diagnostik fisik jantung

Physical diagnosisOfTHE HEART

SYMPTOMSa good clinical history remains the clinicians most valuable diagnostic tool. the diagnosis may be made from the history alone, and examination and investigations are confirmatory.A key objective of history-taking is to establish a clear de-scription of the presenting symptom, and to detect any pattern to episodes of the symptom.the previous medical history, medication and the social history.a useful differential diagnosis list

Common cardiac symptomsChest pain or discomfort is one of the most common symptoms encountered in clinical practice, and is a major cause of admission to hospital.

Differential diagnosis of acute chest pain/discomfortCardiovascular CAD Unstable - stable angina Myocardial infarction Variant angina Syndrome X (microvascular angina) NON_CAD Aortic dissection Rupture of thoracic aortic aneurysm Myopericarditis, pericarditis

Pulmonary Pulmonary embolism Pneumonia (usually lobar) Pleuritis

Gastrointestinal Oesophagitis Oesophageal spasm Hiatus hernia Peptic ulcer disease Biliary colic Pancreatitis Pneumothorax Acute asthma PneumomediastinumOthers Chest wall muscle pain Psychogenic chest pain Costochondritis Cervical spondylosis

angina pectorisThe typical description of angina is a tight, heavy or constricting discomfort in the centre of the chest. This sometimes radiates to the neck or jaw, and to one or both shoulders or arms. Presentation can vary, however, and some patients complain of back pain, epigastric pain, or isolated jaw or arm painOther ischaemic pattern : atypical angina equivalent angina

Canadian Cardiovascular Society functional classificationApplies to angina onlyClass I No angina on ordinary activity Angina on strenuous, rapid, or prolonged exertionClass II Slight limitation of ordinary activity Angina when walking up stairs briskly, or walking on a cold or windy dayClass III Marked limitation angina when walking at normal pace up a flight of stairs, or walking one or two blocksClass IV Angina on minimal exertion or at rest

BreathlessnessAlmost all types of cardiac illness can cause breathlessness. It is most helpful to consider the following broad categories: pulmonary oedema reduced cardiac output obstruction to cardiac output arrhythmiaDD :Central - PsychiatricRespiratory appResp app golgimetabolic

New York Heart Association functional classificationApplies to fatigue, dyspnoea and anginaClass I No limitations during ordinary activityClass II Slight limitation during ordinary activity (e.g. mild or occasional angina/dyspnoea)Class III Marked limitation of normal activities without symptoms at restClass IV Unable to undertake physical activity without symptoms Symptoms may be present at rest

cardiac syncope caused by arrhythmia or reduced cardiac output from structural disease. inappropriate vasodilatation (including vasovagal syncope) neurogenic syncope (e.g. epilepsy, cerebrovascular ischaemia) metabolic syncope (e.g. hypoglycaemia).Palpitationis used by patients to describe various sensations, some of which are related to cardiac rhythm. Dizziness and syncopeDizziness is a nonspecific symptom that is common in cardiac patients. It affects about one-third of patients aged over 65 years.

The key to Practice points diagnosis is establishing a clear description of the nature and pattern of symptom episodes New chest pain or discomfort requires prompt assessment it may reflect serious pathology such as MI, aortic dissection or pulmonary embolism Dizziness is a common symptom in the elderly and may be multifactorial; drug treatment may be a contributing factor Syncope of cardiac origin is associated with high mortality; identification of underlying structural and electrical disease is important in the evaluation of syncope

Clinical examination of the heartmaking an initial anatomical diagnosisrapidly assessing cardiac function and progress at the bedsideThe skill of examination is best learned at the bedside from a practitioner already experienced in it, and is best perfected by practice the traditional sequence of inspection, palpation and auscultation is valuable

Jugular venous pulseThe jugular venous pulse (JVP) gives important information about right heart function, and thereby about left heart function.

Arterial pressure and pulseBlood pressure Sphygmomanometry is often performed poorly. The standard cuff is 5 inches (about 12.5 cm) wide, but this may not be appropriate for all patientsArterial pulse should be examined for rate, rhythm, amplitude and waveform, and the character of the arterial wall should be assessed.Rate heart rate is a simple means of detecting bradycardia (< 60 beats/minute) or tachycardia (> 100 beats/minute) arising physiologically (e.g. exercise, emotion) or as a forewarning of dysrhythmia.

Rhythm two abnormal rhythms are common and are sometimes confused: atrial fibrillation multiple extrasystoles.They are characterized by differences in periodicity and volume, but clinical differentiation may be difficult.Volume a low-volume pulse can result from low blood pressureWaveform it is best to seek an abnormal waveform in an artery larger than the radial arteryPalpation of the cardiac impulse normal hyperdynamic sustained

Heart soundsA comfortable, practical stethoscope with a diaphragm and a bell is needed. Practice in use of the stethoscope and in interpretation of what is heard are more important Low-frequency and medium-frequency sounds (e.g. third and fourth heart sounds, mid-diastolic murmurs) are more easily heard with the bell applied lightly to the chest wall. The diaphragm is more appropriate for high-frequency sounds (e.g. first and second heart sounds, opening snap, ejection and some regurgitant murmurs). Pressing hard with the bell tightens the skin and converts the bell into a diaphragm.The traditional method of placing the stethoscope over the mitral, aortic, pulmonary and tricuspid areas is of value only in determining which valve is most likely to be the source of the murmur.

First heart sound: S1 marks the onset of systole. It is produced mainly by mitral valve closure and, to a lesser extent, by tricuspid valve closure. Timing of the heart sounds is aided by gently palpating the carotid pulse with the fingers of the left hand

Second heart sound: S2 is produced by closure of the aortic and pulmonary valves, and marks the end of systole and the beginning of diastole.

The valves close asynchronously; the aortic valve closes first. The aortic component of S2 is accentuated: by systemic hypertension in thin-chested individuals with a forward- projecting aorta.

The aortic component of S2 is reduced in intensity in patients with: poorly mobile cusps (e.g calcification) aortic root dilatation (e.g. syphilitic aortitis).

Pulmonary hypertension accentuates the pulmonary component.

The intensity of S1 varies with the position of the valve cusps at the onset of ventricular contraction. Their position is determined by the volume and pressure of blood on either side of the valve; the wider apart the cusps at the onset of systole, the louder the sound produced.Any change in cusp position at the onset of systole affects the sound produced it varies with, for example: PR interval rate of valve closure valve mobility force of ventricular systole.

Heart sounds and their relationship to the first (S1) and second (S2) soundsSplitting of S2Splitting of S1Fourth, presystolic, heart soundThird heart soundEjection click (preceding aortic or pulmonary systolic murmur)Opening snapMid-systolic ejection

Splitting physiological splitting becomes greater with inspiration,because pulmonary vascular impedance is reduced during inspiration in relation to systemic impedance, but it becomes fixed in: atrial septal defect left-to-right and bidirectional shunts right heart failure.In reversed splitting (P2 precedes A2), the splitting is maximum in expiration. Common causes are left bundle branch block and pacing. Prolonged ejection time in aortic stenosis also causes reversed splitting

Third and fourth heart sounds: additional heart sounds may occur in early diastole (S3) and late diastole (presystole S4). They result from rapid ventricular filling; S3 when the atrioventricular pressure gradient is high, and S4 as atrial contraction gives a boost to ventricular filling.Heart muscle can be viewed as thixotropic; it can be slowly stretched using little force, but sudden stretching

Murmursare graded on a four-point or, more commonly a six-point scale is: grade 1 audible with difficulty grade 2 faint but recognizable grade 3 moderate intensity grade 4 loud grade 5 louder, but still needing a stethoscope grade 6 audible without a stethoscope.It is a common misconception that the intensity of the murmur indicates the severity of the valve defect.

Common heart murmurs

Aortic systolic ejection following an ejection clickPansystolic murmur of mitral regurgitationEarly aortic diastolic murmurMid-diastolic and pre-systolic murmurs of mitral stenosisIt is a common misconception that the intensity of the murmur indicates the severity of the valve defect

Auscultation of the heart sounds provides a helpful clue.

If A2 is clearly audible at the apex, it is likely to be a systolic ejection murmur. If A2 is audible at the base but not at the apex, it is probably a systolic regurgitant murmur. An ejection systolic murmur is accentuated by a post-ectopic beat; a regurgitant murmur remains unchanged. Sustained handgrip, by increasing blood pressure, accentuates systolic regurgitant murmurs but diminishes systolic ejection murmurs. Aortic systolic murmurs often radiate to the neck. Mitral systolic murmurs often radiate to the axilla.

Innocent murmurs : increased flow through a normal valve in pregnancy, anaemia or thyrotoxicosis. Young children with a thin chest wall sometimes have a precordial vibratory murmur of no pathological significance.

Papillary muscle rupture and dysfunction, or chordal rupture, produces a loud crescendodecrescendo murmur heard widely over the precordium.

Diastolic murmurs occur early, during mid or late diastole.

Early diastolic murmur, beginning immediately following S2, arises from aortic or pulmonary regurgitation and rapidly diminishes in a decrescendo manner.

Mid-diastolic murmurs are produced by rapid LV filling through a stenosed mitral or tricuspid valve, or when a left atrial myxoma or severe aortic regurgitation (Austin Flint murmur) impedes LV filling.

Late (presystolic) murmurs arise when atrial systole ejects blood through a stenosed mitral or tricuspid valve; patients with mitral stenosis and atrial fibrillation thus do not have a presystolic murmur.

Other sounds sometimes heard in diastole are the continuous murmur of patent ductus arteriosus, and a pericardial friction rub in perica