Physical Examination in Cardiovascular Diseases PDF

History, physical examination and diagnostic methods in cardiovascular diseases











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History, physical examination and diagnostic methods in cardiovascular diseases











Dr. Abdullah Erdem Istanbul Medipol Univercity, Medical Faculty  method  Anamnesis  Physical examination  ECG (Holter, event recorder, loop recorder…)  Telecardiography  Hyperoxy test  Biochemical investigation (BNP, CPK-MB, Troponin…)  Echocardiography (TEE, IVUS…)  CT  MRI  Nuclear medicine  Catheter Angiography  Identity information Name- Surname Birt date; age is important in pediatri Gender; Birthplace Telephone Adress Note; From whom the story is taken First of all you have to be sure to whom you are talking. Or who is your patient?  Anamnesis It is the history of the patient about the present and past medical events disease or what he had operation accidents etc… It is the medical information of the patient, doctor listens from himself or a relative of a patient. – Unconscious , uncooperable – Very small to talk Anamnesis is the latin word that means remembrance of past.  Importance of the history The richest source of information concerning the patients’ illness Establishes a bond with the patient & improves his co-operation Allows evaluation of the impact of the disease 5  Anamnesis Complaints History of present illness or complaints Personal history – Prenatal, natal, postnatal Family history  Taking a History

Chieff complaint Prenatal, perinatal and postnatal history Family historry Feeding patterns Fatigue Edema Dyspnea/tachypnea Cyanosis Growth and Development Medications Psychosociall history  Complaints Symptom; subjective evidence of disease or physical disturbance which the patient is noticed. – Cyanosis – Dyspnea – Fatigue – Chest pain ( Chest discomfort) – Palpitation – Syncope  Complaints Sign;Any abnormality indicative of disease, discoverable on examination of the patient; an objective indication of disease, in contrast to a symptom, which is a subjective indication of disease. – Odema – Dyspnea – Tachypnea – Tachycardia – Cyanosis  Details of Complaints When How long How / what type Radiation Similarity Degree Past medication drugs Past investigations Aggreveting factors  Past history of patient; Prenatal Clue Basic Patholgy Specific Finding Gestational infection Rubella PDA VSD PPS Maternal Disease DM Asymetric septal hypertrofi, VSD, TGA SLE Konjenital AV bloc Maternal medication Phenitoin VSD Alcohol VSD ve/veya PS Aspirin PH Lithium Ebstein anomali Preterm PDA Syndromic baby Down AV channel defect Aortic coarctation Turner Pulmonary stenozis Noonan Past history of a patient could be divided under 3 main headlines. ;Prenatal, natal and postnatal.  Fetal Alcohol Syndrome Short upper limp, VSD  Down sendromu Cardiac examinationis recommended routinely for Down syndrome patients since the heart defects are ferequently present. 40 % of Down sydrome have CHD. The most common pathology is AVCD. Association of syndromes with heart defects  Syndromes and CHD association  Down – AV canal and VSD  Turner – CoA, AS  Trisomies 13 and 18 – VSD, PDA →  Fetal alcohol – L R shunts, ToF  CHARGE – conotruncal (ToF, truncus)  Digeorge syndrome- Conotruncal anomalies  Lithium use in pregnancy- Ebstein anomaly  Hereditery Dis. and CHD association Marfan (AD)– aortic root aneurysm ± dissection, MVP, MR, AI HCM (AD) – outflow tract obstruction, arrhythmias Noonan (AD) – HCM, PS, aortic coarctation DMD/BMD (X-link) – DCM (>12 y.o.) Williams (AD) – supravalvar AS, Periferic Pulmonary stenosis Tuberous sclerosis – rhabdomyoma Romano-Ward – AD LQTS Jervell & Lange-Nielsen – AR LQTS & deafness  Family History CHD in family or relatives ( parents; siblings…) Familial hereditery disorders and Metabolic disorders Sudden death, Conjenital deafness Rheumatic fever  Family history Sudden cardiac death at young age Athlete death – Aryhtmias; Long QT, Brugada syndrome, CPVT… – HCMP – Hypercholesterolemia – Metabolic disorders affecting heart Carnitine deficiency Pompe disease (Lysosomal glycogen storage disease) 

Family history

CHD in family
– The risk of having a child with CHD of a mother who had already a child with CHD is increased to 2-5%. – The risk is more increased to 20-30 % percent if the first and second child had CHD The incidence of moderate and severe forms of CHD is about 8/1,000 live births; 1/125  CHD risk in a sibling of a child with heart defects. ANOMALY RİSK (%) Ventricular Septal Defect 3.0 Patent ductus arteriosus 3.0 Atrial Septal defect 2.5 Pulmonary Stenozis 2.0 Aortic Stenozis 2.0 Fallot tetralogy 2.5 Transposition (D-TGA) 1.5 Tricuspit atrezisi 1.0 Hypoplastic sol kalp sendromu 2.0 Risk startification in off springs of mother or father with CHD; ____________________ Mother % Baba% Anomali VSD 6 2 PDA 3.5 - 4 2.5 ASD 4 - 4.5 1.5 TOF 6 - 10 1.6 KOA 4 2 AS 13 - 16 3 AV KANAL 14 1 PS 4.5 - 6.5 2 __________________________________________________________________ *Nora JJ. Maternal transmission of congenital heart disease: New reccurence risk figures. Am J Cardiololgy.  You can expand history as much as you could do It is mainly dependent to your skill, time and cooperation of the patient Sometimes it is the only clue which you diagnose the disease; FMF, trauma, Psychological disorders, intoxication  5 year old boy came with syncopy to emergency room. He was normal until breakfast. He got berakfast at 10 oclock in the morning. He was bradycardic and all the other findings were normal.  He ate honey more than usual. Honey intoxication Honey intoxication occurs following the intake of honey produced from the nectar of Rhododendron Ponticum. Additionally, intoxication can occur if either the leaves or flowers of this plant are consumed. The toxin causing this condition is Andromedotoxin (Grayanotoxin) and is named ‘mad honey’ by the rural population Physical examination inspection Palpation Percussion auscultation  Behave appropriate for the age and character of child. Be careful about your hands are warm Giving toys or having toys with color and sounding could enable the children being more co operable. 
Physical examination – Before starting exam Evaluate mental and motor development Notice any syndromic appearance Do not disturb if the baby is sleeping  Carefull about … Weight, lenght Arterial tension Pulse palpation – Must be measured and noticed – Percentile must be determined  Inspection; Examine for Dispnea; intercostal retractions, Nose Flaring Tachypnea; age is important for definition Pale appearance; anemia Cyanosis Clubbing Xhantoma Chest abnormality  RESPIRATORY DISTRESS
For our purposes, two types of respiratory distress can be defined: – tachypnea; abnormally rapid respirations: and – dyspnea; difficult breathing. 
Rapid respirations

Tachypnea > 60/min in 0-2mth >50/mt in 2mth to 1yr >40/mt 1-5 yr in calm child Happy tachypnea- tachypnea with out much retractions  Grunting (a form of positive end-expiratory pressure)  In cyanotic heart disease rapid respirations may be due to associated brain anoxia and not CHF - treatment for these two conditions is entirely different Fever especially with a pulmonary infection may produce rapid respirations.  Breathlessness(dyspnoea) abnormally uncomfortable awareness of breathing regarded as abnormal only when it occurs – at rest or – at level of physical activity not expected to cause it associated with diseases of – heart – lungs – chest wall – respiratory muscles also associated with anxiety 33  Breathlessness(dyspnoea) Exertional dyspnoea – Comes on during exertion and subsides with rest – Commonly due to HF or lung disease Orthopnoea (mainly symptom of adult) – breathlessness on lying flat – A symptom of left ventricular failure – due to redistribution of fluid from the lower extremities to the lungs 34  Orthopnoea
Sensation of breathlessness on lying flat. Orthopnoea occurs because of increased venous return and a redistribution of interstitial oedema throughout the lungs. Patients who are prone to orthopnoea may report using several pillows (ask how many) to prop themselves upright in bed, or may even resort to sleeping in a chair.  Paroxysmal nocturnal dyspnoea The development of breathlessness while the patient is lying down asleep, waking the patient and usually forcing them to sit upright or even lean out of an open window to regain their breath. It results from the development of orthopnoea while the patient is sleeping.  Breathlessness(dyspnoea) Paroxysmal Nocturnal dyspnoea – a variant of orthopnoea – patient awakes from sleep severely breathless persistent cough, may have white frothy sputum – a manifestation of left ventricular failure 37  NYHA Functional heart failure classification  Praecordium Inspection – visible veins – obstruction of SVC – praecordial bulge or prominence – long standing cardiac enlargement before puberty – abnormalities of the chest wall – Praecordial hyperactivity – suggests severe valvular abnormality – Apex beat 39  Jugular venous pulse observed from the right internal jugular vein usually examined with patient at 45° sitting position 2 major pulsations can be observed – ‘a’ and ‘v’ waves measurement of the JVP – height above the sternal angle – usually < 4cm Abdomino-jugular reflux – seen in right heart failure 40  Causes of raised JVP – Rt heart failure – Tricuspid incompetence – Pericardial effusion – SVC obstruction – Constrictive pericarditis – Tricuspid stenosis  Waves a - presystolic; produced by right atrial contraction. c - bulging of the tricuspid valve into the right atrium during ventricular systole (isovolumic phase). v - occurs in late systole; increased blood in the right atrium from venous return. Descents x - a combination of atrial relaxation, downward movement of the tricuspid valve and ventricular systole. y - the tricuspid valve opens and blood flows into the right ventricle. Pectus carinatum Clubbing  Capillary Refill Time

Evaluated by compressing the extremity with moderate pressure and noting the time required for the blanched area to reperfuse Normal refill time is about 3 seconds Prolonged refill may be associated with poor systemic perfusion or a cool ambient temperature  Blood pressure use of a sphygmomanometer – inflatable cuff connected to mercury or aneroid manometer – stethoscope over the branchial artery – inflate cuff above the POP – reduce the pressure in the cuff slowly – reappearance of Korotkov sound – systolic pressure – disappearance of Korotkov sounds – diastolic pressure 52  Blood pressure Pitfalls in BP measurement – apparatus small cuff – overestimation of the BP by 20 - 30 mmHg large cuff – underestimation of the blood pressure calibration of the sphygmomanometer – Patient emotional state of the patient anxiety(white coat hypertension) posture and the position of the sphyg – observer auscultatory gap 53  Assessing Blood Pressure
Normal blood pressure is lower in children than adults Upper extremities are the preferred site Document location and be consistent 4 extremity blood pressure should be obtained during initial assessment  Is it necessary to measure both upper and lower limp blood pressure in children ? WHY? Dinamap, pulse method , flush method  Assessing Blood Pressure
Sitting position preferred with midpoint of arm at level of heart Palpate brachial artery and place index line of cuff inline with the pulse Rolling up a shirt sleeve may act as a tourniquet and give false BP or pulse assessments  Cuff Size Determination The cuff should cover two third of the upper arm length and the bladder of the cuff should encircle 80–100 % of the circumference of the arm What are the three most common clinical presentations in infants with CHD ? (1) murmur, (2) cyanosis, (3) respiratory difficulty.  cyanosis Central cyanosis is caused by increased deoxyhemoglobin content (greater than 5 g/dl) fetus lives without a serious problem in utero, despite a low (65 percent) oxygen saturation. Even when a congenital anomaly such as transposition of the great arteries is present, birth weight is usually normal.  central cyanosis Arterial oxygen saturation is lower than normal limits Three common causes of central cyanosis are ; cardiac disease, pulmonary disease, central nervous system (CNS) depression.  Crying may improve the cyanosis caused by lung diseases or CNS depression; however, crying usually worsens cyanosis in patients with cyanotic heart defects.  Pulse Oxymetry Pulse oximetry is a non-invasive method of indirectly evaluating arterial oxygenation through measurement of peripheral saturation of haemoglobin. The basic rationale behind pulse oximetry is that hypoxaemia may be detected early and treatment can begin before serious or irreversible adverse effects occur. Because pulse oximetry is non-invasive it can used in wards and continuously thus reducing the need for arterial blood gases (ABGs). Screening is extremely important for critically ill patients. Pulse Oxymetry  hyperoxygenation test In some cyanotic patients the hyperoxygenation test may assist the physician in making this distinction. Arterial oxygenation should be greater than 150 mm Hg if a child is allowed to breathe 100% oxygen for 10 minutes and there is a respiratory cause for the hypoxia. Values less than 100 mm Hg suggest congenital heart disease with a mixing lesion as the cause for the hypoxia.  What are the ohter causes of cyanosis ? If No respiratory, No cardiac disease No CNS disease  Methemoglobinemia Pulmonary arteriovenoz fistula Persistant pulmonary circulation Does systemic arteriovenous fistula cause cyanosis?  What do you think does anemia make easy to evaluate cyanosis or difficult?  7 year old boy came to emergency with severe cyanosis after local anesthesia for circumcision. – No past history of disease – Entirely normal before this event Diagnosis?  PERIPHERAL EDEMA

Infants and young children differ strikingly from adults in the development of peripheral edema in congestive heart failure. Pretibial and presacral edema are late developments in the child's congestive circulatory failure picture, apparently due to difference in tissue turgor. When peripheral edema due to heart failure does develop in an infant, it first appears periorbitally, usually preceded by other manifestations such as tachypnea, tachycardia, dyspnea, and liver enlargement.  Oedema Causes of peripheral oedema – cardiac failure – Chronic venous insufficiency – Hypoalbuminaemia – nephrotic syndrome, liver disease, protein losing enteropathy – Drugs retaining sodium (fludrocortisone, NSAID) increasing capillary permeability (nifedipine) 73  Praecordium: palpation apex beat – lowermost and outermost point of cardiac impulse – normally in the 4-5 LICS at the mid-clavicular line – when displaced suggests cardiac enlargement – heaving apex – LVH – tapping apex beat (palpable 1st heart sound) – mitral stenosis 74  Praecordium: palpation Right ventricle – left parasternal heave indicate RVH Palpable sounds – Palpable 2nd heart sound –loud P2 or A2 Thrills – palpable murmurs with low frequency components 75  Pulse character and volume

pulse character and volume are not easily assessed at the radial pulse because it is so far from the heart (so the pulse has become quite ‘damped’). In most cases it is easier and better to assess pulse character and pulse volume using the brachial pulse or, even better, the carotid pulse.  The pulse has been studied for Information gained: – Frequency, regularity – Patency of peripheral arteries – Characteristics of the arterial pressure pulse wave The arterial pulse contour changes to the periphery: – Resistance: viscosity, vessel geometry opposes flow; HR independent – Inertia: mass opposes rate of change of flow, HR dependent – Compliance: distensibility opposes changes of blood volume, HR -dependent  Normal Pulse – The normal central aortic pulse wave is characterized by a fairly rapid rise to a somewhat rounded peak. – The anacrotic shoulder, present on the ascending limb, occurs at the time of peak rate of aortic flow just before maximum pressure is reached. – The less steep descending limb is interrupted by a sharp downward deflection, coincident with AV closure, called incisura. – The pulse pressure is about 30-40 mmHg.  What is pulse pressure ? When it İncreases? When it Decreases?  Pulsus Parvus The pressure is diminished, and the pulse feels weak and small, reflecting decreased stroke volume (e.g. heart failure), restrictive pericardial disease, hypovolemia, mitral stenosis, and increased peripheral resistance (e.g. exposure to cold, severe CHF). Pulsus Parvus et Tardus (weak and delayed): → Aortic Stenosis  Bounding Pulses water-hammer pulse or the Corrigan pulse. Most commonly in chronic, hemodynamically significant AR. Seen in many conditions associated with increased stroke volume: PDA, large arteriovenous fistula, hyperkinetic states, thyrotoxicosis anemia, and extreme bradycardia. Not seen in acute AR, since SV may not have increased appreciably.  Pulsus Alternans Variation in pulse amplitude occurring with alternate beats due to changing systolic pressure. When the cuff pressure is slowly released while taking BP, phase I Korotkoff sounds are initially heard only during the alternate strong beats; with further release of cuff pressure, the softer sounds of the weak beat also appear. Degree of pulsus alternans can be quantitated by measuring the pressure difference between the strong and the weak beat.  Pulsus Paradoxus Pressure drop > 20 mmHg during inspiration. Normally, systolic arterial pressure falls 8-12 mmHg during inspiration. Evaluated with sphygmomanometer: – when the cuff is slowly released the systolic pressure at expiration is first noted. With further slow deflation of the cuff, the systolic pressure during inspiration can also be detected.  Pulsus Paradoxus Causes: – Cardiac Tamponade – COPD, hypervolemic shock – infrequently in constrictive pericarditis and rescrictive cardiomyopathy. Mechanism: – Decreased LV-SV due to an increased RV-EDV and decreased LV-EDV during inspiration. – In cardiac tamponade, the interventricular septum shifts toward the LV cavity during inspiration (reverse Bernheim’s effect) b/c of increased venous return to RV, decreasing the LV preload. – Decrease in pulmonary venous return to the LV during inspiration also contributes to decreased LV preload.  Cardiac auscultation Areas for auscultation – cardiac apex – right and left sternal borders interspace by interspace – Be carefull about dextrocardia 85  Auscultation
URSB – Aortic valve ULSB – pulmonic valve LLSB – Tricuspid valve Apex – Aortic or mitral valve  Assessing Heart Rate
Listen with stethoscope to apical pulse for at least 1 minute Listen for fast rates, slow rates or an irregular rhythm Palpate pulse for 1 minute Brachial pulse forr infants Radial pulse for children  Heart Rate
Heart rates of children are more variable than those of adults Fever, exercise, tension, crying, stress may elevate heart rate  Heart sounds 4 basic heart sounds other sounds i.e. Murmurs, clicks, prosthetic valve sounds, friction rub time the sounds with palpation of the carotid artery 90  Systole The time between the S1 and S2 sounds is: Lub------------Dub 1. The ventricles contracting 2. Blood flowing from the heart to the lungs and body 3. Blood flowing across the Pulmonic and Aortic valves  Diastole
Dub----------Lub The time between S2 and S1 is : 1. The blood is flowing from the atria to the ventricles. 2. The blood flowing across the mitral and tricuspid valves. 3. The atrial contraction also occurs now.  S1- What is it ? The “lub” in the lub – dub. This sound is primarily because of the closing of the Mitral and tricuspid valves. Anatomically they are located between the atria and the ventricles They close because the ventricles contract The Pulmonic and Aortic valves are opening and blood is being forced into the arteries  S2- What is it ? S2 is the “dub” in the lub- dub The sounds are because of the closing of the Pulmonic and Aortic valves as the pressure from the arteries is greater then the pressure in the ventricles. This is the end of systole  Heart sound 1st heart sound – two major components – due to closure of the atrio-ventricular valves – loud in tachycardia short PR interval short circle lengths in AF mitral stenosis with a pliable leaflet 2nd heart sound – due to closure of the semi-lunar valves – normally two components A2 and P2 – splitting of the 2nd heart sound in inspiration 96  2nd Heart sound: abnormal splitting single 2nd heart sound – inaudible pulm. component pulmonary atresia due to emphysema severe pulm. stenosis – inaudible aortic component severe calcific aortic stenosis aortic atresia – persistent synchrony of the two components Eisenmenger’s complex 97  2nd Heart sound: abnormal splitting Persistent splitting – delay in the pulm. component complete RBBB – early timing of the first component mitral regurgitation Fixed splitting – ostium secundum atrial septal defect Paradoxical splitting – complete LBBB – right ventricular pacemaker – severe aortic outflow obstruction – a large aorta-to-pulmonary artery shunt 98  2nd Heart sound: abnormal intensity Increased A2 – systemic hypertension increased P2 – pulmonary hypertension 100  3rd heart sound due to sudden limitation of ventricular expansion during early diastolic filling – heard normally in children – and in patients with high cardiac output – in patients over 40 years old an S3 usually indicates – impairment of ventricular function – AV valve regurgitation – other conditions that increase the rate or volume of ventricular filling 101  4th heart sound a low-pitched, presystolic sound produced in the ventricle during ventricular filling it is associated with an effective atrial contraction and is best heard with the bell piece of the stethoscope absent atrial fibrillation occurs when diminished ventricular compliance increases the resistance to ventricular filling seen in – patients with systemic hypertension – aortic stenosis – hypertrophic cardiomyopathy – ischemic heart disease – acute mitral regurgitation 102  Murmurs result from vibrations set up in the blood stream and the surrounding heart and great vessels as a result of turbulant flow A murmur is a physical finding and not a structural problem within the heart itself. Treatment is aimed at the underlying condition ıf there is a pathology. 103  Murmurs graded I – VI – grade I faint, heard only with special effort – grade II soft – grade III loud – grade IV loud with thrill – grade V audible with stethoscope barely touching the chest – grade VI murmur is audible with the stethoscope removed from contact with the chest  Murmurs for a murmur, determine its – timing – intensity – pitch – site of maximal intensity – radiation – configuration – relationship with posture and respiration 105 three major categories of murmurs

– systolic;pan systolic, systolic ejection, mid systolic – Diastolic; early diastolic, middiastyolic – continuous  What kind of murmur Do you hear in Atrial septal defect? Gradient turbulent Flow  Murmur  Systolic murmurs There are three types of systolic murmur: ejection systolic Pansystolic late systolic.  ejection systolic murmur grows in loudness during early systole, peaks in mid -systole, and diminishes during late systole (‘crescendo-decrescendo’). Ejection systolic murmurs result from: aortic stenosis pulmonary stenosis hypertrophic obstructive cardiomyopathy increased flow (‘fl ow murmur’) of pregnancy anaemia fever  There are two types of diastolic murmur:

early diastolic mid-diastolic – An early diastolic murmur peaks at the start of diastole and then gradually diminishes in loudness. aortic regurgitation, ! pulmonary regurgitation. A – A mid-diastolic murmur is a low-pitched ‘rumbling’ murmur which is loudest in the middle of diastole.  Early diastolic murmurs The early diastolic murmur of aortic regurgitation is usually best heard at the lower left sternal edge, and is enhanced with the patient sitting forward and in expiration. The murmur of pulmonary regurgitation is sometimes called a Graham Steell murmur and is generally found in the context of pulmonary hypertension.  Mid-diastolic murmurs mitral stenosis tricuspid stenosis (rare). The mid-diastolic murmur of mitral stenosis is best heard at the apex, and is enhanced with the patient rolled onto their left side.  Innocent Murmurs Diastolic murmurs are never innocent Innocent murmurs are present in at least 50 % of normal children – Still’s murmur : low pitched, vibratory, systolic ejection, increases with the supine position. – Venous hum: continuous murmur in supraclavicular region, reduces on lying down or with pressure on neck.  Innocent murmurs Peripheral pulmonic stenosis (PPS) – Heard in newborns – disappears by one year of age (often earlier) – Soft SEM at ULSB w/ radiation to axilla and back (often heard best in axilla/back) – Need to differentiate b/w PPS and actual pulmonic stenosis. PS often associated with a valvular click and heard best over precordium  Innocent Heart Murmurs History – normal growth and development, normal exercise tolerance – no history of cyanosis Physical Examination – Grade II or less, localized – varies with position (decreased with upright posture) – normal precordium – normal pulses Lab – normal EKG, normal CXR 
Biochemical tests Cardiac enzymes Brain natriüretic peptides in emercency; indicates heart failure Electrolite imbalance because of cardiac drugs Blood gas analysis could show methemoglobinemia Renal function; urea and creatinine in aortic coarctation …  Classic Radiologic Signs of Congenital Cardiovascular Abnormalities A number of imaging signs of congenital cardiovascular abnormalities have been widely described in the radiology literature and are generally recognized to be clinically important. But as a cardiologist we mainly benefit from x- ray to exclude any other pathology (especially with lungs….)  In view of cardiology chest x-ray is important to decide if the pulmonary flow is increased or not. Associating problems Any special clue To assessment of cardiomegaly Different amounts of PBF
(Truncus vs ToF) Egg-on-a-String Sign Snowman Whatis your diagnosis Your Diagnosis ?  The most common reasons for obtaining EKGs in children are – chest pain, – suspected dysrhythmias, – seizures, – syncope, – drug exposure, – electrical burns, – electrolyte abnormalities, – and abnormal physical examination findings.. Essentials in looking at an ECG Rhythm (sinus….nonsinus) Rate, Atrial and ventricular rates. QRS axis, T axis, QRS-T angle Intervals: PR. QRS, and QT P wave amplitude and duration QRS amplitude and R/S ratio Q wave St- Segment and T wave abnormalities Pediatric ECG differs from adult ECG  Echocardiogram

Cardiac ultrasonography is one of the most versatile of cardiac investigations, revealing detailed information about cardiac structure and function. In transthoracic echo (TTE) an ultrasound probe is applied to the anterior chest wall to obtain 2-D (and, where available, 3-D) moving images of the heart, and also to assess blood fl ow using the Doppler principle.  Echocardiogram

There are many indications for TTE, including the assessment of: breathlessness (e.g. left ventricular failure, pulmonary hypertension) heart murmurs infective endocarditis prosthetic valves Cardiomyopathy pericardial disease (e.g. pericardial effusion) congenital heart disease.  Transoesophageal echo Transoesophageal echo (TOE or TEE) uses the same principles as TTE, but the probe is passed into the patient’s oesophagus. This provides clearer images, making TOE particularly useful when higher resolution imaging is necessary (such as the detection of small vegetations in suspected infective endocarditis).  Which kind of cardiac imaging is more useful during cardiac operation?  indications for TOE assessment of: cardiac source of emboli suspected or proven infective endocarditis aortic diseases (e.g. aortic dissection/trauma) regurgitant heart valves, to judge suitability for surgical repair prosthetic valves (especially those in the mitral position) cardiac masses congenital heart disease and intracardiac shunts.  Cardiac computed tomography

Multislice computed tomography (MSCT) is used to image the heart. multiple image ‘slices’ are obtained as the patient is moved through the gantry during the scan. The slices are then processed to generate images of the heart in any plane and from any angle, either as a three-dimensional volume rendered image or as cross-sectional slices.  Cardiac computed tomography

Cardiac CT scanning is very fast (it takes just a few seconds to acquire the images) but processing and reporting the images usually takes 10–30 minutes. The main use of cardiac CT is in assessment of the coronary arteries. A calcium score can be obtained (refl ecting the amount of calcifi cation present in the coronary arteries) and this correlates with the patient’s risk of future cardiovascular events. With the injection of an intravenous contrast agent, the coronary arteries themselves can be imaged (CT coronary angiography).  Cardiac CT scanning is very fast (it takes just a few seconds to acquire the images) but processing and reporting the images usually takes 10–30 minutes. The main use of cardiac CT is in assessment of the coronary arteries. A calcium score can be obtained (refl ecting the amount of calcifi cation present in the coronary arteries) and this correlates with the patient’s risk of future cardiovascular events. With the injection of an intravenous contrast agent, the coronary arteries themselves can be imaged (CT coronary angiography).  Cardiac magnetic resonance imaging
Cardiac magnetic resonance imaging (MRI) is a highly versatile technique for cardiac imaging and provides both anatomical and functional information. Examples of its many uses include the assessment of:  Cardiac magnetic resonance imaging

cardiac chamber dimensions and function valvular heart disease cardiomyopathies cardiac masses congenital heart disease pericardial disease aortic abnormalities.  Cardiac magnetic resonance imaging

Although cardiac MRI does not involve exposure to ionizing radiation, it does use a powerful magnetic field and is therefore contraindicated in patients with certain types of metallic implants (e.g. pacemakers, implantable defibrillators and cerebrovascular aneurysm clips) TAPVR  Which type of cardiac imaging is contraindicated in a patient with pacemaker?  Cardiac nuclear medicine Cardiac nuclear medicine is useful in diagnosing and assessing coronary artery disease. It is also used to evaluate cardiomyopathy and identify possible damage to the heart from chemotherapy or radiotherapy. Nuclear medicine imaging procedures are noninvasive and, with the exception of intravenous injections, are usually painless medical tests that help physicians diagnose and evaluate medical conditions. These imaging scans use radioactive materials called radiopharmocetuticals or radiotracer.  Cardiac nuclear medicine Myocardial perfusion imaging uses a radiopharmaceutical (e.g. thallium-201 or a technetium- 99m-labelled radiopharmaceutical), administered intravenously, to assess myocardial blood flow, providing valuable information about coronary artery disease with a high degree of sensitivity and specificity. Radionuclide ventriculography assesses ventricular function using red blood cells labelled with technetium- 99m. The count-rate of the radioactivity can be measured using a gamma camera at different stages of the cardiac cycle, and from this an accurate measure of ejection fraction can be derived.  Cardiac catheterization Diagnostic 50 % – Coronary angiography Therapeutic 50 % – Balloon – Stent – Device embolization or defect closure