Cardiology
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A 65 year old man, with a known history of poorly controlled hypertension, presents to ED with sudden onset ‘ripping’ chest pain that radiates through to his back. The pain is severe and was maximal at onset. His observations are:
- Heart rate: 105 beats/minute
- Blood pressure: 175/110 mmHg
- Respiratory rate: 20 breaths/minute
- Oxygen saturations: 95% on air
What is the most likely diagnosis?
Answer:
The usual presentation is a patient in their 50s with hypertension, but the condition may occur in younger patients who have a connective-tissue disorder, or a recent history of heavy lifting or cocaine use. Aortic dissection should be suspected when an abrupt onset of tearing or ripping chest or back pain is reported. Patients may be haemodynamically stable or in hypovolaemic shock. Blood pressure differences in the upper extremities or pulse deficits in the lower extremities should be sought. Neurological deficits may indicate involvement of cerebral or intercostal vessels. There may be depressed mental status, limb pain, paraesthesia, weakness, or paraplegia. Symptoms of visceral ischaemia may be present. Occasionally, a diastolic decrescendo murmur may be discovered, indicating aortic insufficiency. There may be symptoms or signs of heart failure, pericardial tamponade, or a left pleural effusion.Aortic Dissection
Cardiology
Last Updated: 6th September 2022
Aortic dissection describes the condition when a separation has occurred in aortic wall intima, causing blood flow into a new false channel composed of the inner and outer layers of the media.
Dissection may be classified as Stanford type A or B:
- Type A: involves the ascending aorta with or without involvement of the arch and descending aorta.
- Type B: does not involve the ascending aorta; predominantly involves only the descending thoracic (distal to the left subclavian artery) and/or abdominal aorta.
Risk factors
- Hypertension
- Atherosclerotic aneurysmal disease
- Marfan syndrome
- Ehlers-Danlos syndrome
- Bicuspid aortic valve
- Annuloaortic ectasia
- Coarctation of the aorta
- Smoking
- Family history of aortic aneurysm or dissection
Clinical features
The usual presentation is a patient in their 50s with hypertension, but the condition may occur in younger patients who have a connective-tissue disorder, or a recent history of heavy lifting or cocaine use. Aortic dissection should be suspected when an abrupt onset of tearing or ripping chest or back pain is reported.
The pain associated with aortic dissection may be located retrosternally, interscapularly, or in the lower back. Anterior chest pain is typically associated with an ascending dissection; interscapular pain usually occurs with a descending dissection. Pain may migrate through the thorax or abdomen, and the location of pain may change with time as the dissection extends. A minority of patients present with syncope or without pain. It is important to recognise that no single symptom of aortic dissection is pathognomonic of the condition, as there is overlap with cardiac, pulmonary, abdominal, and musculoskeletal disorders.
Patients may be haemodynamically stable or in hypovolaemic shock. Blood pressure differences in the upper extremities or pulse deficits in the lower extremities should be sought. Neurological deficits may indicate involvement of cerebral or intercostal vessels. There may be depressed mental status, limb pain, paraesthesia, weakness, or paraplegia. Symptoms of visceral ischaemia may be present. Occasionally, a diastolic decrescendo murmur may be discovered, indicating aortic insufficiency. There may be symptoms or signs of heart failure, pericardial tamponade, or a left pleural effusion.
Investigations
- Initial work-up includes chest x-ray, ECG, and cardiac enzymes to exclude pneumonia or myocardial infarction.
- Blood tests including a complete metabolic panel and full blood count, including blood type and crossmatch, should also be requested.
- If aortic dissection is suspected because of the patient's history or widened mediastinum on chest x-ray, computed tomography angiography (CTA) is the primary modality used for diagnosis. CTA has a sensitivity greater than 90% and specificity greater than 85%. The diagnosis is made by imaging an intimal flap separating 2 lumens. If the false lumen is completely thrombosed, central displacement of the intimal flap, calcification, or separation of intimal layers are definitive signs of aortic dissection. CTA also allows visualisation of the extent of dissection and involvement of side-branches.
- Transthoracic echocardiography (TTE) may be done in the emergency department, intensive care unit (ICU), or operating theatre for acute proximal dissections if the patient is clinically unstable and there is any question about the diagnosis, or if CTA is unavailable or contraindicated.
Differential diagnosis
- Acute coronary syndrome
- Pericarditis
- Aortic aneurysm
- Pulmonary embolism
- Musculoskeletal pain
- Mediastinal tumour
Management
- Initial management:
- Local resuscitation protocols should be followed. Supplemental oxygen and haemodynamic support with intravenous fluid resuscitation and judicious use of inotropes is recommended in cases of incipient renal failure and hypovolaemic shock.
- Initial management of both type A and B dissections involves intensive monitoring and anti-impulse therapy. Intravenous beta blockade is used to achieve a heart rate less than 60 beats per minute and systolic blood pressure less than 120 mmHg. If beta blockade alone fails, vasodilator therapy (such as sodium nitroprusside or a calcium channel blocker) should be added.
- To decrease sympathetic tone and facilitate hemodynamic stability, pain should also be controlled with intravenous opioids. It should be noted that morphine causes vasodilation and reduces the heart rate by increasing vagal tone.
- Appropriate treatment is determined by accurate diagnosis of aortic dissection according to the following criteria:
- Type A (ascending)
- Type A dissections require urgent surgical replacement of the diseased aorta. Depending on the extent of retrograde extension, the aortic valve may or may not need to be repaired or replaced in order to prevent cardiac tamponade or fatal exsanguination from aortic rupture.
- Uncomplicated type B (descending)
- Patients with uncomplicated type B aortic dissection are usually managed medically with blood pressure and pain control during the acute phase (less than 14 days). However, updated analysis of data from the International Registry of Aortic Dissection suggests that there may be some benefit to endovascular intervention in patients with refractory pain and hypertension.
- Type B (descending) with end-organ ischaemia
- Urgent surgical or endovascular intervention is required if the patient's course is complicated by rupture, visceral or extremity ischaemia, aneurysmal expansion, or persistent pain. Although both open and endovascular therapies are acceptable options, the endovascular approach is gaining preference over the open technique for patients presenting with complications.
- Type A (ascending)
- Continued treatment:
- Blood pressure control is continued after discharge from hospital. Beta-blockers and ACE inhibitors are usually required, with additional antihypertensives such as diuretics or calcium-channel blockers used if necessary. A systolic blood pressure less than 120 mmHg and heart rate less than 80 beats per minute should be targeted.
Complications
- Pericardial tamponade
- Occurs when an ascending aortic dissection extends proximally with rupture into the pericardial space.
- Aortic incompetence
- Occurs when dissection propagates proximally, leading to loss of commissural support for the valve leaflets.
- Myocardial infarction
- Occurs when the dissection propagates proximally and coronary ostial occlusion occurs.
- Aneurysmal degeneration/rupture
- Complications from distal aortic dissection occur in 20% to 50% of patients.; this occurs due to continued pulsatile force (dP/dt) on already-thinned walls of the false channel or new dissection
- Regional ischaemia
- Cerebral, renal, visceral, spinal cord, or lower-extremity ischaemia occur when the dissection propagates distally and true lumen occlusion occurs
- Left arm ischaemia/subclavian steal syndrome
- Occurs when the left subclavian artery is covered after endovascular aortic repair in approximately 15% of patients
- Endoleak
- The risk of endoleak following thoracic endovascular aortic repair is low (estimated at 4.7%)
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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 |
