cardiovascular investigation

7/29/2019 Cardiovascular Investigation

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Dr. Lamia El Wakeel, PhDLecturer of Clinical Pharmacy


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A careful patient history & physical examination are

extremely important in diagnosing CVD & should be

done prior to any test

A careful patient history & physical examination are

extremely important in diagnosing CVD & should be

done prior to any test

Every 36 seconds 1 person dies from CVD

In the US, 2,500 people die every day

CVD exceeds the next four leading causes of death

combined (cancer, lung disease, accidents &diabetes)


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1. History taking

2. Physical examination

3. Prognostic & diagnostic testing


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Cornerstone of a cardiovascular workup The elements of a comprehensive history include;

9Chief complaint (CC); exact complaint, duration, severity,limitation of daily activities, character & location of complaint &what brings on the complaint.

9Present problems

9Past medical history

9History of Present Illness (HPI)

9Review of systems (ROS)

9Family history (FH)

9Social history


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Cardiovascular PE is divided into 4 categories:

1. Global examination of the patient for signs of CVD & a review of all

body systems2. Observation & assessment of physical findings (JVP)

3. Measurement of parameters of CVD function (P, B.P)

4. Auscultation, percussion &palpation of the chest & related cardiacstructures.

A. Heart sounds

B. Peripheral circulation & arterial pulsesC. Heart rate


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1. Normal heart sounds

a. 1st heart sound S1; closure of AV valves (tricuspid& mitral); beginning of systole (loudest at apex) ; lub

b. 2nd heart sound S2; closure of SL valves (pulmonic

& aortic);. ending of systole (loudest at base); dub .Splitting; P2 & A2 sounds

2. Abnormal heart sounds

a. S3; heard at the end of the rapid filling interval of the diastoledenoting volume overload

b. S4; indicating an increased resistance to filling(noncompliantventricle or an increased volume)

S3 is normal in children & young adults. Horse gallop,while S4 may be normal above 40 yrs

c. Murmur; auditory vibrations heard on auscultation (due toturbulent blood flow within the heart chambers or valves)Classified by; timing & duration (systolic, diastolic & continuous),

location, intensity, pitch (frequency) & radiation.

Fever, anxiety, anemia, hyperthyroidism & pregnancyexacerbate physiologic murmurs

Auscultated areas;apex or base of the heart (mitral sounds) lower left sternal border (tricuspid sounds)second left interspace (pulmonic sounds)second right interspace (aortic sounds) S1 & S2 heard at all


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The JVP is used as anindirect measure of RAP

measured in cms from thesternal angle

best visualized with thepatients head rotated to theleft

Report; extent of elevation &

pt position JVP; cms above the

manubrium, or this value +5-7 cm to indicate the rise of

the JVP above the rightventricle.

Elevated in HF degree of elevation; used to

assess severity &management


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Arterial pulses are evaluated & characterized bilaterally by;observation, palpation & auscultation for presence, character,

pattern & rhythm. Patterns;pulsus alternans , & paradoxical pulse & others.

Pts overall peripheral circulation is recorded;

9 presence9 degree of edema

9 or skin changes

Capillary refill (N; < 2 seconds); depress nail bed until itblanches , release pressure & watch for color return(indicating blood flow)


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Described by both rate & rhythm

Arterial pulse; taken at the radius, but other arterial

pulses may be usedHealthy; count pulse for 15 seconds & multiply by 4

Pts with irregular rhythms, the pulse should be takenover an extended period (1-2 minutes), In patients withAF apical pulse should be counted

Pts with a rapid ventricular rate (SVT, AF, VT);

9 extremity pulses (radial) may be slower than true rate

9more accurate; listen to ventricles with stethoscope (usuallyat the apex) or counting from an ECG.


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1. Chest radiography

2. Electrocardiogram ECG

3. Ambulatory ECG monitoring (AECG) (Holter)4. Exercise stress (tolerance) testing (ETT)

5. The echocardiogram (ECHO)

6. Nuclear cardiology7. Positron emission tomography PET

8. Pharmacologic stress testing

9. Computed tomography CT10. Catheterization


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Does not provide details of internal cardiacstructures but general information about position

& size of heart & surrounding anatomy.

Standard chest radiographs are ;standing posteroanterior & lateral views taken atmaximal inspiration (AP in Bed)

Lack of inspiratory effort & obesity lead to a

poor-quality chest radiograph

2 perspectives:

(a)Observation (b) clinical correlation

Observation; size & placement of the heart,chamber enlargement, pulmonary vasculature,

airfluid levels & diaphragm. Cardiac

enlargement (cardiothoracic ratio)


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ECHO; the use of US to visualizeanatomic structures (valves) &describe wall motion

Indications: valvular dysfunction,Global or segmental wall motionabnormalitiesassociated withcardiomyopathy or ischemia,respectively.

Segmental wall motion abnormalitiesare graded as; akinetic, hypokinetic,dyskinetic, and hyperkinetic.

ECHO in clinical practice: can be Transthoracic (TTE) ortransesophageal (TEE)

Estimated parameters: chamber wall thickness, left ventricleejection fraction, ventricular function & abnormalities of thepericardium (effusions or thickening).


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TEE ; patients in whom TTE is limited(MV, obesity), more accurateassessment of valvular structure /function or to visualize intracardiac

masses (tumors or thrombi). CI of TEE; patients with esophagealabnormalities.

Doppler and color-flow Doppler

technology Principle; reflecting sound off amoving object (RBCs)

Used with ECHO for analysis of ;

9 valvular function (aortic regurgitation,mitral stenosis) or blood flow patterns

9 measurement of transvalvularpressure gradients, valve area, and

pressure changes on either side of thevalve.


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ETT ; evaluates clinical & CVS responsesto exercise (ability of HR to increaseappropriately during exercise)

Method: done on treadmill or bicycleergometer while patient ECG, HR &

hemodynamics are assessed Degree of stress delivered in a graded &

calibrated manner Protocols customized ; an exercise time of

6 - 12 min & HR of 85% - 90% of

maximum predicted (target HR= 220-age) Principle; increase myocardial oxygendemand > myocardial oxygen supply &coronary reserve provoking ischemia

Ischemia; pt symptoms, ECG changes,and/or hemodynamic changes

AE: arrhythmias, sudden death, hypotension & MI

CI: UA, CHF, untreated life threatening arrhythmias

Measurements; peak heart rate, predicted max HR & HR recovery afterexercise testing (N; rapid fall of HR during 1st 30 sec after exercise).


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An alternative in pts unable to undergo ETT

Agents produce stress by;

9 hyperemic (vasodilator) response;

dipyridamole & adenosine

9 increasing myocardial oxygen demand (HR &

contractility); dobutamine

Evaluates; wall motion abnormalities &perfusion

Can be performed using; thallium, MRI,

ECHO, etc


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Dobutamine

Mechanism; inc. HR & CO; inc myocardial oxygen demand (Ischemiadevelops in stenotic areas)

Detection; Ischemia detected by ECHO or thallium . Dose of stress test; doses of 10 - 40 mcg/kg/min; dose titrated at 3-min intervals

in increments of 10 mcg/kg/min

Atropine may be given to augment HR response

Monitoring; ECG & BP; continuously ,ECHO ;last minute of each dose level &during recovery

D.C -Blocker & CCBs prior to test (interfere w HR response)

D.C if; severe CP, extensive new wall motion abnormalities, ST-segment dist

(ischemia), tachyarrhythmias, & symptomatic reductions in BP CI; aortic stenosis, uncontrolled HTN & severe ventricular arrhythmias.


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Dipyridamole & adenosine Principle;9 Dipyridamole inhibits adenosine cellular reuptake

9 Adenosine is a potent CA VD & increase perfusion 4-5 times > baseline

9 Areas distal to CA obstruction show relative hypoperfusion vs normal

9 Acutely, these areas will appear as cold spots,

9 On redistribution scans; defects will fill, indicating viable but jeopardizedmyocardium.

Dose; Dipyridamole IV; 0.142 mg/kg/min over 4 min. Adenosine; over 6min at a dose of 0.140 mcg/kg/min

Imaging (thallium scanning) can follow immediately to heighten theredistribution defects.

ADR; dipyridamole; CP, headache, dizziness & N (give xanthines;adenosine bocker) Caffeine products and theophylline must be avoided for about 24 hrs prior to

the test.

CI; history of bronchospasm.


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technetium-99m (99mTc); t ; 6 hrs (multiple dosing); gamma ray emission

Evaluation of bld pool & myocardial perfusion (EF, cardiac shunts, volumes & wallmotion)

99mTc-PYP; for presence & extent of damaged myocardium after MI

Uptake into infarcted tissue depends on; regional blood flow, myocardial calciumconcentration, degree of irreversible myocardial injury & time after infarction

Attaches to calcium deposited in the infarcted area;hot-spot scanning

False hot spots; necrotic myocardial tissue (detected after 4 hrs of coronaryocclusion)

Scans prior 4hrs are ve, +ve 12 hrs after

99mTc-PYP is a useful late marker of infarction


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Thallium-201 (201Tl); t ; 73 hrs; energy emitted x-ray

Thallium is a potassium analog taken up into normal myocardium by passivediffusion & active transport via Na+-K+ATPase pump.

Uptake depends on regional blood flow; high uptake occurs in perfused myocardium& vise versa

A repeat scan 4 -6 hrs after initial scan may show a redistribution; these defects arereferred to aspartial defects (areas hypoperfused during stress but viable

myocardium at rest) Areas of nil distribution are calledcold spots orfixed defects (MI)

For postop evaluation of angioplasty procedures & in conjunction with ETT (injectat ETT peak & exercise continues for another 30-60 sec


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Priniciple; CT uses series of X-rays takenfrom different directions & info presented as

cross sections of organ viewed giving 3

dimensional images (w or w out I2 dye)

Uses; determination of chamber volume, size& myocardial wall thickness, localized areas

of infarction, abnormal perfusion

Most sensitive to;

9 differentiate types of pericarditis,

9 estimate pericardial fluid volume,

9 evaluate cardiac masses

9 Calculate; EF, LVV, SV


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Principle; PET measures emissions from radioactively labeledmetabolically active chemicals, data computer processed; 2-3

dimensional images of distribution in organs.

Types of studies;

Myocardial perfusion study; (82Rb), ([13N]H3) & 15O2-

labeled H2O. Uptake of 82 Rb via Na+ K+ ATPase pump

(viable cells)

Myocardial substrate metabolism; [11C]palmitate,

[11C]acetate, and [18F]2-deoxyglucose (FDG) Fasting & PP cell metabolism (ischemic & N)

Hibernating vs infarcted (decision for angioplasty)

Uses;

9measure regional myocardial uptake of exogenous (glu & FA)

9 quantitate FFA metabolism

9 define perfused myocardium energy source(s)

Adv; non invasive, repeat scans over short time (t ;


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Priniciple; for vascular access to CA,percutaneous through brachial or femoral

artery till site then dye injected

Types of procedures;1. Lt sided catheterization; access to aorta, LV

& LA

For coronary angiography & ventriculography

2. Rt sided catheterization; coronary sinus,pulm arteries,

Determination of cardiac performance


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Prior to Procedure; fasting, D.C warfarin, heparin

(6hrs prior to procedure), ACS; UFH, LMWH,

sedatives (pt aware)

During procedure; HD, BP, HR & ECG continuousmonitoring

After procedure; pt remains still 6-8 hrs, discharged

same day or w in 24 hrs, CPK troponin elevated

Complications;9 Thrombotic (depend on)

9 Bleeding

9 Heart perforation

9 Vagal reflex w hypotension, brady cardia(atropine)

9 MI (risk; DM, UA)


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Cardiac catheterization is the GOLD standard fordiagnosis & assesment of CAD

Used w PTCA & or drug therapy in management

of ACS assessment of valvular function & computation of

cardiac performance parameters; CO, SV, SVR,

bld flow

Drug administration for;1. Thrombolytics to assess CA patency

2. VD for CP

3. Diagnosis; ergonovine for coronary spasm


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Angiographic study

Radiographic visualization of coronary

vessels after injection of radio opaque

contrast media

Angiography determines

9morphology of a stenotic lesion

9& degree of luminal obstruction

9Collateral circulation

9Dynamic; vasospasm

Extent of disease depends on; no of

vessels

75% or more; seen on angiography

50 % or >; significant marrowing40-60% ; are CA lesions prone

rupture or form thrombus

Lesions are simple or complicated

Ventriculographic study

Injection of radioopaque contrast

media into the ventricles &

determines;

9 contour of the heart

9 regional wall motion

9 filling defects

9Presence of mural thrombi


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Left coronaryLeft coronary

arteryarteryRight coronaryRight coronary

ArteryArtery

DiastoleDiastoleSystoleSystole


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Measurement of electrical activity in the heart;by Willem Einthoven

Procedure of 1st choice for evaluation of; chest pain, dizziness, or syncope

Used for; rhythm abnormalities, evaluate ischemia, monitor responses toantiarrhythmic agents or pts receiving drugs with potential cardiac effects.

ECG characterizes;9rhythms & conduction abnormalities

9by inference; info about; anatomy & structures of heart, HD of CVS

ECG abnormalities are earliest sign of ADE, ischemia & electrolyte abnormalities

ECG findings shd be correlated w clinical & pathologic states

Prior & /or serial ECGs in; pts with cardiac disease or on meds that alter ECG


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Transmembrane potential; Na+, K+, Ca++, Cl-Na+; conc & electrical gradientK+; conc gradient


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Cardiac Cycle


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Principle

ECG utilizes 12 leads which are composed of 6 limb leads & 6 precordial leads

1. Limb leadsare: I, II, III, aVR, aVL, andaVF


Lead I

Lead II Lead III

Left ArmRight Arm

Left Foot

+-

+

--

+

I +

IIIII

(0 degrees)

(60degrees)(120degrees)

++


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Principle

ECG utilizes 12 leads which are composed of 6 limb leads & 6 precordial leads



For a heart with a normalECG and a mean electricalaxis of +60, the standard

limb leads will appear asfollows:


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Principle

1. Limb leadsare: I, II, III, aVR, aVL, and

aVF

1. Limb leadsare: I, II, III, aVR, aVL, and

aVF

augmented leads use one of the electrodes as positive (lt foot, r arm, or lt arm) & other

2 electrodes as negative;

Leads Sensor used as Positive Sensors used as Negative

aVL Left Arm L. Foot and R. ArmaVR Right Arm L. Foot and L. ArmaVF Left Foot L. Arm and R. Arm

The resulting vectors appear as follows:


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Principle


1. Limb leadsare: I, II, III, aVR, aVL, andaVFaugmented leads use one of the electrodes as positive (Lt foot, Rt arm, or Lt arm) &

other 2 electrodes as negative.

aVL

aVR

aVF


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Principle




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Principle

2. Chest leadsare: V1, V2, V3, V4, V5, V62. Chest leadsare: V1, V2, V3, V4, V5, V6

TransitionalZone


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Analyzing the ECGRateRhythm

Regularity

AxisIntervals

o P wave

o PRo QRS

o QT

Morphology

o P waveo QRS


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1. Rate


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The part of the heart controlling the activationsequence

Regular

P followed byQRS

2. Rhythm & Regularity


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Irregular

No P wave

Regular


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TachycardiaWide

QRSIf P is seen:after theQRS,inverted, or

dissociated


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Normal SinusRhythm

Sinus arrhythmia

Sinus Tachycardia



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4. Axis


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4. Axis


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5. Intervals

5 I l


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5. Intervals

6 M h l


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6. Morphology

6 M h l


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6. Morohology

RBBB

LBBB


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AECG (Holter monitoring); detect & document ECG abnormalities overextended periods of time detects random abnormal cardiac electrical activity during daily activity &

relates to pt symptomatology Types;9Noninvasive; pt activated, duration; (hrs- days)9Invasive; implanted & removed later, duration; yrs uses; screening for asyptomatic ischemia limitation; analysis of xxs day to day stimulation is hard Three types of monitors are available:(a)continuous monitors; record ECG strip over test duration(b)event or intermittent recorders; continuously monitor ECG but only record

preprogrammed abnormal ECG events or are pt activated based on symptoms(pt diary); occurrence, duration & severity of symptoms + activities/interventions(c)real-time analytical recorders; record throughout the monitoring period &

analyze each beat as it occurs

cardiovascular investigation

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