Cardiology Flashcards
Define ischaemic heart disease (IHD) (aka coronary heart disease)
Cardiac myocyte damage (and eventual death) due to insufficient supply of oxygen-rich blood
In ascending order of severity: stable angina> unstable angina > NSTEMI > STEMI
What are the 3 main causes of IHD?
Atherosclerotic plaque, aortic stenosis (often caused by atherosclerotic plaque) and anaemia (supply cannot match demand)
Describe the process of atherogenesis.
- Endothelial cell injury, low density lipoproteins accumulate in intima
- Leukocytes (macrophages, T-lymphocytes) migrate and accumulate in intima
- Macrophages take up LDLs forming foam cells > formation of fatty streaks
- Foam cells rupture, releasing lipids, and smooth muscle cells migrate from media to intima > SMC proliferation
- Formation of fibrous cap with necrotic core
- This plaque can partially occlude the lumen which restricts blood flow → ischemia
- If plaque rupture → thrombus formed →lumen is fully occluded → infarction
Which arteries does atherogenesis affect most commonly?
Left anterior descending artery
Circumflex
Right coronary artery
What are the risk factors for atherosclerosis (therefore IHD)?
Non-Modifiable Risk Factors
- Older age
- Family history
- Male
Modifiable Risk Factors
- Smoking
- Alcohol consumption
- Poor diet
- Low exercise
- Obesity
- Poor sleep
- Stress
- Diabetes
- Hypertension
Define stable angina
A condition where a narrowing of the coronary arteries reduces blood flow to the myocardium.
During increased oxygen demand e.g., exercise, insufficient supply to meet demand > ischaemia > angina symptoms
What are the symptoms of stable angina?
- Constricting chest pain with/without radiation to jaw or arms, brought on by exposure to cold/exercise
- Lasts 1-5 minutes
- Pain relieved by rest/GTN (glyceryl trinitrate) spray
What investigations/tests would you carry out for a patient with suspected stable angina?
Gold standard: CT Coronary Angiography - CT image with heartbeat so coronary arteries can be viewed
Baseline investigations
- Physical Examination (heart sounds, signs of heart failure, BMI)
- ECG
- FBC (check for anaemia)
- U&Es (before ACEi and other meds)
- LFTs (prior to statins)
- Lipid profile
-Thyroid function tests (check for hypo / hyper thyroid)
- HbA1C and fasting glucose (for diabetes)
What is the management plan for stable angina?
R – Refer to cardiology (urgently if unstable)
A – Advise them about the diagnosis, lifestyle changes, management and when to call an ambulance
M – Medical treatment
P – Procedural or surgical interventions
What is used for immediate symptom relief in stable angina?
- GTN spray, repeat after 5 minutes if no relief
- Call ambulance if no relief after repeat dose
What is used for long-term symptom relief in stable angina?
Use one or a combination if uncontrolled on one:
Beta blocker (e.g. bisoprolol) and/or Calcium channel blocker (e.g. amlodipine)
What is used for primary prevention of stable angina?
- Lifestyle changes
- Low-dose aspirin (75mg once daily)
What is used in secondary prevention of stable angina?
- Aspirin (i.e. 75mg once daily)
- Atorvastatin 80mg once daily
- ACE inhibitor
- Already on a beta-blocker for symptomatic relief.
Define acute coronary syndrome (ACS)
Acute Coronary Syndrome is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery.
Three types:
- Unstable angina
- ST Elevation Myocardial Infarction (STEMI)
- Non-ST Elevation Myocardial Infarction (NSTEMI)
What are the symptoms of ACS?
Symptoms:
- Chest pain
Central, ‘heavy’, crushing pain
Radiation to the left arm or neck - Certain patients, such as diabetics, may not have chest pain (‘silent MI’)
- Shortness of breath
- Sweating
- Nausea and vomiting
- Palpitations
- Anxiety: often described as a ‘sense of impending doom’
What are the signs of ACS?
SIgns:
- Hypo- or hypertension
- Signs of heart failure: red flag
- Systolic murmur: if mitral regurgitation or a ventricular septal defect develops
What investigations/tests are used to diagnose ACS?
- ECG
- Measurement of troponin levels (not specific to ACS)
- Diagnostic investigation of choice: CT coronary angiogram
Plus:
- Physical Examination (heart sounds, signs of heart failure, BMI)
- ECG
- Bloods: FBC, U&Es, LFTs, Lipid profile, Thyroid function tests, HbA1C and fasting glucose
- Chest x-ray
- Echocardiogram
What would the ECG and troponin levels show in a patient with unstable angina?
ECG normal
Troponin level not raised
What would the ECG and troponin levels show in a patient with NSTEMI?
- ECG - ST depression or T wave inversion or pathological Q waves
- Troponin level raised (released during heart muscle damage)
What would the ECG and troponin levels show in a patient with STEMI?
- ECG - ST elevation or new left bundle branch block
- Troponin level raised (released during heart muscle damage)
What are the symptoms of ACS?
- Central, constricting chest pain associated with:
- Nausea and vomiting
- Sweating and clamminess
- Feeling of impending doom
- Shortness of breath
- Palpitations
- Pain radiating to jaw or arms
- Symptoms persist for 20+ mins and are not resolved by GTN spray
What might an atypical presentation of ACS look like?
Usually affects diabetic patients, known as silent MI:
- no pain
- low-grade fever
- pale, cool, clammy skin
- hyper/hypotension
What is the immediate treatment/management for STEMI?
Immediate management:
D - dual antiplatelets: aspirin (300mg) + clopidogrel
A - analgesia - morphine
N - nitrate - glyceryl trinitrate
S - SpO2 < 94% O2 therapy
As well as acute management for STEMI, what other first-line treatments should be considered?
- Primary PCI: symptom onset < 12hrs and available within 2hrs
- Thrombolysis: symptoms onset > 12 hours and PCI unavailable within 2hrs
- PCI: Percutaneous coronary intervention is first-line method of revascularization
- Insertion of a catheter via the radial or femoral artery to open up the blocked vessels using an inflated balloon (angioplasty), and a stent may also be inserted
2) Anticoagulation and further antiplatelet therapy:
- Aspirin + clopidogrel
- Unfractionated heparin and a glycoprotein IIb/IIIa inhibitor
STEMI: what treatment would be provided if the patient is unsuitable for PCI?
1) Thrombolysis e.g. alteplase or tenecteplase
- Offered if symptom onset is greater than 12h OR PCI not available within 120 mins
- IV administration of a thrombolytic or ‘clot-busting’ agent
2) Anticoagulation
- Unfractionated heparin
3) ECG: if the ECG shows residual ST elevation after 60-90 minutes of thrombolysis, offer immediate angiography and PCI
What is the acute treatment/management for unstable angina and NSTEMI?
Immediate management:
1) Oxygen: if SpO2 is <94%, and aim for 94-98%, unless the patient has COPD (88 - 92%)
2) Analgesia: morphine and sublingual glyceryl trinitrate
3) Dual antiplatelets:
Aspirin 300mg
AND
- Clopidogrel if not undergoing PCI
OR - Fondaparinux: offer to all patients unless undergoing immediate coronary angiography
- Unfractionated heparin: alternative to fondaparinux if renal impairment.
Remember ‘MONAC’ (Morphine, Oxygen (if sPO2 <94%), Nitrates, Aspirin, Clopidogrel)
Describe the secondary prevention medical management for ACS?
6As
- Aspirin 75mg once daily
- Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
- Atorvastatin 80mg once daily
- ACE inhibitors (e.g. ramipril)
- Atenolol (or other beta blocker)
- Aldosterone antagonist for those with clinical heart failure
ACS: what are some lifestyle changes that patients can make as secondary prevention?
- Stop smoking
- Reduce alcohol consumption
- Mediterranean diet
- Cardiac rehabilitation (a specific exercise regime for patients post MI)
- Optimise treatment of other medical conditions (e.g. diabetes and hypertension)
Why do we use anti-platelet meds such as aspirin, clopidogrel and ticagrelor in treating ACS?
Because when a thrombus forms in a fast flowing artery it is made up mostly of platelets.
What are the possible complications of MI?
Heart Failure (DREAD)
- D – Death
- R – Rupture of the heart septum or papillary muscles
- E – “Edema” (Heart Failure)
- A – Arrhythmia and Aneurysm
- D – Dressler’s Syndrome
Define heart failure (HF)
The inability of the heart to deliver blood and thus oxygen at a rate that matches the requirements of the body
What is chronic HF?
Chronic heart failure = chronic acute heart failure.
Caused by:
- Impaired left ventricular contraction (“systolic HF”) - aka HFrEF
- Impaired left ventricular relaxation (“diastolic heart failure”) - aka HFpEF
What is the pathophysiology of HF?
- HF can result from structural/functional defects that impair the heart’s function
- When the heart fails, the following systems compensate to maintain CO and perfusion. However, these compensatory mechanisms eventually lead to cardiac remodelling, which further exacerbates heart failure.
- Sympathetic system activation - BP falls → detected by baroreceptors → sympathetic activation → positively inotropic/chronotropic → CO increases
- Increased catecholamine release
- RAAS system activation
What is the aetiology of HF?
- Ischemic heart disease - main cause
- Cardiomyopathy
- Valvular heart disease (aortic stenosis/mitral regurgitation)
- Hypertension
- Alcohol excess
- Cor pulmonale
- Anaemia
- Arrhythmias
- Hyperthyroidism
What is congestive HF?
Congestive HF = both-sided HF
Congestive refers to sodium and water retention
What is cor pulmonale?
Right-sided heart failure caused by respiratory disease
Disease of lung/pulmonary vessels → pulmonary hypertension → RV hypertrophy → RHF with venous overload, peripheral oedema, hepatic congestion
What is left-sided HF?
LV weakened/stiffened > cannot pump oxygen-rich blood from lung to body properly, causing backflow into the pulmonary circulation
Causes: increased LV afterload (e.g. HTN) or increased LV preload (e.g. aortic regurgitation)
What is right-sided HF?
RV weakened/stiffened > inability to pump blood to and from the lungs > backflow into systemic veins
Causes: increased RV afterload (e.g. pulmonary HTN) or increased RV preload (e.g. tricuspid regurgitation)
What are the different types of HF?
- Acute/chronic
HF can be further classified as follows:
- HF with reduced ejection fraction where LVEF <40% (HFrEF) - traditionally known as systolic HF
- HF with mildly reduced ejection fraction (HFmrEF) - LVEF 41% to 49%
- HF with preserved ejection fraction (normal or near-normal left ventricular function) (HFpEF)
where LVEF > 50% - traditionally known as diastolic HF - Left-sided heart failure
- Right-sided heart failure
What are the risk factors for acute HF?
-Previous CVD
- Older age
- Prior HF
- Family history of IHD or cardiomyopathies
- Hypertension
- Diabetes
- Smoking
- Excess alcohol intake
What are the main risk factors for chronic HF?
- Myocardial infarction (MI)
- Hypertension
- Diabetes mellitus
- Dyslipidaemia
What signs and symptoms might a patient with acute HF present with?
3 non-specific cardinal signs:
Shortness of breath
Ankle swelling (peripheral oedema)
Fatigue
What signs and symptoms might indicate left-sided heart failure?
Symptoms:
- Shortness of breath
- Fatigue and weakness
- Cough (frothy white/pink sputum)
Signs:
- Peripheral or central cyanosis
- Displaced apex beat
- Tachycardia + tachypnoea
- 3rd Heart Sound
- Bilateral basal crackles (sounding “wet”) on auscultation
- Hypotension in severe cases (cardiogenic shock)
What signs and symptoms might indicate right-sided heart failure?
Symptoms:
- Swelling of legs
- Abdominal distention
- Fatigue and weakness
Signs
- Raised Jugular Venous Pressure (JVP) - a backlog on the right side of the heart leading to an engorged jugular vein in the neck
- Peripheral oedema (ankles, legs) + pitting
- Hepatosplenomegaly
- Ascites
What signs and symptoms might indicate congestive heart failure?
Symptoms of both LV and RV failure
What signs and symptoms might a patient with chronic HF present with?
- SOB worsened by exercise
- Orthopnea (SOB when lying down)
- Cough - with pink/white sputum
- Paroxysmal Nocturnal Dyspnoea (waking up at night with severe attack of SOB, cough and wheezing)
- Peripheral oedema (swollen ankles)
What investigations and tests are carried out to diagnose acute HF?
1) FBC: anaemia as possible cause of HF
2) U&Es: renal failure as possible cause of HF
3) Arterial blood gas: type 1 respiratory failure.
4) B-type natriuretic peptides (BNP) levels raised
5) ECG: assess for abnormalities such as arrhythmias and myocardial infarction
6) Chest x-ray:
A - Alveolar oedema (batwing opacities)
B - Kerley B lines (lines seen at lung periphery
C - Cardiomegaly
D - Dilated upper lobe vessels
E - Pleural Effusion
What investigations and tests are carried out to diagnose chronic HF?
1) Transthoracic echocardiogram
2) ECG - abnormal, broad QRS complexes with evidence of LV hypertrophy
3) CXR:
- A - Alveolar oedema (batwing opacities)
- B - Kerley B lines
- C - Cardiomegaly
- D - Dilated upper lobe vessels
- E - Pleural Effusion
4) B-type natriuretic peptide (BNP) test - raised BNP levels
What is the treatment/management for acute HF?
OMFFG
oxygen, morphine, furosemide, fluid restriction (<1.5L a day), GTN spray (not routine)
Surgery:
- If acute HF is due to aortic stenosis, then surgical aortic valve replacement
- Mechanical assist device
What is the treatment/management for chronic HF?
Conservative management- lifestyle changes
- stop smoking!
-eat less salt, optimise weight and nutrition
- avoid NSAIDs/verapamil
Medical management: AABCDD
1st line: ACE-I + B-blocker
2nd line: ARB + nitrate
3rd line: cardiac resynchronization or digoxin
diuretics: furosemide (symptom relief)
Define cor pulmonale
Right-sided heart failure caused by respiratory disease
What is the pathophysiology of cor pulmonale?
Disease of lung/pulmonary vessels → pulmonary hypertension → RV cannot pump blood out effectively > RV hypertrophy to compensate → RHF with venous overload, peripheral oedema, hepatic congestion
What are the respiratory causes of cor pulmonale?
- Most common: COPD
- Pulmonary Embolism
- Interstitial Lung Disease
- Cystic Fibrosis
- Primary Pulmonary Hypertension
What symptoms might a patient with cor pulmonale present with?
Symptoms:
- Early cor pulmonale - asymptomatic
- Main symptom is SOB, but non-specific as SOB can be caused by the chronic lung disease that leads to cor pulmonale
- Peripheral oedema
- Breathlessness on exertion
- Syncope
- Chest pain
What investigations/tests might you carry out for a patient with suspected cor pulmonale?
Examine the patient for signs of cor pulmonale:
- Hypoxia
- Cyanosis
- Raised JVP (due to a back-log of blood in the jugular veins)
- Peripheral oedema
- Third heart sound
- Murmurs (e.g. pan-systolic in tricuspid regurgitation)
- Hepatomegaly due to back pressure in the hepatic vein
What is the treatment/management for cor pulmonale?
- Treat symptoms
- Treat underlying cause
- Long-term oxygen therapy
Prognosis is poor unless there is a reversible cause
Define abdominal aortic aneurysm (AAA)
- Dilation of the abdominal aorta, with a diameter of more than 3cm.
- > 90% originate below the renal arteries
- The mortality of a ruptured AAA is around 80%
What is the pathophysiology of AAA?
- Histologically - degradation of collagen and elastin and loss of smooth muscle cells in 3 layers - tunica intima, media and adventitia > vessel dilatation
- Infiltration of lymphocytes and macrophages and neovascularisation
What is the difference between a true AAA and false AAA?
- A true aneurysm involves all 3 layers of the arterial wall
- False aneurysm (or pseudoaneurysm) is formed by only a single layer of fibrous tissue - 1% of AAA
What are the risk factors for AAA?
- Men are affected significantly more often and at a younger age than women
- Increased age
- Family history
- Smoking
- Hypertension
- Existing cardiovascular disease
How are AAA classified?
AAAs are classified by size as it corresponds to severity:
Normal: less than 3cm
Small aneurysm: 3 – 4.4cm
Medium aneurysm: 4.5 – 5.4cm
Large aneurysm: above 5.5cm
How would a patient with an unruptured AAA present?
Most patients are asymptomatic, detected incidentally during routine screening.
Other ways it can present include:
- Non-specific abdominal pain
- Pulsatile and expansile mass in the abdomen when palpated with both hands
- As an incidental finding on an abdominal x-ray, ultrasound or CT scan
Or they can present when the aneurysm ruptures.
What is a possible differential diagnosis for AAA that also present with non-specific abdominal pain?
Acute appendicitis - pain often periumbilical and is localised to the lower right quadrant
How will a patient with a ruptured AAA present?
- Severe abdominal pain that may radiate to the back or groin
- Haemodynamic instability (hypotension and tachycardia) - RED FLAG!
- Grey-Turner’s sign - flank bruising secondary to retroperitoneal haemorrhage
- Pulsatile and expansile mass in the abdomen
- Collapse
- Loss of consciousness
AAA = surgical emergency - do not delay treatment!
What investigation is used to diagnose AAA?
1st line investigation: aortic ultrasound
What is the treatment/management for a patient with a non-ruptured AAA?
Conservative management by managing risk factors for aneurysm < 5.5cm in diameter
- Stop smoking
- Healthy diet and exercise
- Optimising the management of hypertension, diabetes and hyperlipidaemia
How often do patients with AAA receive follow-up scans?
- Yearly for patients with aneurysms 3-4.4cm
- 3 monthly for patients with aneurysms 4.5-5.4cm
Abdominal Aortic Aneurysm: For which groups of patients do NICE guidelines recommend elective repair?
- Patients with symptomatic aneurysm
- If aneurysm diameter is >4cm and growing more than 1cm per year
- If aneurysm diameter above 5.5cm
Abdominal Aortic Aneurysm: What procedures are used in surgical repair?
Surgical repair involves inserting an artificial “graft” into the section of the aorta affected by the aneurysm. Two methods to insert the graft:
- Open repair via a laparotomy
- Endovascular aneurysm repair (EVAR) using a stent inserted via the femoral arteries
When is urgent surgery indicated for AAA?
1) Urgent surgical repair: for a symptomatic AAA
- Management is same as elective surgery but performed urgently!
2) Urgent surgical repair: for a ruptured AAA
- NICE 2020 guidelines: EVAR is preferred for women, and men > 70 for an infrarenal AAA. Otherwise, open repair is preferred.
Define pulmonary embolism (PE)
- A condition where a blood clot (thrombus) forms in the pulmonary arteries.
- Usually due to deep vein thrombosis (DVT) that developed in the legs > embolise to venous system> right side of the heart > pulmonary arteries in the lungs.
- Embolism block blood flow in pulmonary arteries > blood unable to reach the lungs > extra strain on the right side of heart
Define DVT
A deep vein thrombosis (DVT) is the formation of a blood clot in the deep veins of the leg or pelvis.
DVTs and PEs are collectively known as?
Venous thromboembolism (VTE).
What are the risk factors for DVT/PE?
The risk factors for DVT and PE are dependent on Virchow’s triad An abnormality in any one of the three components can result in thrombus formation.
1) Hypercoagulability:
- Pregnancy
- Hormone therapy with oestrogen
- Malignancy
- Polycythaemia (high RBCs)
- Systemic lupus erythematosus
- Thrombophilia (blood more likely to clot)
2) Venous stasis e.g. immobility, long-haul flights
3) Endothelial damage e.g. smoking, recent surgery or trauma
What signs and symptoms might a patient with PE present with?
Signs and symptoms can be subtle.
- Shortness of breath
- Cough with or without blood (haemoptysis)
- Pleuritic chest pain (inflammation of the tissue between the lungs and ribcage)
- Hypoxia
- Tachycardia
- Raised respiratory rate
- Low-grade fever
- Haemodynamic instability > hypotension
Might be S+S of DVT: unilateral leg swelling and tenderness
What signs and symptoms might a patient with DVT present with?
1) Unilateral calf pain, redness and swelling
2) Oedema
3) Tender and redness over affected area, particularly over deep veins)
4) Distention of superficial veins
What investigations/tests would you carry out for a patient with suspected DVT?
D-dimer is a sensitive (95%), but not specific, blood test for VTE:
- Raised in DVT
- However also raised in conditions such as pneumonia, malignancy, heart failure, surgery or pregnancy.
So further investigations needed:
Wells score ≥ 2 (DVT likely):
- Doppler ultrasound of the leg is required to diagnose deep vein thrombosis.
- Repeat USS if negative - 6 - 8 days after if positive D-dimer and wells score ≥ 2
Wells score ≤ 1 (DVT unlikely):
- D-Dimer with 4-hour result
- If D-Dimer is raised: duplex ultrasound within 4 hours
- If D-Dimer is normal: a DVT is unlikely, consider alternative diagnosis
What investigations/tests would you carry out for a patient with suspected PE?
Perform a Wells score and proceed based on the outcome:
- Likely: perform a CT pulmonary angiogram
- Unlikely: perform a d-dimer and if positive perform a CTPA
Tests for definitive diagnosis:
- Gold standard is CT pulmonary angiogram - chest CT scan with IV contrast to highlight the pulmonary arteries
Alternative cause assessment: Hx, examination, CXR
ECG change: normal sinus rhythm/ sinus tachycardia, new right bundle branch block, S1Q3T3 pattern (deep S wave in lead 1, pathologic wave in lead 3, inverted T wave in lead 3
What is the Wells score?
It is used to predict the risk of a patient presenting with symptoms of DVT or PE actually having the disease. It takes into account risk factors and clinical findings e.g., tachycardia and haemoptysis.
Score ≤ 4 = PE unlikely
Score > 4 = PE likely
Signs and symptoms of a DVT - 3.0
PE is the number 1 diagnosis or equally likely - 3.0
Tachycardia (>100 BPM) - 1.5
Immobilisation for more than three days or surgery in the previous four weeks - 1.5
Previous, objectively diagnosed PE or DVT - 1.5
Haemoptysis - 1.0
Malignancy with treatment within the last 6 months, or palliative - 1.0
What is the initial management for DVT/PE?
- Apixaban or rivaroxaban (anticoagulation)
- LMWH as alternative if renal impairment
What is the long-term management for PE/DVT?
Long term anticoagulation
- Warfarin
- NOACs/DOACs (direct-acting oral anticoagulants) such as apixaban (okay for cancer paitents)
- LMWH as an alternative if renal impairment
Continue anticoagulation for:
- 3 months if there is a reversible cause (then review)
- Beyond 3 months if the cause is unclear, there is recurrent VTE, or there is an irreversible underlying cause such as thrombophilia
- 3-6 months in active cancer (then review)
What is the treatment/management for massive PE?
Thrombolysis - injecting a fibrinolytic medication (clot buster by breaking down fibrin!)
Massive risk of bleeding = dangerous
Only use in patients with massive PE where benefits > risks
Thrombolytic agents e.g., alteplase
Define aortic dissection
Aortic dissection is when a break or tear forms in the aortic wall intima, causing blood flow into a new false lumen formed between the intima and media.
Three layers - intima, media and adventitia
Which section of the aorta is most often affected by aortic dissection?
Ascending aorta and aortic arch - as under the most stress from blood exiting the heart
What are the risk factors for aortic dissection?
- Most common - chronic hypertension!
- Increasing age
- male sex
- smoking
- poor diet (high in saturated fat and sugars)
- Reduced physical activity
- Raised cholesterol
What conditions can increase the risk of developing aortic dissection?
- Atherosclerotic aneurysmal disease
- Bicuspid aortic valve
- Ehlers-Danlos Syndrome
- Marfan’s Syndrome
Aortic dissection: what is the Standford system?
A classification system for aortic dissection:
-Type A – affects the ascending aorta before the brachiocephalic artery (~first 10cm of aorta)
- Type B – affects the descending aorta after the left subclavian artery
Aortic dissection: what is the DeBakey system?
A classification system for aortic dissection:
- Type I – begins in the ascending aorta and involves at least the aortic arch, if not the whole aorta
- Type II – isolated to the ascending aorta
- Type IIIa – begins in the descending aorta and involves only the section above the diaphragm
- Type IIIb – begins in the descending aorta and involves the aorta below the diaphragm.
What signs and symptoms might a patient with aortic dissection present with?
- Acute severe chest pain (tearing or ripping pain)
- Interscapular (between shoulders) and lower pain
- Differences in blood pressure between the arms (more than a 20mmHg difference is significant)
- Radial pulse deficit (the radial pulse in one arm is decreased or absent and does not match the apex beat)
What investigations/tests would you carry out for a patient with suspected aortic dissection?
- CT (chest, abdomen, and pelvis) = initial investigation to confirm the diagnosis - intimal flap
- ECG + chest x-ray to rule out other causes e.g., STEMI
- Echocardiography - intimal flap
What are some differential diagnoses for acute severe chest pain seen in aortic dissection?
- Myocardial infarction
- Acute coronary symdrome
- Aortic aneurysm
What is the treatment/management for aortic dissection?
- ABCDE, O2 therapy (aim SpO2 94%, 88% - 92% COPD), IV resuscitation
- Surgical emergency! The type of surgery depends on the type of aortic dissection
- Analgesia (e.g., morphine)
- Beta-blockers to control BP and HR to reduce stress on aortic walls.
What type of surgery is usually carried out for type A aortic dissection?
Open surgery (midline sternotomy) to remove the affected section of the aorta and replace it with a synthetic graft. The aortic valve might need to be replaced too.
What type of surgery is usually carried out for type B aortic dissection?
Thoracic endovascular aortic repair (TEVAR).
A stent graft is inserted into the affected section of the aorta via a catheter in the femoral artery
What are the main complications of aortic dissection?
- Cardiac tamponade
- Myocardial infarction
- Aortic valve regurgitation
- Stroke
- Paraplegia (motor or sensory impairment in the legs)
- Death
Define peripheral arterial disease (PAD) (aka peripheral vascular disease)
The narrowing of the arteries supplying the limbs and periphery, which reduces the blood supply to these areas. It usually refers to the lower limbs, resulting in symptoms of claudication.
What is the aetiology of PAD?
The main cause is atherosclerosis
What are the risk factors for developing PAD?
1) Non-modifiable risk factors:
- Older age
- Family history
- Male
2) Modifiable risk factors:
- Smoking
- Alcohol consumption
- Poor diet (high in sugar and trans-fat and low in fruit, vegetables and omega 3s)
- Low exercise / sedentary lifestyle
- Obesity
- Poor sleep
Stress
What is the pathophysiology of PAD?
Atherosclerotic plaques in the arterial walls are caused by chronic inflammation and activation of the immune system in the artery wall.
This can lead to the following:
- Stiffening > hypertension > strain on heart
- Stenosis > reduced blood flow
- Plaque rupture > thrombus > ischaemia in distal limb
What signs and symptoms might a patient with PAD present with?
- Most patients are asymptomatic, so look out for the presence of risk factors
- Intermittent claudication - due to limb ischaemia
- Thigh or buttock pain with walking that is relieved with rest
What is end-stage PAD and what symptoms might be present?
This is known as critical limb ischaemia- caused by inadequate supply of blood to a limb to allow normal function at rest
6 Ps
Pain
Pallor
Pulseless
Paralysis
Paraesthesia (abnormal sensation or “pins and needles”)
Perishing cold
What is a possible complication of PAD?
Acute limb ischaemia - sudden onset of ischaemia in a limb.
Typically due to a thrombus blocking arterial supply to a distal limb.
What investigations/tests would you carry out for a patient with suspected PAD?
Ankle-brachial pressure index (ABPI)
Duplex ultrasound – ultrasound that shows the speed and volume of blood flow
Angiography (CT or MRI) – using contrast to highlight the arterial circulation
What does ABPI measure?
The ratio between the systolic blood pressure (SBP) in the ankle (around the lower calf) compared with the systolic blood pressure in the arm.
Taken using a Doppler probe
For example: ankle SBP of 80 vs. arm SBP of 100 gives a ratio of 0.8 (80/100).
What does a ratio of 0.9 - 1.3 on an ABPI indicate?
Normal - no presence of PAD
What does a ratio of 0.6 - 0.9 on an ABPI indicate?
Mild peripheral arterial disease
What does a ratio of 0.3 - 0.6 on an ABPI indicate?
Moderate to severe peripheral arterial disease
What does a ratio less than 0.3 on an ABPI indicate?
Severe PAD to critical ischaemic.
What is the management for intermittent claudication?
- Lifestyle changes
- Exercise training - walking to near maximal claudication, then rest and repeat
- Optimise management of co-morbidities (such as hypertension and diabetes)
Medical treatments:
- Atorvastatin 80mg
- Clopidogrel 75mg once daily (or aspirin)
- Naftidrofuryl oxalate (peripheral vasodilator)
What is the management for chronic limb ischaemia?
Revasculation surgery:
- Endovascular angioplasty and stenting
- Endarterectomy (removal of fatty deposits)
- Bypass surgery (new path around affected artery)
- Amputation of the limb if it is not possible to restore the blood supply
What is the management for acute limb ischaemia?
- Endovascular thrombolysis – catheter inserted through the arterial system to apply thrombolysis directly into the clot
- Endovascular thrombectomy – catheter inserted through the arterial system, and thrombus is removed by aspiration or mechanical devices
- Surgical thrombectomy – cutting open the vessel and removing the thrombus
- Amputation of the limb if it is not possible to restore the blood supply
Define pericardial effusion
Pericardial effusion is where excess fluid (more than 50ml) collects within the pericardial cavity. Pericardial effusion can be acute or chronic.
What is the pathophysiology of pericardial effusion?
The pericardium consists of visceral (inner) and parietal (outer) layers.
Between them is the pericardial cavity, which has potential space
Pericardial effusion = pericardial cavity filled with fluid > inward pressure on the heart which makes it difficult for it to expand during diastole.
What is the aetiology of pericardial effusion?
- Pericarditis can causes inflammation > pericardial effusion
- Pericarditis can result from:
- Infection (e.g., tuberculosis, HIV, EBV)
- Autoimmune and inflammatory conditions (e.g., SLE and RA)
- Injury to the pericardium
Conditions which cause increased venous pressure, reducing drainage from the pericardial cavity:
- Congestive heart failure
- Pulmonary hypertension
What is a complication of pericardial effusion?
Cardiac tamponade - pericardial effusion large enough to raise intra-pericardial pressure > heart cannot fill properly during diastole > decreased CO > medical emergency!
What symptoms might a patient with pericardial effusion present with?
It depends on how quickly the effusion develops:
- Rapid onset - cardiac tamponade can cause haemodynamic compromise and collapse
- Slowly developing, chronic effusions may initially be asymptomatic.
As pressure rises, symptoms can include:
- Chest pain
- Shortness of breath
- A feeling of fullness in the chest
- Orthopnoea (shortness of breath on lying flat)
What are the clinical signs of cardiac tamponade?
- Tachycardia
- Hypotension
- Distant heart sounds
- Elevated jugular venous pressure
- Pulsus paradoxus (decrease in systolic arterial pressure) >10 mmHg.
What investigations and tests are used to diagnose pericardial effusion?
The investigation of choice is echocardiogram as it can:
- Diagnose pericardial effusion
- Assess the size of the effusion
- Assess the effect on the heart function (haemodynamic effect)
Fluid analysis is performed on the pericardial fluid to diagnose the underlying cause
What investigations and tests are used to diagnose cardiac tamponade?
- ECG - electrical alternans i.e., varying amplitude of QRS complexes
- Transthoracic echocardiogram - large pericardial effusion
- CXR - enlarged heart
- FBC - raised WBC count and inflammatory markers might indicate pericarditis
What is the treatment/management for pericardial effusion without cardiac tamponade?
Treatment of the underlying cause with aspirin, NSAIDs, colchicine or steroids (e.g., infection)
Drainage of larger effusion:
- Needle pericardiocentesis (echocardiogram guided)
- Surgical drainage
What is the treatment for a patient with hemodynamically unstable cardiac tamponade?
Urgent pericardiocentesis!
Define Tetralogy of Fallot (TOF)
A combination of four pathologies affecting the heart:
- Pulmonary valve stenosis
- Right ventricular hypertrophy
- Ventricular septal defect (VSD)
- Overriding aorta
What is the pathophysiology of TOF?
- Pulmonary valve stenosis - narrowing of the pulmonary valve makes it difficult for deoxygenated blood to leave the right ventricle into the pulmonary circulation
- Right ventricular hypertrophy - RV compensates for increased resistance by undergoing hypertrophy (boot-shaped heart)
- Ventricular septal defect (VSD) - gap between the RV and LV, which allows shunting of blood between them. Due to RV hypertrophy, pressure in the RV > LV and deoxygenated blood is shunted from RV to LV
- Overriding aorta - aorta entrance sits above the septal defect, meaning that a greater proportion of deoxygenated blood enters the aorta and systemic circulation from RV
What are the risk factors for TOF?
- Rubella infection
- Increased age of the mother (over 40 years)
- Alcohol consumption in pregnancy
- Diabetic mother
What investigations are used to diagnose TOF?
Investigation of choice: echocardiogram
Echo produces coloured pictures of the heart - doppler flow studies to assess the severity, gives you audio and visuals of blood flow through heart.
Chest x-ray - boot-shaped heart due to RV hypertrophy
What signs and symptoms might a patient with TOF present?
Most TOF cases are picked up at antenatal scans before the baby is born
- Ejection systolic murmur due to pulmonary stenosis - newborn baby check
- HF in severe cases present < 1 years old
- Milder cases will present in older children as signs and symptoms of HF develop:
- Cyanosis (blue discolouration of the skin due to low oxygen saturation)
- Clubbing
- Poor feeding
- Poor weight gain
- Ejection systolic murmur heard loudest in the pulmonary area (second intercostal space, left sternal border)
- “Tet spells”
What are tet spells?
Intermittent symptomatic periods where the right to left shunt becomes temporarily worsened, precipitating a cyanotic episode.
What can help alleviate the symptoms of a tet spell?
- Children might squat or put their knees to their chest as this increases peripheral vascular resistance by bending the femoral arteries which encourage blood to enter the pulmonary arteries.
What is the treatment/management for TOF?
Definitive treatment choice - total surgical repair by open heart surgery
Neonates - given prostaglandin infusion to keep ductus arteriosus open to allow LV > RV shunt
Prognosis - 90% will live to adulthood if surgery successful
Define coarctation of the aorta
- Coarctation of the aorta is a congenital condition with narrowing of the aortic arch, usually around the ductus arteriosus (70% cases infant, 30% adults)
- Severity of the coarctation (or narrowing) can vary from mild to severe.
- Often associated with an underlying genetic condition, particularly Turners syndrome (one X chromosome in females)
What is the pathophysiology of coarctation of the aorta?
Narrowing of the aorta reduces the pressure of blood flowing to the arteries that are distal to the narrowing. It increases the pressure in areas proximal to the narrowing, such as the heart and the first three branches of the aorta.
What is the pathophysiology of infant aortic coarctation?
- Ductus arteriosus remains patent (open), allowing RV to LV shunt
- Pressure in aorta after coarctation is lower than in pulmonary arteries > deoxygenated blood from RV goes to LV via ductus arteriosus into the lower extremities
Results in lower limb cyanosis in infants
What is the pathophysiology of adult aortic coarctation?
- Ductus arteriosus is closed and forms the ligamentum arteriosum
- No mixing of deoxygenated and oxygenated blood
- Pressure higher in areas proximal to narrowing, pressure lower in areas distal to narrowing
- Upstream - increased flow into aortic branches > increased pressure in upper limbs and head > increased risk of berry aneurysm and aortic dissection
- Downstream - lower pressure so inadequate blood flow to lower limbs = weak pulses
- Results in claudication
- Kidneys respond to low blood flow by activating RAAS > hypertension
What signs and symptoms might a patient with coarctation of the aorta present with?
- Neonates = weak femoral pulses often only symptom
- Perform four limb blood pressure check:
- High BP in limbs supplied by arteries before the coarctation
- Low BP in limbs supplied by arteries that come after the coarctation
- Systolic murmur below left clavicle and scapula
Signs might include:
- Tachypnoea and increased work of breathing
- Poor feeding
- Grey and floppy baby
