The HEART

Dr Georges Ghorayeb
Internal Medecine InterventionalCardiologist

The Cardiovascular System

A closed system of the heart and blood vessels
The heart pumps blood

Blood vessels allow blood to circulate to all parts of the body

The function of the cardiovascular system is to deliver oxygen and nutrients and to remove carbon dioxide co2 and other waste products
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Slide 11.1

The Heart
Location
Thorax between the lungs (MEDIASTINUM) Pointed apex directed toward left hip

About the size of your fist

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Slide 11.2a

The Heart

Figure 11.1
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Slide 11.2b

The Heart: Coverings

Pericardium a double serous membrane
Visceral pericardium :Next to heart

Parietal pericardium :Outside layer

Serous fluid fills the space between the layers of pericardium

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Slide 11.3

The Heart: Heart Wall

Three layers
Epicardium
Outside layer This layer is the parietal pericardium Connective tissue layer

Myocardium
Middle layer Mostly cardiac muscle

Endocardium
Inner layer Endothelium
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Slide 11.4

External Heart Anatomy

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Figure 11.2a

Slide 11.5

The Heart: Chambers

Right and left side act as separate pumps Four chambers
Atria Receiving chambers
Right atrium Left atrium

Ventricles Discharging chambers

Right ventricle Left ventricle
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Slide 11.6

Blood Circulation

Figure 11.3
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Slide 11.7

The Heart: Valves

Allow blood to flow in only one direction Four valves
Atrioventricular valves between atria and ventricles
Bicuspid valve ,the mitral valve(left) Tricuspid valve (right)

Semilunar valves between ventricle and artery

Pulmonary semilunar valve Aortic semilunar valve
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Slide 11.8

The Heart: Valves

Valves open as blood is pumped through Held in place by chordae tendineae (heart strings)

Close to prevent backflow

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Slide 11.9

Operation of Heart Valves

Figure 11.4
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Slide 11.10

The Heart: Associated Great Vessels

Aorta
Leaves left ventricle

Pulmonary arteries
Leave right ventricle

Vena cava
Enters right atrium

Pulmonary veins (four)

Enter left atrium
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Slide 11.11

Coronary Circulation
Blood in the heart chambers does not nourish the myocardium The heart has its own nourishing circulatory system
Coronary arteries Cardiac veins Blood empties into the right atrium via the coronary sinus
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Slide 11.12

Coronary Arteries

The left and right coronary arteries and their branches supply arterial blood to the heart. These arteries originate from the aorta just above the aortic valve leaflets.
The heart has large metabolic requirements, extracting approximately 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 first major branch is called the left main coronary artery. two bifurcations arise off the left main coronary artery 2- left anterior descending artery (LAD), which courses down the anterior wall of the heart 3-circumflex artery, which circles around to the lateral left wall of the heart.

The right side of the heart is supplied by the right coronary artery, which progresses around to the bottom or inferior wall of the heart. The posterior wall of the heart receives its blood supply by an additional branch from the right coronary 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 artery disease (CAD), can develop myocardial ischemia (inadequate oxygen supply) when the heart rate accelerates.

The Heart: Conduction System

Intrinsic conduction system (nodal system)

Heart muscle cells contract, without nerve impulses, in a regular, continuous way

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Slide 11.13a

The Heart: Conduction System

Special tissue sets the pace
Sinoatrial node Pacemaker Atrioventricular node Atrioventricular bundle Bundle branches

Purkinje fibers
Slide 11.13b

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Heart Contractions

Figure 11.5
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Slide 11.14b

Filling of Heart Chambers the Cardiac Cycle

Figure 11.6

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Slide 11.15

The Heart: Cardiac Cycle

Cardiac cycle events of one complete heart beat
SYSTOLE = CONTRACTION (S1-lub) DIASTOLE= RELAXATION (S2-dub)

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Slide 11.17

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

Atria contract simultaneously Atria relax, then ventricles contract simultaneously

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Slide 11.16

The Heart: Cardiac Output

Stroke volume:Volume of blood pumped by the ventricles in one contraction.

The percentage of the volume that is ejected with each stroke is called the ejection fraction EF = 50-70%. Cardiac output (CO) :sv of the heart in one minute : = (heart rate /min) x stroke volume [SV]
5-6 liter/min

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Slide 11.18

Contractility is a term used to denote the force

generated 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

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

also called the fight-or-flight-or-freeze response, hyperarousal, or the acute stress response ADRENALINE

Cardiac Output Regulation

Figure 11.7
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Slide 11.19

The Heart: Regulation of Heart Rate

Increase heart rate
Sympathetic nervous system Crisis/Stress Low blood pressure Hormones Epinephrine Thyroxine Exercise Decreased blood volume
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Slide 11.21

The Heart: Regulation of Heart Rate

Decrease

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 Venules Veins
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Slide 11.23

BLOOD VESSEL: ANATOMY Three layers (tunics)

Tunica intima Endothelium Tunica media Smooth muscle Controlled by sympathetic nervous system Tunica externa Mostly fibrous connective tissue

The Vascular System

Figure 11.8b
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Slide 11.24

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 Through Vessels

Most arterial blood is pumped by the heart Veins use the milking action of muscles to help move blood

Figure 11.9
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Slide 11.27

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 the onset and severity of chest discomfort, associated symptoms, current medications, and allergies. At the same time, observes the patients general appearance 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, left ventricular 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.
S1First Heart Sound. Closure of the mitral and tricuspid valves creates the first heart sound (S1), S2Second Heart Sound. Closing of the aortic and pulmonic valves produces the second heart sound (S2).

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, a defect between the aorta and the pulmonary artery

 Pulse pressure wave of blood Monitored at pressure points where pulse is easily palpated
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Slide 11.35

Blood Pressure
Measurements by health professionals are made on the pressure in large arteries
Systolic pressure at the peak of ventricular contraction Diastolic pressure when ventricles relax

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Slide 11.36

Variations in Blood Pressure

Human normal range is variable
Normal 140110 mm Hg systolic 8075 mm Hg diastolic Hypotension Low systolic (below 110 mm HG) Often associated with illness Hypertension High systolic (above 140 mm HG) Can be dangerous if it is chronic
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Slide 11.41

Diagnostic Evaluation
Laboratory

test (Cardiac Labs) Chest X-ray ECG (electrocardiogram)

CARDIAC

STRESS TESTING ECHOCARDIOGRAPHY

Laboratory Test Rationale

1.

To assist in diagnosing MI 2. To identify abnormalities 3. To assess inflammation

CPK- MB (creatine kinase)

Indicates

myocardial

damage Elevates in MI within 4-6 hours peaks in 18 hours and then declines till 3 days

CPK -MB
0-5%

of total CPK (26174U/L) Normal value is 0-7 U/L

Lactate Dehydrogenase (LDH)

Elevates

in MI in 24 hours peaks in 48-72 hour Normal value is 70-200 IU/L

Myoglobin
Oxygen binding protein Found in both skeletal and

cardiac

muscle Level rises 1 hour after cell death Peaks in 4-6 hours Returns to normal w/in 24-36 hours Not used alone Muscular and RENAL disease can have elevated myoglobin

Troponin I and T +++

Troponin

I has a high affinity for myocardial injury Elevates within 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 injections before obtaining blood sample! Early and late diagnosis can be made!

SERUM LIPIDS
Lipid

profile measures the serum cholesterol, triglycerides and lipoprotein levels Cholesterol= 200 mg/dL Triglycerides =40- 150 mg/dL

SERUM LIPIDS
LDL

130 mg/dL HDL 30-70- mg/dL NPO post midnight (usually 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
A

non-invasive test in which the client wears a Holter monitor and an ECG tracing recorded continuously over a period of 24 hours

Holter Monitoring
Instruct

the client to resume normal activities and maintain a diary of activities and any symptoms that may develop

ECHOCARDIOGRAM
Non-invasive

test that studies the structural and functional changes of the heart with the use of ultrasound No special preparation is needed

Stress Test
A

non-invasive test that studies the heart during activity and detects and evaluates CAD

Stress Test
Treadmill

testing is the most commonly used stress test Used to determine CAD, Chest pain causes, drug effects and dysrhythmias in exercise

Stress Test
Pre-test:

consent may be required, adequate rest , eat a light meal or fast for 4 hours and avoid smoking, alcohol and caffeine

Stress Test

instruct client to notify the physician if any chest pain, dizziness or shortness of breath Observe for ECG changes Confirm if stress test positive or negative

CARDIAC CATHETERIZATION

Insertion of a catheter into the heart and surrounding vessels Obtains information about the structure and performance of the heart valves and surrounding vessels

CARDIAC CATHETERIZATION

Used to diagnose CAD, assess coronary artery patency and determine extent of atherosclerosis

PRE PROCEDURE

Ensure Consent assess for allergy to seafood and iodine Withhold solid food 6-8 hours and liquids for 4 hours document weight and height, baseline VS, blood tests and document the peripheral pulses

PRE PROCEDURE
a

local anesthetic will be administered before insertion

POST TEST
Keep

the leg straight to prevent occlusion

Monitor

for bleeding and hematoma formation

fluid intake to flush out the

Encourage

dye Immobilize the arm if the antecubital vein is used Monitor for dye allergy

CVP

The CVP is the pressure within the SVC Reflects the pressure under which blood is returned to the SVC and right atrium

CVP

is measured with a central venous line in the SVC and balloon flotation catheter in the pulmonary artery Normal CVP is 4 to 8 mmHg / 4-12 cm H2O

INCREASED CVP

increase in blood volume as a result of Na and water retention, excessive IV Fluid or heart / renal failure

DECREASED CVP

May indicate decrease in circulating blood volume and may be to hypovolemia, hemorrhage and severe vasodilatation

MEASURING CVP
1. 2.

3.

Position the client supine with bed elevated at 45 degrees Position the zero point of the CVP line at the level of the right atrium. Usually this is at the MIDANTERIOR LINE 4th Intercostal space. Instruct the client to be relaxed and avoid coughing and straining.

ECG
NORMAL AND ABNORMAL

Cardiac Conduction
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.

 Before

mechanical contraction, an action potential travels quickly over each cell membrane and down into each cells.

Three physiologic characteristics of two specialized 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 electrical impulse from one cell to another

Cardiac Conduction
(SA) node Fires at 60100 beats/minute Intranodal pathway Atrioventricular (AV) node Fires at 40-60 beats/minute Atrioventricular bundle of His
Sinoatrial

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

Right

and left bundle branches Purkinje fibers

Action Potential

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 The direction of the flow of electricity

Axis

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P wave : atrial depolarization up to 0.12 second in duration . QRS complex : ventricular depolarization normal measure is 0.08-0.12 second T wave : ventricular repolarization , rounded upright, not exceeds 0.2 sec of duration PR interval : the interval between the beginning of p wave and the beginning of R wave it measures between ( 0.12-0.2)

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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
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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.

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 between two 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

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

Rate above 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 Caused by fever, stress, caffeine, nicotine, exercise, or by increased sympathetic tone Treatment is to take care of the underlying cause

Sinus Bradycardia

Rate is lower than 60 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 Caused by beta-blocker, digitalis, or calcium channel blockers. Normal for athletes Dont treat unless there are symptoms. Can use pacing or atropine

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

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

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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 AF
CAUSES

1- myocardial infarction. 2- valvular heart disease . 3- heart failure . 4- thyroid problem 5- lone AF
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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

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 CAUSES

: 1- atrial enlargement . 2-throid problem. 3- myocardial infarction .

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JUCTIONAL RHYTM

This type occurs when SA node & the atria are unable to discharge an impulse to depolarize both atria & ventricles , therefore an ectopic focus in the surrounding 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 its origin .
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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 stimulated by the junctional tissue after activation after or with the activation of the ventricles .
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JUNCTIONAL RHYTHM
CAUSES

: 1- acute myocardial infarction . 2- digoxin toxicity .

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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 impulses discharged prior to the next anticipated sinus rhythm impulse .
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Ventricular Tachycardia
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 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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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 normal conduction pathway but there is a delay in the process .
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Second degree av block mobitz-1 Occurs when conduction through the AV junction become progressively difficult with each successive impulse until finally a ventricular depolarization doesnt occur .

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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 .

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 CAUSES

: 1-rheumatic fever . 2- myocardial infarction . 3- drug 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 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 .

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 CAUSES

: 1- degenerative changes in conduction system 2- anterior myocardial infarction . 3- coronary artery disease .

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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 block involve the junctional tissue , the idiodventricular rhythm arises .

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 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 )
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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- myocardial infarction . 2- digoxin toxicity . 3- degeneration of conduction system .

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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 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.

Atherosclerosis is responsible for the majority of deaths in our society. It is also responsible for a huge amount of morbidity. If one studies insurance tables, atherosclerosis causes a large contribution to years of potential life lost. Atherosclerosis is predominantly a disease of arteries both large and medium-sized. It affects elastic and muscular vessels. Atherosclerosis may also involve veins when they become vein grafts and are exposed to arterial pressure.

Risk factors for atherosclerosis include those, which are modifiable, and those, 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 this is a disease present since infancy. Gender atherosclerosis is present more in males, however females catch up after menopause.( Some old dated thinking regarded females as having less atherosclerosis than males. However, it is recognized now that females do develop significant atherosclerosis. Estrogen is protective as it has multiple effects including effects on lipids, nitric oxide, vascular tone and antioxidant properties.) Smoking - causes multiple malignancies and accelerates and initiates atherosclerosis. Many effects on the endothelial cell including poor vascular tone with 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 atherosclerosisthe buildup of cholesterol and other fatty substances in the arteries.
When the arteries narrow, blood flow is reduced. The reduced blood flow (ischemia) causes the heart muscle to receive less oxygen in certain areas. 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 lasts for 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 minutes or more.

Pain that lasts less than 30 seconds and goes away 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. 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 as shortness 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 Angina

There are three primary types of angina: Stable angina The attacks are predictable, and the triggers that cause them can be identified. They do not occur when you are resting or relaxed, and symptoms will usually disappear after a few minutes of rest. 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 when symptoms occur more frequently, last longer, or are precipitated more easily. You should call your doctor immediately if you experience symptoms at 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
drugs: aspicot,plavix Thrombolytic treatment: drug that can lyses the clot of MI: streptokinase 1.5 MU in 30-60 min metalyse kg? push Primary angioplasty of occluded coronary artery : insertion of balloon and stent
Antiplatelets

Congestive Heart Failure

inability of the heart to pump blood into the circulatory system. usually due to inability of the ventricles to pump blood leading to Pulmonary congestion Pulmonary hypertension

CHF
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

CHF
right ventricle will pump harder just to pass blood into the congested pulmonary capillaries resulting to right ventricular hypertrophy Right Ventricular Failure (Cor Pulmonale)

CHF
blood will be congested into the right side right sided heart failure will follow Venous congestion distended neck veins, hepatomegaly, portal hypertension splenomegaly, pancreatomegaly, esophageal varices, hemorrhoids, ascites, caput medusa, weight gain

CHF
venous pooling in the lower extremities bi-pedal edema, varicosities, DVT until all venous system becomes congested with fluid periorbital edema or generalized edema ANASARCA

RIGHT-SIDED HEART FAILURE

CHF

Predisposing Factors: Myocardial Infarction Arrhythmias Pregnancy Pulmonary Embolism Anemia Renal Failure

Diagnosing CHF:

CHF

Daily weighing reveals unexplained weight gain Abdominal girth measurement shows ascites EKG detects heart strain Chest X-ray may highlights cardiomegaly and pleural effusion CVC Central Venous Catheter and Swan-Ganz Catheter are able to record high pressure in the chambers and pulmonary capillaries.

SWAN-GANZ

CHF

Complications: Acute Pulmonary Edema Treatment: Bed rest and maintain high fowlers position O2 therapy Morphine administration to dilate blood vessels Dopamine to increase myocardial contractility and CO Diuretics to reduce blood volume Steroids to reduce inflammation

CHF
Complications:
Cardiac

Arrhythmias Disturbances in regular rate and rhythm due to changes in electrical automaticity or conduction Irregular HR, rhythm and regularity

Cardiac Arrhythmias
ATRIAL A. Premature atrial contraction (PAC) more than 100 bpm 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 PVCs Ventricular fibrillation (vfib) extremely rapid and erratic impulse formation

AV Block Impulse is delayed from SA node to AV node 1st degree 2nd degree

Mobitz type I asymptomatic (ventricular contraction is adequate) Mobitz type II critical (atrial contraction is not synchronized with the ventricle) Cardiac monitor must be in-placed Anti-arrhythmic drugs administration Defibrillator standby Pacemaker

Treatment:

Cardiac Arrest Heart stops beating or contraction is ineffective Watch-out for tissue perfusion manifestations: 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 skin Cyanosis Shock

Cardiac Arrest Treatment: Increase CO Cardiovascular drugs and mechanical equipment utilization 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 sedative 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)

Cardiovascular Drugs

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

Cardiovascular Drugs
Digitalis,

Digoxin Positive Inotropic (Increases contraction of the heart)

Increase emptying capacity of the heart

Negative

chronotropic (Decreases HR) AV node control

Increase CO (improves stroke volume)

S.E.

GIT disturbance, CNS depression and flashes of light

Cardiovascular Drugs
diuresis effect Increase Na excretion (kidney) Vasodilators Norepinephrine effect Dobutamine Increase CO More potent on contraction
Dopamine

Cardiovascular Drugs

Diuretics Spironolactone (Aldactone) K sparer Furosemide (Lasix) K waster

Anti hypertensive ACE inhibitors Captopril (Capoten)

Cardiovascular Drugs

Anti dysrhythmic drug Lidocaine (Xylocaine) for PVC Atropine for Mobitz type I Isoproterenol (Isuprel) for sinus bradycardia Norepinephrine (Levophed) powerful vasoconstrictor Epinephrine increase conduction, contractility and automaticity Quinidine for atrial fib

Cardiovascular Drugs

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

Cardiovascular Drugs

Blood thinner Heparin prevent formation of new clot (4-8T IU/30 min) Check APTT Antidote Protamine Sulfate
Warfarin (Coumadin) decrease viscosity of blood (PO) home meds Dont give to pregnant Check PT or INR Antidote Vitamin K

CARDIOVASCULAR SKILLS

Cardiac Disorders
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
Diminished

O2 supply to the myocardium Myocardial Infarction Absent of O2 supply to the myocardium

 Hyperlipidemia
Group

of metabolic disorders that lead

to: Elevated serum total cholesterol (hypercholesterolemia) Elevated low density lipoprotein Elevated triglycerides (hypertriglyceridemia)

 Cardiogenic

Shock Occurs when the heart muscle loses its contractile power Extensive damage to left ventricle due to MI may lead to shock Infective Endocarditis Infection of the inner lining due to direct invasion of bacteria May lead to deformity of valve leaflets

 Rheumatic

Endocarditis Valvular problem Valvular insufficiencyvalve leakage causing regurgitation Valvular stenosisnarrowing causing the heart to exert more effort to eject blood

 Myocarditis
Inflammation Pericarditis

of the myocardium

Pericardial effusion-fluid in the pericardial cavity Constrictive pericarditis-thickening of the pericardium compressing the heart

 Cardiomyopathy

Idiopathic 3 Groups Dilated Hypertrophic Restrictive

 Heart

Failure or Congestive Heart Failure Hearts inability to pump blood Acute Pulmonary Edema Presence of excess fluid in the lung, either in the alveoli or interstitial space

 Cardiac

Dysrhythmias 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 occlusion of the vein or destruction of valves leading to venous stasis. Stasis Ulcers Excavation of the skin surface produced by sloughing of 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 Buergers 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 Raynauds 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 peripheral resistance factor

Cardiac Pacemakers INVASIVE

An

electrical impulse generator that transmits 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 the atrium 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 EKG baseline 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 cardiopulmonary resuscitation 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 an 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 correct placement by auscultating lung sounds. It must be equal to both lungs

Advance Cardiac Life Support (A C L S) INVASIVE

Almost

the same with BLS except for the following: Done inside the hospital Uses defibrillator machine/precordial thump

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 until CPR is stopped Can be given in ETT 1 amp in 10 ml NSS q 3-5 min if there is no IV line

Advanced Cardiac Life Support (A C L S) INVASIVE

Lidocaine
50100

mg, 1mg/kg IVPush Then start drip at 2mg/min, maximum of 200 mg Atropine 0.51 mg IV stat, maximum of 3mg (3 ampules) May be given in ETT with 10 ml NSS

Advanced Cardiac Life Support (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 the electrical activity within the heart allowing SA node to resume its normal function This is used when other methods have failed Commonly done during atrial flutter/fib, and ventricular tachydysrhythmias to convert to sinus rhythm It is a synchronized discharge of electricity through the heart by giving a bolus of 25-50 watt-second delivered on the R wave of QRS complex

Cardioversion (Synchronized) INVASIVE

Charge the defibrillator and grease the paddles before using it Attach cardiac monitor to determine cardiac status Set the prescribed energy level Check energy-level gauge to see if the paddles are fully charged Place one paddle to the right of midsternum and the other to the left lower rib cage for female use the 5ICS midaxillary to avoid the breast

Cardioversion (Synchronized) INVASIVE

When in place do not move the paddles and 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 the handles

Cardioversion (Synchronized) INVASIVE

Repeat the procedure if necessary Then continue to give ACLS After the procedure turn off the defibrillator and discharge the remaining current on the paddles 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 be done at any given situation not unless there is cardiac activity It is also given on a higher dose around 200-300 watt-seconds