Ebook Tips and tricks of bedside cardiology (first edition): Part 2

(BQ) Part 2 book Tips and tricks of bedside cardiology presents the following contents: Exertional dyspnea, cyanosis and fainting, fever with chills and petechial spots; exertional dyspnea and sudden hemiparesis; retrosternal discomfort upon climbing stairs; recent increase in angina frequency;...

Patient Profile

Chief Complaints

• Progressively increasing dyspnea on exertion for the last 1 year

• Coldness of hands and blueness of fingers since 3 months

• Fainting on 2 occasions in the preceding 1 month

• No pallor or jaundice or ankle edema

• Cyanosis and clubbing of the finger-nails

• Pulse: 88 BP: 104/ 70 Temp.: 98 Resp.: 24

• Pulse: regular, low in volume and feeble

• JVP: 5 cm above angle of Louis at 45 degrees

Prominent ‘a’ wave observed

• CVS: Normal apex beat, sustained left parasternal heave

Systolic pulsations visible in the pulmonary area

S1 normal, P2 loud and audible upto the apex

No S3 or S4 gallop sound heard

Gr II /VI soft systolic murmur adjacent to the sternum

• Chest: clear on auscultation, no rhonchi or crepts

Exertional Dyspnea, Cyanosis and Fainting 30

Case

An ECG was obtained.

ECG Findings:

• Tall R wave in leads V1 to V3

• Deep S wave in leads V4 to V6

• Peaked P wave; P pulmonale

An X-RAY was also ordered

X-RAY Findings:

• Right ventricular enlargement

Exertional Dyspnea, Cyanosis and Fainting 119

• Prominent pulmonary artery

• Normal pulmonary vasculature

• Causes of pulmonary hypertension are:

– Increased pulmonary flow

lt to rt shunt; ASD, VSD, PDA

– Raised left atrial pressure

mitral valve disease, LV dysfunction

– Chronic pulmonary disease

bronchitis, emphysema, fibrosis

– Obstruction to pulmonary flow

thromboembolic, veno occlusive

– Primary pulmonary hypertension.

• In pulmonary hypertension due to Eisenmenger complex with left- right shunt, chest X-ray features are RV hypertrophy, prominentpulmonary artery and increased pulmonary blood flow (pulmonaryplethora) In mitral valve disease, there is straightening of the left heart

to-border due to prominent left atrial appendage In chronic pulmonarydisease the bronchovascular markings are accentuated and there ispulmonary emphysema.

Clinical Pearls

• The presence of cyanosis indicates the presence of chronic lungdisease or a right-to-left cardiac shunt In primary pulmonaryhypertension, cyanosis is caused by right-to-left shunt across a patentforamen ovale

• A prominent ‘a’ wave in the jugular venous pulse indicates right atrialcontraction against a noncompliant hypertrophic right ventricle It isobserved in both pulmonary stenosis as well as in pulmonaryhypertension

• A sustained heave on palpation in the left parasternal area indicatesthe presence of right ventricular hypertrophy It is also observed inpulmonary stenosis

• A loud pulmonary component (P2) of the second heart sound (S2) is aclassical indicator of pulmonary hypertension In pulmonary stenosis,the P2 is muffled The fact that the P2 is heard even at the cardiac apex is

in itself indicative of pulmonary hypertension

• Prominent systolic pulsations felt with a soft systolic murmur heard inthe second left intercostal space adjacent to the sternum (pulmonaryarea), indicates dilatation of the main pulmonary artery

Patient Profile

Chief Complaints

• High grade fever with chills for the past 10 days

• Malaise, arthralgias, anorexia and weight loss

• Ill-looking, toxic, restless and tachypneic

• Petechiae under finger-nails (Splinter hemorrhages)

• Painful nodules on the finger-tips (Osler nodes)

• Hemorrhages on thenar eminences (Janeway lesions)

• Subconjunctival petechiae in both eyes (Roth spots)

• Pulse: 104 BP: 110/ 60 Temp.: 100.8 Resp.: 24

• CVS: Normal precordium, heaving apex beat

S1 loud, ejection click +, high pitched S2, no S3 sound

Gr II /VI ejection systolic murmur, left sternal border

• Chest: normal sounds; no rhonchi or crepts

• Abdo.: no hepatosplenomegaly or ascites

An ECHO was performed

Fever with Chills & Petechial Spots 31

Case

ECHO Finding:

• Nodular echo-reflective masses,

attached to the aortic leaflets

Lab Investigations

• Blood counts: Hb 8.8, TLC 13800, N83 L15, ESR 52

• Biochemistry: Glucose 78, Urea 32, Creatinine 1.1,

ASLO titer 220 IU, CRP level 80 mg/ LBilirubin 2.2, SGOT 42, SGPT 48Cholesterol 178, LDL 110, TSH 2.2

• Bacteriology: Throat swab culture: no growth

Blood culture grew Streptococcus viridans

Fever with Chills & Petechial Spots 123 Diagnosis

AORTIC VALVE ENDOCARDITIS

Discussion

• Endocarditis is inflammation of the inner surface of the heart, includingthe lining of heart valves Inflammatory and infected materialaccumulates to cause discrete lesions called vegetations Vegetationsare made up of tissue debris fibrin, platelets and leukocytes

• Endocarditis may be caused by an infective pathogen or due to anoninfective disease:

Infective causes:

– Bacterial : Streptococcus, Staphylococcus

– Fungal : Aspergillus, Candida

– Others : Coxiella, Chlamydia

Noninfective causes

– Malignant disease : Marantic endocarditis

– Collagen disorder : Libman-Sacks endocarditis

– Rheumatic fever : Rheumatic pancarditis

• On echo, vegetations appear as mobile, irregular echoreflective massesattached to a valve cusp or a cardiac shunt The valve may be native orprosthetic and is usually a left- sided mitral or aortic valve

• Vegetations vary in size from few mm to several cm Those less than

2 mm in size are difficult to visualize Large vegetations are associatedwith fungal or tricuspid endocarditis They shrink as they heal althoughrapid shrinkage is indicative of embolization

• Vegetations move in concert with the leaflet, and do not impair itsexcursion They may be sessile (nodular) or pedunculated and irregular

or smooth Fresh vegetations are lumpy but they smoothen as they heal.Fresh vegetations are isoechoic with the leaflet but they get brighter asthey heal

Clinical Pearls

• In the clinical setting of rapid onset of dyspnea and palpitation with afebrile illness, an infectious process must be considered Acute rheumaticfever and subacute bacterial endocarditis are the main possibilities Anacute viral pericarditis or myocarditis or pneumonitis must also beexcluded

• The indications for performing serial echoes in endocarditis are:– diagnosis of vegetations

– looking for complications

– detecting predisposing lesion

– evaluating response to treatment

– timing of surgical intervention

• Endocarditis can lead to valve destruction, valvular regurgitation,appearance of a new murmur or change in a preexisting murmur Thisoccurs due to prolapse, perforation or rupture of a valve leaflet Therecan be abscess formation around a valve ring or in the interventricularseptum which can cause conduction block

• Healed vegetations differ from fresh ones by being smaller, smootherand hyperechoic Shrinkage of vegetations alone does not indicate curewhile rapid shrinkage suggests embolization Increase in vegetation sizeindicates persistence of infection and ineffective antimicrobial therapy.The risk of embolization persists for as long as 6 months even afterbacteriological cure

• How often serial echos should be done while the patient is receivingantibiotics is a matter of debate It is difficult to justify frequent echosunless this will clearly alter clinical decisions in management However,repeat echo should be definitely carried out if there is deterioration inthe patient’s clinical condition

Patient Profile

Chief Complaints

• High-grade fever with chills and night sweats for 3 weeks

• Malaise, easy fatigability, anorexia and 6 kg unintentional weight loss

• Mild breathlessness on physical exertion for the same duration

Relevant History

• No history of cough, hemoptysis or chest pain

• No urinary complaints or altered bowel habits

• No history of orthopnea, nocturnal dyspnea or palpitation

• He was a college drop-out who was presently not engaged inany gainful employment

• He admitted to be a smoker and alcoholic on a regular basis

• On further questioning he confessed having taken drug-snortsand intravenous injections of illicit drugs, once in a while

Physical Examination

• Drowsy, confused and slightly dyspneic

• Multiple needle-prick marks on forearms

• Neck veins distended; mild pedal edema

• Moderate anemia, mild jaundice, no cyanosis

• Pulse: 106 BP: 104/ 70 Temp.: 101.6 Resp.: 24

• CVS: Pansystolic murmur in parasternal area

No gallop sound or pericardial rub heard

• Chest: normal breathing, few rhonchi/crepts

• Abdo.: hepatomegaly with jugular reflux;

no ascites or splenomegaly

An ECHO was performed

Fever with Chills

& Illicit Drug Abuse 32

Case

ECHO Finding:

• Rounded mass in the right atrium,

prolapsing into tricuspid valve

Lab Investigations

• Blood counts: Hb 9.2, TLC 14600, N78L21, ESR 48

• Urinalysis: Albumin +1, WBCs 2-3, RBCs nil

• Biochemistry: Glucose 86, Urea 38, Creatinine 1.2,

Cholesterol 158, SGOT 24, SGPT 28ASLO titer 180 IU, CRP level 79 mg

• Bacteriology: Staph epidermidis grown in 2 out of 3

blood culture bottles

Throat swab culture: no growth

Fever with Chills & Illicit Drug Abuse 127 Diagnosis

TRICUSPID VALVE ENDOCARDITIS

Discussion

• Endocarditis related to intravenous drug abuse is drastically differentfrom endocarditis due to other causes in terms of clinical picture,bacteriology and prognosis

• Staphylococcal species introduced by contaminated needles from theskin into the venous system, is the most common causative organism inthis variety of endocarditis In most other forms of endocarditis,

Streptococcus viridans is the predominant pathogen

• Septic pulmonary embolism is a consequence of right- sided endocarditiswhile systemic embolism occurs in left- sided endocarditis These embolican turn into lung abscesses, if inadequately treated Septic emboli aretreated with antimicrobials and not anticoagulants

Clinical Pearls

• Tricuspid valve involvement occurs in the majority of drug-abuse relatedendocarditis and is rare in non-addicts Besides intravenous drug-abuse,other portals of entry of bacterial contaminants into the right side of theheart are an indwelling Swan-Ganz venous line or a right ventricularpacing lead

• Metastasis from renal cell carcinoma can spread along the inferior venacava to gain access into the right atrium They give a characteristic

“pop- corn on string” appearance Right atrial myxomas are relativelyrare Other rare right atrial masses are congenital remnant of the Chiarinetwork and Eustachian valve guarding the inferior vena cava

• Right-sided endocarditis is associated with a much lower mortality than

is left-sided endocarditis On appropriate therapy, the survival rate is ashigh as 90%

Patient Profile

Chief Complaints

• Fatigue, joint pains, malaise and low-grade fever for 6 months

• Unintentional weight-loss of 5 kg in the preceding 3 months

• Occasional breathlessness on exertion and fainting spells

• Sudden onset of blueness in the left hand noticed 2 days back

Relevant History

• She gave no history of chills or rigors

• She was not orthopneic and denied nocturnal dyspnea

• There was no history of cyanotic spells or squatting attacks during herearly childhood

• There was neither a history of joint pains nor prolonged fever

• She denied smoking tobacco, alcohol intake or illicit drug abuse

Physical Examination

• Mild pallor, slightly dyspneic, not in pain or distress

• Weak left radial pulse, cold hand, cyanotic fingertips

• Pulse: 92 BP: 130/ 80 Temp.: 99.6 Resp.: 22

• CVS: Low-pitched diastolic murmur in mitral area

S1 and S2 normal; high-pitched S3 audible

• Chest: clear on auscultation

An ECHO was performed

Constitutional Symptoms & Sudden Hand Cyanosis 33

Case

ECHO Findings:

• A Rounded mass in the left atrium

• B Prolapse into mitral valve orifice

Lab Investigations

• Blood counts: Hb 9.6, TLC 11200, N74 L23, ESR 52

• Urinalysis: Albumin +, RBCs nil, WBCs nil

• Biochemistry: Glucose 78, Urea 28, Albumin 3.8, Globulin 4.2,

SGOT 32, SGPT 42, ASLO < 200, CRP < 10

• Bacteriology: Blood culture : sterile

Throat swab : no growth

Constitutional Symptoms & Sudden Hand Cyanosis 131 Diagnosis

LEFT ATRIAL MYXOMA

PERIPHERAL EMBOLISM

Discussion

• Myxoma is a gelatinous and friable cardiac tumor of connective tissueorigin It is mostly single and occurs three times more often in the leftatrium than in the right atrium It is commonly seen in middle-agedwomen Although benign in the neoplastic sense, myxoma is far frombeing benign in its clinical effects

• Effects of left atrial myxoma relate to:

– Valvular obstruction: breathlessness and palpitation

– Peripheral embolism: bits of friable tissue breaking away

– Constitutional symptoms: fever, arthralgias and weight loss– Inflammatory features: anemia, leukocytosis and high ESR

• On 2- D echo, the myxoma is seen as a mass in the left atrial cavity It is 2

to 8 cm in size usually pedunculated, rarely sessile and attached to themargin of foramen ovale It is a lobulated mass of variable echodensity;the center is echolucent due to necrosis and the periphery is echo-reflectivedue to calcification Most myxomas are mobile and prolapse into themitral valve orifice in diastole An atrial myxoma is nonprolapsing if it iseither sessile or too large in size

• Since the extent of prolapse of the myxoma into the mitral valve inflowtract varies with posture, the 2- D, M- mode and Doppler findings willchange significantly, with the patient’s position

Clinical Pearls

• Left atrial myxoma needs to be differentiated from a thrombus at this site.Unlike a myxoma, LA thrombus is close to the LA posterior wall, notpedunculated and stays in the atrial cavity without prolapsing It isrounded in shape with a more echogenic center and the mitral valve isdiseased

Differences between LA thrombus and LA myxoma

LA thrombus LA myxoma

Left atrial myxoma is a masquerader of several clinical entities:

• On the basis of 2- D echo, myxoma needs to be differentiated from aleft atrial thrombus On M- mode, myxoma resembles mitral stenosisfrom which it can be differentiated by an early echo-free zone

• When the myxoma prolapses into the mitral valve, the auscultatoryfindings resemble those of mitral stenosis A mid-diastolic murmurpreceded by a ‘tumor plop’ resembles an opening snap followed by adiastolic rumble

• The constitutional features of myxoma such as fever, arthralgia andanemia need to be differentiated from those due to other clinicalconditions including bacterial endocarditis, collagen disorder andoccult malignancy

Patient Profile

Chief Complaints

• Sudden onset of weakness of the right-sided limbs 6 hours back

• Long-standing fatigability, exertional dyspnea and orthopnea

• Episodic palpitation with dizziness and occasional fainting spells

Relevant History

• No recent febrile illness, ear-discharge or trauma to the head

• No history of cyanotic spells or squatting attacks in childhood

• She admitted having had sore throat requiring medication repeatedlyduring her schooling years

• She was incapacitated with joint pains for 1 month at age 14

• Her daily medication included digoxin 0.25 mg and furosemide 40 mg

• She had also received monthly shots of injectable penicillin until theage of 30 years

Physical Examination

• Pallor, mild tachypnea, anxious appearance

• Pulse: 110 BP: 106/ 70 Temp.: 98.4 Resp.: 18

• Pulse: irregular, low in volume

• JVP: raised, Thyroid: normal, Edema: mild

• CVS: Rumbling diastolic murmur in mitral area

S1 variable, P2 loud, no S3 heard

• Chest: scattered basilar rales bilaterally

• CNS: right- sided hemiparesis; power Gr II/ V

An ECHO was performed

Exertional Dyspnea & Sudden Hemiparesis 34

Case

ECHO Findings:

• Thickened mitral valve leaflets

• Diastolic doming anterior leaflet

• Restricted opening of valve

• Dilatation of the left atrium

Lab Investigations

• Blood counts: Hb 10.8, TLC 8800, ESR 22

• Urinalysis: Albumin nil, no RBCs or WBCs

• Biochemistry: ASLO titer & CRP level normal

• Bacteriology: Blood culture : sterile

Throat swab : no growth

Exertional Dyspnea & Sudden Hemiparesis 135 Diagnosis

MITRAL STENOSIS

LEFT ATRIAL THROMBUS

CEREBRAL EMBOLISM

Discussion

• A stenotic mitral valve with a dilated left atrium, especially in the presence

of atrial fibrillation, is an ideal setting for the formation of a left atrialthrombus

• The thrombus appears as a well-defined rounded mass arising from theposterior atrial wall or floating freely A thrombus in the atrial appendagecan only be identified by transesophageal echo (TEE)

• Besides a thrombus, other causes of a mass in the left atrium are an atrialmyxoma, a dilated coronary sinus and a flail mitral leaflet Linearstructures rarely seen in the left atrium are supravalvular ring, cortriatriumand anomalous pulmonary veins

Differences between LA thrombus and LA myxoma

LA thrombus LA myxoma

Clinical Pearls

• The risk of thromboembolism in mitral stenosis is very high, particularly

if atrial fibrillation is present and more so if it is intermittent Mitralstenosis can be safely assumed to be the cause of cerebral infarction even

if a left atrial thrombus is not demonstrable

• A thrombus that is too small for detection, thrombus in the atrialappendage or one that has already embolized may be missed on echo Insuch patients anticoagulants can be initiated rightaway provided there

is no systemic contraindication and cerebral hemorrhage has beenexcluded by a cranial CT scan

• Occasionally, an echo may show a large left atrial ball thrombus which ispotentially fatal if it suddenly obstructs the mitral valve Such a

‘ball- valve’ thrombus is an indication for urgent surgical intervention

Patient Profile

Chief Complaints

• Severe retrosternal discomfort of 4 hours duration, 4 days back

• Associated suffocation, choking, profuse sweating and dizziness

a strong family history of coronary artery disease

• He did not restrict his dietary caloric intake, led a sedentary life withoutexercise and had a particularly stressful job

• He denied any past history of dyspnea, palpitation or syncope

Physical Examination

• Pulse: 104 BP: 100/ 60 Temp.: 98.8 Resp.: 24

• Pulse: fast and regular, low and variable volume

• JVP : raised 4 cm above angle of Louis at 30 degrees

• CVS: Apical impulse diffuse, double and displaced

S1 loud, S2 normal, S3 gallop appreciated

No murmur or pericardial rub audible

• Chest: few basilar crepts over lower lung-fields

An ECHO was performed

Displaced & Diffuse

Apical Impulse 35

Case

ECHO Findings as:

• Pedunculated mass protruding into

the left ventricular cavity

• Dyskinesia of the apical IV septum and LV apex

Displaced & Diffuse Apical Impulse 139 Diagnosis

• A pedunculated ventricular thrombus appears as a well-defined roundedmobile stalked mass, that protrudes into the ventricular cavity Themobility of the thrombus is not synchronous with the left ventricular freewall

• A mural ventricular thrombus is a flat, laminated mass, contagious withthe ventricular wall with which it moves synchronously It is moreechogenic than the adjacent myocardium and less likely to embolize

• Thrombus always has a clear identifiable edge while an artefact caused

by stagnated blood has a hazy appearance On color flow mapping, theflow stops abruptly at the edge of a thrombus but not at the edge of anartefact

Clinical Pearls

Left ventricular thrombus is a masquerader of several other mass lesions:

• Other causes of a mass in the left ventricle are rhabdomyoma, falsetendon and prominent papillary muscle

• Mural thrombus can be distinguished from localized myocardialthickening since myocardium thickens during systole while athrombus does not

• Thrombus can be differentiated from a cardiac tumor by the fact thatadjacent wall motion is almost always abnormal in case of thrombusand often normal in case of tumor

Indications for Echo in stroke patients are:

• Young patient (< 50 years) with cerebral infarction

• Older patient (> 50 years) without cerebrovascular disease

or an obvious cause of CVA (TIA/ stroke)

• Strong clinical suspicion of cardiac embolism

e.g recurrent peripheral or cerebral embolic events

• Clinical evidence of structural heart disease, e.g

mitral stenosis, or dilated left ventricle

• Clinical suggestion of conditions causing embolism,

e.g bacterial endocarditis or left atrial myxoma

• Abnormal ECG indicating underlying heart disease,

e.g Q waves, loss of R waves or ST-T changes and arrhythmias such

as atrial fibrillation and ventricular tachycardia

• He denied pain at rest or nocturnal pain and the typical discomfort hadnot increased in frequency, severity or duration since 1 year.

• He had smoked one pack of cigarettes per day for the last 20 years andhad a strong family history of premature coronary artery disease aswell as of diabetes mellitus

• He had no history of hypertension and had never undergone a serumlipid profile analysis

• His job entailed long working hours and high level of mental stress

Physical Examination

• Pulse: 82 BP: 130/ 80 Temp.: 98.4 Resp.: 16

• Pulse: regular, average in volume, normal character

• JVP: not raised, Thyroid: normal, Ankle edema: nil

• CVS: Normal precordium and apex beat location

S1 and S2 normal; no S3, S4 gallop or murmur

• Chest: normal breath sounds; no rhonchi or crepts

An ECG was obtained:

Retrosternal Discomfort upon Climbing Stairs 36

Case

ECG Findings:

• S-T depression in leads V4, V5 and V6

• T wave inversion in leads V5 and V6

Lab Investigations

• Blood counts: Hb 12.4, TLC 7200, N63 L37, ESR 12

• Urinalysis: Albumin traces, RBCs and WBCs nil

• Biochemistry: Glucose 98, Urea 24, Creatinine 0.9,

Uric acid 6.7, SGOT 21, SGPT 28CRP 4.8, CPK 92, CPK (MB) 4Cholesterol 224, LDL 134, HDL 36Triglyceride 220, VLDL 44

Retrosternal Discomfort upon Climbing Stairs 143 Diagnosis

CORONARY ARTERY DISEASE (CAD)

CHRONIC STABLE ANGINA (CSA)

Discussion

• Coronary artery disease is the most important cause of S-T segmentdepression The degree of S-T segment depression (greater than 1 mm)correlates with the severity of coronary insufficiency

• Besides being depressed, the morphology of the S-T segment withincreasing severity of myocardial ischemia, can be classified as:

A Isolated J point depression (upsloping S-T segment)

B Horizontality of S-T segment (sharp ST-T junction)

C Plane S-T depression (horizontal S-T depression)

D Sagging depression (hammock- like S-T segment)

• Depression of the S-T segment constitutes the most useful criterion for thepositivity of the exercise ECG test (stress test) using a treadmill or bicycleegometer The degree of positivity of the stress test (mild, moderate orsevere) can be gauged from these parameters of S-T segment depression:– Onset during exercise and duration into recovery

– Magnitude and nature of S-T segment depression

Clinical Pearls

• Angina pectoris is described as a feeling of retrosternal heaviness ortightness with a sensation of suffocation or choking The pain is of acrushing or squeezing nature along with restlessness, sweating,palpitation, shortness of breath or extreme weakness The pain mayradiate to both shoulders and arms, down the inner aspect of left arm or

to the neck and lower jaw

• Pain arising from the musculoskeletal system of the chest is described as

a dull ache or a sharp pricking sensation The pain increases on deepinspiration, turning to one side or on bending forwards The pattern ofradiation and accompaniments that characterize angina pectoris aretypically absent

• Conventional risk factors for coronary artery disease are:

– Physical inactivity – Mental stress

• Non-conventional risk factors are elevated levels of:

– C- reactive protein [hs CRP]

– Lipoprotein (a)[Lp(a)]

– Homocysteine

– Fibrinogen

• Over the preceding 2 weeks, his angina had become unstable with increase

in frequency, severity and duration of episodes He also admitted havingpost-prandial and nocturnal chest discomfort

• Patient had smoked 15 to 20 cigarettes per day for the last 24 years andhad a strong family history of premature coronary artery disease aswell as of diabetes mellitus

Physical Examination

• Mild distress, tachypneic, sweating +

• Yellow-colored papules around the eye lids (xanthelasma)

• Purple-black velvety areas in the neck- creases (acanthosis nigricans)

• Pulse: 92 BP: 160/ 96 Temp.: 99 Resp.: 20

• Pulse: irregular, missed- beats, bounding in character

• JVP: not raised, Thyroid: normal, Pedal edema: nil

• CVS: Normal precordium and apex beat location

S1 and S2 normal; no S3, S4 gallop or murmur

• Chest: few crackles over basal lung fields

An ECG was obtained

Recent Increase in Angina Frequency 37

Case

ECG Findings:

• S-T segment coving and depression

• Symmetrical inversion of the T wave

Lab Investigations

• Biochemistry: Glucose(fasting) 166, Urea 38, Creatinine 1.3,

Uric acid 7.8, HbA1c 9.2, MAUria 240/ 24 hrsCPK 480, CPK (MB) 64, Troponin T +veCholesterol 244, LDL 158, HDL 42,Triglyceride 220, Lp(a) 48, CRP 4.8

Recent Increase in Angina Frequency 147 Diagnosis

NON ST-ELEVATION MYOCARDIAL INFARCTION

(NSTEMI)

Discussion

• Coronary artery disease causing myocardial ischemia or infarction is themost important cause of T wave inversion Acute coronary insufficiencyproduces coving (convexity) of the S-T segment and T wave inversion Innon-Q myocardial infarction, a similar ST-T pattern is observed

• The two conditions can be differentiated by the fact that in acute coronaryinsufficiency, the chest pain is of short duration, cardiac enzyme titers(CPK, SGOT) are normal and the ECG changes rapidly revert to normal

In non- Q myocardial infarction, there is history of prolonged chest pain,cardiac enzymes levels are raised and the ECG changes persist for alonger period

• Non- Q wave myocardial infarction is also referred to as subendocardialinfarction, non- ST- elevation MI or NSTEMI Thrombolytic therapy isstandard treatment for ST- elevation MI (STEMI), but contraindicated inNSTEMI

• Predictors of increased mortality after non-Q MI are:

– Recurrent post-hospitalization after angina

– Persistent S-T segment depression

– High titers of cardiac enzymes

– Serious ventricular arrhythmias

– Hemodynamic instability

Clinical Pearls

On echocardiography, the systolic inward motion of the ischemic orinfarcted myocardial segment is reduced in extent, altogether absent oreven paradoxically outward The regional wall motion abnormality can

be classified as:

• Normal motion : full inward motion

• Hypokinesia : < 50% inward motion

• Akinesia : no inward motion

• Dyskinesia : outward movement

• Aneurysmal : outpouching of wall

From the location of the regional wall motion abnormality (RWMA),

it is possible to identify the occluded coronary artery

• He was markedly obese and also diagnosed to have systemic hypertensionand diabetes mellitus However, he was irregular with his medicationand did not follow-up with his doctor periodically.

• He did not undergo a blood lipid analysis, despite requests from hisdoctor and wife A treadmill test done over a year earlier was inconclusivesince he had failed to achieve the target heart rate

• Patient led a sedentary life without any physical exercise or dietary triction Recently he had been complaining of frequent bouts of

res-‘indigestion’ which in retrospect, appeared to be attributable tomyocardial ischemia

Physical Examination

• In distress, diaphoretic and mildly tachypneic

• Pulse: 104 BP: 104/ 74 Temp.: 99.4 Resp.: 24

• Pulse: irregular, “skipped- beats”, low in volume

• JVP: normal, Thyroid: not enlarged, Edema: nil

• CVS: Precordium and apex beat unremarkable

S1 and S2 normal; soft S3 gallop audible

Gr II /VI systolic murmur at cardiac apex

• Chest: crepts over lower- third of lung fields

An ECG was obtained

Severe Chest Pain, Sweating and Sinking 38

Case

ECG Findings:

• S-T segment elevation in leads LII, LIII and aVF

• Reciprocal S-T depression in leads LI and aVL

Lab Investigations

• Biochemistry: Glucose(F) 144, HbA1c 9.4, Creatinine 1.6

Troponin T +ve, CPK 1840, CPK (MB) 357Cholesterol 264, LDL 148, HDL 38Triglyceride 290, Lp(a) 66, CRP 6.8

Severe Chest Pain, Sweating and Sinking 151 Diagnosis

ST-ELEVATION MYOCARDIAL INFARCTION

(STEMI)

Discussion

• In the hyperacute phase of myocardial infarction, there is S-T segmentelevation (convex upwards) along with tall T waves, the proximal limb ofthe T wave blending with the elevated S-T segment This phase is followed

by serial evolution of ECG changes with appearance of Q waves, settlingdown of the S-T segment and inversion of the T waves Because ofmyocardial necrosis due to coronary occlusion, the serum levels of cardiacenzymes (CPK, SGOT) are raised

• The phases of acute myocardial infarction are:

of cardiac enzymes are not raised as there is no myocardial necrosis

Location of Q wave Area of infarction

V1-6LIaVL Extensive anterior

LIILIIIaVF Inferior

Clinical Pearls

• Q-Wave myocardial infarction is also referred to as transmural infarction,ST- elevation MI or STEMI Thrombolytic therapy or primary angioplasty

is standard treatment for STEMI

• Myocardial infarction results in a central necrotic core surrounded by azone of injury and skirted by a water- shed area of myocardial ischemia.These areas form the pathological basis of ECG changes observed in MI

• The location of myocardial infarction can be identified from the ECGleads showing the classical changes

thrombo-• On the 5th day of admission, he became breathless and was unable tolie flat in bed An observant resident doctor detected a new murmur.

Physical Examination

• Apprehensive, diaphoretic and mildly dyspneic

• Extremities cold, clammy and pale in color

• No anemia, cyanosis, jaundice or edema

• Pulse: fast and regular, low in volume

• Pulse: 104, BP: 104/ 76, Temp.: 98.8, Resp.: 22

• CVS: Normal precordium and apex beat location

S1 and S2 normal, no S3 gallop or rub audible

Gr III /VI pansystolic murmur along left sternal border

Radiation of murmur towards right side of chest

• Chest: few crackles over lower lung fields

An ECG was obtained

Myocardial Infarction & New Murmur on Day 5 39

Case

ECG Findings:

• QS in V1 to V4; qR in V5 to V6

• Coving of the S-T segment

• Symmetrical T wave inversion

An ECHO was also performed

ECHO Findings:

• Color flow map across interventricular septum

• Hypokinesia of the mid and apical IV septum

Myocardial Infarction & New Murmur on Day 5 155 Diagnosis

MYOCARDIAL INFARCTION

VENTRICULAR SEPTAL RUPTURE

Discussion

• After acute myocardial infarction, causes of a new murmur are:

– Papillary muscle dysfunction

– Papillary muscle rupture

– Ventricular septal rupture

• A breach in the continuity of the interventricular septum (IVS) followingacute myocardial infarction (AMI) leads to an acquired ventricular septaldefect (VSD) Septal rupture usually occurs in the first week after infarctionand may occur after anterior or inferior wall MI It is commonly locatedclose to the cardiac apex, in the lower apical septum

• Acquired ventricular septal defect can be accurately diagnosed by 2- DEcho and Color Doppler On 2- D Echo, the VSD causes an echo drop-outfrom the lower septum or aneurysmal bulging of the septum during systole.Pulsed- wave and Color- Doppler can pick up a velocity signal and color-

flow map extending from the left ventricle to the right ventricle.

Clinical Pearls

• Clinically, an acquired VSD produces a systolic murmur along the leftsternal border It may be difficult at the bedside to distinguish this murmurfrom that of mitral regurgitation secondary to papillary muscledysfunction or rupture

• One differentiating feature is that the murmur of MR radiates towardsthe left axilla while the murmur of VSD radiates towards the right side ofthe chest

• A significant amount of blood shunting from the left ventricle to the rightventricle across the septal defect produces right ventricular volumeoverload Impairment of right ventricular function is a prominent markerfor the development of cardiogenic shock and carries a grave prognosiswith high mortality