Murmurs Made Easy

For the purpose of this post, I shall fast forward the examination of the heart to auscultation of the heart murmurs. 

We begin auscultation of the precordium by placing the stethoscope over the mitral area. 

A hand drawn picture of the anterior chest with the location of each valves

One very important step which is often overlooked or neglected by medical students is the instruction to the patient to breathe in and breathe out slowly. Personally, I would let my stethoscope to remain over each valve area for a total duration of 2 breathing cycles (i.e. breathe in-breathe out-breathe in-breathe out) before moving to the next valve area. 

Let us recap the basic physiological changes that affect murmurs during breathing. During inspiration, the increased thoracic cavity volume lowers intrathoracic pressure thus increases venous return to the right side of the heart. This will cause an increase in murmur intensity for tricuspid and pulmonary valve disorders. 

On the other hand, expiration reduces the thoracic cavity volume and thus increases arterial outflow from the left side of the heart. This will cause an increase in murmur intensity for mitral and aortic valve disorders. 

This basic concept is very important and will help guide you to eliminate and narrow down possible differentials for every murmur heard over any particular valve area as I will explain next. 

Let us begin at the mitral valve area. Place the diaphragm of the stethoscope over the mitral valve area. Regardless whether you hear any murmurs or not, I would encourage you to do the breathing manouvres for at least 2 breath cycles as mentioned above. If there are any soft murmurs, this manouvre will enhance or increase the murmur intensity. 

If there is a murmur heard over the mitral area, below are the possible causes:

1. Mitral regurgitation (MR)

2. Mitral stenosis (MS)

3. Aortic stenosis (AS)

4. Tricuspid regurgitation (TR)

5. Ventricular septal defect (VSD)

To help differentiate between the causes, here is how the breathing manouvre will help narrow down the diagnoses. 

If during inspiration, the murmur heard over the mitral area becomes louder, then it can be concluded that the murmur is actually originating from the neighbouring tricuspid valve. Therefore the murmur detected over the mitral valve can be ignored. The murmur will then be best heard over the tricuspid area after completing the mitral valve examination. 

If during expiration, the murmur heard over the mitral area becomes louder, then it can be concluded that the murmur is unlikely to originate from the tricuspid valve or VSD. Only 3 possibilities remain i.e. MR, MS or AS. To differentiate between the 3 possible source of the expiratory phase murmur heard over the mitral valve area, the student will need to time the murmur by palpating the carotid or radial pulse. If the expiratory murmur coincides with the diastolic phase, then the only diagnosis possible would be a MS murmur. Next step is to listen and verify that the murmur is indeed a mid diastolic murmur (MDM) of MS i.e. switching to the bell of the stethoscope and listening for the MDM with the patient lying left lateral.

If the expiratory murmur coincides with the systolic phase, then you have ruled out MS. So all that is left would be either MR or AS. To differentiate between this two, listen to the systolic murmur carefully and decide if its a pansystolic murmur (PSM) or an ejection systolic murmur (ESM). A PSM would classically have a soft S1 with the systolic murmur extending throughout systole. An ESM, on the other hand, would have a clearly heard S1 and the systolic murmur would be heard in mid systole. 

If it is a PSM, then the diagnosis would be a MR. This can be further confirmed by auscultating the axillae for radiation of the MR murmur. If it is a ESM, then the only diagnosis possible would be an AS murmur. An AS murmur can sometimes be heard all the way to the left axillae as well. This phenomenon is called the Gallarvardin phenomenon. 

If there no variation in the murmur intensity between inspiration and expiration, time the murmur by palpating the carotid or radial pulse. A systolic murmur that does not vary with inspiration or expiration heard over the mitral area can only be caused by a VSD. Once you have completed the mitral valve examination, confirm the earlier heard murmur which will be best heard over the lower left sternal edge. This will confirm the presence of a VSD. 

 

Over the tricuspid valve area, the same manouvres as above should be applied. If a PSM is heard over the tricuspid valve area, there are only 3 possibilities: a TR, a VSD or a loud MR. Remember, the chest cavity and specifically the heart isnt a very large structure. Therefore any loud murmur can practically be heard everywhere. If the PSM increases intensity during inspiration, the PSM is confirmed to be from the tricuspid valve i.e. a TR. If the PSM is louder during expiration, then the murmur is a radiation from the mitral valve i.e. a MR. But if the murmur does not change with either inspiration or expiration, then the PSM could be from a VSD. 

 

Over the pulmonary valve area, it is unusual to hear a PSM. But you could detect a ESM of pulmonary stenosis (PS). This is, however, uncommon for undergraduate examinations. An early diastolic murmur (EDM) of pulmonary regurgitation (PR) is even more rare. Both PS and PR murmurs will be louder during inspiration. Also, do look out for machinery or continuous murmurs near the pulmonary valve area. This may indicate presence of a Patent Ductus Arteriosus (PDA). The machinery murmur of a PDA is often heard over the upper left chest area just below the left clavicle. This area is often close to the pulmonary valve area.

Over the aortic valve area, it is also uncommon to hear a PSM. Look out for ESM of aortic stenosis (AS) and EDM of aortic regurgitation (AR). Both AR and AS murmurs will be louder during expiration. AR murmur can be further verified by presence of EDM which is best heard over the Erb's space or second aortic space over the left sternal edge with the patient leaning forward. AR murmurs are usually accompanied by other peripheral signs like Corrigan's sign (bilateral prominent carotid arterial pulsations), a collapsing pulse as well as wide pulse pressure. AS murmurs can sometimes radiate to both carotid arteries and this feature should be looked for and examined routinely in patients with AS murmurs. However, AS due to aortic sclerosis (degenerative cause) may not always have radiation to both carotids. The ESM murmur may be localised to the aortic valve area only. It is important to take note of this. In real life practice, the ESM of AS can sometimes be heard over the pulmonary valve area as well. This may confuse the unsuspecting student. However this confusion can be avoided when patient is asked to inspire and expire slowly. If the ESM heard over the pulmonary valve area is louder during inspiration as mentioned earlier, then the ESM is likely due to PS. If the ESM over the pulmonary valve area is louder during expiration, then the ESM is likely to originate from the neighbouring aortic valve i.e. an AS.

CCE.

Cushing's syndrome

Cushing's syndrome is a favourite appearance in the medical examinations. 

Often, the stem would be to "look and proceed". Often the diagnosis would be easily suspected. 

From head to toe, the clinical findings are as below:

1. Depression or psychosis

2. Cataracts

3. Acne

4. Rounded facies

5. Hirsuitism in females

6. Central obesity

7. Increased supraclavicular fat pads

8. Increase dorso-cervical fat pad

9. Acanthosis nigricans

10. Purple striae at anterior abdomen or axillary skin folds or thighs

11. Easy skin bruising

12. Osteoporosis

13. Diabetes mellitus (look for finger prick marks at finger tips, funduscopy for diabetic retinopathy changes)

14. Hypertension (offer to check patient's blood pressure using manual sphygmomanometer)

15. Hypogonadism (menstrual disturbances, impotence)

16. Proximal muscle weakness (myopathy)

17. Thin arms and legs

Once the diagnosis of Cushing's syndrome is made, investigations will be focused on determining the aetiology of Cushing's syndrome i.e ACTH-dependent (ACTH secreting pituitary tumours/ ectopic ACTH-secreting tumours) versus ACTH-independent (adrenal causes or exogenous steroid exposure). A differential of a person with Cushingoid appearance would be pseudo-Cushing's which can be seen with persons with obesity or chronic alcoholism.

CCE.

Diabetes Mellitus - How to Approach a Patient with Diabetes Mellitus in the Long Case Examination (History Taking)

Diabetes Mellitus (DM) is a common entity nowadays and therefore it should be well known by every healthcare practitioner particularly the clinicians. 

Similarly, diabetes mellitus is also a common appearance in the medical examinations. They may appear in various forms e.g.  target organ damage, complications related to treatment, as well as psychosocial issues surrounding the condition itself. 

For the undergraduate final examinations, students can expect to encounter cases where a patient presents with a particular complaint related to a target organ damage. For example the patient may present with numbness affecting the feet or even blurred vision affecting one or both eyes. The student is expected to get a competent and complete history pertaining to the presenting complaint as well as establish the diagnosis of diabetes mellitus and whether there are presence of other target organ damage occurring concomitantly with the presenting complaint.

So, let us refresh our memories with regards to diabetes mellitus and its complications.

Diabetes mellitus are broadly categorised into 2 types (for the undergraduate level, at least):

Type 1 - Autoimmune cause, due to premature loss of pancreatic beta islet cells

Type 2 - Acquired cause, usually due to insulin resistance as a result of increased adipocity, hormonal dysregulation etc.

There are other types as well e.g Maturity Onset of Diabetes in the Young (MODY), Gestational diabetes, Double Diabetes (mixture of both Types 1 and 2 in the same patient) etc. But those are for another topic and discussion as it can be complex. 

In general, the differentiating factor between Types 1 and 2 Diabetes Mellitus is age of onset. Type 1 typically occur in the young, usually pre adolescent age whereas Type 2 diabetes occur in adulthood (in general). However this distinctive factor is no longer clearcut and we are seeing younger patients with Type 2 diabetes due to lifestyle and the ever increasing waistline among youngsters. 

After tackling the presenting complaint, you can add the following information within the history of presenting illness (HOPI) segment. 

Enquire and explore regarding complications resulting from diabetes mellitus:

MACROVASCULAR:

• Coronary artery disease
• Ask about chest pains (categorise according to Canadian Cardiovascular Society classification), dyspnoea (categorise according to New York Heart Association classification), pedal oedema, orthopnoea, paroxysmal nocturnal dyspnoea etc
• Cerebrovascular disease
• Ask about facial assymetry, unilateral limb weakness, speech impairment, dysphagia, memory impairment (vascular dementia)
• Peripheral arterial disease
• Claudication pains, resting pains, digital cyanosis or gangrene

MICROVASCULAR:

• Retinopathy
• Ask about scotomas, blurred vision, floaters, visual field defects
• Nephropathy
• Ask about frothy urine, pedal oedema, facial puffiness, periorbital oedema, dyspnoea, uremia (nausea/ vomiting/ anorexia/ chest pains (pericarditis) / abdominal pains (uremic peptic ulceration)/ altered sensorium or seizures (uremic encephalopathy), dialysis, renal transplantation)
• Neuropathy - somatic and autonomic
• Ask about numbness affecting extremities especially the foot, pressure ulcers, digital gangrene, foot deformities, postural giddiness, recurrent vomiting (gastroparesis)
• Sexual dysfunction - erectile dysfunction (a sensitive issue due to the taboo among Asian customs, but if approached professionally and you are able to obtain information regarding this issue, many patient's will be grateful and of course, impress the examiners)

METABOLIC:

• Hyperglycemia
• Ask about polyuria, polydipsia, unintentional weight loss, nocturia (not to be mistaken with prostatism - diabetic polyuria have good amd large volume urine stream due to osmotic diuresis whereas prostatism nocturia have weak urine stream with the usual lower urinary tract symptoms e.g. terminal dribbling, hesitancy etc). 
• Diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic syndromes (HHS)
• Ask about symptoms of hyperglycemia plus dyspnoea (may suggest acidotic breathing), sweet fruity breath smell (ketone breath), altered sensorium (HHS) or involuntary limb movements (hemichorea hemiballismus due to HHS) ** diabetic emergencies will not appear for exams, rest assured 😏
• Hypoglycemia
• Ask about hand tremors, hunger pangs, diaphoresis, agitation/ anxiety/ restlessness, syncope and coma (unlikely to appear in the exams as you wont be able to clerk the patient!!) 

In the review of systems segment, can explore regarding any health problems from head to toe which may be the cause of diabetes mellitus e.g. connective tissue disorders e.g. SLE/  rheumatoid arthritis or chronic lung disease (asthma/COPD) (chronic steroid usage), acromegaly, Cushing's syndrome. If the patient is young, presence of concomitant connective tissue disease (s) may suggest an autoimmune cause of DM. 

In the family history segment, explore about strong family history of DM. 

For past medical history or surgical history segment, enquire about history of pancreatitis, pancreatic tumours or pancreatic surgery. Also about any pituitary tumour resection (pituitary Cushing's or Acromegaly), adrenal tumour (Adrenal Cushing's) resections. 

In the drug history section, can check with the patient regarding their medication list and compliance. Patients may know the medications they are on and the dosages. Alternatively, patients may be provided a prescription slip and will be instructed to show the medical student upon request. If there is element of non-compliance, be sure to enquire the reason behind the behaviour. Very often, the patient may inform of some adverse side effects as a result of taking that particular medication which causes the non-compliance. For example, the patient may be non-compliant to metformin because of bloating or frequent loose stools. 

Physical examination of the patient with diabetes mellitus requires a comprehensive approach from head to toe similar to history taking. There will be many areas to cover and therefore, it will be covered in the next post "Diabetes Mellitus - How to Approach a Patient with Diabetes Mellitus in the Long Case Examination (Physical Examination)". 

CCE. 

Chest Pains - Approach to a Patient with Chest Pain for the Long Case Examinations

Chest pain is a common exam question especially for the long case in undergraduate level exams. 

As in any scenario, usage of common sense is important and this will help you use time more effectively in the 60 mins designated for the long case exam. 

Differential diagnoses will depend on the anatomical location of the chest pain:

Skin:

Herpes zoster

• Fever, rash (usually in dermatomal location), history of varicella zoster infection, enquire about immune suppressed states: DM, malignancies, chronic steroid therapies or immune suppressive therapies 

Muscle:

Hematoma or soft tissue injury 

• history of chest wall trauma 
• Signs of external injuries: bruises, abrasions, deformities 
• Tender on palpation

Bone:

Costochondritis 

• recent exertion involving chest wall movement 
• Pain aggravated by thoracic wall movements (leaning forwards or backwards, rotatory movements, breathing in/ out movements)

Rib/ sternal fractures

• recent trauma to chest wall
• Chest wall deformities or signs of external injuries
• Chest spring will be positive over the fracture site 

Lung:

Pneumonia

• fever, cough, dyspnoea 
• Chest pain is usually described as pleuritic in nature nature 
• Usually associated with bronchial breathing and reduced breath sounds with coarse creps over the pain area 

Pneumothorax

• history of fever, cough, dyspnoea preceding or concurrent with pain onset 
• chest pain is usually described as sharp and sudden in onset for spontaneous pneumothorax
• history of recent chest wall trauma 
• history of pneumothorax 
• History of chronic lung disease 
• Look for chest tube scars or thoracotomy scars 
• Tall stature with long limbs suggestive of Marfanoid feature

Empyema

• Usually will have associated high grade fever, cough, dyspnoea
• Cough productive of purulent or blood stained sputum 
• Usually unwell appearance (septic looking)
• Chest pains due to empyema are usually pleuritic in nature
• Reduced chest expansion over the pain site 
• Reduced breath sounds with pleural effusion like findings 

Pleural effusion/ hemothorax

• similar to empyema except patient may be less septic looking on presentation
• the complaint may be more of dyspnoea or chest tightness as compared to chest pain
• may have other features of fluid overload: congestive heart failure, nephrotic syndrome, liver cirrhosis 
• Recent Chest wall trauma with evidence of external chest wall injury e.g. bruises, chest wall deformities, positive chest spring on palpation

Heart:

Angina

• pressing or crushing retrosternal chest pains (usually left sided) with typical radiation to i psi lateral shoulder or upper limbs and neck with associated diaphoresis, nausea, vomiting with/without syncope 
• History of similar attacks, or history of exertional angina 
• Risk factors: Age, family history of coronary artery disease, cigarette smoking, alcohol, DM, HPT, dyslipidemia, CKD

Dissecting aneurysm 

• usually present with back pains
• described as tearing pain
• History of high BP
• Check discrepancy in UL pulses
• Look for Marfanoid features 
• Look for new onset aortic valve murmurs
• Patient usually unwell 

Gastrointestinal tract:

GERD

• burning type retrosternal chest pains 
• May originate from epigastric region and extend superiorly to the throat 
• Assoc with acid or water brash
• May or may not have hoarseness or voice 
• Preceding heavy meals, spicy or oily foods 
• Usually symptoms have been ongoing for a long time 

FB 

• ask about bony fish meals or accidental or deliberate swallowing of any foreign bodies recently (if yes, you may need to explore suicidal tendencies and major depression). 

Spine:

Radiculopathies

• pain is usually circumferential ie radiating from the back around the sides to the front of the thorax. It is important to clarify this with patient so they may give you a clear description with regards to the nature and origin of the pain (on a personal note, I have encountered a case that was referred for chest pains suspecting to be unstable angina only to discover that the pain is actually from a collapsed thoracic vertebra due to TB spondylitis causing nerve root compression of the exiting thoracic spinal nerve). Radiculopathies can be caused by compression of the exiting spinal nerve root by a prolapsed intervertebral disc, a spinal cord tumour, paraspinal abscess or a collapsed vertebra as mentioned above, etc
• This type of pain may be aggravated by certain manouvres eg coughing, straining etc. 

Psychiatry:

Anxiety

• chest pains can be felt like a central anterior chest tightness sensation when experiencing a panic attack. It is usually accompanied by other supporting symptoms like feeling extreme fear, light headedness, palpitations, hand tremors, and the patient may or may not have a clear precipitating event or stressor. 

Major depression

• A depressed person may have multiple psychosomatic complaints. Pain may not necessarily be limited to the chest. Pain may also affect other body parts. Enquire about other depressive symptoms e.g. low mood, suicidal ideations, anhedonia, anorexia, etc. 

The list of chest pain aetiology mentioned above may seemed a lot and you may wonder if you will ever have time to explore each differential within the 60 min time frame. This is a valid concern. Therefore you need to be selective and use common sense and try narrow down the differentials based on the patient in front of you. As the clerking progresses, you’ll be able to gain more information to help you cross off the differentials one by one quickly. 

Lastly, practice makes perfect. So go out there and clerk many cases of dyspnoea. There are many such cases in the medical wards as it is a common presenting complaint. Happy learning. 

CCE. 

Right Eye Horner's Syndrome

This elderly male patient presented with chronic coughing associated with dyspnoea and weight loss. 

Examination noted partial ptosis of the right eye but no ophthalmoplegia.

Further examination of the eyes noted reduced pupil size over the right eye compared to the left eye. 

The left eye pupil size was normal.

A diagnosis of right Horner's syndrome was made. 

Respiratory examination noted bronchial breathing over the right lung apex with tracheal deviation to the contralateral side suggestive of a right pancoast tumour. 

Therefore the unifying diagnosis was Right pancoast tumour causing Right eye Horner's syndrome. 

CCE. 

Cranial Nerve 3 Palsy - Surgical CN3

The picture below shows a young girl with complete ptosis of the left eye. She presented with progressive and worsening ptosis affecting her left eyelid. At the same time, she reported having diplopia as well. 

Upon elevating her left upper eyelid, her left eyeball is displaced inferolaterally in neutral position. This finding is consistent with a left CN 3 (occulomotor) palsy. The eyeball is deviated in such a manner due to unopposed action of the left lateral rectus and left superior oblique muscles which are innervated by the left CN 6 (abducens) and left CN 4 (trochlear) nerves respectively. 

It is also important to take the opportunity to assess the left pupil size to determine the possible cause of her left CN 3 palsy. In this picture, it can be seen that her left pupil is dilated compared to the right pupil. This suggests that she may have a space occupying lesion compressing the CN3. In most cases, a cerebral aneurysm (particularly from the posterior communicating (PCOM) artery) need to be looked for. The pathogenesis of a dilated pupil in such a scenario is that an aneurysm arising from the PCOM artery compresses on the CN 3 putting pressure on, and damaging the parasympathetic nerve fibres that innervate the constrictor pupillae muscle that is responsible for pupillary constriction. These parasympathetic nerve fibres run on the surface of the CN 3, therefore when there is an external compression onto the CN3, the parasympathetic nerve fibres would be affected as well.

Once a surgical cause i.e. an aneurysm has been excluded, then a medical cause can still be possible. Bear in mind, the parasympathetic nerve fibres that innervate the constrictor pupillae muscle that is responsible for pupillary constriction is also supplied by tiny blood vessels called vasa nervorum. The vasa nervorum are equally susceptible to damage from medical diseases e.g. connective tissue disorders, diabetes mellitus, atherosclerosis etc like other arteries elsewhere in the body. Once the blood supply to the parasympathetic nerve fibres are disrupted, there will be ischemic damage followed by impaired parasympathetic nerve function resulting in a dilated pupil.

CCE.

Koilonychia

Dear students, welcome back. 

This image shows koilonychia i.e. spoon shaped nail deformities. The typical description is that such nail changes will be able to hold a drop of water. Such abnormal nail changes are usually seen in chronic iron deficiency anemia.

This photo was taken from the hand of a patient diagnosed with Hereditary Hemorrhagic Telangiectasis. As a result of chronic occult bleeding, he was admitted for symptomatic anemia and required blood transfusions. 

It is important to look out for koilonychia when encountering a patient with chronic anemia. Remember to get a complete history regarding chronic blood loss e.g. menorrhagia or bleeding per rectum etc. A complete dietary history confirming reduced iron intake is also important.

CCE.

Dyspnoea - Approach to a patient with dyspnoea for the long case examination

Dyspnoea is a common complaint encountered both in the exams and real clinical practice. 

To approach a patient with dyspnoea, you need to have a list of possible differentials in your mind to enable you to start off the interview smoothly without wasting much time. It is advisable to conduct your long case examination in a "hybrid" manner, whereby after clerking the patient for several minutes, you may proceed with physical examination while taking more relevant history concurrently. This will save you lots of time when comparing to compartmentalising your long case session into history taking, followed by physical examination, then drafting out your management plan.

The causes of dyspnoea are numerous and can be broadly categorized into the systems. This way, it will be easier to draw out a longer list of differentials which you may tackle during history taking and physical examination:

1. Respiratory 

- Asthma:

• Enquire about diurnal variation of symptoms (worse at night or early mornings, symptoms less during afternoons)
• Enquire about atopy: eczema, allergic rhinitis
• Enquire about triggers: dustmites, pollen, animal dander, environmental pollutants (smoke, dust, chemical aerosols etc), respiratory tract infections
• Enquire about family history of asthma or atopy
• Important to enquire about asthma control - frequency of symptoms and exacerbations (will impact treatment plan)
• Look for triggers causing exacerbations in current setting: respiratory tract infections, recent exposure to allergens, non compliance to inhalers or oral medications
  
• Examine for atopy: eczema at the joint flexures (commonly at antecubital fossa or popliteal fossa), nasal turbinate hypertrophy (allergic rhinitis)
• Examine the lungs for ongoing bronchospasm: signs of respiratory distress (tachypnoea, tripod positioning, tracheal tug, intercostal and subcostal recessions), expiratory wheezing or prolonged expiratory phase.  
• Remember to examine the sputum pot if provided in the exams. Look for purulent  sputum to suggest pneumonia 

- Chronic lung disease (Chronic obstructive airways disease/ interstitial lung disease):

• Enquire about symptoms without diurnal variation
• Enquire about history of cigarette smoking
• Enquire about occupation: shipyard workers/ painters (asbestos), sawmill workers, quarry workers, clearners, farmers
• Enquire about previous lung infections e.g. pulmonary tuberculosis, recurrent lung infections that may lead to pulmonary fibrosis/ bronchiectasis due to scarred lung tissue
• If the patient has fertility issues with bronchiectasis, consider Kartagener's syndrome
• Examine for barrel shaped or hyperinflated chest wall, clubbing, asterixis (Co2 toxicity), palmar erythema (chronic Co2 retention), nicotine staining (cigarrete smoking)
• Examine the lungs for ongoing bronchospasm: signs of respiratory distress (tachypnoea, tripod positioning, tracheal tug, intercostal and subcostal recessions), expiratory wheezing or prolonged expiratory phase.
  
• Remember to examine the sputum pot if provided in the exams. Look for purulent or blood stained sputum to suggest bronchiectasis 
  

- Pneumothorax:

• Enquire about chest trauma
• Enquire regarding previous pneumothorax
• Enquire about any thoracic procedures e.g. chest tube, decortication, pleurodesis
• Enquire about family history
• Enquire about patient's height and proceed to examine height and arm span if there is a clinical suspicion of Marfan's. 
• Enquire about history of chronic lung disease or connective tissue disorders
• Enquire about ongoing current lung infection: fever, cough, pleuritic chest pains
• Examine for tension pneumothorax which can be life threatening (unlikely to appear in exams but it is good practice in clinical setting): tracheal shift to contralateral side, displaced cardiac apex beat, reduced chest expansion with increased percussion resonance over the affected side, cyanosis, tachypnoea
  

- Pleural effusion:

• Enquire about lung infection: fever, cough, pleuritic chest pains (parapneumonic effusions)
• Enquire about lung malignancy: anorexia, weight loss
• Enquire about pulmonary TB symptoms: chronic coughing, hemoptysis, drenching night sweats, anorexia, weight loss, PTB contact
• Enquire about heart failure symptoms: reduced effort tolerance, pedal oedema, orthopnoea, paroxysmal nocturnal dyspnoea, cough with frothy pinkish sputum 
• Enquire about chronic liver disease symptoms: yellow discoloration of the eyes, generalised itching, easy bruising, hemoptysis, epistaxis, abdominal distension, pedal oedema, alcohol consumption, sharing of intravenous syringes, multiple sexual partners
• Enquire about kidney disease: frothy urine, hematuria, facial puffiness, scrotal swelling, pedal oedema, nausea/ vomiting, generalised itching

- Airway obstruction/ restriction

• Enquire about foreign body aspiration/ choking episodes prior to onset of dyspnoea
• Examine for stridor 
• Enquire about oral cavity or upper airway swellings: allergic reaction, chemical burns, smoke inhalation, trauma
• Enquire about neck compression: large goitre, large tumour/ hematoma/ subcutaneous emphysema
• Enquire about fatigability: ptosis/ diplopia more prominent towards the evening or night, proximal upper/ lower limb weakness (all these suggestive of Myasthenia gravis)
• Enquire about lower limb paralysis as well; if ascending pattern, suspect Gullain-Barre syndrome (need to check precipitating factors e.g. recent viral infection) and examine for absent reflexes. 

2. Cardiovascular

- Congestive heart failure

• Enquire about reduced effort tolerance, its best to classify severity using the NYHA classification
• Enquire about orthopnoea, paroxysmal nocturnal dyspnoea, leg swelling, cough with frothy pinkish sputum to suggest pulmonary oedema
• History of myocardial infarctions or coronary artery intervention procedures e.g. stenting or bypass grafting surgery
• History of valvular heart diseases or any valvular surgeries
• History of endocarditis or rheumatic fever/ heart disease
• History of congenital heart disease (usually the uncorrected ones will likely progress to decompensated heart failure at a later age)
• Clarify with the patient regarding instruction by health provider concerning fluid restriction and whether patient is compliant to fluid restriction advice
• Any precipitating factor to suggest cardiac decompensation: look for infection, anemia, new myocardial ischemia

 

 

- Myocardial ischemia/ angina

• Enquire about crushing retrosternal chest pains or left sided chest pains with typical radiation to left shoulder/ arm, jaw/ neck and associated nausea/ vomiting/ diaphoresis
  
• Expect atypical presentation in special groups e.g. elderly, diabetic patients
• Enquire about reduced effort tolerance, exertional angina, try classify according to Canadian Cardiovascular Society (CCS) classification. 

- Venous thromboembolism

• Usually dyspnoea will be sudden onset
• May be associated with pleuritic chest pains (as a result of pulmonary infarction)
• Enquire about precipitating conditions e.g. prolonged immobilisation (long haul flights), recent pelvic or lower limb /trauma or surgeries, on combined oral contraceptive pills, history of thrombophilia (unprovoked venous thrombosis, arterial thrombosis, early pregnancy loss, connective tissue disease)
• Examine for pulmonary hypertension (loud P2, left parasternal heaving, tricuspid regurgitation)
• Examine for pleural rubs (pulmonary infarction)
• Examine abdomen for pelvic masses or intra-abdominal tumours
• Examine the lower limbs for any painful calf swellings to suggest deep vein thrombosis
• Look for recent surgical scars over the abdomen and lower limbs
• Look for signs of connective tissue disease: malar rash, discoid rash, peripheral joint deformities, alopecia, Raynaud's phenomenon, sclerodactyly etc. 

3. Hematological

- Anemia

• Enquire about dizziness, headaches, pale look, palpitations, reduced effort tolerance
• Enquire about blood loss: gastrointestinal bleeding, menorrhagia, hematuria, bleeding wounds
• Enquire about fever, bleeding tendencies (may suggest reduced leucocytes or platelets as well, thus pointing towards a hematological or connective tissue disorder)
• Enquire about dietary habits: pure vegetarian, lack of iron in diet etc
  
• Examine for pallor, bruises, hepatomegaly, splenomegaly, lymphadenopathies
• Look at the nails for koilonychia (chronic iron deficiency)
  
• May offer to do rectal examination to look for melena
  

- Hyperviscosity - polycythemia, thrombocytosis, leucocytosis

• On the other hand, excessive blood cells can also cause dyspnoea when there is hyperviscosity
• Ask about headaches, blurred vision, thrombotic episodes e.g. stroke, angina, claudication pains etc
• Ask about bleeding tendencies as well (thrombocytosis can manifest as bleeding) 
• Examine the patient for plethora (polycythemia), hepatomegaly, splenomegaly (may be massive in Myelofibrosis or any of the other Myeloproliferative neoplasms)
• Examine for enlarged lymphadenopathies as well (to suggest a hematological disorder)
• Examine for gum hypertrophy (may suggest acute myeloid leukemia)

4. Endocrine

- Diabetic ketoacidosis

• The severe metabolic acidosis usually seen in DKA can manifest as dyspnoea. The patient may be tachypnoiec as a compensatory mechanism to the metabolic acidosis. Acidotic breathing also known as Kussmaul breathing is different compared to the usual hyperventilation or tachypnoea. You will need to see several or multiple such presentations to be able to appreciate Kussmaul breathing. However, rest assured, such a case will not appear in your exams. 
• Get history about diabetes mellitus and any osmotic symptoms (weight loss, polydipsia, polyuria).
• Enquire about any precipitating factors: infection, trauma, fasting (dehydration), surgery, angina etc
• Do bear in mind that any condition that causes organ failure resulting in metabolic acidosis can also manifest as dyspnoea

- Thyroid disorders

• Paarticularly hypothyroidism. Hypothyroidism causes reduced muscle strength (including respiratory muscle weakness), fatigue and reduced effort tolerance. 
• Hypothyroidism can also cause weight gain and is also associated with obstructive sleep apnoea which can cause dyspnoea as well

5. Drugs

- Drug overdoses - 

• Certain drugs like salicylates (common example is aspirin) can cause high anion gap metabolic acidosis which may result in Kussmaul breathing. 
• Opioid toxicity can suppress the respiratory drive and lead to dyspnoea in toxicity. However opioids if used appropriately can reduce dyspnoea (commonly used by palliative teams everywhere). 
• Therefore it is important to get a proper drug history and explore regarding possible drug toxicity. If there is suspicion of toxicity, it is also prudent to explore regarding possible deliberate self harm. 

6. Psychiatry

- Anxiety:

• The anxious patient may have palpitations, sweating, hand tremors, feeling fearful constantly together with dyspnea 
• In a panic attack, patients may be hyperventilating which may result in carpopedal spasms, so ask about muscle spasms or cramps usually affecting the hands and feet. 
• Patients may complaint of perioral numbness with or without numbness affecting their extremities. If present, this may further suggest an anxiety aetiology. 
• Try to enquire about concomitant major depression symptoms, which may accompany patients suffering from anxiety. 

It may seem like so much to do when seeing a patient with dyspnoea. This is where practice is important and it helps you to go through your differentials more effectively. Also, tailor the differentials to the patient in front of you. Not every differential will be applicable. For example, a young patient who is lean without a barrel shaped chest is unlikely to have chronic lung disease (therefore you need not dwell too long in excluding this differential). A reminder also to examine the patient while taking the patient's history concurrently to save time. You cannot afford to be too compartmentalized in the exams due to time constraint. 

Happy practising. 

CCE.

Apex Beat Missing - What to do?

Looking for the cardiac apex is an important part in the cardiovascular examination, be it the long case or short case examination.

If the cardiac apex is not palpable in the supine position (patient propped up at 45 degrees of course), then the next step is to request the patient to raise the left arm above his or her head and turn to the left lateral position. This enables the cardiac apex to be closer to the thoracic wall thus easier to be palpated.

However, in some situations, the cardiac apex remain elusive in its usual expected anatomical location. Some possible causes are:

1. Thick chest wall

- the thick subcutaneous tissue makes it difficult to feel the apex 

2. Emphysema

- the overlying hyperinflated lung tissue masks the cardiac apex and makes it more difficult to detect

- a hyperinflated chest wall can be suspected when the antero-posterior chest thickness is similar or greater than the distance between the nipples (this is an informal tip, and I do not think it is verified or supported in any medical textbook to my knowledge). 

3. Pericardial effusion

- Increased fluid accumulation in the pericardial layers may "muffle" the cardiac apex making it less easy to detect by palpation over the precordium. 

- However, a significant pericardial effusion may be required to be present before causing "loss" of apex beat. Thus there may be other signs to suggest a significant pericardial effusion e.g. reduced pulse volume, elevated jugular venous pressure and muffled heart sounds. 

4. Dextrocardia

- After satisfying yourself that the cardiac apex is not located within the left hemithorax, try looking for it on the right side instead. 

5. Is the patient "alive"?

- This possibility is unlikely in the exam setting, but of course, just to be sure, ensure there is spontaneous breathing and peripheral pulses are also palpable (especially the carotid pulse) at the same time. 😆

- However this scenario may be possible in the regular medical ward, particularly in the acute cubicle where there are critically ill patients. Some years ago, I have come across a house officer (HO) trying to palpate for the apex beat during morning ward rounds and the poor HO requested for assistance as he was unable to find the apex despite numerous attempts. Upon attending by the senior medical officer, the patient was found to have no spontaneous circulation and immediate resuscitative attempts were started. 😅

CCE. 

Atrial Fibrillation

Atrial fibrillation is a common occurrence in the medical examination. It can appear either as a short case examination or part of the long case examination.

Atrial fibrillation can be easily missed especially if there is bradycardia or tachycardia. However with practice, it can be detected rather easily. 

The 3 key features of atrial fibrillation that a student should be able to identify are:

1. Irregularly irregular rhythm

2. Variable pulse volume

3 Pulse deficit*

* A pulse deficit is when there is discrepancy between the peripheral pulse rate and the heart rate. Depending on which medical article you refer to, pulse deficit can vary between 5 to 10 beats per minute to be considered significant. 

Once atrial fibrillation is detected, a good student will go on to try to determine its cause or associated features:

1. Thyrotoxicosis

- look for signs of hyperthyroidism: exophthalmos, hand tremors, proximal myopathy, goitre with bruit

2. Elderly

- Elderly patients are more prone to have atrial fibrillation

3. Valvular heart disorders

- Examine the heart for any murmurs; commonly mitral stenosis or even mitral regurgitation

4. Heart failure

- Chronic atrial fibrillation may progress to heart failure especially if the heart rate is inadequately controlled. Conversely, patients with heart failure are also prone to develop atrial fibrillation. 

CCE.