The Heart

Basis of life…….?
1
Functions of the Heart
 Regulate Blood circulation

 Systemic circuit: vessels that transport blood to and from

all the body tissues
 Pulmonary circuit: carry blood to and from the lungs

 Generates blood pressure

 Ensures one-way blood flow: Heart valves ensure one-way

flow
Continue……..
Regulates blood supply

 Changes in contraction rate and force match blood

delivery to changing metabolic needs

 Most healthy people can increase cardiac output by

300–500% (Cardiac reserve)

Heart failure is the inability of the heart to provide enough

blood flow to maintain normal metabolism
Volume of blood in human body is approx. 5 liters.

The heart pumps about 280 liters/ hour, 7200 liter/

24 hours,
Brain

or 2,688,000 liters per year!

Vena cava

4
 Heart Anatomy
 Approximately the size of your fist
 Wt. = 250-300 grams
 Location
 In the mediastinum b/w the lungs
 Superior surface of diaphragm

 ⅔’s of it lies to the left of the midsternal line

 Anterior to the vertebral column, posterior to the

sternum surrounded by membrane called
Pericardium
 Pericardial space is fluid-filled to nourish and
protect the heart.
 HEART ANATOMY

 The heart has four chambers.

 Two atria act as collecting reservoirs

 Two ventricles act as pumps.

 The heart has four valves for:

 3-tricuspid + 1 Bicuspid
Pumping action of the heart.
Maintaining unidirectional blood flow.

6
 Chambers of the heart

Two atria-divided by
interatrial septum
Right atrium
Left atrium

Two ventricles-
divided by
interventricular septum
Right ventricle
Left ventricle
7
 Structure of Heart Wall
Left ventricle – 3-times
thicker than right

Exerts more pumping force

Flattens right ventricle into a

crescent shape

Thicker myocardium due to greater work load

Systemic circulation supplied by left ventricle is a higher

pressure system and thus requires more forceful contractions
 Heart Valves: Tricuspid and bicuspid
 “Tricuspid” valve: RA to RV
 Pulmonary or pulmonic valve: RV to pulmonary trunk
 Mitral valve (the bicuspid one): LA to LV
 Aortic valve: LV to aorta

(cusp means flap)

9
Function of AV valves
Mitral valve

chordaetendineae

Papillary

 The leaflets of the mitral and tricuspid valves are also supported by tough, fibrous strings
called chordae tendineae, attached with small muscles, called papillary muscles, 10
Function of semilunar valves
(Aortic and pulmonic valves)

11
Heart valves Disease: can have one of two malfunctions:
Regurgitation

Valve(s) does not close completely, causing the blood to flow backward instead of
forward through the valve.

Stenosis: The valve(s) opening becomes narrowed or does not form properly,
inhibiting the flow of blood out of the ventricle or atria.

The heart is forced to pump blood with increased force in order to move blood
through the stiff (stenotic) valve(s).

When heart valves fail to open and close properly, hampering the heart’s ability to
pump blood adequately through the body.

Heart valve problems are one cause of heart failure.

12
 How Does Blood Travel Through the Heart?
 Arteries. carry oxygen-rich blood away from the heart to all tissues
-branch several times, becoming smaller

 Capillaries: small, thin blood vessels that connect the arteries and the
veins.

-thin walls allow O2, nutrients, CO2, and other waste products to pass to and
from cells.

 Veins- blood back to the heart, become larger as they get closer to the
heart, superior vena cava and the inferior vena cava brings blood back

This vast system of blood vessels -- arteries, veins, and capillaries -- is over 60,000
miles long
-long enough to go around the world more than twice!
13
Microscopic Anatomy of Heart Muscle

 Cardiac muscle is striated, short, fat, branched, and

interconnected
 The connective tissue endomysium acts as both tendon
and insertion
 Intercalated discs anchor cardiac cells together and
allow free passage of ions
 Heart muscle behaves as a functional syncytium

14
Microscopic Anatomy of Heart Muscle

15
Figure 18.11
Cardiac Cycle- Output
 Heart is two pumps that work together, right (pulmonary) and
left (systemic) half

 Repetitive, sequential contraction (systole) and relaxation

(diastole) of heart chambers

 Contraction of heart produces the pressure

CO: the amount of blood pumped by each ventricle in one minute

-the product of heart rate and stroke volume

 Continue……
 CO = HR (75 beats/min) x SV (70 ml/beat

 CO = ……… ml/min (…… L/min)

If HR increases to 150 b/min and SV increases to 120 ml/beat,

then
 CO = 150 b/min x 120 ml/beat
 CO = 18,000 ml/min or 18 L/min …..up to 35 L/min in
athlete
 Heart Rate
Pulse = surge of pressure in artery
 infants have HR of 120 bpm or more
 young adult females avg. 72 - 80 bpm
 HR rises again in the elderly

Tachycardia: resting adult HR above 100

 stress, anxiety, drugs, heart disease or  body temp.

Bradycardia: resting adult HR < 60

 in sleep and endurance trained athletes
 Essential functions - secured by integration of electrical and
mechanical functions of the heart

Cardiac output (CO) = heart rate (HR) x stroke vol.(SV)

- changes of the heart rate

- changes of stroke volume

•Control of HR:
- autonomic nervous system
hormonal(humoral) control
•Control of SV: - preload
- contractility
- afterload
 Adaptive mechanisms of the heart to increased load

Frank - Starling mechanism

states that the SV of the heart increases in response to an increase in the volume of
blood filling the heart (the end diastolic volume) when all other factors remain
constant.

1:Ventricular hypertrophy
– increased mass of contractile elements  strength
of contraction

 2: Increased sympathetic adrenergic activity

– increased HR, increased contractility

3: Incresed activity of R–A–A system

 Conduction system
 Specialized heart cells - generate and coordinate the transmission
of electrical impulses to myocardial cells

 The result is sequential AV- contraction - provides the most

effective flow of blood , thereby optimizing cardiac out put

Characteristics of Cardiac Conduction Cells

 Automaticity: ability to initiate an electrical impulse

 Excitability: ability to respond to an electrical impulse
 Conductivity: ability to transmit an electrical impulse from one
cell to another
Cardiac Conduction System
Initiates and coordinates contraction: Four basic components
 Sinu-atrial node (SA node)
 Atrioventricular node (AV node)
 AV-bundle with its right and left bundle branches (Bundle of
His)
 Subendocardial plexus -the Purkinje fibers)
 Internal Control of Heart Rate
 Cardiac muscle beats involuntarily, beat of each cell of heart
muscle is in synchrony or in pace with the beat of every other heart
muscle cell.

 Nervous impulses from a specialized bundle of nervous tissue

called the SA Node

 SA Node: control the rate of the heart beat and also synchronize
the beating of all cardiac cells.
 Continue…..
 The sinoatrial or SA node is known as the pacemaker.

 The SA node causes a wave of contraction to start in both the atria.

 -causes the AV- node to initiate contractions of the ventricles.

 The bundle of HIS carries the nervous stimuli to all parts of the
ventricle via Purkinje Fibres which brings the impulse to each
cardiac cell.
The SA node: at 72 beats/min which can be considered a “normal”
resting heart rate.

Medulla Oblangata in the brain controls the nerves that influence HR

Chemoreceptors: O2 and CO2 concentration levels

Baroreceptors: pressure sensetive receptor in the arteries respond to

changes in the BP

a. Increased or accelerated HR by stimulation of the

sympathetic nerve.
b. Decreased or slowing of the HR -stimulation of the
parasympathetic nerve
 Factors Affecting Heart Rate
Increase Physical Activity = Increase in HR
Increase in Emotions = Increase in HR
1. Nicotine
2. Adrenaline
3. Thyroxin
4. Caffeine

Tachycardia: When your heart beats more than 72 beats/ minute.

Bradycardia:When the heart beats very slowly, less than 72 beats/minute

 Heart Sounds
Heart sounds (lub-dup) are associated with closing of heart valves
 First sound occurs as AV valves close and signifies beginning
of contraction
 Second sound -SL valves close at the beginning of ventricular
diastole

BP: pressure the blood exerts against the inner wall of the blood
vessels.
BP = CO X PR

Normal BP: 120 / 80 mm Hg

Systolic = 120:
Diastolic= 80
28
 Measurement of BP
The BP cuff is wrapped around the arm and inflated until the cuff
pressure exceed the systolic BP.
At this point blood flow is stoped, then the pressure gradually
reduced to listen the sound with a stethoscope.

First soft tapping sound are heard when small ammt of blood is
spurting through constrict artery.

Second: As the pressure is further reduced the sound ,clear and

finally disappear, as blood flow freely.

The pressure at which the sound disappear is recorded as DP.

Disorders of the Heart
 Hypertension

 Arrythmia

Coronary artery disease (Heart Attack):

 Atherosclerosis – fatty deposit
 angina pectoris – chest pain
 Myocardial Ischemia – blocked coronary artery
 Hypertension

Secondary Hypertension
Primary/Essential Hypertension - Elevated BP with a cause-
DM, Obesity
- Unknown cause
-Smocking and alcoholism
- 90% to 95% of all cases
- 5% to 10% in adults
-May involved -  SNS activity
 Renal disease
 Endocrine disorders

31
Essential Hypertension
- Contributing factors:
 SNS activity
due to -Obesity, Diabetes mellitus
 Sodium intake
Excessive alcohol intake

Secondary Hypertension: Contributing factors:

 Renal disease
 Endocrine disorders
 Neurologic disorders
 Coarctation of aorta- common in Turner syndrome

32
 RISK FACTORS

Age
Low physical activity
Obesity and DM
Family history / Genetic factors
Smocking and alcohol
Lower education & socioeconomic status
*Stress, anxiety
 Food habit - High sodium intake
sleep apnea, drug induced causes,
 chronic kidney disease,

33
 Hypertension

Cardiac Total Systemic

Mean BP = Output X
Vascular Resistance

Increased Cardiac Output Increased

Intravascular Volume Vasoconstriction Decreased
 Glomerular filtration  Adrenergic Stimuli Vasodilation
 Prostacyclin
 Sodium excretion  Angiotensin II
 Nitric oxide
 Extracellular Fluid  Endothelin
 EDHF*
 Renal Nerve Activity  Endothelium-derived
Myocardial Performance Contracting Factors
 Thromboxane
 Adrenergic Activity

34
PATHOPHYSIOLOGY:

The normal BP is maintained by four mechanisms:

 Sympathetic nervous system activities

 Vascular endothelium

RAAS-Activities of renal system

Endocrine system

35
 Symptoms:

Asymptomatic - does not causes any symptoms, known as silent

killer disease

Head ache, Dizziness, Nausea/Vomiting

-Blurred vision Fatigue

-Shortness of breath

- Irregular heart beat

36
Diagnostic / Clinical Tests
Symptoms/signs of hypertension/coexistent illnesses: Chest pain,
shortness of breath, palpitations, claudication, peripheral edema, headaches,
blurred vision, nocturia, hematuria, dizziness

Symptoms suggestive of secondary hypertension: Muscle weakness/tetany,

cramps, arrhythmias (hypokalemia/primary aldosteronism), flash pulmonary edema
(renal artery stenosis), sweating, palpitations, frequent headaches
(pheochromocytoma),

-snoring, daytime sleepiness (obstructive sleep apnea), symptoms suggestive of

thyroid disease

37
38
 Measurement of BP
The BP cuff is wrapped around the arm and inflated until the cuff
pressure exceed the systolic BP.
At this point blood flow is stoped, then the pressure gradually
reduced to listen the sound with a stethoscope.

First soft tapping sound are heard when small ammt of blood is
spurting through constrict artery.

Second: As the pressure is further reduced the sound ,clear and

finally disappear, as blood flow freely.

The pressure at which the sound disappear is recorded as DP.

 Blood Pressure Classification
BP Classification SBP mmHg DBP mmHg

Normal < 120 and < 80

Pre-hypertension* 120-139 or 80-89

Stage 1 Hypertension 140-159 or 90-99

Stage 2 Hypertension > 160 or > 100

*newly recognized, requiring

lifestyle modifications
 Isolated Systolic Hypertension
 If your SBP is higher than 140 but your DBP is under
90,'called isolated systolic hypertension.

 SBP should be primarily considered during treatment and not

just diastolic BP.

 Systolic BP is more important cardiovascular risk factor after

age 50.
Mean arterial pressure (MAP)

MAP = (CO X SVR) X SVP

where: CO: is cardiac output: SVR is systemic vascular resistance

SVP: is central venous pressure and usually small enough to be

neglected in this formula.

1. MAP =DP + 1/3 PP (SP- DP)

SBP=170: DBP=105: ?

2. Equation: MAP = [(2 x diastolic)+systolic] / 3

 Pre Hypertension -Treatment

Changing your lifestyle can help control and manage high blood
pressure.
Eating a heart-healthy diet with less salt
Getting regular physical activity
Maintaining a healthy weight or losing weight if you're overweight
or obese
Limiting the amount of alcohol you drink

But sometimes lifestyle changes aren't enough.

If diet and exercise don't help, recommend medication to lower your
blood pressure.

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 Antihypertensive Drugs
1:Diuretics: Thiazides: Hydrochlorothiazide, chlorthalidone
High ceiling: Furosemide:
K+ sparing: Spironolactone, triamterene and amiloride
MOA: Acts on Kidneys to increase excretion of Na and H2O – decrease in
blood volume – decreased BP
2: ACE inhibitorsm:Captopril, lisinopril., enalapril, ramipril
MOA: Inhibit synthesis of Angiotensin II – decrease in peripheral resistance
and blood volume
3: AT1- blockers: Losartan, candesartan, valsartan and telmisartan
MOA: Blocks binding of Angiotensin II to its receptors

4: ß-adrenergic blockers:
Non selective: Propranolol (others: nadolol, timolol, pindolol, labetolol)
Cardioselective: Metoprolol (others: atenolol, esmolol, betaxolol)

5: α – adrenergic blockers:Prazosin, terazosin, phenoxybenzamine

Diuretics
-Excretion, Inhibit NaCl reabsorption
-E,g: Thiazides- cholorthoiazide, Hydrochlorothiazide
Loop diuretics-Furosemide
Used: to treat hypertension, edems, CHF, Nephrotic syndrome
glomerulonephritis, and chronic renal failure
Side effects: Electrolyte imbalances: ↓ Na, ↓ Cl, ↓ K** (advise K
rich foods)
-Fluid volume depletion -orthostatic hypotension, Impotence,
decreased libido

Loop diuretics- used to treat hypertension and edema often due

to CHF or CKD.

45
 RAAS
Aliskarin
Renin
Angiotensinogen Ischemia/
JG cells renal

Ang-1

ACE

Ang-II

Non- Aldosterone
RAAS EC-constriction

Na+ -water

B.P
46
 2:SNS:Alpha-beta -blockers

Alpha-1 selective
Alpha and Non -selective
Beta

Prazocin, Dox,
Alfuz, Terazo, Labetalol, Phenoxybenzami
Tamsulosin Carvedilol ne, Phentolamine

CHF
Emergency
Raynaud BHP, BP,
syndrome PTSD
47
Diuretics
-Excretion, Inhibit NaCl reabsorption
-E,g: Thiazides- cholorthoiazide, Hydrochlorothiazide
Loop diuretics-Furosemide
Used: to treat hypertension, edems, CHF, Nephrotic syndrome
glomerulonephritis, and chronic renal failure
Side effects: Electrolyte imbalances: ↓ Na, ↓ Cl, ↓ K** (advise K
rich foods)
-Fluid volume depletion -orthostatic hypotension, Impotence,
decreased libido

Loop diuretics- used to treat hypertension and edema often due

to CHF or CKD.

48
Cardiac Arrest:

-is the sudden cessation of normal heart rhythm which can include a No.
of pathologies such as

1)tachycardia-extremely rapid heart beat which prevents the heart

from effectively pumping blood, an irregular and ineffective heart rhythm,

2)asystole, which is the cessation of heart rhythm entirely.

Cardiac Attack (Heart Attack): a coronary artery disease:

-If blood flow isn’t restored quickly, the section of heart muscle begins to die.

49
Heart attacks: can be associated with or lead to severe health problems, such
as heart failure and life-threatening arrhythmias.

Heart failure: the heart can't pump enough blood to meet the body's needs.
Arrhythmias: irregular heartbeats
50
Cardiac -tamponade:

is a condition in which the fibrous sac surrounding the heart fills

with excess fluid or blood, suppressing the heart's ability to beat
properly.

Tamponade is treated by pericardiocentesis, the gentle insertion of

the needle of a syringe into the pericardial sac on an angle, usually
from just below the sternum, and gently withdrawing the fluids.

51
 Coronary Artery Disease
 Occurs when the coronary arteries that supply the heart muscle
become blocked.

 Partially blocked it causes angina, fully blocked resulted necrosis

-myocardial infarction or a heart attack

Atherosclerosis → buildup of fat, cholesterol and other substances

on your artery walls.

Arteriosclerosis → hardening of medium or large arteries.

Arteriolosclerosis → a hardening of arterioles.

 Myocardial Infarction
Myocardial Infarction: rapid myocardial necrosis by a critical imbalance b/w
O2 supply and demand to the myocardium.

prolonged ischemia irreversible, myocardial cell death & necrosis occurs

 Thrombosis: formation of a blood clot inside a blood vessel

 A clot, or a piece of the clot, that breaks free and begins to travel -
embolus.

The severity of an MI is dependent of three factors

 The level of the occlusion in the coronary
 The length of time of the occlusion
 The presence or absence of collateral circulation
 Classification
Acute coronary syndromes include
 ST-elevation MI (STEMI)
 Non ST-elevation MI ( NSTEMI)
 Unstable Angina

Cardiac markers in circulation indicates myocardial infarction

and help categorize MI and is a useful adjunct to diagnosis
 Myocardial infarction
Clinical manifestations

Symptoms
 Pain is the cardinal symptom of an MI

 Anxiety and fear of impending death

 Nausea and vomiting

 Breathlessness

 Collapse/syncope
Continue……….
 Nausea with and without vomiting

 Diaphoresis or sweating

 Syncope or near syncope

 Elderly present, fatigue, syncope or weakness

 As many as half of MI are clinically silent

Cardiac Biomarkers
Cardiac biomarkers are protein molecules released into the blood
stream from damaged heart muscle
1.Creatinine Kinase-MB): Begins to rise 4-6 hours:Peaks 24
hours (Normal reference values for serum: range from 3 to 5%
(percentage of total CK) or 5 to 25 IU/L)
2. Myoglobin: Damage to skeletal or cardiac muscle release
myoglobin into circulation
3. Troponint T and I. These isoforms are very specific for cardiac
injury: Cardiac troponin T: < 0.1 ng/mL. Cardiac troponin I: <
0.03 ng/mL (troponin is between 0 and 0.4 -0.9 ng/mL
4. Lactate Dehydronase (LDH): 120-240 IU/L
 ECG, electrocardiogram
ECG is a representation of the electrical events of the cardiac cycle
Electrical depolarization and repolariztaion is recorded

P wave=atrial depolarization
QRS=ventricular depolarization
T wave=ventricular repolarization
PR interval or PQ interval: 0.16 sec:Can indicate damage to conducting
pathway or AV node if greater than 0.20 sec (200 msec)

59
60
Rhythm: The intervals between the two P and two R waves will occur
in a consistent pattern:

Rate: Both the atrial and ventricular rate will be between 60 and 100 beats.

P wave configuration: The P waves will have the same shape and are
usually upright in deflection on the rhythm strip. A P wave will appear in
front of every QRS complex
.
PR interval: The PR interval measurement will be between 0.12 and
0.20 second, which is within normal limits. Each PR interval will be the
same, without any variations.

QRS duration and configuration: The QRS duration and configuration

measurement will be between 0.06 and 0.10 second, which is within normal
limits.

Each QRS duration and configuration will be without any variations from
PQRST complex to complex.
The width of the QRS complex often indicates the location of the originating
electrical impulse.

QT interval represents a complete ventricular cycle of depolarization and

repolarization. The QT interval is measured from the beginning of the QRS complex to
the end of the T wave.

A prolonged QT is associated with a high incidence of arrythmia and sudden death.

ST segment is located between the QRS complex and the T wave. The ST segment
shows early repolarization of the ventricles
 ECG interpretation
 Quality of ECG?

 Rate
 Rhythm
 Axis

 P wave
 PR interval
 QRS duration
 QRS morphology
 Abnormal Q waves
 ST segment
 T wave
 QT interval
Small box is equal to 0.04 seconds. Count no of the small boxes b/w the two P or
two R waves divide the number into 1500 to calculate the heart rate.

The ventricular rate is determined in the same manner except you will need to
count the number of boxes between the QRS complexes
 Rate
 300/number of big squares between R
waves

 Rate is either:
- normal
- bradycardic
- tachycardic
66
Identifying the P Wave Configuration
Analyzing P waves and their relationship with the QRS complex is necessary
to determine the type of dysrhythmia. The P wave reflects the atrial Contraction and
how the electrical current is moving through the atria.

The Relationship between the P wave and QRS complex provides information
Regarding the coordination between atrial and ventricular contractions.

The PR interval is determined by measuring from the beginning of the P wave, or its
up slope, to the beginning of the QRS complex. This is the first indication of
ventricular depolarization.
The PR interval measurement will be between 0.12 and 0.20 second.
 PR interval
 Start of P wave to start of QRS complex

 Normal = 0.12 - 0.2 seconds (3-5 small squares)

 Decreased = can indicate an accessory pathway

 Increased = indicates AV block (1st/2nd/3rd)

 QRS complex
 Normal = <0.12 seconds
 >0.12 seconds = Bundle Branch Block
 QT interval
 Start of QRS to end of T wave

 Needs to be corrected for HR

 Normal QTc = < 400ms

 Long QT can be genetic or iatrogenic

71
 SINUS BRADYCARDIA

• Less than 60 bpm

• If profound, could have decreased cardiac output
• Treatment:
- None if uncomplicated
- Atropine, Pacing
 SINUS TACHYCARDIA

• Greater than 100 bpm

•  Myocardial oxygen demand and may  coronary
artery perfusion resulting in angina in CAD
• Decreased cardiac output could be exhibited
Sinus Bradycardia : a rhythm of less than 60 beats per minute
• Decreased urinary output of less than 30 cc in one hour
• Hypotension
• Pale skin
• Skin cool and

Both the atrial and ventricular rates will be the same, between 100 and 150 beats
per min.
 ATRIAL FLUTTER

• Saw toothed pattern; 200-350bpm atrial rate

• Can convert to atrial fibrillation
 ATRIAL FIBRILLATION

• Chaotic atrial dysrhythmia; atrial rate can be 350+ bpm

• Higher ventricular response = cardiac output

• Treatment:
- Drugs (Digitalis, Verapamil, Beta blocker)
- Anticoagulation therapy
- Cardioversion
Atrial flutter (A flutter) occurs when a rapid impulse originates in the atrial tissue.
The ectopic focus may be originating from ischemic areas of the heart with
enhanced automaticity or from a reentry pathway.

The P-P interval or flutter-to-flutter waves will be regular. The atrial rate will be
between 250 and 350 beats per minute.
P wave configuration: P waves are not seen, and only flutter waves are
present. These flutter waves resemble a “sawtooth” or “picket fence.”

160 and 180 beats per minute: the P waves cannot be identified: There is chaotic
electrical activity, or “f” waves may be seen.
First degree AV block is a delay in electrical conduction from the SA
node
to the AV node, usually around the AV node, which prevents an electrical
impulse from traveling to the ventricular conduction system

With first degree atrioventricular block, the PR interval is constant

and measures greater than 0.20 second.
The R-R interval will be irregular due to the blocked impulse(s).

There will be a P wave for every QRS complex, but there will be extra P
waves.
QRS is dropped
3rd Degree Heart Blocked

Looking at the ECG you'll see that:

•Rhythm - Regular
•Rate - Slow
•QRS Duration - Prolonged
•P Wave - Unrelated
•P Wave rate - Normal but faster than QRS rate
•P-R Interval - Variation
•Complete AV block. No atrial impulses pass through the
atrioventricular node and the ventricles generate their own rhythm
 Torsade de pointes:
Torsade de pointes: is an uncommon and distinctive form of polymorphic
ventricular tachycardia characterized by a gradual change in the amplitude and
twisting of the QRS complexes around the isoelectric line
 QT-prolonging drugs such as clarithromycin, levofloxacin, or haloperidol, when
taken concurrently with CYP-P450 inhibitors, such as fluoxetine, cimetidine, or
particular foods including grapefruit can result prolong the QT interval and therefore
increase a person's risk of developing torsades de pointes.
Treatments includes: isoproterenol infusion, cardiac pacing, and intravenous
atropine.
Intravenous magnesium sulfate, a relatively new mode of theray, was proven to be
extremely effective and is now regarded as the treatment of choice for this arrhythmia

81
Rate: Atrial rate cannot be determined because the P-P interval
cannot be
recognized. The ventricular rate is between 100 and 200 beats per minute.
P wave configuration: The P wave is usually absent; therefore, no
analysis of the P wave can be done.
PR interval: The PR interval cannot be measured because the P wave
is not able to be identified.
QRS duration and configuration: The QRS duration and configuration
measures greater than 0.12 second and will have a bizarre appearance
with an increase in amplitude. The T wave will be in the opposite direction
Ventricular Fibrillation (VF)

Looking at the ECG you'll see that:

•Rhythm - Irregular
•Rate - 300+, disorganized
•QRS Duration - Not recognizable
•P Wave - Not seen
•This patient needs to be defibrillated!! QUICKLY
ECGs, Normal and Abnormal
 ECGs, Abnormal

Arrhythmia: conduction failure at AV node

No pumping action occurs

 Myocardial Infarction
Rationale for therapy
 A main goal of intervention for myocardial infarction is to limit the size
of the infarcted area

 Early recognition and intervention in a MI have been shown to

significantly improve the outcome and reduce mortality in patients.

 If employed in the early stages of MI, antiplatelet-aggregating drugs

such as aspirin/clopiderol

 -and clot-dissolving agents such as streptokinase and tissue

plasminogen activator may be very effective at improving myocardial
blood flow and limiting damage to the heart muscle.
Newer Antiplatelet-aggregating drugs

The class of antiplatelet drugs include:

1: Irreversible cyclooxygenase inhibitors
 Aspirin, Triflusal (Disgren):

Triflusal is a selective platelet antiaggregant through; blocks COX, thereby

inhibiting thromboxane A2, and thus preventing aggregation

-blocks phosphodiesterase thereby increasing cAMP concentration, thereby

promoting anti-aggregant effect due to inhibition of calcium mobilization

2:Adenosine diphosphate (ADP) receptor inhibitors:

-These drugs antagonize the P2Y12 platelet receptors and therefore prevent the
binding of ADP to the P2Y12 receptor.

This leads to a decrease in aggregation of platelets, prohibiting thrombus formation.

-Ticlopidine, clopidogrel and prasugrel

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3: Glycoprotein IIb/IIIa inhibitors: is a class of antiplatelet agents:
 In medicine, glycoprotein IIb/IIIa (GPIIb/IIIa, also known as integrin αIIbβ3)
is an integrin complex found on platelets.

 It is a receptor for fibrinogen and von Willebrand factor and aids platelet
activation.
 The complex is formed via calcium-dependent association of gpIIb and gpIIIa, a
required step in normal platelet aggregation and endothelial adherence.
 Platelet activation by ADP leads to the aforementioned conformational change in
platelet gpIIb/IIIa receptors that induces binding to fibrinogen.

Several GpIIb/IIIa inhibitors exist: Abciximab (abcixifiban), eptifibatide, tirofiban,

roxifiban etc

4: Terutroban is an antiplatelet agent developed by Servier Laboratories.

It is a selective thromboxane prostanoid (TP) antagonist, blocks thromboxane
induced platelet aggregation and vasoconstriction
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 Glycoprotein IIb/IIIa Antagonists
 Potent inhibitors of platelet aggregation
 Use during PCI and in patients with high risk features ACS have
been shown to reduce the composite end points of death,
reinfraction and the need for target lesion
 is a class of antiplatelet agents.
 abciximab , eptifibatide
 tirofiban
They do so by inhibition of the GpIIb/IIIa receptor on the surface of
the platelets.
They may also be used to treat acute coronary syndromes, without
percutaneous coronary intervention, depending on TIMI risk.
 Treatment
 Oxygenation, Supportive treatment (Pain, anxiety and
apprehension): Opoids analgesic or diazepam I,v.
 Maintenance of Blood vol, tissue perfusion: Dextran, saline
infusion, correction of acidosis (lactic acid depot) NaHCO3 I.V.
 PUMP Failure: Inc. C.O or dec. filling pressure without unduly
incr cardiac work or red. B.P
 Furesemide: Dec cardiac preload
 Vasodilator: GTN, Nitroprusside
 Dobutamine, Dopamine
 Anti-platelet (Aggregator inhibitor): Aspirin, clopidogrel
 Thrombolytic agents: Streptokinase, Alteplase,
Urokinase etc
 ACE/ ARB: prevention of remodeling

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 Byvalson (nebivolol and valsartan)

Company: Allergan
Approval Status: Approved June 2016
Specific Treatments: hypertension
Therapeutic Areas Cardiology/Vascular Diseases

Byvalson (nebivolol and valsartan 5 mg/ 80 mg tablet) is a fixed-dose combination

of nebivolol - a beta-adrenergic receptor blocking agent that is preferentially beta-
1 selective, and valsartan - an angiotensin II receptor blocker.

Yosprala (aspirin and omeprazole): Aralez Pharmaceuticals: 2016

Yosprala is a combination of aspirin, an anti-platelet agent, and omeprazole, a proton

pump inhibitor
Yosprala is specifically indicated for patients who require aspirin for secondary
prevention of cardiovascular and cerebrovascular events and who are at risk of
developing aspirin associated gastric ulcers.

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