Cardiology
Question 60 of 148
A 65 year old woman presents to the Emergency Department following a fall at home. She has a past medical history of obesity and hypertension. On examination you note she has a regular pulse and an ejection systolic murmur. She gets shortness of breath and complains of back pain when you lean her forward to palpate the apex beat. What is the most likely diagnosis?
Answer:
Aortic stenosis can be a cause of shortness of breath and syncope due to reduced cardiac output. Post-fall back pain is very common and is simply due to trauma in this case. Ejection systolic murmurs are the classic sign of aortic stenosis, as blood is ejected through the narrowed valvular orifice under enough pressure to generate turbulent noise. The most common cause of aortic stenosis is age-related calcification.Valvular Heart Disease
Cardiology
Last Updated: 24th October 2023
Aortic stenosis
- Definition:
- Aortic stenosis is defined as restricted opening of the valve cusps causing an obstruction to left ventricular (LV) outflow.
- LV outflow obstruction can also be produced by a congenital abnormality above the valve (supravalvular aortic stenosis) or by subvalvular obstruction due to muscular hypertrophy as seen in hypertrophic cardiomyopathy.
- AS is severe once the valve area has decreased to 1 cm2 or less (normal 3-4 cm2). Once symptoms occur prognosis is poor without surgical treatment. Almost all patients with heart failure are dead within two years.
- Pathophysiology:
- As the aortic valve area reduces a systolic pressure gradient develops between the left ventricle (LV) and the aorta. The progressive outflow obstruction requires the LV to contract more forcefully (increased myocardial contractility) to maintain stroke volume eventually resulting in LV hypertrophy. As long as the mitral valve is functioning normally the pulmonary circulation is protected and the patient may be asymptomatic for years. In severe disease the ventricle can no longer respond and LV function becomes abnormal. At this stage (i.e. critical aortic stenosis) the balance between cardiac output and myocardial muscle oxygen demand can be easily disrupted causing acute decompensation and severe pump failure.
- Causes:
- Congenital (commonest cause in young adults)
- Rheumatic (commonest cause worldwide)
- Age-related degenerative calcific (commonest cause in UK)
- Rare causes: rheumatoid involvement, irradiation and obstruction due to infected vegetations
- Clinical features:
- Classic triad: Breathlessness, chest pain and exertional syncope
- Pulse: Slow rising small volume with a sustained peak (pulsus parvus et tardus)
- Cardiac impulse: Sustained heaving apical impulse with a precordial thrill, laterally displaced apex beat indicates onset of heart failure
- Auscultation: Harsh systolic ejection murmur 2nd intercostal space right sternal edge and radiating to the carotids, single second heart sound (S2) in moderate AS, paradoxical splitting of S2 or soft/obscured by murmur in severe AS, fourth heart sound “gallop rhythm”
- ECG: Left ventricular hypertrophy criteria (or strain pattern) but may be absent despite severe obstruction, may show RBBB or LBBB
- CXR: May show normal sized heart and a dilated proximal ascending aorta, late signs are of LV/LA dilatation and pulmonary oedema, calcium in the aortic valve of a patient <45 is indicative of AS
- ED Management:
- Pulmonary oedema can be treated with diuretics and continuous positive airways pressure (CPAP) to reduce preload and improve ventilatory function. Nitrates and ACE inhibitors may cause a drop in after load and a significant drop in blood pressure and should be avoided.
- Recent excessive diuretics, vasodilator therapy or hypovolaemia may be responsible for the acute decompensation and require corrective measures.
- New onset AF can be treated with digoxin to slow ventricular response and improve stroke volume.
- Chest pain may be relieved by beta blockers which reduce myocardial oxygen demand and may improve coronary blood flow.
- Patients in heart failure are likely to need emergency surgery and have a higher operative mortality than the patients with AS who have preserved LV function. However they still have a better outcome from surgery than from medical management.
- Up to 6% of older patients present in cardiogenic shock. These patients need aggressive medical therapy and emergency surgery.
Aortic regurgitation
- Definition:
- Aortic valve incompetence results from failure of the valve to prevent leakage (regurgitation) of some of the stroke volume back into the left ventricle from the aorta. It can occur because of aortic valve leaflet pathology or because of aortic root disease or a combination of these factors. Aortic regurgitation can be acute or chronic.
- Pathophysiology:
- Regurgitation of blood into the left ventricle during diastole causes volume overloading. The pathophysiology of acute and chronic AR is different.
- In acute AR there is a sudden increase in the volume of blood in the LV during diastole. The left ventricle volume can only increase marginally in response to this acute change so left ventricular end diastolic pressure rises sharply. LA and pulmonary venous pressure rises and results in acute heart failure.
- In chronic AR there is time for compensation and the LV progressively dilates and hypertrophies to maintain the ejection fraction. Tachycardia decreases the diastolic filling time and so reduces the regurgitant volume. During early stages of the disease the heart is able to respond to exertion with an appropriate increase in cardiac output. As a result AR can be tolerated for years.
- Causes:
- Acute AR
- Aortic dissection
- Infective endocarditis
- Prosthetic valve dysfunction
- Rupture of an aortic valve leaflet e.g. during trauma
- Chronic AR
- Congenital
- Calcific degeneration
- Aortic root dilatation
- Rheumatic fever/previous infective endocarditis
- Rare causes: Connective tissue diseases e.g. Marfan’s syndrome, Ehlers-Danlos; Autoimmune diseases e.g. rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis; Syphilis
- Acute AR
- Clinical features:
- Symptoms: Palpitations, chest pain, fatigue, heart failure, angina
- Pulse: Rapid rise and quick collapse (water hammer pulse), double impulse, wide pulse pressure, Corrigan's sign (visible carotid pulsation), Traube's sign (pistol shot sound heard over femoral artery), Quincke's pulse (capillary pulsation visible on shining a light through fingertips)
- Cardiac impulse: Hyperdynamic, maybe visible
- Auscultation: Soft blowing early diastolic murmur left sternal edge, best heard with the patient sitting forward in fully held expiration, duration of the murmur in diastole correlates with severity of AR; Austin Flint murmur (apical mid-diastolic murmur) may be seen in severe AR, produced by the partial closure of the mitral valve by the regurgitant jet and rapid rising LV diastolic pressure
- ECG: May be normal, non-specific ST-T changes and sinus tachycardia, LVH with or without strain pattern in moderate/severe disease
- CXR: May be normal sized heart and pulmonary oedema, or cardiomegaly with LV prominence and possible dilated aorta
- ED management:
- In acute severe AR secondary supportive management is needed while the underlying cause is being treated. Blood cultures should be taken unless there is an obvious underlying cause (e.g. aortic dissection or AMI)
- In acute AR supportive measures are directed at reducing pulmonary venous pressure and increasing cardiac output. They will include the use of vasodilators, intubation and positive pressure ventilation. Inotropic support may be needed but can worsen the AR. Nitrates and diuretics have little effect and the intra-aortic balloon pump is contraindicated.
- Any patient with known AR presenting in heart failure will need admission for evaluation and consideration of aortic valve replacement.
- In an acute presentation of a patient with chronic AR adjustment of medical therapies such as diuretics, vasodilators, rate and rhythm control is needed acutely.
Mitral stenosis
- Definition:
- Mitral valve narrowing restricts the flow of blood from the left atrium into the ventricle impairing left ventricular filling. Symptoms may not occur until the valve area is reduced to 1-1.5 cm2 (normal 4-6 cm2). Once the valve area is <1 cm2 the patient almost always has significant heart failure and very poor survival rates without surgery.
- Pathophysiology:
- The obstruction to atrial emptying in MS causes an elevation in left atrial and pulmonary venous pressure, leading to reduced lung compliance and breathlessness on exertion. Reactive pulmonary arterial hypertension causes right ventricular hypertrophy and failure. Progressive stenosis cause left atrial dilatation and consequent atrial fibrillation which will further impair the function of the atrium. Left ventricular filling becomes impaired and cardiac output becomes compromised.
- Causes:
- Rheumatic heart disease (commonest cause worldwide)
- Infective endocarditis
- Calcification of the mitral annulus
- SLE
- Carcinoid syndrome
- Clinical features:
- Symptoms: Exertional breathlessness, orthopnoea, PND, pulmonary oedema, atrial fibrillation, haemoptysis, fatigue
- Pulse: Small volume, irregular (usually AF)
- Cardiac impulse: Tapping apex due to palpable first heart sound
- Auscultation: Loud first heart sound (in sinus rhythm), opening snap and rumbling mid-diastolic murmur heard loudest over apex; early diastolic murmur of pulmonary regurgitation may occur (Graham Steell murmur)
- ECG: Broad or biphasic p wave best seen in Lead 2 indicating LA hypertrophy, right axis deviation, AF common, RV hypertrophy in later stages
- CXR: Straightening of the left heart border indicating a dilated LA (‘double atrial shadow’), pulmonary congestion
- Other features: Mitral facies (pink/purple patches on the cheeks reflecting reduced cardiac output and vasoconstriction)
- ED management:
- Any cause of tachycardia may result in an acute deterioration. Symptoms will be improved by slowing the heart rate and allowing better ventricular filling during diastole. Atrial fibrillation can precipitate acute heart failure and may be difficult to treat.
- Diuretics may be needed to relieve pulmonary congestion but addressing the shortened diastolic filling caused by any tachycardia will be of most benefit in the emergency setting.
- Rate control with beta blockers, digoxin or calcium channel blockers will be required for rapid atrial fibrillation. Any consideration of cardioversion must recognise the significant incidence of atrial thrombus and the risks of embolisation.
- Acute haemoptysis is relatively rare but can be severe. It is caused by vessel rupture due to venous congestion and may require referral to a cardiothoracic surgeon.
- ll MS patients in atrial fibrillation should be on long term anticoagulants. There is little benefit to those in sinus rhythm. Systemic embolisation may be due to subtherapeutic anticoagulation therapy. Patients may also present with complications of overanticoagulation.
Mitral regurgitation
- Definition:
- Mitral regurgitation is backflow of blood from the left ventricle into the left atrium during systole. This causes volume overloading of the left atrium and an increased workload for the ventricle to maintain the ejection fraction. As with aortic valve incompetence mitral regurgitation may be acute or chronic. Mitral valve regurgitation occurs in about 2% of the population. Acute MR is a cardiovascular emergency.
- Pathophysiology:
- During systole, a portion of the ejection fraction regurgitates into the left atrium. The portion is known as the regurgitant volume. This can also be expressed as the regurgitant fraction which is the regurgitant volume/ejection volume. Moderate MR is said to be present when the regurgitant fraction is in the range of 30 to 50%; severe MR is defined as a regurgitant fraction >50%.
- In acute MR there is sudden volume and pressure overloading of the LA and pulmonary veins leading to acute pulmonary congestion. The LV stroke volume increases to maintain cardiac output but in acute myocardial infarction the ventricle may fail leading to cardiogenic shock.
- Causes:
- Acute MR
- Ruptured chordae tendineae or partial or complete papillary muscle rupture (e.g. due to acute myocardial infarction, trauma or infective endocarditis)
- Chronic MR
- Rheumatic heart disease
- LV dilatation secondary to ischaemic heart disease or cardiomyopathy
- Myxomatous degeneration
- Mitral valve prolapse
- Acute MR
- Clinical features:
- Symptoms: With progressive leaking of the mitral valve in chronic MR the left side of the heart has time to adapt. Both the LA and LV will enlarge to cope with the increase in blood volume and the LV will hypertrophy to deliver the increase in stroke volume needed to maintain cardiac output. With acute MR the patient will be acutely unwell with signs and symptoms of acute pulmonary oedema as well as signs of the underlying cause
- Pulse: Tachycardia, AF common, prominent 'v' wave in JVP
- Cardiac impulse: Hyperdynamic , diffuse and laterally displaced apex beat, systolic thrill at apex
- Auscultation: Pansystolic murmur radiating to the axilla and back, 3rd heart sound
- ECG: No changes, acute MI, LA/LV hypertrophy, AF
- CXR: Pulmonary oedema, normal sized heart or increased LA/LV size
- ED management:
- Acute papillary muscle rupture in acute myocardial infarction is associated with a 75% mortality without surgery within 24 hours. Rapid recognition of this complication of myocardial infarction is important.
- Treat acute myocardial infarction if underlying cause.
- Treat pulmonary oedema. This may be difficult if the patient is in cardiogenic shock. Intubation and positive pressure ventilation should be considered early. CPAP can be helpful. Reduce preload and afterload with nitrate infusion and ACE inhibitors if tolerated. Diuretics and inotropes may also be needed. Patients with cardiogenic shock with acute MR may benefit from intra aortic balloon pump.
- Acute presentations of chronic MR are usually related to the onset of AF. Therapy is directed at reducing afterload to reduce LV work and controlling AF. Acute presentation of a patient with known chronic MR may indicate they require surgical intervention.
Mitral valve prolapse
- Definition:
- MVP is prolapse of a portion of the valve leaflets into the left atrium during systole associated with a small amount of regurgitation of blood. The condition is found in between 2-5% of the population and occurs more commonly in women.
- Pathophysiology:
- One or both of the mitral valve leaflets show fibromyxomatous changes. At the end of diastole the valve closes normally but as the pressure in the LV rises the leaflet prolapses back into the LA. Strain on the papillary muscles can lead to mitral regurgitation.
- Causes:
- Most cases are idiopathic. It can be acquired secondary to IHD, Rheumatic heart disease and hypertrophic cardiomyopathy.
- Clinical features:
- Although most patients are asymptomatic, a wide variety of symptoms have been associated with MVP such as chest pain, breathlessness and palpitations.
- Pulse: Normal
- Cardiac impulse: Normal
- Auscultation: Midsystolic click – a high pitched sound caused by sudden tensing of the mitral valve apparatus as the leaflet prolapses
- ECG: Normal
- CXR: Normal
- ED management:
- Attribution of symptoms to MVP is controversial. A patient with significant associated MR may have symptoms and signs related to this. Otherwise, when MVP has previously been diagnosed or is suspected, the role of emergency care is to exclude another acute cause for presenting symptoms. In the absence of another cause needing immediate treatment, the patient should be referred back to their own doctor for follow up or further investigation.
Tricuspid regurgitation
- Definition:
- Both the tricuspid and pulmonary valves can be stenotic or regurgitant. In the emergency setting, the most important presentation is tricuspid regurgitation secondary to either infective endocarditis in intravenous drug users or chronic obstructive pulmonary disease (COPD) with pulmonary hypertension and subsequent right ventricular failure/dilatation.
- Causes:
- Congenital (Ebstein's anomaly)
- RV dilatation – RV infarction, pulmonary hypertension
- Infective endocarditis (intravenous drug abuse)
- Marfan’s syndrome
- Clinical features:
- Patients are usually asymptomatic unless right heart failure develops and the patient complains of oedema, ascites and abdominal pain from liver congestion.
- Pulse: AF common, large 'v' waves in JVP
- Auscultation: Soft pansystolic murmur at left sternal edge louder on inspiration, third heart sound
- ECG: No specific changes
- CXR: Cardiomegaly, pleural effusion
- Other features: Tender enlarged pulsatile liver
- ED management:
- Tricuspid endocarditis in a drug abuser needs blood cultures and aggressive antibiotic therapy covering staphylococcal infection. Early surgery may be needed.
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- Biochemistry
- Blood Gases
- Haematology
| Biochemistry | Normal Value |
|---|---|
| Sodium | 135 – 145 mmol/l |
| Potassium | 3.0 – 4.5 mmol/l |
| Urea | 2.5 – 7.5 mmol/l |
| Glucose | 3.5 – 5.0 mmol/l |
| Creatinine | 35 – 135 μmol/l |
| Alanine Aminotransferase (ALT) | 5 – 35 U/l |
| Gamma-glutamyl Transferase (GGT) | < 65 U/l |
| Alkaline Phosphatase (ALP) | 30 – 135 U/l |
| Aspartate Aminotransferase (AST) | < 40 U/l |
| Total Protein | 60 – 80 g/l |
| Albumin | 35 – 50 g/l |
| Globulin | 2.4 – 3.5 g/dl |
| Amylase | < 70 U/l |
| Total Bilirubin | 3 – 17 μmol/l |
| Calcium | 2.1 – 2.5 mmol/l |
| Chloride | 95 – 105 mmol/l |
| Phosphate | 0.8 – 1.4 mmol/l |
| Haematology | Normal Value |
|---|---|
| Haemoglobin | 11.5 – 16.6 g/dl |
| White Blood Cells | 4.0 – 11.0 x 109/l |
| Platelets | 150 – 450 x 109/l |
| MCV | 80 – 96 fl |
| MCHC | 32 – 36 g/dl |
| Neutrophils | 2.0 – 7.5 x 109/l |
| Lymphocytes | 1.5 – 4.0 x 109/l |
| Monocytes | 0.3 – 1.0 x 109/l |
| Eosinophils | 0.1 – 0.5 x 109/l |
| Basophils | < 0.2 x 109/l |
| Reticulocytes | < 2% |
| Haematocrit | 0.35 – 0.49 |
| Red Cell Distribution Width | 11 – 15% |
| Blood Gases | Normal Value |
|---|---|
| pH | 7.35 – 7.45 |
| pO2 | 11 – 14 kPa |
| pCO2 | 4.5 – 6.0 kPa |
| Base Excess | -2 – +2 mmol/l |
| Bicarbonate | 24 – 30 mmol/l |
| Lactate | < 2 mmol/l |
