lecture cardio physiotherapy 1

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The HEART

Dr Georges GhorayebInternal Medecine

InterventionalCardiologist



The Cardiovascular System

Slide 11.1 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

A closed system of the heart and bloodvessels

The heart pumps bloodBlood vessels allow blood to circulate to all

parts of the body

The function of the cardiovascular system is to deliver oxygen andnutrients and to remove carbon dioxideco2 and other waste products



The Heart

Slide11.2a

Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Location

Thorax between the lungs(MEDIASTINUM)

Pointed apex directed toward left hip

About the size of your fist



The Heart

Slide11.2b


Figure 11.1



The Heart: Coverings


Pericardium – a double serousmembrane

Visceral pericardium :Next to heart

Parietal pericardium :Outside layer

Serous fluid fills the space between thelayers of pericardium



The Heart: Heart Wall


Three layers

Epicardium

Outside layer

This layer is the parietal pericardium

Connective tissue layer

Myocardium

Middle layer

Mostly cardiac muscleEndocardium

Inner layer

Endothelium



External Heart Anatomy

Slide 11.5 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Figure 11.2a



The Heart: Chambers


Right and left side act as separate pumps Four chambers

Atria

Receiving chambers Right atrium

Left atrium

VentriclesDischarging chambers

Right ventricle

Left ventricle



Blood Circulation


Figure 11.3



The Heart: Valves


Allow blood to flow in only one direction Four valves

Atrioventricular valves – between atria andventricles

Bicuspid valve ,the mitral valve(left)

Tricuspid valve (right)

Semilunar valves between ventricle andartery

Pulmonary semilunar valve

Aortic semilunar valve



The Heart: Valves


Valves open as blood is pumped

through Held in place by chordae tendineae

(―heart strings‖)

Close to prevent backflow



Operation of Heart Valves

Slide11.10


Figure 11.4



The Heart: Associated GreatVessels

Slide11.11


AortaLeaves left ventricle

Pulmonary arteries

Leave right ventricle

Vena cava

Enters right atrium Pulmonary veins (four)

Enter left atrium



Coronary Circulation

Slide11.12


Blood in the heart chambers does notnourish the myocardium

The heart has its own nourishingcirculatory system

Coronary arteries

Cardiac veins

Blood empties into the right atrium via thecoronary sinus



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%).



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.



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.



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.



The Heart: Conduction System

Slide11.13a


Intrinsic conduction system(nodal system)

Heart muscle cells contract, without nerveimpulses, in a regular, continuous way



The Heart: Conduction System

Slide11.13b


Special tissue sets the pace

Sinoatrial node Pacemaker

Atrioventricular node

Atrioventricular bundle

Bundle branches

Purkinje fibers



Heart Contractions

Slide11.14b


Figure 11.5



Filling of Heart Chambers – the Cardiac Cycle

Slide11.15


Figure 11.6



The Heart: Cardiac Cycle

Slide11.17


Cardiac cycle – events of one completeheart beat

SYSTOLE = CONTRACTION (S1-lub)

DIASTOLE= RELAXATION (S2-dub)



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 from

the left ventricle Equated with systemic vascular resistance (SVR)



The Heart: Cardiac Cycle

Slide11.16


Atria contract simultaneously

Atria relax, then ventricles contractsimultaneously



The Heart: Cardiac Output

Slide11.18


• Stroke volume:Volume of blood pumped by the

ventricles in one contraction.

• The percentage of the volume that is ejectedwith each stroke is called the ejection fraction EF = 50-70%.

• Cardiac output (CO) :sv of the heart in oneminute : = (heart rate /min) x stroke volume [SV]

5-6 liter/min



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 ventricular ejection is called systemic vascular resistance.

The resistance of the pulmonary BP to right ventricular ejection is called pulmonary vascular resistance

.



also called the fight-or-flight-or-freeze response,

hyperarousal, or the acute stress response

ADRENALINE

is responsible for stimulation of "rest-and-digest" or "feed

and breed― activities that occur when the body is at rest,

especially after eating, including sexual arousal, salivation,

lacrimation (tears), urination, digestion and defecation

ACETHYLCHOLINE

http://en.wikipedia.org/wiki/Sexual_arousal

http://en.wikipedia.org/wiki/Salivation

http://en.wikipedia.org/wiki/Tears

http://en.wikipedia.org/wiki/Urination

http://en.wikipedia.org/wiki/Digestion

http://en.wikipedia.org/wiki/Defecation

http://en.wikipedia.org/wiki/Defecation

http://en.wikipedia.org/wiki/Digestion

http://en.wikipedia.org/wiki/Urination

http://en.wikipedia.org/wiki/Tears

http://en.wikipedia.org/wiki/Salivation

http://en.wikipedia.org/wiki/Sexual_arousal



Cardiac Output Regulation

Slide11.19 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Figure 11.7



The Heart: Regulation of Heart

Rate


Increase heart rate

Sympathetic nervous system

Crisis/Stress

Low blood pressure

Hormones

Epinephrine

Thyroxine

Exercise

Decreased blood volume

Th H t R l ti f



The Heart: Regulation of

Heart RateDecrease heart rate

Parasympathetic nervous system (vagus

nerve)

High blood pressure / blood volume

Decreased venous return



Blood Vessels: The Vascular System


Taking blood to the tissues and back

Arteries

Arterioles

Capillaries

VenulesVeins



BLOOD VESSEL: ANATOMY

Three layers (tunics)Tunica intima

Endothelium

Tunica mediaSmooth muscle

Controlled by sympathetic nervoussystem

Tunica externa

Mostly fibrous connective tissue



The Vascular System


Figure 11.8b

DIFFERENCES BETWEEN



DIFFERENCES BETWEEN

ARTERIES & VEINS

VEINS

Larger lumen, thinner

walls

Lower pressure Carry deoxygenated

blood

(+)VALVES

ARTERIES

Smaller lumen,

thicker walls

Higher pressure Carry oxygenated

blood

(-)VALVES

*Walls of capillaries are only one cell layer thick to

allow for exchanges between blood and tissue

capillaries -



Movement of Blood ThroughVessels


Most arterial blood is

pumped by the heart Veins use the milking

action of muscles to

help move blood

Figure 11.9



Patient Assessment:

Cardiovascular System



HEALTH HISTORY AND

CLINICAL MANIFESTATIONS

For the patient experiencing an acute MI, obtains the

health history using a few specific questions about theonset and severity of chest discomfort, associated

symptoms, current medications, and allergies.

At the same time, observes the patient’s generalappearance and evaluates hemodynamic status (heart

rate and rhythm, BP).



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)



ANGINA

A heavy or constricting feeling in the chest. This pain or discomfort can spread anywhere between the belly

button and the jaw, including to the shoulder, arm, elbow or hand (usually on the left side)

The type of pain caused by angina is continuous, not stabbing

Breathlessness, especially following exercise

Nausea or dizziness.



• Fatigue (earliest symptom associated with several

cardiovascular disorders)

• Dizziness and syncope or loss of consciousness (postural

hypotension, dysrhythmias, vasovagal

effect,cerebrovascular disorders)



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



HEART SOUNDS



HEART SOUNDS:

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

the closing of the heart valves.

S1—First Heart Sound. Closure of the mitral and tricuspid valvescreates the first heart sound (S1),

S2—Second Heart Sound. Closing of the

aortic and pulmonic valves

produces the second heart

sound (S2).

Murmurs are created by the turbulent flow of blood.



y

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, a defect between the

aorta and the pulmonary artery




Pulse – pressure waveof blood

Monitored at―pressurepoints‖ wherepulse is easilypalpated

Bl d P



Blood Pressure

Slide11.36


Measurements by health professionalsare made on the pressure in largearteries

Systolic – pressure at the peak of ventricular contraction

Diastolic – pressure when ventricles relax



Variations in Blood Press re



Variations in Blood Pressure

Slide11.41


Human normal range is variable

Normal

140 –110 mm Hg systolic

80 –75 mm Hg diastolic

Hypotension

Low systolic (below 110 mm HG)

Often associated with illness

HypertensionHigh systolic (above 140 mm HG)

Can be dangerous if it is chronic

Diagnostic Evaluation



Diagnostic Evaluation

Laboratory test (Cardiac Labs)

Chest X-ray

ECG (electrocardiogram)CARDIAC STRESS TESTING

ECHOCARDIOGRAPHY

Laboratory Test



Laboratory Test

Rationale

1. To assist in diagnosing MI2. To identify abnormalities

3. To assess inflammation



CPK- MB (creatine kinase)

Indicates myocardialdamage

Elevates in MI w ithin 4-6 hours

peaks in 18 hours and then dec l ines t i l l 3 days



CPK -MB

0-5% of total CPK (26-

174U/L)

Normal value is 0-7

U/L

Lactate Dehydrogenase



Lactate Dehydrogenase

(LDH) Elevates in MI in 24 hours

peaks in 48-72 hour Normal value is 70-200 IU/L

M l bi



Myoglobin

Oxygen binding proteinFound in both skeletal and cardiac

muscle

Level rises 1 hour after cell deathPeaks in 4-6 hours

Returns to normal w/in 24-36 hours

Not used aloneMuscular and RENAL disease can

have elevated myoglobin

Troponin I and T +++



Troponin I and T +++

Troponin I has a high affinity for

myocardial injury

Elevates w ith in 3-4 hours , peaks

in 4-24 hours and persists for 7 days to 3 weeks !

Troponin I < 0.11 ng/mL

Troponin T 0-0.2ng/mL



if myocardial infarction suspected

REMEMBER to AVOID IM

inject ions before obtain ing

blood sample! Early and late diagnosis can be

made!



SERUM LIPIDSLipid profile measures the

serum cholesterol,

triglycerides andlipoprotein levels

Cholesterol= 200 mg/dL

Triglycerides =40- 150mg/dL

SERUM LIPIDS



SERUM LIPIDS

LDL 130 mg/dL

HDL 30-70- mg/dL

NPO pos t m idn igh t

(usual ly 12 hours )



ELECTROCARDIOGRAM



(ECG)A non-invasive procedure that

evaluates the electrical activity

of the heart Electrodes and wires are

attached to the patient

ELECTROCARDIOGRAM



(ECG)Tell the patient that there is

no risk of ECG

Avoid muscular contraction/movement



Holter Monitoring



Holter Monitoring

A non-invasive test inwhich the client wears a

Holter monitor and anECG tracing recordedcontinuously over aperiod of 24 hours

Holter Monitoring



Holter Monitoring

Instruct the client to

resume normal activities

and maintain a diary of

activities and any

symptoms that maydevelop



ECHOCARDIOGRAM



ECHOCARDIOGRAM

Non-invasive test thatstudies the structural and

functional changes of theheart with the use of ultrasound

No special preparation isneeded



Stress Test



Stress Test

A non-invasive test thatstudies the heart during

activity and detects andevaluates CAD

Stress Test



Stress Test

Treadmill testing is themost commonly used

stress testUsed to determine CAD,

Chest pain causes, drug

effects and dysrhythmias inexercise

Stress Test



Stress Test

Pre-test: consent may berequired, adequate rest ,

eat a light meal or fastfor 4 hours and avoid

smoking, alcohol andcaffeine



Stress Test



Stress Test

• instruct client to notify thephysician if any chest pain,dizziness or shortness of breath

• Observe for ECG changes

• Confirm if stress test positiveor negative

CARDIAC



CATHETERIZATION Insertion of a catheter into

the heart and surrounding

vessels Obtains information about

the structure and

performance of the heartvalves and surrounding

vessels

CARDIAC



CATHETERIZATION Used to diagnose CAD,

assess coronary artery

patency and determineextent of atherosclerosis



PRE PROCEDURE



PRE PROCEDURE

Ensure Consent assess for allergy to seafood and

iodine

Withhold solid food 6-8 hours andliquids for 4 hours

document weight and height,

baseline VS, blood tests anddocument the per ipheral pu lses

PRE PROCEDURE



PRE PROCEDURE

a local anesthetic will beadministered before

insertion

POST TEST



POST TEST

Keep the leg straigh t to prevent occ lus ion

Monitor for bleeding and

hematoma formation Encourage fluid intake to flush out the

dye

Immobilize the arm if the antecubitalvein is used

Monitor for dye allergy

CVP



CVP

The CVP is the pressurewithin the SVC

Reflects the pressureunder which blood is

returned to the SVC andright atrium

CVP



CVP is measured with a central

venous line in the SVC andballoon flotation catheter in

the pulmonary arteryNormal CVP is 4 to 8 mmHg /4-12 cm H2O

INCREASED CVP



INCREASED CVP increase in blood volume as a

result of Na and water retention, excessive IV Fluid

or heart / renal failure

DECREASED CVP



DECREASED CVP May indicate decrease in

circulating blood volume andmay be to hypovolemia,

hemorrhage and severevasodilatation

MEASURING CVP



MEASURING CVP1. Position the client supine with bed

elevated at 45 degrees

2. Position the zero point of the CVP line

at the level of the right atrium. Usually

this is at the MIDANTERIOR L INE 4 th

Interco stal space.

3. Instruct the client to be relaxed and

avoid coughing and straining.



ECG

NORMAL AND ABNORMAL

Cardiac Conduction



Cardiac Conduction

To pump effectively, large portions of cardiac muscle must receive an action

potential nearly simultaneously.

Special cells that conduct action potentialsextremely rapidly are arranged in

pathways through the heart.



Before mechanical contraction, an actionpotential travels quickly over each cell

membrane and down into each cell’s.



Three physiologic characteristics of twospecialized electrical cells, the nodal cells and

the Purkinje cells, provide this synchronization:

Automaticity: ability to initiate an electrical

impulse

Excitability: ability to respond to an electrical

impulse

Conductivity: ability to transmit an electricalimpulse from one cell to another



Cardiac Conduction



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

Action Potential



Action Potential



12 L d ECG



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



Saturday, 8 June 2013 131



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 thebeginning of p wave and the beginning of Rwave it measures between ( 0.12-0.2)

135



ST segment : the isoelectric line between

the end of QRS and the beginning of T

wave

QT interval : the interval between the

beginning of Q wave and the end of T

wave , it measures ( 0.32 – 0.40 )

second

136



Steps to reading ECGs

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



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.

Rate



Rate

Look at complexes in a 6-second strip andcount 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.



Normal Sinus Rhythm



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

Sinus Tachycardia



Sinus Tachycardia

Rate above 100 beats/minute The rhythm is regular


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

The P waves all look the same

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

increased sympathetic tone

Treatment is to take care of the underlying cause

Sinus Bradycardia



y

Rate is lower than 60 beats/minute The rhythm is regular


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

The P waves all look the same Caused by beta-blocker, digitalis, or calcium channel

blockers. Normal for athletes

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

atropine



Premature Atrial Contraction(PAC)



(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

S t i l T h di



Supraventricular Tachycardia

(SVT)

Rate is between 150 and 250 beats/minute

The rhythm is regular

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



CAUSES :

1- hypothyroidism .

2- anxiety .

3- pericarditis .

4- heart failure .5- structural abnormality .


Atrial Fibrillation



Atrial Fibrillation

Atrial rate is between 350 and 600beats/minute; ventricular rate can vary

The rhythm is irregular

There is no PR interval; QRS may benormal

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




Atrial Fibrillation AF



CAUSES

1- myocardial infarction.

2- valvular heart disease .3- heart failure .

4- thyroid problem

5- lone AF


Atrial Flutter Af



Atrial Flutter Af

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



CAUSES :

1- atrial enlargement .

2-throid problem.3- myocardial infarction .


JUCTIONAL RHYTM



This type occurs when SA node & the

atria are unable to discharge an impulseto depolarize both atria & ventricles ,therefore an ectopic focus in thesurrounding junctional tissue take the

responsibility as apace maker at a rate of ( 40-60 ) bpm .

The P wave may be absent, inverted &

next QRS complex ; depends upon itsorigin .





JUNCTIONAL RHYTHM



1-RHYTHM : regular .

2- RATE : 50 bpm , ( 40 – 60 ) bpm .

3-P WAVE : Absent .

4- QRS COMPLEX : normal configuration& duration .

5- T WAVE : normal .

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





JUNCTIONAL RHYTHM



CAUSES :

1- acute myocardial infarction .

2- digoxin toxicity .


Premature Ventricular

Contractions (PVC)



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



Multi focal means that the ectopic beat has

more than one foci , that discharge many

shapes of QRS & T .




That means that 2 consequences impulses

discharged prior to the next anticipated

sinus rhythm impulse .




Ventricular Tachycardia



y

Rate is between 100 and 200 beats/minute

The rhythm is regular , but can change to

different rhythms

No PR interval; QRS is wide and aberrant

There may be a P wave, but it is not related

to the QRS



Ventricular Fibrillation Rapid, irregular rhythm made by stimuli from many

different foci in the ventricule



different foci in the ventricule

Produces no pulse, blood pressure, or cardiac output Can be described as fine or coarse

Most common cause of sudden

cardiac death



Occurs when there is a delay in the

transmission of electrical impulse

through the AV node to the ventricles .




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 .Saturday, 8 June 2013 171



Second degree av b lock mob itz-1

Occurs when conduction through the AV

junction become progressively difficultwith each successive impulse until

finally a ventricular depolarization

doesn’t occur .




1-Ventricular and atrial rate :Depends on the

underlying rhythm

2- RHYTHM : atrial regular , but ventricular irregular .

3- P WAVE : normal .

4-P-R INTERVAL : lengthening with each successive

beat .

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 .




CAUSES :

1-rheumatic fever .

2- myocardial infarction .3- drug toxicity .




In this arrhythmia : 2 or more atrial

impulses conducted normally , then the

next impulse blocked without warning .

Block may occur occasionally or atregular intervals . ( for every third beat )

( 3:1) .




1-Ventricular and atrial rate :Depends on the

underlying rhythm

2- RHYTHM : P-P interval regular , R-R interval

irregular .

3- P WAVE : normal . 5- QRS COMPLEX : normal,

some dropped beats .

7- CONDUCTION : Third atrial impulse is blocked .




CAUSES :

1- degenerative changes in conduction

system

2- anterior myocardial infarction .

3- coronary artery disease .


COMPLETE HEART BLOCK



Occurs when the electrical impulses

above the AV node are blocked ,

therefore no impulses conducted to the

ventricles , if SA node blocked the

junctional rhytm arises , if the blockinvolve the junctional tissue , the

idiodventricular rhythm arises .




1-1-Ventricular and atrial rate :Depends

on the underlying rhythm

2- RHYTHM : P-P interval regular , R-R

interval regular .

3-P WAVE : normal .

4-P-R INTERVAL : absent ( no relation

between atria& ventricles )




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 .




CAUSES :

1- myocardial infarction .

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


Cardiovascular



Disorders

Heart Attack (Myocardial Infarction)

Description

This image shows clearly the damage caused by a heart attack. To the right of the image, you

can see the back wall of the left ventricle where there is an extensive area of dead tissue

(infarct).

The central part of the infarct shows the yellow appearance of dead tissue (necrosis) and



The central part of the infarct shows the yellow appearance of dead tissue (necrosis), and

bordering on this is an outer reddish area which suggests partial healing by early scar tissue. The

front wall of the left ventricle (on the left of the image) appears normal.

Where the reddish area curves around the yellow dead tissue at the top, you can see the right

coronary artery, which is considerably narrowed due to artherosclerosis (hardening of the artery

walls). A blood clot has formed in this narrowed area and was responsible for the heart attack.



Risk factors for atherosclerosis include those, which are modifiable, andthose, which are not.

Age - in general, atherosclerosis increases with age. The earliest lesions of

atherosclerosis are present after the age of 10 years old and some believe that thisis a disease present since infancy.



p y

Gender – atherosclerosis is present more in males, however females catch up aftermenopause.( Some old dated thinking regarded females as having lessatherosclerosis than males. However, it is recognized now that females do developsignificant atherosclerosis. Estrogen is protective as it has multiple effects includingeffects on lipids, nitric oxide, vascular tone and antioxidant properties.)

Smoking - causes multiple malignancies and accelerates and initiatesatherosclerosis. Many effects on the endothelial cell including poor vascular tonewith vasoconstriction, oxidation, and prothrombotic products.

Hypertension - accelerates the development of atheroma

Hyperlipidemia

Inactivity and obesity

Diabetes – affects endothelium and lipids

Family history – probably multifactorial based on many of the above factors



ARTERIOSCLEROSIS OF THE EXTREMITIES



ARTERIOSCLEROSIS

OF THE EXTREMITIES

Arteriosclerosis of the extremities is a disease of the peripheral blood vessels

that is characterized by narrowing and hardening of the arteries that supply the

legs and feet. The narrowing of the arteries causes a decrease in blood flow.

Symptoms include leg pain, numbness, cold legs or feet and muscle pain in the

thighs, calves or feet.



Hypertension



Coronary artery disease (CAD)is caused by a

narrowing or constriction of the arteries that supply the heart muscle with blood. This narrowing

is a result of atherosclerosis—the buildup of

cholesterol and other fatty substances in the

http://healthlibrary.epnet.com/GetContent.aspx?token=de6453e6-8aa2-4e28-b56c-5e30699d7b3c&chunkiid=12031




yarteries.

When the arteries narrow, blood flow is reduced.

The reduced blood flow (ischemia ) causes the

heart muscle to receive less oxygen in certainareas. If the blood flow is completely cut off, a

heart attack ( myocardial infarction) will

occur, and the heart muscle will be permanently

damaged.

Blocked Coronary Artery





• ANGINA

•Duration of pain – In general, anginal pain lastsfor only a few minutes and is relieved by rest or



nitroglycerin.

•MYOCARDIAL INFARCTION (HEART ATTACK)•Heart attack pain is usually more severe than

anginal pain, and may last longer, often 15 minutesor more.

•Pain that lasts less than 30 seconds and goesaway with a few deep breaths or a change in

position is usually not angina.

•External factors – • Anginal pain is often brought on by exercise or activity,emotional tension, dreams, cold or windy weather, low blood sugar, or even eating.



g , g•Your symptoms can subside when you alter the behavior or environmental trigger.

•Heart attack pain will usually not subside with rest and

may be accompanied by other symptoms such asshortness of breath, nausea, or sweating.

•The elderly or people with diabetes may have less

typical or more subtle symptoms signaling angina or heart attack. Some people may have ―silent ischemia‖ and experience no symptoms.

Types of AnginaThere are three primary types of angina:

•Stable angina – The attacks are predictable, and the triggers that causethem can be identified. They do not occur when you are resting or relaxed,and symptoms will usually disappear after a few minutes of rest.



a d sy pto s usua y d sappea a te a e utes o est

•Unstable angina – The symptoms are less predictable. Chest pain may occur while resting or even sleeping (nocturnal angina), and the discomfort may last longer and be more intense. Stable angina becomes unstable whensymptoms occur more frequently, last longer, or are precipitated more

easily. You should call your doctor immediately if you experience symptomsat rest, or a worsening pattern of symptoms.

•Variant or Prinzmetal's angina – This is usually caused by the spasm of a coronary vessel. It occurs when you are at rest, and often in the middle of the night. It can be quite severe. It may indicate that you have one of the

following conditions:

•Coronary artery disease•Extremely high blood pressure•Hypertrophic cardiomyopathy (disease of the heart muscle)•Diseases of the heart valves





CLOSE WINDOW



ST-segment (V1 to V4) elevation myocardial infarction.



TREATMENT OF MI

A ti l t l t d i t l i



Antiplatelets drugs: aspicot,plavix… Thrombolytic treatment: drug that can

lyses the clot of MI:

streptokinase… 1.5 MU in 30-60 minmetalyse … kg? push

Primary angioplasty of occluded coronary

artery : insertion of balloon and stent



Congestive Heart Failure

inability of the heart to pump blood into the



inability of the heart to pump blood into thecirculatory system.

usually due to inability of the ventricles to

pump bloodleading to

↓

Pulmonary congestion↓

Pulmonary hypertension

CHF

left sided heart failure will manifest



left sided heart failure will manifest

↓

Pulmonary in Nature

dyspnea, labored breathing,

orthopnea,

moist hacking cough, bi-basilar

crackles,

increased PAWP

LEFT-SIDED HEART FAILURE



CHFright ventricle will pump harder just to



pass blood into the congested pulmonary

capillaries

↓ resulting to right ventricular hypertrophy

Right Ventricular Failure (Cor Pulmonale)

↓

CHFblood will be congested into the right side

↓



↓

right sided heart failure will follow

↓

Venous congestiondistended neck veins, hepatomegaly,

portal hypertension

splenomegaly, pancreatomegaly, esophagealvarices, hemorrhoids, ascites,

caput medusa, weight gain

↓

CHF

venous pooling in the lower extremities



venous pooling in the lower extremitiesbi-pedal edema, varicosities, DVT

↓

until all venous system becomes congestedwith fluid

↓

periorbital edema or

generalized edemaANASARCA

RIGHT-SIDED HEART FAILURE



CHF

Predisposing Factors:



Predisposing Factors:

Myocardial Infarction

Arrhythmias

Pregnancy

Pulmonary Embolism

Anemia Renal Failure

CHF Diagnosing CHF:



Daily weighing reveals unexplained weight gain

Abdominal girth measurement shows ascites

EKG detects heart strain

Chest X-ray may highlights cardiomegaly andpleural effusion

CVC Central Venous Catheter and Swan-Ganz

Catheter are able to record high pressure in thechambers and pulmonary capillaries.

SWAN-GANZ



CHF

Complications:



Complications: Acute Pulmonary Edema

Treatment:

Bed rest and maintain high fowler’s position

O2 therapy Morphine administration to dilate blood

vessels

Dopamine to increase myocardial contractility

and ↑ CO Diuretics to reduce blood volume

CHF

Complications:



Complications:

Cardiac Arrhythmias

Disturbances in regular rate and

rhythm due to changes in electrical

automaticity or conduction

Irregular HR, rhythm and regularity

Cardiac ArrhythmiasATRIAL A.

Premature atrial contraction (PAC) – more than 100bpm



Premature atrial contraction (PAC) more than 100bpm

Atrial flutter – 250-300 bpm

Atrial fibrillation – higher than 500 bpm

VENTRICULAR A.

Premature ventricular contraction (PVC) – most

common due to dec. K, dec. Calcium and MI Ventricular tachycardia (vtach) – 3 or more PVC’s

Ventricular fibrillation (vfib) – extremely rapid anderratic impulse formation

AV Block Impulse is delayed from SA node to AV node

1st degree –

2nd degree –



2nd degree Mobitz type I – asymptomatic (ventricular contraction

is adequate)

Mobitz type II – critical (atrial contraction is not

synchronized with the ventricle)

Treatment:

Cardiac monitor must be in-placed

Anti-arrhythmic drugs administration

Defibrillator standby

Pacemaker

Cardiac Arrest

Heart stops beating or contraction is ineffective

Watch-out for ↓ tissue perfusion manifestations:

Restlessness (early sign)



Restlessness (early sign)Tachycardia and tachypnea

Shallow respirations

Palpable BP

Drop in BP (systolic is only 30)

Narrowing BP (cerebral anoxia)

Decreased urine output

Cold, pale, clammy skinCyanosis

Shock

Cardiac Arrest Treatment:

Increase CO

Cardiovascular d rugs and mechanical equipment

uti l izat ionC di l D



uti l izat ion Cardiovascular Drugs:

IV Dopamine (vasopressor)

IV Dobutamine (diuretic effects)

IV Epinephrine (vasoconstrictor)IV Nitroprusside (vasodilator)

Mechanical:

IABP intra aortic balloon pump (improve

coronary perfusion)Defibrillator (arrhythmias can be stopped)

Cardiac monitor (to detect arrhythmias)



THANK YOU

Cardiovascular Drugs

Anti Anginal

Opiate Analgesic – Morphine Sulfate

↓ cardiac workload and BP improve LOC and



↓ cardiac workload and BP, improve LOC andsedative effect

Vasodilators

Nitroglycerin NTG Relax smooth muscle, dec. BP and alleviate

headache

Increase blood vessel diameter and improves

blood flow S.E. – hypotension, dizziness and flushing

Can be given SL or IV (Isordil) and topical(Nitrobid)


Calcium Channel Blockers



Nifidepine (Procardia) Diazepam (Cardizem)

Decrease muscle tone, interferes contraction,decrease BP

S.E. – bradycardia, diarrhea and rashes

Beta Blocking Agent

Propranolol

Decrease workload Blocks beta receptors and capable of decreasing

HR

S.E. – vomiting, nausea and depression


Digitalis Digoxin Positive Inotropic (Increases contraction of



Digitalis, Digoxin Positive Inotropic (Increases contraction of

the heart) Increase emptying capacity of the heart

Negative chronotropic (Decreases HR) AVnode control Increase CO (improves stroke volume)

S.E. – GIT disturbance, CNS depression

and flashes of light


Dopamine – diuresis effect



Dopamine diuresis effect Increase Na excretion (kidney)

Vasodilators

Norepinephrine effect

Dobutamine

Increase CO More potent on contraction


Diuretics



Diuretics

Spironolactone (Aldactone) – K

sparer

Furosemide (Lasix) – K waster

Anti hypertensive

ACE inhibitors – Captopril

(Capoten)


Anti dysrhythmic drug



Anti dysrhythmic drug Lidocaine (Xylocaine) for PVC

Atropine for Mobitz type I

Isoproterenol (Isuprel) for sinusbradycardia

Norepinephrine (Levophed) powerfulvasoconstrictor

Epinephrine – increase conduction,contractility and automaticity

Quinidine for atrial fib


Thrombolytic/Fibrinolytic Agent



Thrombolytic/Fibrinolytic Agent

Streptokinase – lyses the clot (20T

IU IV bolus or 4T IU/min drip)

Urokinase – avtivates plasminogen

to plasmin (intracoronary)

TPA – tissue plasminogen activator

Antidote – Amino Caproic Acid


Blood thinner



Heparin – prevent formation of new clot(4-8T IU/30 min)

Check APTT

Antidote – Protamine Sulfate

Warfarin (Coumadin) – decrease viscosityof blood (PO) home meds

Don’t give to pregnant Check PT or INR

Antidote – Vitamin K

CARDIOVASCULAR



CARDIOVASCULARSKILLS

Cardiac Disorders

Coronary Artery Disease



Coronary Artery Disease

Accumulation of fatty deposits in the

innermost layer of the coronary arteries

Atheroma or plaque can lead to

narrowing of the lumen decreasing

coronary blood flow and inadequate O2

supply to heart muscles

Angina



Angina

Diminished O2 supply to the

myocardium

Myocardial Infarction

Absent of O2 supply to the myocardium

Hyperlipidemia

Group of metabolic disorders that lead

to: El t d t t l



to Elevated serum total

cholesterol

(hypercholesterolemia)

Elevated low density

lipoprotein

Elevated triglycerides(hypertriglyceridemia)

Cardiogenic Shock

Occurs when the heart muscle loses its

contractile power



p

Extensive damage to left ventricledue to MI may lead to shock

Infective Endocarditis Infection of the inner lining due to direct

invasion of bacteria

May lead to deformity of valveleaflets

Rheumatic Endocarditis



Valvular problem

Valvular insufficiency—valve

leakage causing regurgitation

Valvular stenosis—narrowing

causing the heart to exert more effort to

eject blood

Myocarditis



y

Inflammation of the myocardium

Pericarditis

Pericardial effusion-fluid in the

pericardial cavity

Constrictive pericarditis-thickening of

the pericardium compressing

the heart

Cardiomyopathy



y p yIdiopathic

3 Groups

DilatedHypertrophic

Restrictive

Heart Failure or Congestive Heart



gFailure

Heart’s inability to pump blood

Acute Pulmonary Edema

Presence of excess fluid in the lung,

either in the alveoli or interstitial space

Cardiac Dysrhythmias



y y

Disturbances in regular rate/rhythm due

to changes in electrical

automaticity or conduction

Vascular Disorders

VEIN



Venous Thrombus

Phlebitis

Inflammation in the wall of a vein Phlebothrombosis

Formation of thrombi in the vein

Deep Vein Thrombosis Thrombosis of deep veins

VEIN Chronic Venous Insufficiency



Chronic Venous Insufficiency

Chronic occlusion of the vein or destruction of valvesleading to venous stasis.

Stasis Ulcers

Excavation of the skin surface produced by sloughingof inflammatory

necrotic tissue

Caused by vascular insufficiency

Varicose Veins Dilatation and elongation of saphenous veins, deeper

veins are normal

ARTERY Arteriosclerosis



Loss of elasticity and hardening of vessel wall

Atherosclerosis

Common type of arteriosclerosis, manifested by formation of atheromas

Thromboangitis Obliterans or Buerger’s Disease Inflammation of arterial wall followed by thrombosis

Also affects adjacent veins and nerves

Aneurysm

Distension of an artery due to weakening of arterial wall

High pressure in the lumen due to plaque deposits Aneurysm can enlarge

Acute Arterial Occlusion Sudden interruption of blood supply lead to gangrene formation



Raynaud’s Phenomenon or Vasospastic Disorder

Unusual sensitivity to cold or emotional stress

Intermittent vasoconstriction leads to coldness, pain, pallor of

fingertips, toes, tip of the nose Hypertension

CNS factor

Renin-angiotensin/aldosterone system factor

ECF volume

Increased cardiac output plus increased peripheralresistance factor

Cardiac Pacemakers

INVASIVE

An electrical impulse generator that



p gtransmits rhythmic impulses when the

heart is unable to do its normal

conduction of impulses (SA Node and AV Node)

It may be temporary or permanent

Cardiac Pacemakers

INVASIVE



Cardiac Pacemakers

INVASIVE

Temporary Pacemakers



Consist of wire connected to an external

battery-operated pulse generator box

Wire is threaded via the SVC into theatrium or ventricle, where it remains to

initiate impulses

Sometimes insertion is done under fluoroscopy

Cardiac Pacemakers

INVASIVE

Permanent pacemakers



Smaller and the box is implanted under

the skin (chest or abdomen) under

surgery

Cardiac Pacemakers

INVASIVE

Electrical impulses seen on ECG



Generated by the pacemaker cause a

straight and upright

deflection (pacer spike) on the EKGbaseline

A spike precedes every QRS

complex stimulated by the pacemaker

BLS

Basic Life Support (B L S) INVASIVE



Emergency first aid focused on

recognizing cardiac and respiratory

arrest and to provide cardiopulmonaryresuscitation

1 Rescuer = 15:2 C:V

2 Rescuers = 5:1 C:V

C = compression, V = ventilation

BLS

Open the airway



Head-tilt or chin-lift

Head-tilt or neck-lift

Jaw-thrust without head-tilt when neck

or spinal injury is suspected

(Never hyperextend the head)

BLS

Give Mouth-to-Mouth Resuscitation



If there is no expansion of the chest

suspect airway obstruction

Insert an Artificial Airway

Keep the tongue from falling back that

may occlude airway

Use an ambu bag

BLS

Always use an oropharyngeal airway with anambu bag



ambu bag

Insert an ETT

Once intubated the lungs are checked with

stethoscope for bilateral ventilation Make sure the cuff is inflated to prevent air

leaks and aspirating gastric contents

The tip must be checked for correctplacement by auscultating lung sounds. Itmust be equal to both lungs

Advance Cardiac Life Support

(A C L S) INVASIVE

Almost the same with BLS except for th f ll i



the following:

Done inside the hospital

Uses defibrillator machine/precordialthump

Advanced Cardiac Life Support

(A C L S) INVASIVE

Drugs are also given like:



Epinephrine

1mg/amp give 1-2 amp IV stat, q 3-5

min until there is cardiac rhythm or untilCPR is stopped

Can be given in ETT 1 amp in 10 ml

NSS q 3-5 min if there is no IV line


(A C L S) INVASIVE

Lidocaine



50 –100 mg, 1mg/kg IVPush

Then start drip at 2mg/min, maximum of

200 mg

Atropine

0.5 –1 mg IV stat, maximum of 3mg (3

ampules)

May be given in ETT with 10 ml NSS


(A C L S) INVASIVE

NaHCO3



1 amp 1 meq/kg

Consider administration if the heart has

stopped more than 15 min

Cardioversion (Synchronized)

INVASIVE

An electrical current wipes out all of theelectrical activity within the heart allowing SA



y gnode to resume its normal function

This is used when other methods have failed

Commonly done during atrial flutter/fib, andventricular tachydysrhythmias to convert tosinus rhythm

It is a synchronized discharge of electricitythrough the heart by giving

a bolus of 25-50 watt-second delivered onthe R wave of QRS complex


INVASIVE

Charge the defibrillator and grease thepaddles before using it



paddles before using it

Attach cardiac monitor to determine cardiacstatus

Set the prescribed energy level Check energy-level gauge to see if the

paddles are fully charged

Place one paddle to the right of midsternumand the other to the left lower rib cage for female use the 5ICS midaxillary to avoid thebreast


INVASIVE

When in place do not move the paddles andsmear the lubricants (electrical current may



smear the lubricants, (electrical current may

follow the path of the conducting material that

may lead to burns)

SHOUT ―stand clear.‖

Apply 25 lbs pressure to each paddle and

discharge the energy simultaneously by

depressing the buttons located on thehandles


INVASIVE

Repeat the procedure if necessary Then continue to give ACLS



Then continue to give ACLS

After the procedure turn off the defibrillator

and discharge the remaining current on thepaddles

Wash the paddles with soap and water

Dry the paddles thoroughly and place them

on the charge plates

Never use alcohol when cleaning the paddles

it may lead to corrosion of the rubber

Defibrillation (Unsynchronized)INVASIVE

Same as above except that it can bedone at any given situation not unless



done at any given situation not unless

there is cardiac activity

It is also given on a higher dose around

lecture cardio physiotherapy 1

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