.

 Types of Electrocardiogram Recording
1. Bipolar/standard limb leads:
• Record voltage b/n two electrodes
(leads) placed on the wrists and
legs. These leads include:

Lead I= LA-RA, measures electric

potential difference b/n Lft arm &
Rt arm.

Lead II =LL-RA, measures electric Bipolar limb leads

potential difference b/n Lft leg &

Rt arm.
Einthoven Triangle
• is defined as an equilateral triangle that is used as a model of
standard limb leads used to record electrocardiogram.
• Heart is presumed to lie in the center of Einthoven triangle.
• Electrical potential generated from the heart appears
simultaneously on the roots of the three limbs, ( left arm,
right arm and the left leg).
Einthoven triangle. C = Center of electrical activity, RA = Right arm, LA = Left
arm, LL = Left leg, LI, LII and LIII = Standard limb leads.
Einthoven Law
• If electrical potentials of any two of the three leads are given,
the 3rd one can be determined.
• Amplitude (electrical potential) of QRS complex in one lead
can be mathematically calculated, by summing up or
subtracting the amplitude in other two leads
• Eg. amplitude of QRS in lead II = I + III

• the amplitude of QRS in lead III = II – I.

. Normal Electrocardiograms recorded from the bipolar limb leads
2. Unipolar leads
• Voltage is recorded b/n a single “exploratory electrode” placed
on the body and an electrode that is built into the
electrocardiograph and maintained at zero potential.
A. Unipolar Limb Leads/Augmented Limb Leads
• Two of the limbs are connected through electrical resistances
to the negative (indifferent) terminal of the electrocardiograph
and the 3rd limb is connected to the positive terminal.
• When positive terminal is placed on right arm, the lead is
designated as aVR; when on the left arm aVL, and when on left
leg, aVF .
Normal Electrocardiograms recorded from the unipolar
limb leads
 B. Precordial (Chest) Leads

• Unipolar leads labeled V1, V2, V3, V4, V5 and V6.

• One electrode is connected to the positive terminal of the

Electrocardiograph and the negative electrode (indifferent
electrode) is connected through equal electrical resistances to
the right arm, left arm, and left leg.

• Electrodes are placed on the chest as shown in the next fig..

Fig. 8. Position of electrodes for chest leads (V1 to V6)
• QRS in V1, V2, are negative because the chest electrodes are
nearer the base of the heart (direction of electronegativity).
• V3 is in b/n.
• QRS of leads V4-V6 are positive because they are nearer the
apex (direction of electropositivity).
PLACEMENT OF Electrocardiograph (ECG) Leads
 Principles of Vectorial Analysis of
Electrocardiograms
• Cardiac vector( cardiac axis) is the direction

at which electrical potential generated in

the heart travels at an instant.

• Vector is represented by an arrow.

• Arrowhead shows the direction of current

flow Instantaneous mean vector when

current flows through
• Length of the arrow represents the interventricular septum of the heart

amplitude (magnitude or voltage) of

electrical potential.
Mean Electrical Axis of the Heart
• is the vector showing current flows from base of
ventricles(negative) toward apex (positive).
• The mean electrical axis of the normal ventricles is 59 degrees.
• It varies between -30° and 90°.

• Electrical axis is determined from standard limb leads .

• A positive vector in a lead causes recording in the ECG above the
zero line, while a negative vector causes ECG recording below the
zero line.
Plotting the mean electrical axis of the ventricles from two
electrocardiographic leads (leads I and III).
Polarity convention
• Upward deflection: when voltage difference between two
electrodes is more positive.
• Downward deflection: when voltage difference between two
electrodes is more negative.

1. A wave of depolarization traveling toward a positive

electrode results in a positive deflection in the ECG trace.
2. A wave of repolarization traveling toward a negative
electrode results in negative deflection.
3. A wave of depolarization or repolarization oriented
perpendicular to an electrode axis has no net deflection.
 Approach to Determining Axis
• There are multiple methods to determine the
electrical axis.
• The main QRS complexes to evaluate are
those in leads I, II, and aVF. The positive ends
of these three leads fall within the normal axis
region.
• The positive ends of leads I, II, and aVF are
0 degrees, +60 degrees, and +90 degrees,
respectively. .
 Cont…
• 0 degrees to +90 degrees is normal axis,
• +90 degrees to 180 degrees is RAD,
• 0 degrees to -90 degrees is LAD, and
• 90 degrees to 180 degrees is extreme axis.
• Therefore, if leads I and aVF are both positive,
then the axis falls within the normal axis range
 Cont…
• If lead I is positive and lead aVF is negative,
then there is LAD.
• If lead I is negative and lead aVF is positive,
then there is RAD.
• And, if both leads I and aVF are negative, then
the axis falls within the extreme axis range
Cont…
 ECG Conventions
• ECG machine amplifies electrical signals produced from the
heart .
• It records these signals on a moving ECG paper.
• ECG paper has horizontal and vertical lines at regular intervals
of 1 mm.
• Every 5th line (5 mm) is thickened.
 Cont…

Height = millivolts
Width = Time

1 mm x 1 mm
Cont…
A normal electrocardiogram
• Duration of different ECG waves is plotted horizontally on
X-axis (1 mm = 0.04 sec.,5 mm = 0.20 sec.
• Normal Paper speed =25mm/sec.
• Amplitude of ECG waves is plotted vertically on Y-axis.

(1 mm = 0.1 mV ,5 mm = 0.5 mV
• 10mm deflection → 1mV
 WAVES OF NORMAL ECG

• The normal electrocardiogram is composed of

• P wave,
• QRS complex, and
• T wave.

Intervals and Segments of the a normal electrocardiogram

„ ‘P’ WAVE
• ‘P’ wave is positive and the first wave in ECG.
• it is produced due to the depolarization of both atria.
• Atrial repolarization is not recorded as a separate wave in
ECG because it is obscured by the QRS complex.
• Normal duration is 0.12 second.
• Normal amplitude is 0.1 to 0.12 mV.
‘QRS’ COMPLEX
• is due to depolarization of ventricles. .
• ‘Q’ wave is a small negative wave.

• It is continued as the tall ‘R’ wave, which is a positive wave.

• ‘R’ wave is followed by a small negative wave, the ‘S’ wave.
• ‘Q’ wave is due to the depolarization of basal portion of
interventricular septum.
• ‘R’ wave is due to the depolarization of apical portion of
interventricular septum and apical portion of ventricule
• ‘S’ wave is due to the depolarization of basal portion of
ventricular muscle.
• Normal duration of ‘QRS’ complex = 0.08 - 0.10 second.
• Amplitude of ‘Q’ wave = 0.1 - 0.2 mV.

• Amplitude of ‘R’ wave = 1 mV.

• Amplitude of ‘S’ wave = 0.4 mV.
‘T’ WAVE
• ‘T’ wave is due to the repolarization of ventricles.
• Normal duration of ‘T’ wave is 0.2 second.
• Normal amplitude of ‘T’ wave is 0.3 mV.
U’ WAVE
• Small rounded, upright wave, following T wave.

• ‘U’ wave is not always seen.

• Mostly seen in slow heart rate.

• It is also an insignificant wave in ECG.

• represents repolarization of pukinje fibers.

 Segments- isoelectric period
• PR (PQ)segment :represents the delay in the AV
node
‘S-T’ segment
• is the time interval between the end of ‘S’ wave and the
onset of ‘T’ wave.
• Represents the complete depolarization of ventricles.
• Normal duration is 0.08 second.
P-Q or P-R Interval ( interval= wave +segment )
• The time between the beginning of the P wave and the
beginning of the QRS complex.
• Is the interval between the beginning of excitation of the
atria and the beginning of excitation of the ventricles.
• The average P-Q interval is about 0.16 second.

CVS Monitoring by Timsel and Ayele

Q-T Interval.
• Is the time interval between the onset of ‘QRS’ complex and
the end of ‘T’ wave.
• indicates the ventricular depolarization and repolarization.
• It signifies the electrical activity in ventricles.
• Is about 0.35 second.
„ ‘R-R’ INTERVAL
• Is the time interval between two consecutive ‘R’ waves.
• Signifies the duration of one cardiac cycle.
• Normal duration is 0.83 second.

Determining heart rate from the ECG

• the heart rate is the reciprocal of the time interval between
two successive heartbeats (1/RR interval)
• If the ‘R-R’ interval is 1 second, the heart rate is 60 bpm.

• The normal interval between two successive QRS complexes

or ‘R’ waves in the adult person is about 0.83 second.
• This is a heart rate of 60/0.83 times per minute=72 bpm.
Arrythmia
 Arrhythmia
Definition of Arrhythmia:
It is an abnormal activity of the heart in at least one of the
following
 Origin
 Rate
 Rhythm
• Conduct velocity and sequence
• In arrhythmia, heartbeat may be fast or slow or there
may be an extra beat or a missed beat.
• It occurs in physiological and pathological conditions
 Sinoatrial Node Arrhythmias
Arrhythmias originate in the sinoatrial node.
The ECG features common to all of them are
upright P waves, all similar in appearance;
normal duration PR intervals; and normal-
duration of QRS complexes.
 Those are
, sinus bradycardia, sinus tachycardia, sinus
arrhythmia, sinus pause (sinus arrest), and SA
block.
Normal sinus rhythm
the impulse originates in the sinus node and travels through the
normal conduction pathways within normal time frames.
the P waves will be uniform(small, rounded, and upright in leads I, II,
aVF, and V4 to V6 inverted in lead aVR. In other leads, it can be upright,
inverted, or biphasic (half upright, half inverted)) and since conduction
is normal, one P wave will be in front of every QRS complex.

what is the rate? approx. 90 bpm,

Is it sinus rhythm? Yes, Regular
What is the PR interval? < 0.2 s (normal)
What is the QRS duration? < 0.12 s (normal)
Sinus bradycardia
Characterized by sinus rate below 60 beats/minute and a regular
rhythm.
Sinus bradycardia usually occurs as the normal response to a
reduced demand for blood flow & in a person with a well-conditioned
Heart.

what is the rate? approx 40 bpm

Is it sinus rhythm? Yes

What is the PR interval? < 0.2 s (normal)

What is the QRS duration? < 0.12 s (normal)

 Causes of sinus bradycardia
Sleep hyperkalemia,
Fit and healthy Increased intracranial
Hypoxia (especially in children) pressure, hypothyroid ism,
Vagal stimulation hypothermiaHy
Inferior wall MI(BEZOLD-JARISCH REFLEX) pertension (Marey Reflex)
Drugs (eg suxamethonium, BB etc.)
Valsalva’s maneuver,
Treatment
Treat underlying cause (e.g stop surgical stimulus)
100 %Oxygen
Anticholinergic (e.g. atropine,.02/kg or glycopyrolate .01/kg)
adrenaline 1 mg up to 0.2 mg/kg.
If low BP accompanies bradycardia dopamine infusion at 2
to 10 mcg/kg/min
beta-blocked patients may respond to glucagon(2-10mg
Definetive mngt pacemaker.
Sinus tachycardia
Sinus tachycardia in an adult is characterized by a sinus rate of
more than 100 -160 beats/minute. The rate rarely exceeds 160
beats/minute.

what is the rate? A normal Approx 120 bpm

Is it sinus rhythm? P wave precedes yes
What is the PR interval? each QRS < 0.2 s (normal)
complex. < 0.12 s (normal)
What is the QRS duration?
As the heart rate increases, the P wave may be superimposed on the
preceding T wave and difficult to identify. The QT Interval also
shortens with tachycardia.
Causes of sinus tachycardia
Inadequate anaesthesia
Thyrotoxicosis
Pain
Drugs (including ketamine,
Fever / sepsis
atropine)
Hypovolaemia
Anaphylaxis
Anaemia
Pulmonary embolism
Heart failure
Hypersecretion of catecholamines
Treatment
Treat underlying cause
Deep anesthesia
Carotid massage
Beta blockers (esmolol, 1 mg/kg by iv bolus or propanalol)
calcium channel blockers (verapamil 5 to 10 mg iv)
NOTE Remember that tachycardia is commonly the first sign of a
pulmonary embolism.
Atrial arrhythmias
• Atrial arrhythmias, the most common cardiac rhythm
disturbances, result from impulses originating in areas
outside the SA node.
• These arrhythmias can affect ventricular filling time and
diminish the strength of the atrial kick.
• It result from three mechanisms
• Enhanced automaticity
• Reentry
• Triggered activity
 Premature atrial contractions
• originate outside the SA node and usually result from an irritable
spot, or focus, in the atria that takes over as pacemaker for one or
more beats.
• PACs may be conducted through the atrioventricular (AV) node and
the rest of the heart.

what is the rate? Around 80

Is it sinus rhytm
What is the PR interval? Normal except during PAC
< 0.12s( normal)
What is the QRS duration?
• PACs may occur in bigeminy (every other beat is a PAC), trigeminy (every
third beat is a PAC), or couplets (two PACs in a row).
 The nicotine in
cigarattes can cause
PACs. Yuk!
Causes
coronary or valvular heart
Triggering factors
disease,  alcohol,
acute respiratory failure,  nicotine,
hypoxia,  anxiety,
pulmonary disease,  fatigue,
digoxin toxicity, and  pain
certain electrolyte imbalances  fever, and infectious
diseases.
Treatment
As most PACs are benign it not need trx.
Treating underlying condition
BB
CCB
Atrial flutter
is characterized by an atrial rate of 250 to 350bpm, although it’s
generally around 300bpm. Atrial flutter is commonly associated
with second-degree block. characterized by abnormal P waves
that produce a saw-toothed appearance
The clinical significance of atrial flutter is determined by the
number of impulses conducted through the node(conduction
Ratio).

what is the rate? approx 75 bpm(ventricular)

Is it sinus rhythm? no
What is the PR interval? no normal P waves
What is the QRS duration? < 0.12 s (normal)
NOTE in AF pt you may note that His/her peripheral or apical
pulse is normal in rate and rhythm. why???
 Causes of atrial flutter
• Electrolyte disturbances • Hypertension
• Sepsis • Ischaemia
• Thyrotoxicosis • Alcohol
• Excessive sympathetic stimulation • Caffeine
• Mitral valve disease
• Thoracic surgery
• Pericarditis

Treatment
Treat underlying cause
• , consider
- electrical cardioversion (synchronised)
- Carotid sinus massage
- rate control (eg digoxin BB,CCB)
- anticoagulation (Heparin)
-Radiofrequency ablation
Atrial fibrillation (“AF”)
A-fib, is defined as chaotic, asynchronous, electrical activity in atrial
tissue.
common arrhythmia encountered in anaesthetic andsurgical practice.
The ectopic impulses may fire at a rate of 400 to 600bpm, causing the
atria to quiver instead of contract. It eliminates atrial kick.

what is the rate? variable; average 100 (ventricular)

What is the PR interval? unknown
Is it sinus rhythm? No!!! no P wave:QRS r/nship
What is the QRS duration? < 0.12 s (normal)
Remember!!! Never confuse muscle artifact with A-fib if the rhythm is
regular(The irregular conduction of impulses result in irregularly
irregular ventricular response).
When caring for a patient with atrial fibrillation, you may find that the
radial pulse rate is slower than the apical rate.
 Causes of atrial fibrillation (“AF”)
Electrolyte disturbances
Sepsis
Thyrotoxicosis Hypertension
Excessive sympathetic Ischaemia
stimulation Thoracic surgery
Mitral valve disease Alcohol
Pericarditis Caffeine
Treatment
Initial treatment should consist of control of the ventricular response
rate with drugs that slow AV node conduction:   
 esmolol (1 mg/kg by iv bolus) or propranolol.  
 verapamil (5 to 10 mg iv) & Amiodarone 300mg loading dose
 Synchronized DC cardioversion
 flecainide 50 - 100mg
 Radiofrequency ablation
 Treat underlying cause
ventricular arrhythmias
Ventricular arrhythmias originate in the ventricles
below
the bundle of His.
 Ventricular arrhythmias appear on an ECG in
characteristic ways.
 QRS complex is wider
 T wave and the QRS
complex deflect in opposite
directions
 P wave is absent
 Premature ventricular contraction
oPVCs are usually caused by electrical irritability in the ventricular
conduction system or muscle tissue.
• This irritability may be provoked by anything that disrupts normal
electrolyte shifts during cell depolarization and repolarization.
• QRS complex in the premature beat exceeds 0.12 second.
• The T wave in the premature beat has a deflection opposite that of
the QRS complex.

• PVCs are significant for two reasons.

 lead to more serious arrhythmias,
 decrease cardiac output,
 Cause
• electrolyte imbalances • enlargement of the
• metabolic acidosis ventricular chambers
• hypoxia • increased
• MI sympathetic
• drug intoxication stimulation
• myocarditis • caffeine or alcohol
• tobacco use. ingestion
• proarrhythmic effects
of some
antiarrhythmics
 bigeminal uniform PVCs

Premature ventricular contraction – multiform pvc

Premature ventricular contraction –trigeminy

Premature ventricular contraction –quadrigeminy

• Treatment
• If the patient is asymptomatic, the arrhythmia probably
won’t require treatment. Correction of any contributing
causes
• Iv atropine - If sinus rhythm is slow < 50 bpm
• Lignocaine is drug of first choice.
• Amiodarone 300mg iv
• Magnesium sulfate 1–2 g mixed in 50–100 mL of D5W
infused over 5–60 min IV
Ventricular tachycardia (“VT”)
If the myocardium is extremely irritable, the ventricular focus could
speed up and override higher pacemaker sites. This would create what
is essentially a sustained run of PVCs.
This rhythm is called VentricularTachycardia &which is 150-
250bpm.Ventricular tachycardia is significant because of its
unpredictability and potential to cause death.

what is the rate? Approx 167 bpm

Is it sinus rhythm? no (no P waves, but fairly regular
(abnormal) QRS complexes)
What is the PR interval? not known
What is the QRS duration? ‘broad’; > 0.12 s
NOTE Sustained v-tach lasts for more than 30 seconds and requires
immediate treatment to prevent death.
 • VT may be monomorphic or polymorphic( Torsades de pointe)
Causes of ventricular tachycardia (“VT”)
Myocardial ischaemia Fluid overload
Hypoxia Electrolyte imbalance
Hypotension Adrenaline (or other
Drugs catecholamines
Treatment
depends on whether the patient’s pulse is detectable or undetectable.
If there is no pulse, begin CPR and follow ACLS protocol
Treatment for the patient with a detectable pulse depends on
whether his condition is stable or unstable and has monomorphic or
polymorphic QRS complexes.
• If unstable; DC cardioversion
• If stable + monomorphic ; consider
• Epinephrine 1mg, Lignocaine 100mg amiodarone 300mg,
Propranolol 0.5 -1.0mg Procainamide 100mg
• synchronized cardioversion
• Also treat under lying causes like ( electrolyte inbalance stopping
drugs )
 With chronic or recurrent VT
may need ICD
• NOTE Any wide QRS complex tachycardia should be treated as
ventricular tachycardia until definitive evidence is found.
Ventricular fibrillation (“VF”)
chaotic pattern of electrical activity in the ventricles in which
electrical impulses arise from many different foci. It produces no
effective muscular contraction and no cardiac output. It is the
easiest of all the arrhythmias to recognize.
Untreated ventricular fibrillation causes most cases of sudden
cardiac death.

what is the rate? completely chaotic

Is it sinus rhythm? no
What is the PR interval? unknown
What is the QRS duration? unrecognisable
 Causes The 4 ‘H’s and 4 ‘T’s
Untreated VT
underlying heart disease  Hypoxia
acid-base imbalance  Hypovolaemia
electric shock  Hyper/hypokalaemia
severe hypothermia  Hypothermia(untreated )
Brugada syndrome  Tension pneumothorax
drug toxicity,  Tamponade
severe hypoxia.  Thrombo-embolism
 Toxic (eg drugs)
Treatment
CPR must be performed until the defibrillator arrives .
Drugs Such as epinephrine amiodarone, lidocaine, may also be given.
Defibrillation is the most effective treatment.
Identify and treat underlying cause appropriately
ICD
AV block
Atrioventricular (AV) heart block results from an interruption
in the conduction of impulses between the atria and ventricles.
The block can occur at the AV node, the bundle of His, or the
bundle branches.
 We will concentrate on AV node conduction problems
 The heart’s electrical impulses normally originate in the
sinoatrial (SA) node.
 The clinical effect of the block depends on
how many impulses are completely blocked,
how slow the ventricular rate is as a result, and
how the block ultimately affects the heart
First degree heart block (“1 DHB”) st

If each wave of depolarization that originates in the SA node is

conducted to the ventricles, but there is delay somewhere along the
conduction pathway, then the PR interval is prolonged. This is called
‘first degree heart block.

What is the rate? Approx 60 bpm

it sinus rhythm? yes
What is the PR interval? > 0.2 s (prolonged)
What is the QRS duration? < 0.12 s (normal)
NOTE
If the PR interval is extremely long, a longer interval between S1 and S2 may
be noted on cardiac auscultation.
Causes of 1st DHB
Idiopathic (benign)
coronary artery disease,
acute rheumatic carditis,
digoxin toxicity
or electrolyte disturbances.
Treatment
Not require txt in the absence of symptoms
Treat underlying causes.
Atropine – 0.5 – 2 mg IV
Pacemakers
Second degree heart block
(Mobitz Type I / Wenkebach)
when each successive impulse from the SA node is delayed
slightly longer than the previous impulse. That pattern continues
until an impulse fails to be conducted to the ventricles.

what is the rate? Background of 60 bpm with

missed beats
Is it sinus rhythm? yes, but with some missed QRS
complexes
What is the PR interval? prolongs with each successive beat
What is the QRS duration? < 0.12 s (normal)
 Causes of 2nd DHB, Mobitz Type I
coronary artery disease
inferior wall MI,
Rheumatic fever.
Increased vagal stimulation
Drugs( CCB, BB)
Treatment
No treatment is needed if the patient is asymptomatic. For a
symptomatic patient, atropine .5-2mg may improve AV node
conduction.
A temporary pacemaker may be required for long-term relief of
symptoms until the rhythm resolves.
Treat underlying cause.
Second degree heart block (Type II )
is less common than type I but more serious. It occurs when
occasional impulses from the SA node fail to conduct to the
ventricles.
The arrhythmia indicates a problem at the level of the
bundle of His or bundle branches.

what is the rate? 40bpm ,atrial around 100

yes, but with some missed QRS
Is it sinus rhythm?
complexes & P, 2/3 Ps without QRS
What is the PR interval? < 0.2 s (Normal)
What is the QRS duration? < 0.12 s (normal)
Causes of 2nd DHB,
Anterior wall MI,
Degenerative changes in the
conduction system, or
Severe coronary artery disease
Treatment
If the patient is hypotensive, treatment aims to improve
cardiac output by increasing the heart rate.
Atropine, dopamine, or epinephrine may be given for
symptomatic bradycardia.
placement of a pacemaker.
Complete heart block (“CHB”)
3rd degree AV block occurs when impulses from the atria are
completely blocked at the AV node and can’t be conducted to the
ventricles.
Atria is under the control of the SA node, so has a regular rate.The
ventricular rhythm can originate from the AV node and maintain a rate
of 40 to 60 bpm.
Because the ventricular rate is so slow, it is a potentially life-threatening
situation because cardiac output can drop dramatically.

what is the rate? Approx 30 bpm, but atrial 60-

100bpm
Is it sinus rhythm? no (no relationship between P &QRS)
What is the PR interval? no relationship
What is the QRS duration? ~ 0.12 s (borderline prolonged)
 Causes of complete heart block (“CHB”)
Myocardial
ischemia( anterior, inferior)
Structural heart disease
Vagal stimulation
Congenital heart disease
Radiofrequency ablation
Treatment
Therapy aims to improve the ventricular rate .
Stop vagal stimulation
Give atropine
Dopamine and epinephrine may also be indicated.
a temporary pacemaker may be used to restore adequate
cardiac output.
Asystole (arrhythmia of death.)
The last stage of a dying heart is when all electrical activity
ceases.it is ventricular standstill. The patient is completely
unresponsive, with no electrical activity in the heart and no
cardiac output.
Results most commonly from a prolonged period of cardiac
arrest without effective resuscitation.

How would you describe the trace? no cardiac activity seen

 REVERSIBLE causes of asystole (from ALS algorithm)
The 4 ‘H’s and 4 ‘T’s

Hypoxia Tension
Hypovolaemia pneumothorax
Hyper/hypokalaemia Tamponade
Hypothermia Thrombo-
Treatment embolism
Toxic (eg drugs)
The immediate treatment for asystole is CPR. Give
repeated doses of atropine and epinephrine.
Transcutaneous pacing should be initiated as soon as
possible.
Identify and treat underlying cause appropriately
 Pulseless Electrical Activity (PEA)
• Electricity is working, but the mechanics and plumbing
are not.
• ▪The absence of a palpable pulse and absence of
myocardial muscle activity with presence of organized
electrical activity on the cardiac monitor. The patient is
clinically dead despite some type of organized rhythm
on monitor.
Causes: H’s and T’s
•Hypovolemia #1 cause • Toxins
•Hypoxia
•Tamponade (cardiac)
•Hydrogen ions (acidosis)
•Hypo / Hyperkalemia •Tension pneumothorax
•Hypothermia •Thrombosis (coronary or
•Overdose 0f TCA pulmonary)
•Trauma
Treatment •Massive MI
• Determine cause & treat
• ▪CPR
• ▪Initiate ACLS protocol
Myocardial ischaemia &myocardial infarction
• Myocardial ischaemia represents a decrease in the
perfusion of a certain area of the myocardium generally
due to atherothrombosis.
• If significant and persistent, it usually leads to tissue
necrosis MI.
• Horizontal depression of the ST segment, associated with
an upright T wave, is usually a sign of ischaemia as
opposed to infarction
• After a myocardial infarction, the first abnormality seen on
the ECG is elevation of the ST segment (exceeding 1 mm in
the limb leads and 2 mm in the chest leads) Subsequently,
Q waves appear, and the T waves become inverted.
• The ST segment returns to the baseline, usually
within the range 24–48 h. T wave inversion is often
permanent.
• Infarctions causing this pattern of ECG changes are
called ‘ST segment elevation myocardial infarctions’
(STEMIs)
• If an infarction is not full thickness and so does not
cause an electrical window, there will be T wave
inversion but no Q waves.
• Infarctions with this pattern of ECG change are called
‘non-ST segment elevation myocardial infarctions’
(NSTEMIs).
 Signs of ischaemia
ST depression
Ischaemic changes T wave inversion
(cell hypoxia / Possible rhythm disturbance
hypoperfusion) (may be cause or effect)

ST elevation
Acute signs of infarct T wave inversion
(cell death) New conduction abnormalities
Q waves (after a few hours)
Arrhythmias

Signs of a previous Q waves

infarct (mature Flattened T waves
Persistent conduction abnormalities
changes)
 Anterior Wall MI

Anterior Wall infarct: Occlusion of the Left Anterior

Descending Artery (LAD)
•2mm ST segment elevation in two or more of leads V1-
V4
• Reciprocal changes in leads II, III, aVF
•Lethal due to large myocardium involvement
Possible conduction defects:
Bundle Branch Block
2nd Degree Block Type II
CHB
Anterior Wall MI
 Inferior Wall MI(diaphragmatic MI)
Inferior Wall MI: Occlusion of Right Coronary Artery (RCA)
•At least 1mm ST segment elevation in leads II, III, aVF
•Reciprocal ST depression in leads I & aVL or precordial leads
Conduction defects:
•Sinus bradycardia
•Sinus arrest
•1st degree block
•Accelerated Idoventricular rhythm
Inferior Wall MI
 Lateral Wall MI
Lateral Wall MI: results from occlusion of the Left
Circumflex Artery
•At least 1 mm ST segment elevation in leads I,
aVL, V5 & V6 and /or 2 mm ST segment elevation
in V5 & V6
• Reciprocal ST depression in V1
• Sometimes an extension of an Anterior or
Inferior MI
• Conduction defects are rare
Anterior/Lateral Wall MI
 Posterior Wall MI
Posterior Wall MI: Occlusion of the Right Coronary Artery
(RCA) or the Posterior Descending Artery
•No leads that look at the posterior wall
• Leads look at the infarct site from the opposite
side(backwards)
•ST depression in V1 & V2
•Tall R waves in V1 and/or V2
•Most often associated with Inferior MI
*Associated with dangerous conduction disturbances*
Posterior Wall MI
Acute myocardial infarction (“MI”)

How do we know it’s an MI? ST elevation

Which leads are involved? II, III and aVF

Where is the infarction? Inferior MI
Treating arrhythmia
• Anti arrhythmic treatment can be categorized into
two
Non pharmacological
Pacemaker
Defibrillator
cardioversion
Pharmacological
Class I( Na† channel blockers)
Class II(Beta blockers)
Class III ( K† channel blockers)
Class IV ( Ca ††channel blockers)
 pacemakers
• is an artificial device that electrically stimulates the
myocardium to depolarize, which begins a
contraction.
• used when a patient has an arrhythmia, such as
certain bradyarrhythmias and tachyarrhythmias, sick
sinus syndrome, or (AV) blocks & it’s commonly
necessary following MI or cardiac surgery.
• The device may be temporary or permanent.
• Pacemakers consist of three components:
• Pulse generator, the pacing leads, and the electrode
tip.
 Pulse  generator

Direction of current
flow

Electrode
• Permanent pacemakers
A permanent pacemaker is used to treat chronic
heart conditions such as AV block. It’s surgically
implanted.
The leads are placed transvenously,
The power source of generator is lithium batteries
which last about 10yrs & implanted in a pocket made
from subcutaneous tissue.
The pocket is usually constructed under the clavicle.
Permanent pacemakers are programmed during
implantation.
• Temporary pacemakers
• A temporary pacemaker is commonly inserted in an
emergency. is powered by alkaline batteries.
• The temporary pacemaker supports the patient until
the condition resolves.
• Temporary pacemakers are used for patients with
heart block, bradycardia, or low cardiac output.
• Several types of temporary pacemakers are available,
including transvenous, epicardial, and
transcutaneous.
 Working with pacemakers
On an ECG, you’ll notice a pacemaker spike Which is occurs when the
pacemaker sends an electrical impulse to the heart muscle.
That impulse appears as a vertical line or spike.
Depending on the position of the electrode, the spike appears in d/t
locations on the waveform.
When the atria are stimulated the spike is followed by a P wave and
QRS complex and T wave.
When the ventricles are stimulated by a pacemaker, the spike is
followed by a QRS complex and T wave.
When the pacemaker stimulates both the atria and the ventricles,
the first spike is followed by P wave, then a spike, and then
QRS complex.
 Pharmacological

• Antiarrhythmic drugs affect the movement of ions

across the
• cell membrane and alter the electrophysiology of the
cardiac cell.
• They’re classified according to their effect on the
cell’s electrical activity (action potential) and their
mechanism of action.
 Class IV drugs inhibit calcium’s slow
influx during phase 2, which lengthens
the phase. They also depress phase 4
and lengthen phases 1 and 2.

Classes Ia, Ib, and Ic drugs

Class III drugs prolong phase 3,
reduce movement of sodium
which increases repolarization
ions into the cell during
and refractoriness.
phase 0.

Class II drugs inhibit adrenergic stimulation of

cardiac tissue by depressing phase 4
spontaneous
depolarization and slowing sinoatrial node
impulses.
 Class I(Na† channel blockers)

• Block the influx of sodium into the cell & minimizes the
chance of sodium reaching its threshold potential and
causing cells to depolarize.
• Antiarrhythmic drugs in this class are further categorized
as
Class Ia, which reduce conductivity and prolong
repolarization and the action potential .
• Used for atrial fibrillation or flutter, paroxysmal
supraventricular tachycardia, and premature ventricular
contractions (PVCs).
E.g quinidine and procainamide.
 class Ib, which slow phase 0 depolarization, don’t affect
conductivity, and shorten phase 3 repolarization and the
action potential. Used for suppressing ventricular
arrhythmias
E.g lidocaine
class Ic, which markedly slow phase 0 depolarization and
reduce conduction (used only for refractory arrhythmias).
• Because of their proarrhythmic potential, these drugs are
used only for life-threatening or ventricular arrhythmias.
E.g flecainide and propafenone
 Class II antiarrhythmics

• Block SNS beta-adrenergic receptors and thereby

decrease heart rate. Phase 4 depolarization
• Is diminished resulting in depressed SA node
automaticity and increased atrial and (AV) nodal
refractoriness, or resistance to stimulation.
• Used to treat supraventricular and ventricular
arrhythmias, especially those caused by excess
catecholamines.
• E.g esmolol, propanalol
 Class III antiarrhythmics
• They block the movement of potassium during phase
3 of the
• Action potential and prolong repolarization and the
refractory period.
• Used to treat supraventricular arrhythmias,
paroxysmal supraventricular tachycardia caused by
ventricular arrhythmias and accessory pathway
conduction, as in Wolff-
• Parkinson-White syndrome.
• E.g amiodarone hydrochloride (Cordarone), ibutilide
(Corvert), and dofetilide
 Class IV antiarrhythmics
• Block the movement of calcium during phase 2 of the
action potential.
• They prolong conductivity and increase the refractory
period at the AV node. used for paroxysmal
supraventricular tachycardia.
• It also slows the ventricular response in atrial fibrillation
and flutter
• E.g verapamil and diltiazem.
 Monitors of Renal Function
• The vigilance of anesthetist is the first monitor
required to preserve renal function.
• Repeated direct perioperative assessment of renal
hemodynamics, tubular function, or pathogenesis
of perioperative renal dysfunction is impractical.
 Con’t…
• So, indirect assessments, such as serum creatinine
trends, are the best practical currently available
perioperative tool to assess renal function.
• They are referred as traditional (delayed)
biomarkers of acute kidney injury
• obligate delay between the onset of AKI and the
diagnosis of AKI
 Con’t…
• Biomarkers of Kidney Function
• urine volume,
• urine specific gravity,
• urine osmolality,
• serum creatinine level
• serum blood urea nitrogen level
• Inulin clearance
• Creatinine clearance
• etc
 Serum Creatinine Concentration
• Creatine is a product of muscle metabolism that is
nonenzymatically converted to creatinine.
• Creatinine is then filtered but not reabsorbed in
the kidneys.
• reliable indices/marker of GFR
• Unlike BUN, it is not influenced by protein
metabolism or the rate of fluid flow through
renal tubule
• inversely related to GFR
 Con’t…
• Normal range: 0.8–1.3 mg/dL in men and 0.6–1
mg/dL in women…why?
• increased serum creatinine conc without there being
a concomitant decrease in GFR:
e.g. Large meat meals, cimetidine therapy
• late marker of renal injury
• increases in serum creatinine are not typically
noted until GFR has declined by at least 50%
• especially in elderly patients- mild increases
suggest significant renal disease
 Con’t…
• GFR can be estimated from serum creatinine using
Cockcroft-Gault equation:

• For women, this equation must be multiplied by

0.85 to compensate for a smaller muscle mass.
 Blood Urea Nitrogen (BUN)

• Ammonia produced from the deamination of

amino acids is converted into urea by liver.
• late sign of renal injury
• inversely related to GFR
• not a reliable indicator of GFR
• Influenced by protein catabolism
• 40–50% of urea filtrate is normally
reabsorbed
• normal BUN concentration is 10–20 mg/dL
 Con’t…
• Lower values can be seen with starvation or liver
disease
• Increased BUN conc despite a normal GFR:
• high-protein diets, gastrointestinal bleeding,
dehydration, increased catabolism (trauma or sepsis)
• Conversely, BUN Conc can remain normal in the
presence of low-protein diets (hemodialysis patients)
despite decreases in GFR.
 Con’t…
• BUN concentrations greater than 50 mg/dL are
generally associated with impairment of renal
function
• BUN to-creatinine ratio greater than 20 during
dehydration. why?
 Creatinine Clearance
• volume (ml) of plasma that would be completely
cleared of creatinine per minute
• More reliable measurement of GFR than the serum
BUN and creatinine values
• not influenced by body metabolism or dietary
factors
• Normal 110 to 150 mL/min
 Con’t…
• principal disadvantage of this test is the need for
timed urine collections- for 24 hours
• However, 2-hr creatinine clearance
determinations are reasonably accurate and
easier to perform
 Con’t…
• CrCl 40–60 mL/min= Mild impairment of renal function
• CrCl between 25 and 40 mL/min= moderate renal
dysfunction and nearly always cause symptoms
• risk of developing prolonged or adverse responses to
drugs (such as nondepolarizing muscle relaxants)
• CrCl less than 25 mL/min are indicative of overt kidney
failure
 Con’t…
• The reliability of creatinine clearance is
diminished by the variability in tubular
secretion of creatinine.
• So not ideal
 Urine Volume
• The presence of urine (regardless of amount)
confirms blood flow to the kidney
• The reliability of intraoperative urine output
as a sign of pending renal dysfunction is not
clear.
• In contrast to the intraoperative setting,
significant prolonged preoperative or
postoperative oliguria has been proposed as
a diagnostic criterion for AKI, with urine
output (<0.5 mL/kg/hr for longer than 6
hours)
 Con’t…
• The kidney concentrates the ultrafiltrate so that at
maximal concentration, a minimum of 400 to 500
mL of urine
• is required to clear the daily obligatory nitrogenous
wastes.
• However, the urine output criteria for AKI have not
been
• well validated in the clinical literature and remain
controversial.
 Urine Specific Gravity
• Urine concentrating ability
• Reflects the mass of 1 mL of urine compared with 1
mL of distilled water.
• Normal values range between 1.001 and 1.035
• High (e.g., 1.030) during poor perfusion or prerenal
azotemia
• reflecting the kidney’s ability to conserve
sodium and water
 Con’t…
• With a loss of concentrating ability attributable to
ATN, urine specific gravity resembles plasma
osmolarity (e.g., 1.010).
• when interfering substances that raise urine
specific gravity, high urine specific gravity can
provide misleading reassurance that the renal
concentrating ability is preserved
• e.g., glucose, protein, contrast dye
 Con’t…
• The ability of the kidneys to concentrate urine is
impaired in many older patients and many with
chronic kidney disease
• Urine specific gravity is a surrogate for osmolality
 Urine Osmolality
• A measure of the number of osmotically active
particles in solution in the solvent phase
• Theoretically, urine osmolality is physiologically
superior to urine specific gravity as a test of renal
function
• the same substances and conditions that render
urine specific gravity a nonspecific test can also
affect the reliability of urine osmolality
 Con’t…
• Similar to urine-specific gravity, the sensitivity and
specificity of urine osmolality as a test for
predicting or distinguishing ATN from prerenal
azotemia are clinically inadequate.
 Urinary Sodium Concentration
• With decreasing perfusion, the normally
functioning kidney conserves sodium and water.
• Affected by heterogenicity of nephrons, secretion
of aldosterone, secretion of ADH, diuretic therapy,
saline
• It is traditionally accepted that a urinary sodium
level of less than 20 mEq suggests prerenal
azotemia and
• a level of greater than 40 mEq indicates acute
tubular necrosis.
 Con’t…
• It is unreliable indicators of prerenal
azotemia or acute tubular necrosis due
to the complex physiology of sodium
homeostasis.
 Fractional Excretion of Sodium(FeNa)

•First described by Espinel

•Represents the fraction of sodium excreted versus that
filtered by the kidneys

where PCr is the plasma creatinine level, PNa is the plasma

sodium level, UCr is the urinary creatinine level, and UNa is
the urinary sodium level
 Con’t…
• < 1% suggests prerenal azotemia
• > 1% suggests ATN
• FeNa is useful only when oliguria is already present
 Inulin Clearance

• A “gold standard” tool to measure GFR in clinical

practice
• Inulin is a polymer of fructose has been used to
measure GFR because it is filtered freely in the
glomerulus, not reabsorbed or secreted, and is
excreted in the urine.
• It is infuses, and after an equilibration period (usually
1 hour), clearance measurements obtained.
 Con’t…
• The standard formula for calculation of clearance is
as follows:
CI = (U1V) ÷ P1
• Where UI and PI are the urine and plasma
concentrations of inulin, respectively, CI is the rate
of inulin clearance, and V is the urine flow rate
• Other exogenously administered clearance markers
include iohexol, iothalamate, and radiolabeled
ethylenediaminetetraacetic acid (EDTA) and
diethylenetriaminepentaacetic acid (DTPA)
 Urinalysis
• Routinely performed for evaluating renal function
• Includes: pH, specific gravity, detection and
quantification of glucose, protein, and bilirubin
content, and microscopic examination of the
urinary sediment.
• A urinary pH greater than 7.0 in the presence of
systemic acidosis is suggestive of renal tubular
acidosis
 Con’t…
• Glycosuria is the result of either a low tubular
threshold for glucose (normally 180 mg/dL) or
hyperglycemia.
• Proteinuria (excretion of more than 150 mg of
protein per day) is most likely due to abnormally
high filtration rather than impaired reabsorption by
the renal tubules.
 Con’t…
• Microscopic analysis of the urinary sediment
detects the presence of red or white blood cells,
bacteria, casts, and crystals.
• Red cells may be indicative of bleeding due to
tumor, stones, infection, coagulopathy, or trauma.
• White cells and bacteria are generally associated
with infection.
• Disease processes at the level of the nephron
produce tubular casts.
Thanks!!!
 References

• Arrhythmia essentials 2nd edition

• Basic arrhythmias 7th edition
• ECG interpretation made incredibly easy 5 th
edition
• ECG success-exercise interpretation
• Graphics-Sequenced Interpretation of ECG
• Guyton medical physiology 11th edition