skills in cv1 1

8/4/2019 Skills in CV1 1

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Physical Examination Inspection

Anatomical landmarks incardiovascular examination

Body habitus Stature Skin exam Cachectic? Obese? Gait abnormalities

Palpation Percussion Arterial pulses Jugular venous pressure

Congenital problems associated withCV disordersMarfanSyndrome

Aortic aneurysm Aortic regurgitation: classic for

Marfans Mitral regurgitation: can coexist

with AR Pt. tends to be male, tall, with

significant aortic regurgitation

Klinefelter Syndrome Tall stature, long extremities,

eunuchoid Congenital heart diseases

Ventricular septal defect Patent ductusarteriosus Tetralogy of Fallot

Gait AbnormalitiesSeen in:

Cardioembolic strokes Hypertensive CV disease Shy Drager syndrome

Degenerative disease of theautonomic nervous system

Parkinsonian gait

Body Habitus Obesity

Part of metabolic syndrome,which also has hypertension,hypercholesterolemia, diabetes.Can lead to strokes and heartattacks.

Cardiac cachexia, seen in: CHF, especially those with

chronic low output states

Respiration

CHF Orthopnea: patient needs to be

elevated with pillows whilesleeping

Cheyne Stokes respirationwith sleep apnea

COPD The blue bloater of chronic

bronchitis and pink pufferwith emphysema

Cyanosis Peripheral detected in exposed

skin (lips, nose, earlobes, andextremities)

Central cyanosis seen in thetongue, uvula, and buccalmucus membrane Intrapulmonary or

intracardiac right to leftshunting

Edema Generalized edema

Nephrotic syndrome and sepsis Heart problem or vascular

disease Dependent edema

Right heart failure Ascites in the absence of edema of

the lower extremities Liver disease, ie, cirrhosis or

hepatitis

Skin CHF

Slate or bronze pigmentation ofthe skin (hemochromatosis)

Mild jaundice Hypercholesterolemia

Arcus: white rim around iris Xanthelasma

Acute rheumatic fever Erythema marginatum (pink

rings on the trunk and innersurfaces of the arms and legs)

Subject:Physical DiagnosisTopic: Skills in CVS1Lecturer:Dr. TironaDate of Lecture:September 7, 2011

Transcriptionist: Original SinEditor:deray loverPages: 7

SY2011-2012


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Rheumatic nodules Bacterial endocarditis

Conjunctival hemorrhages,purpuric skin rash, petechiallesions, and splinterhemorrhages

Osler nodes (palms, soles of thefeet and pads of the fingers and

toes, tender and result frommicroemboli Janeway lesions (non tender,

raised hemorrhagic nodules onthe palms of the hands andsoles of the feet.

Funduscopy Hypertensive retinopathy

Grade I Minimal irregularity of the

arterial lumen and narrowing

with increased light reflex Grade II AV nicking with more

marked narrowing andirregularity of the arteriolesand distention of veins

Grade III Flame shaped hemorrhages

and fluffly cotton woolexudates

Grade IV Papilledema with another

changes from grades Ithrough III

Below: Grade II

Below: Grade III

Below: Grade IV

Inspection (see diagram on lastpage)

Anatomical landmarks Midsternal line Parasternal borders Midclavicular line Anterior axillary line Midaxillary line Posterior axillary line Suprasternal notch: visible

aortic pulsations and aortic

aneurysms may be visible here Subxiphoid area: enlargement

of left ventricle can beappreciated upon palpation

Aortic area: 2nd ICS,midclavicular line

Pulmonic area Mitral area: 5th ICS,

midclavicular line Tricuspid area: 3rd and 4th ICS

left parasternal border Point of Maximal Impulse (PMI)

5th ICS left midclavicular line In 50% of individuals, it may

not be visible. In whichcase, palpate for apex beat(next)

Apex beat Determined by palpation 5th ICS LMCL

Parasternal borders Midclavicular line

Palpation Pulsations of the heart and great

arteries are transmitted to thechest wall

Precordial movements should betimed with simultaneously palpatedcarotid pulse or auscultated heartsounds

Examination carried out with thechest completely exposed andelevated to 30 degrees

Examination of precordial pulsations Best performed in patients insupine position with head andtrunk elevated 45 degrees

Examiner positioned in the rightside of the supine patient

Rotating the patient in the leftlateral decubitus position with theleft arm elevated over the headcauses the heart to move laterally


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and increases the palpability ofboth normal and pathologicalthrusts of the left ventricle

Above: Structures that can be palpated Short arrow: aortic arc Arched arrow: pulmonary artery Straight and long arrow: left atrial

appendage Open arrows: area of left ventricle

Palpation The left ventricular impulse

Apex beat normally producedby left ventricular contractionand is the lowest and mostlateral point on the chest atwhich the cardiac impulse isappreciated

5th ICS, LMCL (left midclavicularline)

May not be palpable in thesupine position in as many ashalf of all normal subjects, apexbeat is palpable in the leftlateral decubitus position.

Abnormal Precordial Pulsations Pronounced epigastric or

subxiphoid pulsation Right ventricular failure Abdominal aortic aneurysm

A visible pulsation over the right 2nd

ICS or right sternoclavicular joint Aneursym of the ascending

aorta Suprasternal pulsation

Aneurysm of the arch of theaorta

A visible pulsation over the left 2nd

or 3rd ICS Dilated pulmonary artery

Palpation Right ventricle

Subxiphoid area Pulmonary artery

2nd ICS, LMCL (left midclavicularline)

Thrills The flat of the hand or the

fingertips usually bestappreciate thrills which arevibratory sensations that arepalpable manifestations of loudharsh murmurs having low tomedium frequency componentsseen in stenotic valves.

Percussion Palpation is far more helpful than is

percussion in determining cardiacsize

Useful in the absence of apicalsystolic beat Pericardial effusion Dilated cardiomyopathy Heart failure Marked displacement of the

hypokinetic apical beat Percussion carried out from mid to

lateral or vice versa within theintercostals spaces

Normal cardiac area of dullness iswithin 10 cm from midsternal lineto the lowest most lateral border ofthe heart

Examination of the arterial pulse Arterial pulses

Carotid: do one at a time

please lest the patient shouldfaint or stroke

Brachial, radial, and ulnar Femoral, popliteal,

posterialtibial, and dorsalispedis(absent 40% of the time)

Assess Rigidity and elasticity of the

arteries Done by rolling the vessel under

underlying tissue The more rigid the artery,

the less compressible

Arterial pulses rate and rhythm Arrhythmias

Sinus bradycardia, junctionalrhythm, complete AV block

Ventricular premature beats Bigeminies

Atrial fibrillation Irregularly irregular pulses

Arterial pulses: variations in thecharacter of the pulse

Pulsusalterans Alternating strong and weak

pulses in the presence of aregular pulse

Commonly caused by leftventricular systolic failure

Other causes: Aortic stenosis


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Hypertrophic obstructivecardiomyopathy

Ischemia Pulsusparadoxus

Substantial reduction in theamplitude of the pulse duringinspiration

Inspiratory decrease in arterialpressure exceeding 12 to 15mmHg

Causes: Cardiac tamponade COPD Rarely in PE, pregnancy,

marked obesity, partialobstruction of the SVC.

Above:A: Normal. Brisk and rapid upstroke thatoccurs at systole.Dicrotic notchrepresents aortic valve closure.B: Aortic stenosis. Because the aorticvalve does not open up all the way, thereis a delay in the upstroke and theamplitude of the stroke is diminished.

They pulse is delayed and weak, hence,pulsustardus.C: Aortic regurgitation:pulsusbisferiens. There are 2 systolicpeaks.D: Hypertrophic cardiomyopathy: Alsoexhibiting pulsusbisferiens duringsystole, but lower in amplitude than withAR.E: Chronic heart failure: 2 peaks, one insystole and one in diastole.

Above: Pulsusalternans: Alternating

strong and weak pulses. Pulsusparadoxus: substantial

reduction in the amplitude of thepulse during inspiration. It iselicited using asphygmomanometer. Take not ofthe 1stKorotkoff sound. Thereshouldnt be an inspiratorydecrease of >10 mmHg. If there is>10mmHg decrease during normalrespiration that is a (+)pulsusparadoxus. Seen in cardiactamponade, severe COPD,sometimes pulmonary embolismand pregnancy or partialobstruction of SVC.

Arterial Pulses Changes in Contour Pulsustardus

Delayed upstroke in theascending limb of the carotidpulse

Aortic stenosis


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Pulsusparvus Aortic stenosis Small amplitude pulse

Pulsusbisferiens Presence of 2 positive impulses

near the peak of the arterialpulse Aortic regurgitation

Altered Characteristic of the ArterialPulse and their Clinical Significance

Pulsusalternans Suspect acute or chronic

reduction in left ventricularsystolic function

Pulsustardus Suspect fixed left ventricular

outflow tract obstruction suchas valvular aortic stenosis

Pulsusbisferiens Suspect aortic regurgitation,

large PDA, HOCM, completeheart block, hyperkinetic heart

syndrome Pulsusparadoxus

Suspect tamponade,emphysema

Dicrotic pulse Suspect low output syndrome

with increased systemicvascular resistance

Commonly seen in patients withsevere heart failure.

Sign characteristic of severe aortic

regurgitation Corrigan or Water hammer pulse

Abrupt upstroke followed byrapid collapse

Traube sign Pistol shot sounds heard over

the femoral artery when thestethoscope is placed on it

Duroziez sign

Systolic murmur heard over thefemoral artery when the arteryis compressed proximally; adiastolic murmur heard whenthe artery is compresseddistally

Quincke sign Phasic blanching of the nailbeds

Hill sign Systolic pressure in the lower

extremity exceed that in thearms by more than 20 mm Hg

Becker sign Visible pulsations of the retinal

arterioles Mueller sign

Pulsating uvula

Examination of the Jugular venouspulse and pressure

Essential to assess hemodynamicchanges in the right side of theheart

Done with the patient in a 45degree semirecumbent position

IJV pulse located medial to themandibular portion of thesternocleidomastoid muscle

IJV is valveless so is morerepresentative of right atrialpressure than EJV, which has avalve.

Difference between venous andcarotid artery pulsation

Venous pulse Sharp inward movement Double undulation character

during sinus rhythm Gentle compression obliterates

the venous pulse Venous pulse amplitude

decreases on inspiration Carotid arterial pulse

Sharp outward movement Arterial pulse remain visible on

gentle compression Arterial pulse amplitude does

not change on respiration

JVP Normal right atrial pressure is 9 cm

of water

Jugular venous pulse waverecordings

Take note of the uppermost visiblepulsation of the jugular vein and thelandmark used is the sternal angle ofLouis. The measurement that is obtainedwill have 5 cm added to it. (eg,measurement obtained is 3 cm3cm +5cm = 8cm).

Positive waves A wave


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Caused by transmitted rightatrial pressure to the jugularveins during right atrialsystole

Cannon waves seen incomplete heart block

C wave Recognized with the onset of

right ventricular systole andoccurs from bulging of thetricuspid valve into the rightatrium

V wave Caused by the rise of in right

atrial and jugular venouspressure due to continuedinflow of blood to the venoussystem during rightventricular systole when thetricuspid valve is still closed

Tricuspid regurgitation Negative waves X descent Results from right atrial

relaxation Prominent in patients with

cardiac tamponade Y descent Caused by opening of the

tricuspid valve and the rapidflow of blood from the rightatrium to the right ventricle

Rapid and deep in patientswith constrictive pericarditis Kussmaul sign Increase in JVP during

inspiration Seen in: Constrictive pericarditis Right ventricular

infarction Severe right heart failure

Hepatojugular Reflux Test With the patient breathing

normally in the semirecumbentposition, firm pressure is applied

with the palm of the hand to theRUQ of the abdomen for at least 10seconds

Normal patients exhibit slightincrease in JVP with rapid return tobaseline in less than 10 seconds

The abnormal hepatojugular refluxis defined when there is a rapidincrease in JVP that remainselevated by 4 cm or more untilabdominal compression isreleased.

Abnormalities of the venous pressureand pulse and their clinicalsignificance

Positive hepatojugular reflex Suspect CHF, particularly left

ventricular dysfunction Elevated systemic venous pressure

without obvious X or Y descent andquiet precordium andpulsusparadoxus Suspect cardiac tamponade

Elevated systemic venous pressurewith sharp Y descent, Kussmaulsign, and quiet precordium Suspect constrictive pericarditis

because right ventricle is so stiffso it gives rise to a sharp Ydescent.

A prominent A wave with orwithout elevation of mean systemicvenous pressure Exclude tricuspid stenosis, right

ventricular hypertrophy due topulmonary stenosis, andpulmonary hypertension

A prominent V wave with a sharp Y

descent Suspect tricuspid regurgitation Sometimes in severe tricuspid

regurgitation there will bemerging of the C and V wavesto create a CV wave.


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Above: Landmarks__________________________________________________________________________________

End of transcription

skills in cv1 1

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