Cardiology

Clinical Assessment

Taking a History

  • All cardiac histories have two strands (as do all system histories) into the narrative of the current symptoms which is the easier part but do not forget to ask about risk factors. In valvular heart disease this includes rheumatic fever or perhaps recent dental work if endocarditis suspected.
  • For suspected ischaemic heart disease you need to ask about smoking, hypertension, diabetes, cholesterol and family history and present these along with the clinical history of for example chest pain.

General Advice

  • Get a good history of the current presenting complaints and try to get quantitative estimates e.g. distance walked, cigarettes smoked, pillows slept on.
  • Always establish a timeline - patients can be very imprecise but push "A while", "Is that a day, a week, a month, a year..?" "about 6 weeks doctor"
  • Smoking, Hypertension, Family history, Diabetes, Hypercholesterolaemia, Rheumatic fever play a major role in heart disease in many patients and should not be neglected.
  • Don't forget to ask how their disease impacts on their life, can they do stairs at home, are they too breathless to do house work or to even wash and dress themselves, do they need help...
  • When presenting a history of cardiac chest pain always then as part of it present the risk factors. This allows the clinician to work out their a priori risk of actually having IHD. The same pain in a 25 year old women with no risk factors may be assessed quite differently to that in a 60 year old male diabetic chain smoking hypertensive.
  • The commonest symptoms are chest pain, fatigue and breathlessness, palpitations, syncope and presyncope

Chest pain

  • When due to a cardiac cause is usually down to myocardial ischaemia or infarction and reflects a situation in which myocardial oxygen demand is not being met and there is a localised build up of lactate or with infarction there is actual tissue necrosis.
  • With myocardial infarction the pain is worse and there are often additional features such as pallor, nausea and vomiting and the patient is grey and sweaty.
  • By resting to decrease MO2 demand or using perhaps GTN to relax the coronary vessels and reduce myocardial work the pain can be relived. However the presence of rest pain must make one consider myocardial infarction.
  • Classically the pain is central chest and feels like a weight pressing down on the chest. Some will use a clenched fist in front of their sternum to represent the pain.
  • In diabetics and the elderly ischaemia and infarction may be silent and an ACS only present with its complications.
  • Chest pain may also be due to pericarditis but this is more of a constant pain unrelated to exertion and eases on sitting forwards. Worse with deep inspiration and a rub may be heard.
  • A dissecting thoracic aneurysm typically has pain front and back, a tearing interscapular pain, however subtler presentations abound and it is not uncommon for dissections to be treated as ACS or diagnosed at post mortem.
  • Chest pain (Angina), like breathlessness can be graded and scales such as the Canadian cardiovascular society exist but in reality I would rather you tell me exactly what level of exertion provokes pain rather than quote scales. Is it at rest, minimal, moderate or severe exertion.

Breathlessness

  • This is usually associated with heart failure when the bodies needs in terms of primarily oxygen delivery is not being made.
  • It may suggest that there is increased alveolar oedema and incipient pulmonary oedema.
  • Breathlessness can be worse at night when one lies flat due to central redistribution of fluid and this is called orthopnea.
  • Occasionally pulmonary oedema can come on minutes to hours after recumbency and the patient wakes up acutely breathlessness and often has to get out of bed or sit on side of bed or by a window until the breathlessness has eased. This is paroxysmal nocturnal dyspnoea. Oedema
  • Ankle oedema usually suggests right heart failure. As it progressed the oedema climbs until it affects the thigh and even up to the abdomen with scrotal oedema, ascites etc and pleural effusion. Hepatomegaly may also be seen.

Fatigue

  • A subtle sign but often an early feature of heart failure or cardiac impairment but also seen with anaemia, hypothyroidism, malignancy, viral illnesses
  • Often too subtle by itself to be useful but often good to see how a day in a patients life has changed now as it compares with before

Palpitations

  • Abnormal awareness of the heart beat. Get patient to tap it out. Is it regular, fast or slow, associated with symptoms.
  • If fast and stops is there polyuria after (SVT).
  • If it is just a large occasional thump it may simply be due to the heart beat with increased cardiac output after an ectopic which is usually harmless.

Syncope or presyncope

  • Should always be taken very seriously. Look for murmurs and evidence of arrhythmias.
  • Take an accurate history. Know exactly what the patient was doing when the episode happened.
  • Interrogate the patient. Know exactly what happened when they recovered. Do all you can to get a witness report.
  • I have rung neighbours and others to get vital information with the patients consent of course. The history is key.

Investigations where cardiac cause suspected include ECG, Echo, 24 hr tape

Cardiac Causes of syncope

  • Severe aortic stenosis
  • Severe bradycardia e.g. complete heart block or sinus pauses
  • Vasovagal syncope exacerbated by medications
  • Ventricular tachycardia
  • Stokes-Adams attack

Cardiac arrest

By definition there is no cardiac output with no pulse and no breathing.

Causes

  • Pulseless VT
  • Ventricular fibrillation
  • Asystole
  • Electromechanical dissociation

Can be the initial presentation of ischaemic heart disease or hypertrophic cardiomyopathy. Defibrillation of VF/VT can be lifesaving.

Management of Acute onset Chest pain

  • The big diagnoses here are MI, PE, Aortic Dissection
  • Give oxygen 40-60% to enable a saturaion of 94-98%.
  • Check Pulse, BP and O2 saturations
  • Assess patient - quality, onset, severity, exacerbating and relieving factors and consider likely diagnoses
  • Do a 12 lead ECG done. If normal then a cardiac cause less likely.
  • If suggests Ischaemia/infarction then give GTN and/or Diamorphine/Morphine treat as for ACS.
  • Always consider - could this realistically be aortic dissection (Get CT:aortogram)
  • If breathless consider PE (needs CT-PA or VQ scan) or LVF (CXR/Echo)
  • Escalate for PCI. If STEMI and PCI not available consider Aspirin/Clopidogrel/thrombolysis
  • Get a CXR, Dimers if PE suspected, Troponin at 12 hours. A negative dimer may make dissection and PE less likely

Differential of acute chest pain

  • Acute Coronary Syndrome - ECG,Troponin, Echo
  • Pulmonary embolism - D-Dimers, CTPA
  • Aortic Dissection - CXR, CT, TOE
  • Oesophageal rupture - history/ CXR
  • Pneumothorax/ Tension Pneumothorax - Expiratory CXR diagnostic
  • Pleurisy - Pneumonia - CXR, Fever, Systemically unwell
  • Herpes Zoster
  • Rib or Sternal fracture - history

Cardiovascular Examination

Introduction

  • Examination is an active process and one must be thinking and looking for things not expecting them to just jump out at you
  • Even in the exam if you miss a sign or get the diagnosis wrong you may be saved by just talking sensibly and logically about your findings. The corollary that if you get the diagnosis right but talk nonsense you may not be doing yourself any favours either

Inspection

  • Is the patient comfortable, drowsy, agitated or breathless at rest, anaemic, plethoric, jaundiced, cachexic, thin, obese
  • Is there a GTN spray on locker or a packet of cigarettes
  • Midsternotomy scar could suggest cardiac surgery (CABG or valve replacement or correction of congenital abnormality if younger).
  • Connected to drip - IV fluids, IV Nitrates, Inotropes, Insulin
  • Cyanosis suggests > 5g/dl of deoxygenated Hb and if the cyanosis is present centrally may suggest chest disease or a cyanotic heart condition. A sluggish poor circulation can lead to peripheral cyanosis alone with normal central oxygenation.

Face

  • Down's syndrome - AV canal defects
  • Turner's syndrome - Coarctation of Aorta and Biscuspid Aortic valve
  • Mitral facies (malar flush) - suggests Mitral stenosis
  • Lips/Mucosa - Central cyanosis
  • Eyes - xanthelasma and corneal arcus in a younger person suggests hypercholesterolaemia
  • Dentition - potential source of sepsis if rotten (one does not need a dental degree to have a look and comment)
  • Thyrotoxic ? - AF, signs of Grave's disease with eye and skin signs
  • Acromegalic - Hypertension and cardiomegaly
  • Marfan's syndrome : look in mouth for high arched palate

Hands

  • Warm and dilated veins suggests normality or possibly CO2 retention.
  • Cold hands may suggest poor cardiac output or peripheral vascular disease.
  • Nicotine staining in a smoker
  • Clubbing is an important sign: Other than chest causes consider
    • Cyanotic congential heart disease in a young person
    • Infective endocarditis
    • Left atrial myxoma
  • Splinter haemorrhages
    • Can be a sign of nail trauma in a manual worker or endocarditis.
    • Traumatic lesions usually seen mainly in dominant hand
    • Ask about work done if suspicious
  • Osler's nodes - painful lesions in finger pulp suggests endocarditis
  • Janeway lesions - Erythematous lesions on palm suggest endocarditis
  • Nail fold telangiectasia in those with collagen vascular disease.
  • Arachnodactyly "spider fingers" and high arched palate: Marfan's syndrome
  • Elasticated skin and joint flexibility: Ehlers-Danlos (Aortic regurgitation)
  • Elbow and Achilles tendon: Tendon xanthomata in hands and also elbow and over Achilles tendon suggests hypercholesteroleamia

Pulse

Examination

  • Feel character and count the rate.
  • Assess the rhythm and its regularity or lack of.
  • Test to see if it is collapsing.
  • Compared right radial with left radial and femoral artery looking for delay.

Character

  • Good volume - Normal. Bounding - high output e.g. post exercise, thyrotoxicosis, fever.
  • Collapsing pulse - aortic regurgitation or AV fistula. Low diastolic pressure. Wide pulse pressure.
  • Slow rising and plateau - aortic stenosis. Narrow pulse pressure.
  • Jerky pulse - Hypertrophic cardiomyopathy
  • Bisferiens - mixed collapsing and plateau pulse with mixed aortic valve disease
  • Pulsus alternans - alternates large and small beats and suggests severe LV dysfunction
  • Pulsus paradoxus - BP falls > 10 mmHg in inspiration. (Normally falls less than that amount). Tamponade, pericardial constriction and status asthmaticus where inspiration will affect cardiac filling. Pulse weakens during inspiration.
  • Absent - dissection if aorta with ipsilateral subclavian involved, arterial thrombosis or embolism in subclavian or brachial or may be seen post catheterisation (angiography now done via radial artery), Takayasu's disease

Rate

  • Bradycardia (Rate < 60): Sinus bradycardia,
  • Complete heart block, AV Block 2:1, Atrial flutter or fibrillation with AV block, Sinus arrest with Nodal rhythm
  • Tachycardia (Rate > 100): Sinus tachycardia, Supraventricular tachycardia (AVRT, AVNRT), Atrial flutter (Rate = 300 / (2-4)), Atrial fibrillation, Ventricular tachycardia, Ventricular flutter
  • Pulseless: Ventricular fibrillation, Ventricular tachycardia, Asystole, Pulseless electrical activity, death.
  • If atrial fibrillation should actually count rate at the cardiac apex rather than the pulse as some beats will be low volume and undetectable at the wrist.

Rhythm

  • Regular - SR, Sinus tachycardia, Sinus bradycardia, Atrial flutter with 2:1 or 3:1 block, Complete heart block (slow!)
  • Regularly irregular - Bigemini (normal beat followed by ectopic), Mobitz type II block
  • Irregularly irregular - atrial fibrillation (commonest abnormality) , SR with multiple ectopics

Radiofemoral delay

  • Delay suggests coarctation of aorta. Be sure to check blood pressure at arm and leg if suspicious.
  • In an older person and if found more likely to suggest atherosclerosis.

Blood pressure

Physiology

  • Waveform - Arterial pulsation is composed of percussion wave travelling along artery which is at a much higher speed than the actual passage of blood with a dicrotic notch which represents closure of aortic valve
  • Blood pressure is measured using a cuff which inflates above systolic pressure occluding arterial blood flow
  • As the cuff is deflated auscultating over the artery will produce a knocking sound
    • Korotkoff phase 1 sound which comes on when the cuff is inflated to systolic pressure.
    • Korotkov phase 5 signifies diastolic pressure - As the cuff is deflated the sound softens and disappears
  • See section on hypertension for more information

Clinical findings

  • Hypertension BP > 140/90
  • Pulse pressure = systolic - diastolic pressure
  • Aortic stenosis - low pulse pressure
  • Aortic regurgitation - high pulse pressure
  • Right arm pressure > Left arm pressure by 20 mmHg suggests stenosed left subclavian possibly due to dissection or atheroma
  • Left arm pressure > right arm pressure by 20 mmHg suggests stenosed right subclavian possibly due to dissection or atheroma
  • Arm (brachial) pressure >> ankle suggests peripheral vascular disease (See ABPI) or it could suggest a Coarctation of the aorta
  • Right and left arm pressure often varies by 5-10 mmHG in normals

Jugular Venous pressure

Technique

  • The patient should lie back at 45 degrees with the head turned slightly to the left with the head on a pillow so the sternomastoids are relaxed.
  • Examination of the internal jugular vein can take some practice but can give some clues to right sided filling pressures.
  • It is located between heads of sternomastoid. Best seen at right angles with light glancing off. Very high levels seen from the end of bed as the earlobes move with pulse.
  • Do not confuse with the more superficial external jugular vein which has valves and is a poor marker of right atrial pressure.

Differentiating JVP and Carotid pulse

  • Carotid is readily palpable. JVP isn't
  • Carotid has one main waveform, JVP multiple
  • Only the JVP varies with posture and respiration
  • JVP pulsation can be occluded by pressure above
  • Pressure on the abdomen can cause a temporary rise in JVP

Measure the height

  • Determine the height of the JVP by calculating the vertical height above the sternal notch which approximates to the right atrium.
  • If the JVP is not pulsatile then consider SVC obstruction - other veins are often dilated on chest wall and the face and conjunctiva suffused
  • JVP usually falls on inspiration, if it rises consider pericardial tamponade or constrictive pericarditis

Waveform

  • 'a' wave : atrial systole - lost with AF. Increased with pulmonary hypertension/stenosis.
  • 'c' wave : carotid artefact
  • 'v' wave : atria fills while tricuspid valve shut
  • 'x' descent : RAP falls during ventricular systole
  • 'y' descent : Sharp y descent in constrictive pericarditis

Pathological JVP waveforms

  • Pathological giant "V" wave which is a composite of both a and the v wave seen with right ventricular systole and Tricuspid regurgitation
  • Cannon 'a' waves - Complete heart block or VT or frequent Ventricular ectopics where atria may contract against a closed Tricuspid valve.

Causes of an elevated JVP

  • Congestive cardiac failure (LHF+RHF)
  • Right sided failure - Inferior MI
  • Pulmonary embolism
  • Cardiac tamponade
  • Pericardial effusion
  • Constrictive pericarditis
  • IV Fluids and over hydration
  • Superior venal caval obstruction (NON Pulsatile

[picture of jvp]

Praecordial examination

  • Inspect - scar, abnormal motion, deformity
  • Palpate - apex beat, thrills, RV heave
  • Percussion - not usually valuable
  • Auscultate

Palpation

Apex beat

  • Most inferior and lateral point at which apical beat is palpable.
  • Normally is the 5th ICS in the mid-clavicular line. May be difficult to feel if subject is obese, COPD or a pericardial effusion.
  • Feel for the beat and also its character.
  • Dextrocardia is very rare but can sometimes appear in exams

Different types

  • Forceful Heaving - Aortic Stenosis
  • Thrusting and Dynamic - Aortic regurgitation, Post exercise, Dynamic circulation
  • Impalpable - Pericardial effusion, Emphysema, Obesity
  • Tapping - produced by the mitral valve slamming shut in Mitral Stenosis " palpable S1"
  • Dyskinetic asynchronous - Ventricular aneurysm. Place palm of hand flat on chest and feel a sort of rocking sensation
  • Impalpable - obesity, emphysema and barrel chested, pericardial effusion, dextrocardia

Right ventricular heave (the equivalent of LV apex beat)

  • Place palm of hand over left sternal edge and see if one can feel the RV lift which suggests RV Hypertrophy

Thrills

  • Place flat of hand across praecordium and see if one can feel any abnormal pulsations or thrills.
  • Try and get as much information as possible and time it with the pulse

Ausculation

  • Listen and time all sounds with your left index and middle finger on the right carotid or other pulse
  • Listen in all 4 valve places at least. Listen to axilla and along LSE
  • For Mitral stenosis - roll patient on left side and listen just medial to apex - exercise patient if needed
  • For Aortic regurgitation sit patient forward and ask them to exhale slowly and listen along LSE

First Heart sound

Introduction

  • Caused by closure of mitral and tricuspid valves.

Loud S1

  • Usually caused by ventricular systole occurring when the cusps of the mitral valve are far apart and snapped closed by a rapidly rising left ventricular pressure - a bit like a gust of wind catching an open door. Causes the tapping apex beat.
  • Causes
    • Mitral Stenosis
    • Hyperdynamic circulation e.g. anaemia, fever, Left to right shunt
    • Atrial ectopics
    • Short PR

Soft S1

  • Mitral Cusps are close at the time of systole or reduced output.
  • Causes
    • Mitral regurgitation
    • Severe heart failure
    • LBBB
    • Long PR
    • Aortic stenosis

Second Heart sound

About

  • It is produced by the sound of the Aortic valve and then pulmonary valve closing
  • Louder if shuts more forcefully due to increased pressure gradient e.g. hypertension or fast drop in pressure in ventricle e.g. VSD or MR.
  • Softer if reduced flow e.g. severe aortic stenosis

Findings

  • Loud A2 : Systemic hypertension, MR, VSD
  • Loud P2: Pulmonary hypertension, TR
  • Soft A2: Aortic stenosis
  • Soft P2: Pulmonary stenosis
  • Normal splitting of S2
    • Aortic closure and Pulmonary closure
  • Fixed splitting
    • ASD
  • Wide split S2
    • Pulmonary closure delayed with Deep inspiration
    • RBBB
    • Pulmonary stenosis
    • Severe mitral regurgitation
    • VSD
  • Reversed splitting of S2
    • Aortic closure delayed with LBBB
    • Severe Aortic Stenosis
    • Right ventricular pacing,
    • Wolff-Parkinson-White syndrome type B (causes early P2) (similar to LBBB)
    • Patent ductus arteriosus

Third heart sound

Mechanism: Rapid LV filling Normal in those under 30

  • Cadence Sounds like "KENTUCKY" with the
  • S1 ---PULSE--------- S2 S3 S1 -------PULSE------ S2 S3

Causes - Audible with

  • Heart failure
  • Mitral regurgitation
  • Ventricular septal defect
  • Dilated cardiomyopathy

Fourth Heart sound

Mechanism: Atrial systolic kick produces the sound

  • Sounds like "TENNESSEE" with the
  • S4 S1 ------PULSE-------S2 S4 S1 ------PULSE-------S2

Causes - Audible with

  • Hypertension
  • Aortic stenosis
  • HCM
  • Pulmonary stenosis
  • Post MI

Absent S4 with AF.

Prosthetic valves

Metal Prosthetic sounds

  • Metal sounds with pulse = Mitral valve, After is likely to be aortic.
  • Flow murmurs heard. Need warfarin. Longer lasting.

Tissue prosthetic valves

  • sound normal. Do not need warfarin.
  • Last shorter. From pig or homograft.

Other findings

Ejection click

  • Occur as valves open e.g. aortic and pulmonary and suggest bicuspid valves
  • May be heard normally in young.

Mid-systolic click

  • Seen with Mitral valve prolapse. "click murmur syndrome". May be followed by a PSM.

Opening snap

  • As mitral valve opens - associated with mitral stenosis.

Tumour "plop"

  • (Left) Atrial myxoma occluding mitral valve orifice in diastole with a loud S1 and MDM which mimics mitral stenosis

Pacemakers

  • Pacemakers are usually found in the left infraclavicular fossa and should be easily palpable.
  • Usually put on non dominant side. A left handed golfer might end up with his pacemaker on the right.
  • Might actually be an ICD. Should be an overlying scar.
  • Always examine for one in the morgue before you sign a cremation form as unless removed it may explode.
  • If you are unsure look at the CXR which will give you a clue as to what type it is

Murmurs

Introduction

  • Murmurs are caused by turbulent inefficient flow so kinetic energy is converted to sound energy.
  • They may be due to forward flow through a narrowed valve or backward flow through an abnormally open or incompetent valve.

Clinical

  • The timing is intrinsic to diagnosing them. Must always time with one finger on major pulse.
  • With the pulse = systolic. Not with pulse = Diastolic.
  • Listening to murmurs -Traditionally these are the areas but do not really take into account different chest anatomy and physiology and jets of turbulence can be heard outside these areas.
  • Instead of these 4 areas one can just start in the apex and slide the stethoscope across to the tricuspid area, up the LSE to the pulmonary area and over into the aortic areas listening as you go. A sort of sigmoidal shape. Remember to have one finger on a pulse at all times.

Examination

  • Aortic area : 2nd ICS to the right of strernum
  • Pulmonary area: 2nd ICS to the left of the sternum
  • Mitral area : At or just medical to the cardiac apex
  • Tricuspid: at the lower LSE

Grading of murmurs

  • 1. Just audible
  • 2. Quiet but audible with stethoscope
  • 3. Moderately loud
  • 4. Loud
  • 5. Heard all over praecordium + thrill
  • 6. Audible without stethoscope

The five important laws of cardiac auscultation are

  • Murmurs with the pulse are systolic, the rest are diastolic
  • Right sided murmurs get louder with inspiration and left sided murmurs louder with expiration
  • HCM and Mitral valve prolapse murmurs get louder on standing or valsalva.
  • HCM and MVP murmurs disappear with Squatting and leg raising
  • All other murmurs do the opposite to HCM and MVP

Continuous murmur

  • Fallot's tetralogy
  • Coarctation of the Aorta
  • Coronary AV fistula
  • Ruptured sinus of Valsalva Diastolic murmurs are never innocent

Radiation of murmurs

  • Mitral incompetence -> Axilla
  • Aortic stenosis -> Carotids and apex
  • Aortic incompetence -> Sternal edge

At the end of the examination

  • Ask to listen to lung bases for signs of pulmonary oedema
  • Ask to look for hepatomegaly and ascites for right heart failure suspected
  • Ask to check ankles for oedema, may also see vein graft scars confirming sternal scar was for a CABG
  • Offer to examine peripheral pulses