2195Anatomy and Physiology of the Cardiovascular System

8/13/2019 2195Anatomy and Physiology of the Cardiovascular System

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Anatomy and Physiology of

the Cardiovascular System

Prepared by

Miss Fatima Hirzallah


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• The heart is a hollow, muscular organ

situated in the space between

lungs(mediastinum) , its about 12 cm in

length & about 9 cm in width


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Cardiac Muscle

• Contract as a single unit

• Simultaneous contraction due to

depolarizing at the same time

• Automaticity


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• The heart is about the size of a clenched

fist and comprises.

• The heart composd of four layers:

• Endocardium,

• Myocardium,

• Epicardium,• and the pericardium..


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• endocardium is the inner layer and is consistsof endothelial tissue that lines the inner surfaceof the heart and the cardiac valves.

• The myocard ium is the middle layer and is

composed of muscle fibers that enable the heartto pump.

• Epicardium is the outer layer , is tightlyadherent to the heart and the base of the great

vessels.• A thin, fibrous, double-layered sac known as thepericardium surrounds the heart.


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• The outer layer is known as the parietal

per icardium

• and the inner layer is called the visceral

per icardium

• Between these two layers is a small amount ofpericardial fluid (30 to 50 mL) that serves as a

lubricant between the two layers


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• The heart consists of four chambers:

• right and left atrium• right and left ventricles.


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Heart valves

• The cardiac valves are composed of fibroustissue and allow blood to flow in one direction.

• The valves open and close as a result of bloodflow and pressure differences.


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• The tricuspid and mitral valves are known as the

atr ioventr icula r (AV) valves because they are

located between the atria and the ventricles.

• The pulmonic and aortic valves are known as

the semi lunar valves because each has threeleaflets shaped like half-moons.


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Circulation of the blood

• The blood passes through the tricuspid valve

into the right ventricle, which then pumps the

blood through the pulmonic valve into the

pulmonary circulation.• After gas exchange in the lungs, oxygenated

blood returns to the left atrium, passes through

the mitral valve, enters the left ventricle, passes

through the aortic valve, and finally enters theaorta


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Coronary Arteries

• The left and right coronary arteries and their branchessupply arterial blood to the heart. These arteriesoriginate from the aorta just above the aortic valve

leaflets.

• The heart has large metabolic requirements, extractingapproximately 70% to 80% of the oxygen delivered(other organs consume, on average, 25%).


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The left coronary artery has three branches.

1-the artery from the point of origin to the firstmajor branch is called the left main coronaryartery.

two bifurcations arise off the left main coronaryartery

2- left anterior descending artery (LAD), whichcourses down the anterior wall of the heart

3-circumflex artery, which circles around to thelateral left wall of the heart.


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• The right side of the heart is supplied by theright coronary artery, which progresses aroundto the bottom or inferior wall of the heart.

• The posterior wall of the heart receives its bloodsupply by an additional branch from the rightcoronary artery called the posterior

descending artery.


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• The coronary arteries are perfused during

diastole. An increase in heart rate shortens

diastole and can decrease myocardial perfusion.

• Patients, particularly those with coronary arterydisease (CAD), can develop myocardial

ischemia (inadequate oxygen supply) when the

heart rate accelerates.


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Cardiac Output

• Cardiac output is the amount of blood pumpedout of the ventricle .

• The cardiac output in a resting adult is about 5 Lper minute but varies greatly depending on themetabolic needs of the body. Cardiac output is

computed by multiplying the stroke volume bythe heart rate.


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• Stroke volume (SV) :The amount of bloodejected by the left ventricle with eachheartbeat .

• the heart rate is 60 to 80 beats per minute(bpm)

• The average resting stroke volume is

about 70 mL, and Cardiac output can beaffected by changes in either strokevolume or heart rate.


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Cardiac Output/Index

• Cardiac output

– CO = HR (beats/minute) X SV (liters/beat)

– Normal adult: 4-8 liters/minute

• Cardiac index

– CI = CO(liter/minute)/Body surface area (m2)

– Normal adult: 2.8-4.2 liter/minute/m2

– Normalizes liter flow to body size


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Stroke Volume

• Preload

• Afterload

• Contractility


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Stroke Volume

• Preload – The amount of stretch placed on the cardiac muscle just prior

to systole (the amount of the ventricle at end diastole) – Diastole : filling stage of cardiac cycle.

• Afterload

– The force or pressure at which the blood is ejected fromthe left ventricle

– Equated with systemic vascular resistance (SVR)


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• Contractility is a term used to denote the forcegenerated by the contracting myocardium under any

given condition

• The resistance of the systemic BP to left ventricularejection is called systemic vascular resistance.

• The resistance of the pulmonary BP to right ventricularejection is called pulmonary vascular resistance

.


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• The percentage of the end-diastolic

volume that is ejected with each stroke is

called the ejection fraction (EF)

(EF) = 50-70%


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Patient Assessment:

Cardiovascular System


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• HEALTH HISTORY AND

• CLINICAL MANIFESTATIONS

For the patient experiencing an acute MI, the nurse

obtains the health history using a few specific questionsabout the onset and severity of chest discomfort,

associated symptoms, current medications, and

allergies.

At the same time, the nurse observes the patient’sgeneral appearance and evaluates hemodynamic status

(heart rate and rhythm, BP).


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Cardiac Signs and Symptoms

• Chest pain or discomfort (angina pectoris, MI, valvular

heart disease) Shortness of breath or dyspnea (MI, leftventricular failure, HF)

• Edema and weight gain (right ventricular failure, HF)

• Palpitations (dysrhythmias resulting from myocardial

ischemia, stress, electrolyte imbalance)


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•

Fatigue (earliest symptom associated with several

cardiovascularndisorders)

• Dizziness and syncope or loss of consciousness (postural

hypotension, dysrhythmias, vasovagal

effect,cerebrovascular disorders)


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Physical Exam

• Inspection – General appearance

– Jugular venous distension

(JVD) – Skin

– Extremities

• Palpation

– Pulses – Point of maximal impulse

(PMI)

• Percussion

• Auscultation

– Good stethoscope

– Positioning

– Normal tones – S1/S2

– Extra tones – S3/S4

– Murmurs – Rubs


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HEART SOUNDS

HEART SOUNDS

The normal heart sounds, S1 and S2, are produced primarily by

the closing of the heart valves. The time between S1 and S2

corresponds to systole This is normally shorter than thetime between S2 and S1 (diastole). As the heart rate increases diastole

shortens.S1—First Heart Sound. Closure of the mitral and tricuspid valves

creates the first heart sound (S1),

S2—Second Heart Sound. Closing of

the aortic and pulmonic valves

produces the second heart sound (S2).


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• Murmurs are created by the turbulent flow

of blood.

• The causes of the turbulence may be a critically

narrowed valve,

• a malfunctioning valve that allows regurgitant

blood flow,

• a congenital defect of the ventricular wall, adefect between the aorta and the pulmonary

artery,


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Diagnostic Evaluation

• Laboratory test(Cardiac Labs)

• Chest X-ray

• ECG• CARDIAC STRESS TESTING• ECHOCARDIOGRAPHY(ECO)

• Echocardiography is a noninvasive ultrasound test that is

used to examine the size, shape, and motion of cardiacstructures.


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Important Cardiac Labs

• Enzymes – CK, CK-MB, LDH

• Other important cardiac biomarkers that are

assessed include the myoglobin and troponin T or

I. Myoglobin


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•

early marker of MI, is a heme protein with

a small molecular weight. This allows it to

be rapidly released from damagedmyocardial tissue and accounts for its

early increase, within 1 to 3 hours after the

onset of an acute MI. Myoglobin peaks in4 to 12 hours and returns to normal in 24

hours.


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• Lipid studies – Cholesterol, triglycerides

Coagulation studies – PTT and PT/INRI(nternational

• Normalized Ratio (INR). The INR provides astandard method for reporting PT level

• Electrolytes – Potassium, magnesium, and

calcium


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Invasive Tests

• Cardiac catheterization

• Coronary angiography


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Cardiac Conduction


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• To pump effectively, large portions of

cardiac muscle must receive an action

potential nearly simultaneously.

• Special cells that conduct action potentials

extremely rapidly are arranged in

pathways through the heart.


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• Before mechanical contraction, an action

potential travels quickly over each cell

membrane and down into each cell’s.


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• Three physiologic characteristics of two

specialized electrical cells, the nodal cells and

the Purkinje cells, provide this synchronization:

• Automaticity: ability to initiate an electricalimpulse

• Excitability: ability to respond to an electrical

impulse

• Conductivity: ability to transmit an electrical

impulse from one cell to another


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Cardiac Conduction

• Sinoatrial (SA) node – Fires at 60 –100beats/minute

• Intranodal pathway

• Atrioventricular (AV) node – Fires at 40-60beats/minute

• Atrioventricular bundle of His

– Ventricular tissue fires at 20-40 beats/minuteand can occur at this point and down

• Right and left bundle branches

• Purkinje fibers


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Action Potential


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12-Lead ECG

• Limb leads

– Standard leads: I, II, and III

– Augmented leads: aVR, aVL, and aVF

• Precordial leads

– V1,V2,V3,V4,V5, and V6

• Axis – The direction of the flow of electricity


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P wave : atrial depolarizationup to 0.12 second in duration .

QRS complex : ventricular depolarizationnormal measure is 0.08-0.12 second

T wave : ventricular repolarization , roundedupright, not exceeds 0.2 sec of duration

PR in terval : the interval between the beginning

of p wave and the beginning of R wave itmeasures between ( 0.12-0.2

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ST segment : the isoelectric line between

the end of QRS and the beginning of T

waveQT interval : the interval between the

beginning of Q wave and the end of T

wave , it measures ( 0.32 –

0.40 )second

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Normal Timing

• PR interval – 0.12 to 0.20 seconds

• QRS interval – less then 0.12

• QT interval – varies with rate. It is usually

less then ½ the R-to-R distance on the

preceding waves


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Steps to reading ECGs

• What is the rate? Both atrial and ventricular if they are not

the same.

• Is the rhythm regular or irregular?

• Do the P waves all look the same? Is there a P wave for

every QRS and conversely a QRS for every P wave?

• Are all the complexes within normal time limits?

• Name the rhythm and any abnormalities.


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Rate

• Look at complexes in a 6-second strip and

count the complexes; that will give you a

rough estimate of rate

• Count the number of large boxes betweentwo complexes and divide into 300

• Count the number of small boxes between

two complexes and divide into 1500

• Estimate rate by sequence of numbers.


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Normal Sinus Rhythm

• Rate is between 60 and 100 beats/minute

• The rhythm is regular

• All intervals are within normal limits

• There is a P for every QRS and a QRS for

every P

• The P waves all look the same


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Sinus Tachycardia

• Rate above 100 beats/minute



• There is a P for every QRS and a QRS for every P


• Caused by fever, stress, caffeine, nicotine, exercise, or by

increased sympathetic tone

• Treatment is to take care of the underlying cause


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Sinus Bradycardia

• Rate is lower than 60 beats/minute





• Caused by beta-blocker, digitalis, or calcium channel

blockers. Normal for athletes

• Don’t treat unless there are symptoms. Can use pacing or

atropine


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Sinus Arrhythmia


• The rhythm is irregular. The SA node rate can increase or

decrease with respirations




• More common in children and athletes

• Ask the patient to stop breathing and the rate will becomeregular


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Premature Atrial Contraction

(PAC)• Can occur at any rate• The rhythm is irregular because of the

early beat but is regular at other times

• All intervals can be within normal limits

• There is a P for every QRS and a QRS for

every P

• The P waves all look the same except the

P in front of the PAC will be different


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Supraventricular Tachycardia

(SVT)



• QRS intervals can be within normal limits

• There can be a P wave, but more likely it will be

hidden in the T wave or the preceding QRS wave

• Starts and stops abruptly

• Treat with Valsalva maneuver or adenosine IV


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• CAUSES :

1- hypothyroidism .

2- anxiety .

3- pericarditis .

4- heart failure .5- structural abnormality .



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Atrial Fibrillation

• Atrial rate is between 350 and 600

beats/minute; ventricular rate can vary

• The rhythm is irregular

• There is no PR interval; QRS may be

normal

• There are many more f waves then QRS

• Unlike flutter where the f wave will appear

the same, in fib the f waves are from

different foci so they are different


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Atrial Fibrillation

• CAUSES

1- anterior myocardial infarction .

2- inferior myocardial infarction .3- valvular heart disease .

4- heart failure .



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Atrial Flutter• Atrial rate is between 250 and 350 beats/minute.

Ventricular rate can vary

• The rhythm is regular or regularly irregular

• There is no PR interval. QRS may be normal

• 2:1 to 4:1 f waves to every QRS

• There are no P waves; they are now called flutter waves

• Problem: Loss of atrial kick and ventricular conduction is

too fast or too slow to allow good filling of the ventricles


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• CAUSES :

1- atrial enlargement .

2- hyper thyroidism .3- inferior myocardial infarction .

4- anterior myocardial infarction .



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This type occurs when SA node & theatria are unable to discharge an impulseto depolarize both atria & ventricles ,therefore an ectopic focus in thesurrounding junctional tissue take theresponsibility as apace maker at a rate of( 40-60 ) bpm .

The P wave may be absent, inverted &next QRS complex ; depends upon itsorigin .



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JUNCTIONAL RHYTHM


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JUNCTIONAL RHYTHM

1-RHYTHM : regular .

2- RATE : 50 bpm , ( 40 – 60 ) bpm .

3-P WAVE : Absent .

4- QRS COMPLEX : normalconfiguration & duration .

5- T WAVE : normal .

6- CONUCTION : the atria is stimulatedby the junctional tissue after activationafter or with the activation of theventricles .



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JUNCTIONAL RHYTHM


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JUNCTIONAL RHYTHM

• CAUSES :

1- acute myocardial infarction .

2- digoxin toxicity .



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• CAUSES :

1- congestive heart failure .

2- cardiogenic shock .NOTE : this type of arrhythmia start &

end gradually .



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Premature Ventricular


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Premature Ventricular

Contractions (PVC)

• Early beat that is wide (>0.12)

• Originates the ventricles

• No P wave

• Compensatory pause

• Can be defined by couplet or triplet;

anything more would be considered

ventricular tachycardia

• Monomorphic or polymorphic


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• Multi focal means that the ectopic beat has

more than one foci , that discharge many

shapes of QRS & T .



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• That means that 2 consequences impulsesdischarged prior to the next anticipated

sinus rhythm impulse .



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Ventricular Tachycardia


• The rhythm is regular, but can change todifferent rhythms

• No PR interval; QRS is wide and aberrant

• There may be a P wave, but it is not relatedto the QRS


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Ventricular Fibrillation

• Rapid, irregular rhythm made by stimulifrom many different foci in the ventricula

• Produces no pulse, blood pressure, or

cardiac output

• Can be described as fine or coarse

• Most common cause of sudden cardiac

death


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Torsades De Pointes

• Polymorphous ventricular tachycardia

• Caused by long QT syndrome.

• This is an inherited condition or caused by

antiarrhythmic drugs

• Cannot be converted by defibrillation

• Magnesium is the drug of choice

• Overdrive pacing may work also


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• This arrhythmia occurs when all supra

ventricular pace makers ( SA node , AV

junction , bundle of his , bundle branch

) fail to elicit an electrical impulse ; the

ventricles take over as a pace maker ,

firing at their own inherent rate of ( 30 –

40 ) bpm .



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1- RHYTHM : regular R-R interval .

2- RATE :(30-40) bpm .

3- P WAVE : absent .4-QRS COMPLEX : wide & bizarre .

5- CONDUCTION : electrical impulses

arises from the purkinji fibers orventricular myocardium .



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• CAUSES :

1- cardiogenic shock .

2- medication effects like adrenaline .



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• This arrhythmia occurs when the SA

node & AV junction fail to initiate

impulse the ventricles take over the

role as a pace maker at a rate about (

50-100) bpm .



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• 1-RATE : 60 bpm .

• 2- RHYTHM : regular R-R interval .

• 3- P WAVE : absent .• 4- QRS COMPLEX : wide & bizarre .

• 5- T WAVE : caught up in ST segment .

• 6- CONDUCTION : pace maker site is inbundle branch , purkinji fibers or

myocardium Friday, 10 January 2014 102


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• CAUSES :

1- Acute myocardial infarctions .

2- digoxin toxicity .


CCELER TED IDIOVENTRICUL R RHYTHM


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• Occurs when there is a delay in the

transmission of electrical impulse

through the AV node to the ventricles .



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1- RHYTHM : regular .

2- RATE : 45 bpm < 50bpm

3- P WAVE : normal .4- P-R INTERVAL : 0.28 seconds

5- QRS COMPLEX : normal .

6- CONDUCTION : follow normalconduction pathway but there is a

delay in the process .Friday, 10 January 2014 107


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• Occurs when conduction through the

AV junction become progressively

difficult with each successive impulse

until finally a ventricular depolarization

doesn’t occur .



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• 1-Ventricular and atrial rate :Depends

on the underlying rhythm

• 2- RHYTHM : atrial regular , butventricular irregular .

• 3- P WAVE : normal .

• 4-P-R INTERVAL : lengthening witheach successive beat .

• 5-QRS COMPLEX :normal .Friday, 10 January 2014 110


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• 6- CONDUCTION : some of the

impulses from the atria are blocked . P-

R interval gets progressively longer

until one P wave is not followed by

QRST .



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• CAUSES :

1-rehumatic fever .

2- inferior myocardial infarction .3- digoxin toxicity .



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• In this arrhythmia 2 or more atrial

impulses conducted normally , then the

next impulse blocked without warning .

Block may occur occasionally or at

regular intervals . ( for every third beat )

( 3:1) .



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• 1-Ventricular and atrial rate :Depends


• 2- RHYTHM : P-P interval regular , R-Rinterval irregular .

• 3- P WAVE : normal .

• 4- P-R INTERVAL : 0.16 sec , absent inmissed beats .



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• 5- QRS COMPLEX : normal, some

dropped beats .

• 6- T WAVE : normal , some dropped asQRS

• 7- CONDUCTION : Third atrial impulseis blocked .



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• CAUSES :

1- degenerative changes in conduction

system2- anterior myocardial infarction .

3- coronary artery disease .



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• Occurs when the electrical impulses

above the AV node are blocked ,

therefore no impulses conducted to the

ventricles , if SA node blocked the

junctional arises , if the block involve

the junctional tissue , the

idiodventricular rhythm arises .



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• 1-1-Ventricular and atrial rate :Depends


• 2- RHYTHM : P-P interval regular , R-Rinterval regular .

• 3-P WAVE : normal .

• 4-P-R INTERVAL : absent ( no relationbetween atria& ventricles )



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• 5- QRS COMPLEX : depend on the site

of pace maker , ( wide = purkinji fibers )

( normal =junctional tissue )

• 6- T WAVE : absent .

• 7- CONDUCTION : the atria & ventricles

have independent pacemaker ,so there

is no relationship between both .



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• CAUSES :

1-inferior myocardial infarction .

2- digoxin toxicity .3- degeneration of conduction system .



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• THANKS

Documents

2195Anatomy and Physiology of the Cardiovascular System