lecture cardio physiotherapy 1
TRANSCRIPT
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The HEART
Dr Georges GhorayebInternal Medecine
InterventionalCardiologist
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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
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The Heart
Slide11.2a
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Location
Thorax between the lungs(MEDIASTINUM)
Pointed apex directed toward left hip
About the size of your fist
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The Heart
Slide11.2b
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Figure 11.1
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The Heart: Coverings
Slide 11.3 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Pericardium – a double serousmembrane
Visceral pericardium :Next to heart
Parietal pericardium :Outside layer
Serous fluid fills the space between thelayers of pericardium
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The Heart: Heart Wall
Slide 11.4 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Three layers
Epicardium
Outside layer
This layer is the parietal pericardium
Connective tissue layer
Myocardium
Middle layer
Mostly cardiac muscleEndocardium
Inner layer
Endothelium
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External Heart Anatomy
Slide 11.5 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Figure 11.2a
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The Heart: Chambers
Slide 11.6 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Right and left side act as separate pumps Four chambers
Atria
Receiving chambers Right atrium
Left atrium
VentriclesDischarging chambers
Right ventricle
Left ventricle
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Blood Circulation
Slide 11.7 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Figure 11.3
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The Heart: Valves
Slide 11.8 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
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
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The Heart: Valves
Slide 11.9 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Valves open as blood is pumped
through Held in place by chordae tendineae
(―heart strings‖)
Close to prevent backflow
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Operation of Heart Valves
Slide11.10
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Figure 11.4
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The Heart: Associated GreatVessels
Slide11.11
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AortaLeaves left ventricle
Pulmonary arteries
Leave right ventricle
Vena cava
Enters right atrium Pulmonary veins (four)
Enter left atrium
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Coronary Circulation
Slide11.12
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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
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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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The Heart: Conduction System
Slide11.13a
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Intrinsic conduction system(nodal system)
Heart muscle cells contract, without nerveimpulses, in a regular, continuous way
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The Heart: Conduction System
Slide11.13b
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Special tissue sets the pace
Sinoatrial node Pacemaker
Atrioventricular node
Atrioventricular bundle
Bundle branches
Purkinje fibers
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Heart Contractions
Slide11.14b
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Figure 11.5
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Filling of Heart Chambers – the Cardiac Cycle
Slide11.15
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Figure 11.6
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The Heart: Cardiac Cycle
Slide11.17
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Cardiac cycle – events of one completeheart beat
SYSTOLE = CONTRACTION (S1-lub)
DIASTOLE= RELAXATION (S2-dub)
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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 from
the left ventricle Equated with systemic vascular resistance (SVR)
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The Heart: Cardiac Cycle
Slide11.16
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Atria contract simultaneously
Atria relax, then ventricles contractsimultaneously
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The Heart: Cardiac Output
Slide11.18
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
• 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
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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 ventricular ejection is called systemic vascular resistance.
The resistance of the pulmonary BP to right ventricular ejection is called pulmonary vascular resistance
.
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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
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Cardiac Output Regulation
Slide11.19 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Figure 11.7
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The Heart: Regulation of Heart
Rate
Slide11.21 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
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
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The Heart: Regulation of
Heart RateDecrease heart rate
Parasympathetic nervous system (vagus
nerve)
High blood pressure / blood volume
Decreased venous return
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Blood Vessels: The Vascular System
Slide11.23 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Taking blood to the tissues and back
Arteries
Arterioles
Capillaries
VenulesVeins
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BLOOD VESSEL: ANATOMY
Three layers (tunics)Tunica intima
Endothelium
Tunica mediaSmooth muscle
Controlled by sympathetic nervoussystem
Tunica externa
Mostly fibrous connective tissue
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The Vascular System
Slide11.24 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Figure 11.8b
DIFFERENCES BETWEEN
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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 -
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Movement of Blood ThroughVessels
Slide11.27 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
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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Patient Assessment:
Cardiovascular System
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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).
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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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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.
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• Fatigue (earliest symptom associated with several
cardiovascular disorders)
• 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
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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.
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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
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Slide11.35 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Pulse – pressure waveof blood
Monitored at―pressurepoints‖ wherepulse is easilypalpated
Bl d P
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Blood Pressure
Slide11.36
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Measurements by health professionalsare made on the pressure in largearteries
Systolic – pressure at the peak of ventricular contraction
Diastolic – pressure when ventricles relax
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Variations in Blood Press re
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Variations in Blood Pressure
Slide11.41
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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
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Diagnostic Evaluation
Laboratory test (Cardiac Labs)
Chest X-ray
ECG (electrocardiogram)CARDIAC STRESS TESTING
ECHOCARDIOGRAPHY
Laboratory Test
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Laboratory Test
Rationale
1. To assist in diagnosing MI2. To identify abnormalities
3. To assess inflammation
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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
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CPK -MB
0-5% of total CPK (26-
174U/L)
Normal value is 0-7
U/L
Lactate Dehydrogenase
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Lactate Dehydrogenase
(LDH) Elevates in MI in 24 hours
peaks in 48-72 hour Normal value is 70-200 IU/L
M l bi
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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 +++
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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
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if myocardial infarction suspected
REMEMBER to AVOID IM
inject ions before obtain ing
blood sample! Early and late diagnosis can be
made!
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SERUM LIPIDSLipid profile measures the
serum cholesterol,
triglycerides andlipoprotein levels
Cholesterol= 200 mg/dL
Triglycerides =40- 150mg/dL
SERUM LIPIDS
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SERUM LIPIDS
LDL 130 mg/dL
HDL 30-70- mg/dL
NPO pos t m idn igh t
(usual ly 12 hours )
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ELECTROCARDIOGRAM
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(ECG)A non-invasive procedure that
evaluates the electrical activity
of the heart Electrodes and wires are
attached to the patient
ELECTROCARDIOGRAM
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(ECG)Tell the patient that there is
no risk of ECG
Avoid muscular contraction/movement
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Holter Monitoring
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Holter Monitoring
A non-invasive test inwhich the client wears a
Holter monitor and anECG tracing recordedcontinuously over aperiod of 24 hours
Holter Monitoring
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Holter Monitoring
Instruct the client to
resume normal activities
and maintain a diary of
activities and any
symptoms that maydevelop
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ECHOCARDIOGRAM
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ECHOCARDIOGRAM
Non-invasive test thatstudies the structural and
functional changes of theheart with the use of ultrasound
No special preparation isneeded
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Stress Test
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Stress Test
A non-invasive test thatstudies the heart during
activity and detects andevaluates CAD
Stress Test
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Stress Test
Treadmill testing is themost commonly used
stress testUsed to determine CAD,
Chest pain causes, drug
effects and dysrhythmias inexercise
Stress Test
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Stress Test
Pre-test: consent may berequired, adequate rest ,
eat a light meal or fastfor 4 hours and avoid
smoking, alcohol andcaffeine
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Stress Test
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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
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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
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CATHETERIZATION Used to diagnose CAD,
assess coronary artery
patency and determineextent of atherosclerosis
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PRE PROCEDURE
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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
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PRE PROCEDURE
a local anesthetic will beadministered before
insertion
POST TEST
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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
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CVP
The CVP is the pressurewithin the SVC
Reflects the pressureunder which blood is
returned to the SVC andright atrium
CVP
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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
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INCREASED CVP increase in blood volume as a
result of Na and water retention, excessive IV Fluid
or heart / renal failure
DECREASED CVP
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DECREASED CVP May indicate decrease in
circulating blood volume andmay be to hypovolemia,
hemorrhage and severevasodilatation
MEASURING CVP
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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.
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ECG
NORMAL AND ABNORMAL
Cardiac Conduction
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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.
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Before mechanical contraction, an actionpotential travels quickly over each cell
membrane and down into each cell’s.
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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
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Cardiac Conduction
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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
Action Potential
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Action Potential
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12 L d ECG
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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 thebeginning of p wave and the beginning of Rwave 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
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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
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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.
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Normal Sinus Rhythm
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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
Sinus Tachycardia
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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
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y
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
Don’t treat unless there are symptoms. Can use pacing or
atropine
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Premature Atrial Contraction(PAC)
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(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
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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
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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
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Atrial Fibrillation AF
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CAUSES
1- myocardial infarction.
2- valvular heart disease .3- heart failure .
4- thyroid problem
5- lone AF
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Atrial Flutter 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
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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 .
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JUNCTIONAL RHYTHM
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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 .
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JUNCTIONAL RHYTHM
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CAUSES :
1- acute myocardial infarction .
2- digoxin toxicity .
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Premature Ventricular
Contractions (PVC)
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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
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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
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Ventricular Fibrillation Rapid, irregular rhythm made by stimuli from many
different foci in the ventricule
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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 normalconduction pathway but there is a
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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 .
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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 atregular 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
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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 rhytm arises , if the blockinvolve 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
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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
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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.
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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.
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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
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ARTERIOSCLEROSIS OF THE EXTREMITIES
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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.
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Hypertension
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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
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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
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• ANGINA
•Duration of pain – In general, anginal pain lastsfor only a few minutes and is relieved by rest or
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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.
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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.
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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
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CLOSE WINDOW
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ST-segment (V1 to V4) elevation myocardial infarction.
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TREATMENT OF MI
A ti l t l t d i t l i
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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
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Congestive Heart Failure
inability of the heart to pump blood into the
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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
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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
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CHFright ventricle will pump harder just to
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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
↓
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↓
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
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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
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CHF
Predisposing Factors:
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Predisposing Factors:
Myocardial Infarction
Arrhythmias
Pregnancy
Pulmonary Embolism
Anemia Renal Failure
CHF Diagnosing CHF:
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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
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CHF
Complications:
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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:
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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
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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 –
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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)
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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
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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)
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THANK YOU
Cardiovascular Drugs
Anti Anginal
Opiate Analgesic – Morphine Sulfate
↓ cardiac workload and BP improve LOC and
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↓ 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)
Cardiovascular Drugs
Calcium Channel Blockers
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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
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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
Cardiovascular Drugs
Dopamine – diuresis effect
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Dopamine diuresis effect Increase Na excretion (kidney)
Vasodilators
Norepinephrine effect
Dobutamine
Increase CO More potent on contraction
Cardiovascular Drugs
Diuretics
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Diuretics
Spironolactone (Aldactone) – K
sparer
Furosemide (Lasix) – K waster
Anti hypertensive
ACE inhibitors – Captopril
(Capoten)
Cardiovascular Drugs
Anti dysrhythmic drug
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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
Cardiovascular Drugs
Thrombolytic/Fibrinolytic Agent
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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
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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
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CARDIOVASCULARSKILLS
Cardiac Disorders
Coronary Artery Disease
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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
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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
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to Elevated serum total
cholesterol
(hypercholesterolemia)
Elevated low density
lipoprotein
Elevated triglycerides(hypertriglyceridemia)
Cardiogenic Shock
Occurs when the heart muscle loses its
contractile power
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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
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Valvular problem
Valvular insufficiency—valve
leakage causing regurgitation
Valvular stenosis—narrowing
causing the heart to exert more effort to
eject blood
Myocarditis
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y
Inflammation of the myocardium
Pericarditis
Pericardial effusion-fluid in the
pericardial cavity
Constrictive pericarditis-thickening of
the pericardium compressing
the heart
Cardiomyopathy
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y p yIdiopathic
3 Groups
DilatedHypertrophic
Restrictive
Heart Failure or Congestive Heart
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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
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y y
Disturbances in regular rate/rhythm due
to changes in electrical
automaticity or conduction
Vascular Disorders
VEIN
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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
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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
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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
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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
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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
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Cardiac Pacemakers
INVASIVE
Temporary Pacemakers
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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
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Smaller and the box is implanted under
the skin (chest or abdomen) under
surgery
Cardiac Pacemakers
INVASIVE
Electrical impulses seen on ECG
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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
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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
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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
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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
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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
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the following:
Done inside the hospital
Uses defibrillator machine/precordialthump
Advanced Cardiac Life Support
(A C L S) INVASIVE
Drugs are also given like:
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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
Advanced Cardiac Life Support
(A C L S) INVASIVE
Lidocaine
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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
Advanced Cardiac Life Support
(A C L S) INVASIVE
NaHCO3
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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
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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
Cardioversion (Synchronized)
INVASIVE
Charge the defibrillator and grease thepaddles before using it
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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
Cardioversion (Synchronized)
INVASIVE
When in place do not move the paddles andsmear the lubricants (electrical current may
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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
Cardioversion (Synchronized)
INVASIVE
Repeat the procedure if necessary Then continue to give ACLS
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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
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done at any given situation not unless
there is cardiac activity
It is also given on a higher dose around