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
What investigations/tests are used to diagnose coarctation of the aorta?
- ECG - may show normal heart, but may show RVH or LVH
- CxR - may be normal, but may show cardiomegaly and/or posterior rib notching in adults due to vessel enlargement
- Echocardiogram - narrowing in the thoracic aorta; pressure gradient across narrowing - colour doppler will clearly show high velocity turbulent flow after the narrowing
What is the treatment/management for coarctation of the aorta?
- If mild, patients can live symptom-free until adulthood but might need surgery as an adult
- Severe case - emergency surgery shortly after birth
- Prostaglandin E infusion - keeps ductus arteriosus open before surgery - allowing blood flow through the ductus arteriosus into the systemic circulation distal to the coarctation.
- Surgery is then performed to correct the coarctation and to ligate the ductus arteriosus.
Define shock
Shock is a life-threatening, generalised form of acute circulatory failure with inadequate oxygen delivery to cells and oxygen utilisation by the cells.
Causes:
- Decreased blood perfusion of tissues
- Inadequate blood oxygen saturation
- Increased oxygen demand from the tissues
What is hypovolemic shock?
Shock resulting from the loss of intravascular volume
What is cardiogenic shock?
Shock resulting from pump dysfunction where tissue hypoperfusion resulting from loss of cardiac output induces tissue (cellular) inflammation.
What are the causes of hypovolemic shock?
Haemorrhagic causes: gastrointestinal bleeding and trauma.
Non-haemorrhagic causes include burns, dehydration, third-space losses and diabetic ketoacidosis.
What are the causes of cardiogenic shock?
Most commonly occurs after MI, but infections such as sepsis can cause it too.
What signs and symptoms might a patient with hypovolemic shock present with?
Clammy, pale skin, confusion, hypotension and tachycardia
What is the management plan for hypovolemic shock?
ABCDE (airways, breathing, circulation, disability and exposure)
- GIve O2 for airways + breathing
- Give IV fluids
What signs and symptoms might a patient with cardiogenic shock present with?
Heart failure signs such as oedema, increased JVP and S4 heart sound.
What is the treatment for cardiogenic shock?
- ABCDE - fluid resuscitation + O2 therapy etc.
- Treat underlying cause
What is distributive shock?
Shock resulting from the failure of vasoregulation, which results in a fall in systemic vascular resistance with vasodilation and warm peripheries.
Causes include sepsis, anaphylaxis, and brainstem or spinal injury (neurogenic).
What is septic shock, and what causes it?
It is usually a result of a combination of shock:
- Distributive: (failure of vasoregulation): results in a fall in systemic vascular resistance with vasodilation and, classically, warm peripheries.
- Cardiogenic: pump dysfunction
As a result of uncontrolled septicemia (bacterial infection in the bloodstream)
What signs and symptoms might a patient with septic shock present with?
Pyrexia, warm peripheries, bounding (strong) pulse
What is the treatment for septic shock?
- ABCDE - O2 therapy and IV fluids
- Broad spectrum Abx
What is neurogenic shock?
Shock caused by spinal cord injury, e.g., in a road traffic accident. This leads to disrupted SNS but intact PNS.
What signs and symptoms might a patient with neurogenic shock present with?
Hypotension, confusion, bradycardia, hypothermia.
What is the treatment for neurogenic shock?
ABCDE - IV fluids, O2 therapy
IV atropine - block vagal, allows more PNS inhibition and gives a chance for SNS to work
Define anaphylaxis
Anaphylaxis is a life-threatening medical emergency, caused by a severe type 1 hypersensitivity reaction.
This causes a rapid onset of symptoms, with airway, breathing and/or circulation compromise.
What is the pathophysiology of anaphylaxis?
Immunoglobulin E (IgE) mediate type 1 hypersensitivity reactions.
IgE stimulates mast cells to release histamine and other pro-inflammatory chemicals rapidly. This is called mast cell degranulation.
What is the pathophysiology of anaphylaxis?
Immunoglobulin E (IgE) mediate type 1 hypersensitivity reactions.
Two phases:
- Sensitisation - The IgE antibodies are formed in response to an antigen (or allergen); some people have genetic deposition
IgE binds to high-affinity receptors on mast cell surface > primed to react on the second exposure
- Subsequent exposure to allergen:
IgE stimulates mast cells to release histamine and other pro-inflammatory chemicals rapidly. This is called mast cell degranulation.
This causes rapid onset of symptoms with airway, breathing and/or circulation compromise
What are the symptoms of anaphylaxis?
Patients present with a history of exposure to an allergen (although it can be idiopathic). There will be a rapid onset of allergic symptoms:
- Urticaria (hives)
- Itching
- Angio-oedema, with swelling around lips and eyes
- Abdominal pain
Additional symptoms that indicate anaphylaxis are:
- Shortness of breath
- Wheeze
- Swelling of the larynx, causing stridor (noisy breathing)
- Tachycardia
- Lightheadedness
- Collapse
What is the treatment for anaphylactic shock?
- Rapid assessment: ABCDE
- Call for help (resus team or ambulance)
- IM adrenaline (dose based on age)
- If no response after 5 mins - a second IM adrenaline injection + IV bolus (0.9% NaCl solution)
- If no improvement:
- Confirm resuscitation team or ambulance has been called
- Follow refractory anaphylaxis algorithm
What are the doses of IM adrenaline according to age?
- Adult and child >12 years: 500 micrograms IM (0.5 mL)
- Child 6–12 years: 300 micrograms IM (0.3 mL)
- Child 6 months to 6 years: 150 micrograms IM (0.15 mL)
- Child <6 months: 100–150 micrograms IM (0.1–0.15 mL)
What is a biphasic reaction?
Second anaphylactic reaction after successful treatment of the first.
All patients should be assessed and observed for in hospital a period of time after the anaphylactic reaction - 6 - 12 hrs
What confirmatory blood test is needed to confirm anaphylaxis?
Measuring the serum mast cell tryptase, a mast-cell-specific protease.
Elevated serum tryptase levels = massive mast-cell degranulation, 6 hours in blood then disappears.
NICE recommendations:
- As soon as possible after emergency treatment for anaphylaxis
- 1-2 hours after onset of first symptoms of anaphylaxis (and no later than 4 hours)
- Another sample after 24 hours to establish baseline.
Define prevalence
The proportion of a population found to have the disease at a point in time.
Define incidence
The rate at which new cases occur in a population in a certain time period.
What are the risk factors for anaphylaxis?
- Food-induced anaphylaxis = highest in young children
- In < 30 years old = food and exercise
- Atopy (genetic disposition to allergic conditions) /Asthma
- History of anaphylaxis
- Exposure to common sensitizer (e.g. latex in healthcare professionals
Define atrial fibrillation (AF)
A type of supraventricular tachycardia (SVT), characterised by a chaotic irregular atrial arrhythmia.
What is the aetiology of AF?
Mnemonic: PIRATES
- Pulmonary: PE and COPD
- Ischaemic heart disease
- Rheumatic heart disease: any valvular abnormality
- Anaemia, Alcohol, Advancing age
- Thyroid disease: hyperthyroidism
- Electrolyte disturbance: e.g hypo/hyperkalaemia and hypomagnesemia
- Sepsis and Sleep apnoea
What is the pathophysiology of AF?
Normally, the SA node produces electrical activity that coordinates the contraction of the atria and heart.
In AF, the contractions of the atria are uncoordinated and irregular because the uncoordinated electrical discharges produced in the atria override the regular impulses produced in the SA node
What are the risk factors for developing AF?
1) Increasing age: 5% of aged 70-75 years, and 10% aged 80-85 years
2) Diabetes mellitus
3) Hyperthyroidism
4) Hypertension
5) Congestive heart failure
6) Valvular heart disease
7) Coronary artery disease
8) Dietary and lifestyle factors: excessive caffeine intake, alcohol abuse, obesity, smoking, medication use (e.g. thyroxine or beta-agonists)
What are the 4 types of AF?
- First episode
- Paroxysmal: recurrent episodes lasting < 7 days
- Persistent: recurrent episodes lasting > 7 days
- Permanent: continuous atrial fibrillation that is also refractory (does not respond) to treatment.
What is the pathophysiology of AF?
Normally, the SA node produces electrical activity that coordinates the contraction of the atria and heart.
In AF, atrial contractions are uncoordinated and irregular because the uncoordinated electrical discharges produced in the atria override the regular impulses produced in the SA node.
What signs and symptoms might a patient with AF present with?
Symptoms:
- Red flag: chest pain
- Red flag: syncope
- Palpitations
- Dyspnoea
Signs:
- Irregularly irregular pulse
- Red flag: hypotension suggests haemodynamic instability
- Red flag: evidence of heart failure e.g. such as pulmonary oedema
What investigations and tests are used to diagnose AF?
- ECG - irregularly irregular QRS complexes with absent P waves and chaotic baseline
- 24-hour ambulatory ECG monitoring for paroxysmal AF
- If new myocardial ischaemia = immediate DC cardioversion (restoration of normal sinus rhythm)
- KardiaMobile: cardiac event recorder
- NICE recommends it for detecting paroxysmal AF with palpitations
- Serum electrolytes: electrolytes, magnesium, calcium and phosphate
- TFTs: hyperthyroidism is a secondary cause of AF
How would abnormalities would appear on an ECG of a patient with AF?
- Absent P waves
- Irregularly irregular QRS complexes
- Choatic baseline
What is the treatment/management plan for AF?
Rate-control - does not restore sinus rhythm but controls heart rate to reduce the long-term effects on function.
OR
Rhythm control - aims to restore sinus rhythm, known as “cardioversion”, which can be electrical or pharmacological.
Treatment for AF: When is rate control used?
Onset > 48 hours or unknown
Treatment for AF: when is rhythm control used?
Younger age
Onset < 48 hours
No underlying heart disease
Reversible cause of AF
Failure of rate control
Haemodynamic instability acutely
Treatment for AF: what is the first line treatment for rate control?
First line:
Beta-blocker e.g. bisoprolol
Or
Rate-limiting CCB e.g. diltiazem (avoid if HF - use digoxin)
Non-cardioselective beta-blockers (e.g propranolol) should be avoided in asthmatic patients due to the risk of bronchospasm
Treatment for AF: what is the PHARMACOLOGICAL treatment when using rhythm control?
Flecainide or amiodarone: if no evidence of structural/ischaemic heart disease
Amiodarone: if structural/ischaemic heart disease is present
Treatment of AF: what is the second line treatment when using rate control?
Second line: combination therapy with any 2 below:
- Beta‑blocker (e.g. bisoprolol)
- Diltiazem
- Digoxin
Treatment of AF: what is the ELECTRICAL treatment when using rhythm control?
Electrical:synchronised DC (cardioversion) shock with general anaesthesia
- Immediate cardioversion - AF onset < 48 hours or severely haemodynamically unstable.
- Delayed cardioversion - AF onset > 48 hours, and they are stable
- Amiodarone 4 weeks before and up to 12 months after delayed cardioversion to maintain sinus rhythm
What is the surgical treatment when using rhythm control?
Left atrial ablation if drug treatment fails or unsuitable: radiofrequency energy is delivered to pulmonary veins - they supply the area causing premature depolarization - ~75% success rate
Permanent AF: pace and ablate - pacing and AV node ablation
Why are patients with AF prescribed anticoagulants?
AF increases the risk of stroke; anticoagulants lower this risk x2 -3
E.g. warfarin or Direct acting Oral Anticoagulants (DOACS) like apixaban
What are some advantages of DOACs over warfarin?
- No monitoring is required
- No major interaction problems
- Equal or slightly better than warfarin at preventing strokes in AF
- Equal or slightly less risk of bleeding than warfarin
But a lot more expensive.
Why are patients with AF prescribed anticoagulants?
AF increases the risk of stroke; anticoagulants lower this risk x2 -3
E.g. warfarin or Direct acting Oral Anticoagulants (DOACS) like apixaban.
When is emergency electrical synchronised DC cardioversion indicated in AF?
- If the patient is haemodynamically unstable (abnormal BP):
- Shock: hypotension (systolic BP <90 mm Hg)
- Syncope: transient loss of consciousness
- Myocardial ischaemia: chest pain and/or evidence on ECG
- Heart failure: pulmonary oedema and/or raised jugular venous pressure
What conditions are beta-blockers used to treat?
Hypertension, IHD, angina, MI (or ACS), arrhythmias and heart failure
What is the mechanism of action of beta-blockers?
Beta-adrenoceptor blocking drugs (beta-blockers) block the beta-adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, and liver.
Thus, they block the effects of the hormone adrenaline, causing the heart to beat more slowly (negatively chronotropic) and with less force (negatively inotropic), which lowers blood pressure.
Beta blockers also help widen veins and arteries to improve blood flow - useful in IHD
What are some side effects of beta-blockers?
Abdominal discomfort; bradycardia; fatigue, cold peripherals, vivid dreams (fat-soluble), erectile dysfunction
Water-soluble beta-blockers are less likely to enter the brain, unlike fat-soluble ones, so they are less likely to cause sleep disturbances and nightmares
Why does the dose of beta-blockers need to be reduced for patients with renal impairment?
Because beta-blockers are excreted by the kidneys and patients with renal impairment might not excrete the drug as effectively.
What conditions are ACE inhibitors used to treat?
Hypertension, heart failure, prophylaxis after MI
What is the mechanism of action of ACE inhibitors (particularly ramipril)?
ACE inhibitors block the action of angiotensin-converting enzyme, which prevents conversion of angiotensin I to angiotensin II
- Angiotensin II has three main effects:
- Constriction of blood vessels - so ACEis cause blood vessel dilation
- Reabsorption of water by the kidneys - so ACEis lower BV
- Release of the hormone aldosterone, which also causes water re-absorption by the kidneys - so ACEi lower BV
Blood vessel dilation and decreased water reabsorption by the kidney lead to lowered blood pressure.
Which ethnic groups respond less well to ACEis?
People of black African or Caribbean origin as they are usually less dependent on renin so the RAAS is less implicated in MI - give calcium-channel blockers instead.
What are the main side effects of ACE inhibitors?
- Hypotension
- Persistent dry cough
- Hyperkalaemia
- Cause or worsen renal failure
What conditions are loop diuretics (e.g. furosemide) used to treat?
- Chronic heart failure for symptomatic relief of fluid overload
What is the mechanism of action of loop diuretics (particularly furosemide)?
Loop diuretics inhibit water reabsorption from the ascending limb of the loop of Henlé in the renal tubule by inhibiting Na+/K+/2Cl- co-transporters.
What are the main side effects of loop diuretics?
- Dehydration
- Hypotension
- Hyponatremia
- Hypokalaemia
What is hypovolemic shock?
Shock resulting from the loss of intravascular volume
What is AV nodal re-entry tachycardia (AVNRT)?
- A type of supraventricular tachycardia
- Caused by reentry circuit in or around AV node.
- Two separate pathways form the re-entrant circuit:
- Alpha pathway - slow conduction, short refectory period
- Beta pathway - fast conduction, long refectory period
What is the most common type of supraventricular tachycardia?
Atrioventricular nodal re-entry tachycardia (AVNRT) is the most common type of SVT.
Give 4 symptoms of AVNRT.
- Sudden onset/offset palpitations.
- Neck pulsation.
- Chest pain.
- Shortness of breath.
Do you see a P wave in the ECG of a person with AVNRT?
No - the P waves are within the QRS complex.
What is the treatment/management plan for AVNRT?
Acute treatment: vagal manoeuvre and adenosine.
Chronic treatment (prevent further episodes): Amiodarone, Procainamide
Definitive treatment: radiofrequency catheter ablation (RFA) of the slow alpha pathway
Define accessory pathway supraventricular tachycardia
A type of heart arrhythmia caused by an accessory pathway, or an extra electrical conduction pathway, connecting the atria and ventricles
The most common is Wolff-Parkinson-White syndrome.
What is the pathophysiology of Wolff-Parkinson-White syndrome?
“Bundle of kent” - congenital muscle strands connect the atria and ventricles - accessory pathway. This can result in pre-excitation of ventricles
Describe 3 characteristics of an ECG taken from someone with Wolff-Parkinson-White syndrome
- Shorter PR interval (<120ms)
- Delta wave (slurred upstroke to QRS due to pre-excitation of ventricles)
- Longer QRS complex (>110ms)
What is the definitive treatment of Wolff-Parkinson-White syndrome?
Radiofrequency ablation of the accessory pathway (bundle of kent)
Define hypertension
Hypertension is defined as a blood pressure reading of ≥140/90 mmHg (ambulatory blood pressure monitoring ≥135/85 mmHg).
What categories can hypertension be divided into?
Primary (90 - 95%) and secondary.
What is primary hypertension?
Primary hypertension, otherwise known as essential hypertension, has no known underlying secondary cause and is responsible for 90-95% of cases of hypertension.
What are the main underlying causes of secondary hypertension?
R – Renal disease. Most common
O – Obesity
P – Pregnancy-induced hypertension/pre-eclampsia
E – Endocrine. Most endocrine conditions (for example, hyperthyroidism) can cause hypertension but primarily consider hyperaldosteronism (“Conns syndrome”)
What are the risk factors for developing hypertension?
1) Non-modifiable risk factors: increasing age, African heritage, family history
2) Modifiable risk factors: obesity, sedentary lifestyle, alcohol excess, smoking, high sodium intake (>1.5g/day), stress
What signs and symptoms might a patient with hypertension present with?
Symptoms
1) Asymptomatic: most common presentation
2) Headaches: classically occipital and worse in the morning
Signs
1) Malignant hypertension (≥180/120 mmHg):
- Hypertensive retinopathy
- Visual disturbance
- Cardiac symptoms e.g. chest pain
- Oliguria or polyuria
2) Secondary hypertension: signs of the underlying cause
For example, hyperthyroidism causes weight loss, sweating and palpitations
What investigations and tests are used to diagnose hypertension?
1) Blood-pressure reading: both arms
If the clinic blood pressure is ≥140/90mmHg, take a second reading. Record the lower of the 2 measurements as the clinic blood pressure.
Arms pressure difference ≥ 15 mmHg, take higher reading
2) Ambulatory blood pressure monitoring (ABPM):
If patient’s BP between 140/90 mmHg and 180/120 mmHg to confirm the diagnosis
Blood pressure is measured over a 24 hour period, with at least 2 measurements per hour during waking hours
At least 14 measurements are required
3) Home blood pressure monitoring (HBPM):
Offered if ABPM is not appropriate; HPBM involves the patient checking their blood pressure manually throughout the day - over 7 days.
What is white coat syndrome?
Having your blood pressure taken by a doctor or nurse often results in a higher reading. This is commonly called “white coat syndrome”. The white coat effect is defined as more than a 20/10 mmHg difference in blood pressure between clinic and ambulatory or home readings.
What are the 3 stages of hypertension?
1) Stage 1 Hypertension
Clinic Reading: >140/90
Ambulatory / Home Readings >135/85
2) Stage 2 Hypertension
Clinic Reading: >160/100
Ambulatory / Home Readings >150/95
3) Stage 3 Hypertension
Clinic Reading: >180/120
Ambulatory / Home Readings: >180/120
What other investigations are recommended for patients with a new diagnosis of hypertension?
- Fundoscopy: assess for hypertensive retinopathy
- 12-lead ECG: assess for ischaemic changes and evidence of left ventricular hypertrophy
- Albumin:creatinine ratio (ACR) and urinalysis: assessing for renal dysfunction, as evidenced by elevated ACR and proteinuria or haematuria on urinalysis
- Bloods: HbA1c, U&Es, total cholesterol and HDL cholesterol
What is the INITIAL management plan for hypertension?
1) Establish a diagnosis.
2) Investigate for possible causes and end organ damage.
3) Advise on lifestyle. This includes recommending a healthy diet, stopping smoking, reducing alcohol, caffeine and salt intake and taking regular exercise.
What medications are used to treat hypertension?
A – ACE inhibitor (e.g. ramipril 1.25mg up to 10mg once daily)
B – Beta blocker (e.g. bisoprolol 5mg up to 20mg once daily)
C – Calcium channel blocker (e.g. amlodipine 5mg up to 10mg once daily)
D – Thiazide-like diuretic (e.g. indapamide 2.5mg once daily)
ARB – Angiotensin II receptor blocker (e.g. candesartan 8mg to up 32mg once daily)
ARB is used if ACEi is not tolerated or the patient is of Afro-Caribbean or African descent.
What is the medical management for patients with stage 2 hypertension or patients <80 with stage 1 hypertension and Q risk score of 10%, diabetes, renal disease, cardiovascular disease or end organ damage?
There are slightly different guidelines for younger patients and those aged over 55 or black:
Step 1: Aged less than 55 and non-black use A.
Aged over 55 or black of African or African-Caribbean descent - use C.
Step 2: A + C. Alternatively A + D or C + D.
If black then use an ARB instead of A.
Step 3: A + C + D
Step 4: A + C + D + additional (see below)
For step 4, if the serum potassium is ≤ 4.5 mmol/l then consider a potassium-sparing diuretic such as spironolactone.
If the serum potassium is > 4.5 mmol/l, consider an alpha blocker (e.g. doxazosin) or a beta blocker (e.g. atenolol).
Seek specialist advice if the blood pressure remains uncontrolled despite treatment at step 4.
What are the treatment targets for hypertension?
< 80 years
Systolic Target: < 140
Diastolic Target: < 90
> 80 years
Systolic target: < 150
Diastolic target: < 90
What are some complications of hypertension?
1) Coronary artery disease: for every +20/10 mmHg in BP, there is a doubling of mortality related to IHD
2) Cerebrovascular accident
3) Congestive heart failure: hypertensive patients x3 more likely
4) Chronic kidney disease
Define Atrioventricular (AV or heart) block
Atrioventricular (AV) block is a cardiac electrical disorder defined as impaired (delayed or absent) conduction from the atria to the ventricles.
What is first degree heart block?
Delayed atrioventricular conduction through the AV node.
Despite this, every atrial impulse makes it to a ventricular contraction, meaning every P wave results in a QRS complex.
What do you see on an ECG if a patient has first degree heart block?
ECG - PR interval > 0.20 seconds (200ms) (5 small or 1 big square).
What signs and symptoms might a patient with first-degree heart block present with?
Usually asymptomatic
What is the management plan for patients with first-degree heart block?
- Usually no further treatment if asymptomatic, patients are monitored
If symptomatic
- Identify and correct electrolyte imbalance
- Identify and stop AV-nodal blocking medications (e.g. beta-blockers, CCB, digoxin)
What is second-degree heart block?
Some atrial impulses do not make it through the AV node to the ventricles. This means that there are instances where p waves do not lead to QRS complexes. There are different types:
1) Wenckebach’s phenomenon (Mobitz Type 1)
2) Mobitz Type 2
3) 2:1 Block
Describe Wenckebach’s phenomenon (Mobitz type 1) heart block
This is where the atrial impulse becomes gradually weaker until it does not pass through the AV node. After failing to stimulate a ventricular contraction, the atrial impulse returns to being strong. This cycle then repeats.
What would you see on an ECG for a patient with Mobitz type 1 heart block?
ECG - PR prolongation until a QRS complex is dropped, i.e. PR interval progressively elongates
Describe Mobitz type II heart block, including what you would see on an ECG
This is where there is intermitted (random) failure or interruption of AV conduction. This results in missing QRS complexes. There is usually a set ratio of P waves to QRS complexes. For example, 3 P waves to each QRS complex would be a 3:1 block. The PR interval remains normal. There is a risk of asystole (heart stopping) with Mobitz Type 2.
What would you see on an ECG for a patient with Mobitz type II heart block?
PR intervals are consistently prolonged (not consistently prolonging), with randomly dropped QRS complexes.
Describe third-degree heart block.
This is referred to as complete heart block.
Electrical signal from atria to ventricle completely blocked.
P waves and QRS complexes therefore occur independently.
Ventricles: escape beats at ~30bpm
What would see on an ECG if a patient had third-degree heart block?
P waves and QRS complexes occurring independently of each other.
What are ventricular escape beats?
There are pacemaker cells in the ventricles that depolarise at a rate of about 20 - 40 bpm. Under normal conditions, these slower pacemakers are suppressed by the more rapid impulses from above (i.e. sinus rhythm).
However, if the ventricles do not receive a signal from the atria, such as in 3rd-degree heart block, then the ventricular pacemaker cells will kick in, leading to escape beats of about 20 - 40 bpm.
What might cause heart block (first, second (Mobitz subtypes and third-degree)?
First-degree: AV nodal blocking drugs: beta-blockers, CCB, digoxin, adenosine
Second-degree Morbitz type 1: drugs (above), inferior wall MI
Mobitz type II: drugs (above), inferior wall MI, rheumatic fever
Third-degree: acute MI, hypertension, structural heart defects
What signs and symptoms might a patient with Mobitz type I heart block present with?
Usually non but some people can experience light-headedness, dizziness and syncope
What signs and symptoms might a patient with Mobitz type II heart block present with?
Fatigue, dyspnoea, syncope, chest pain
What signs and symptoms might a patient with third-degree heart block present with?
Syncope, confusion, dyspnoea, SEVERE CHEST PAIN
There is a significant risk of asystole (DYING) with third-degree heart block
What is the treatment/management plan for second-degree heart block?
For all: identify and treat electrolyte imbalances + stop AV nodal blocking meds
1) Asymptomatic:
- 1st line is the discontinuation of AV-nodal blocking drugs, identify and treat electrolyte imbalances.
- 2nd line: permanent pacemaker (PPM) implantation for Morbitz type II
2) Symptomatic second or third-degree:
1st line is the discontinuation of AV-nodal blocking drugs, identifying and treating electrolyte imbalances and temp pacing (transcutaneous)
2nd: PPM for MT I and II second-degree and third-degree
Define bundle branch block (BBB).
The branch bundles describe the conduction fibres that run along the ventricular septum - divided into right and left bundle branches. They derive from the Bundle of His which conducts the electrical impulses from the AV node
A Bundle Branch block is the blockage of the electrical signal in the LBB or RBB, preventing the electrical signal from travelling from the atria to the ventricles.
What is the aetiology of RBBB?
Either physiological or the result of damage to the right bundle branch:
- underlying lung pathology (COPD, pulmonary emboli, cor pulmonale)
- Congenital heart disease (e.g. atrial septal defect)
- Ischaemic heart disease
What is the pathophysiology of RBBB?
1) The SA node acts as the initial pacemaker
2) Depolarisation reaches the atrioventricular node
3) Depolarisation through the bundle of His occurs only via the left bundle branch. The left branch still depolarises the septum as normal.
4) The left ventricular wall depolarises as normal.
5) The right ventricular walls are eventually depolarised by the left bundle branch. This occurs by a slower, less efficient pathway.
What is the aetiology of LBBB?
Always pathological!
Left bundle branch block may be due to conduction system degeneration (e.g. fibrosis) or ischaemic heart disease, cardiomyopathy and valvular heart disease.
LBBB may also occur after cardiac procedures which damage the left bundle branch or His bundle.
What is the pathophysiology of LBBB?
1) The sino-atrial node acts as the initial pacemaker
2) Depolarisation reaches the atrioventricular node
3) Depolarisation down the bundle of His occurs only via the right bundle branch. The septum is abnormally depolarised from right to left.
4) The right ventricular wall is depolarised as normal.
5) The left ventricular walls are eventually depolarised by the right bundle branch, this occurs by a slower, less efficient pathway.
Fibrosis of the bundle branch often leads to BBB. What are the most common causes of fibrosis ?
Acute: heart attacks, ischaemia, myocarditis
Chronic: hypertension, IHD, cardiomyopathies
What ECG changes do you see if a patient has LBBB?
WiLLiaM
“W” shape in the QRS complex of lead V1
“M” shape in lead V6
What ECG changes do you see if a patient has RBBB?
MaRRoW
“M” shape in lead V1 (RSR wave)
“W” shape in lead V6 (Deep S wave)
What is the management plan for bundle branch block?
If it has been present since birth and is asymptomatic, then no treatment is needed.
If it is caused by another heart disease, for example, IHD, then optimise treatment for the underlying condition.
If severe, cardiac resynchronization pacemaker implantation.
This device has electrical leads going to both RV and LV. These leads can pace the ventricles at the same time, causing them both to contract at the same time, which helps improve cardiac function.
What is infective endocarditis?
Infective endocarditis (IE) is an infection of the endocardium or other endothelial-lined structures such as heart valves. This usually involves two pathological variables: an abnormal endocardium and a bacterial source.
What are the different types of infective endocarditis?
The mitral valve is most commonly affected
Tricuspid valve most associated with IVDU
1) Acute
- Develops over days to weeks
- Most commonly associated with staph aureus
- Rapid valvular destruction
2) Subacute
- Develops over weeks to months
- Most commonly associated with strep viridans
3) Non-bacterial thrombotic ‘marantic’
- Non-infective cause of endocarditis secondary to thrombus formation on the valvular surface
- Associated with malignancy or SLE (Libman-Sacks endocarditis)
What is the pathophysiology of IE?
1) Rheumatic fever, valvular pathology, prosthetic valves, or congenital heart disease associated with an abnormal endocardium.
2) Any cause of an abnormal endocardium → turbulent blood flow and thrombus formation
thrombus becomes infected due to a bacterial source, such as IV drug use or an infected cardiac device.
Bacterial colonisation of the thrombus → formation of vegetations → valvular damage
What are the risk factors for developing infective endocarditis?
1) Male gender: x2.5 times more likely
2) Previous infective endocarditis
3) Prosthetic heart valves
4) Congenital heart disease
5) Rheumatic heart disease
6) Intravenous drug use (IVDU)
Which 4 groups of people are most at risk of developing infective endocarditis?
1) Elderly.
2) IVDU.
3) Those with prosthetic valves.
4) Those with rheumatic fever
What are the common causative organisms of infective endocarditis?
1) Staph aureus - most common (IVDU, prosthetic valves)
2) Staph epidermis (coagulase-negative staph) (prosthetic valves and indwelling lines)
3) Streptococcus bovis (colon cancer)
4) Strep viridans (alpha haemolytic) (native valves)
5) Strep mitis and sanguinis (viridans streptococci) (poor dental hygiene, infection post-dental procedure)
What are the hallmarks of infective endocarditis?
Vegetation - lumps of fibrin hanging off the heart valves.
Wherevare vegetations most likely in infective endocarditis?
- Atrial surface of AV valves.
- Ventricular surface of semilunar (aortic and pulmonary) valves.
What are the symptoms of infective endocarditis?
1) Fever or chills
2) Headache
3) Shortness of breath
4) Night sweats, malaise, fatigue, weight loss
5) Joint pain: may be due to septic emboli
What are the signs of infective endocarditis?
1) Heart murmur +/- evidence of heart failure
2) Janeway lesions: painless plaques on palms and soles due to septic microemboli
3) Osler’s nodes: painful nodules on fingers or toes due to immune complex deposition
4) Splinter haemorrhages: red-plum lines under the nails due to microemboli
5) Roth’s spots: white centred retinal haemorrhages
6) Mild splenomegaly
What investigations/tests are used to diagnose infective endocarditis?
Diagnosed using modified Duke’s criteria (see specific flashcard).
Investigations:
1) Inflammatory markers: raised WCC (especially neutrophilia), raised CRP and ESR
2) Blood cultures - detects causative organism
3) Echocardiogram (echo): vegetation = confirms diagnosis
- 1st line is transthoracic echo
- TOE is gold standard
4) ECG (prolonged PR interval)
What is the modified Duke’s criteria?
The Modified Duke Criteria requires 2 major criteria, or 1 major and 3 minor criteria, or 5 minor criteria for a diagnosis of infective endocarditis.
Major:
1) ≥ 2 positive blood cultures
2) Echo TOE shows vegetation
Minor:
1) Immunological signs (e.g. Roth’s spots, Olser’s nodes)
2) 1 positive blood culture
3) Pyrexia ≥ 38c
4) IVDU
5) Predisposing heart condition
6) Septic emboli
What is the management plan for infective endocarditis?
First line:
IV antibiotics:
- 4 weeks
- 6 weeks for patients with prosthetic valve
Second line:
Surgery: aim to remove infected tissue and repair or replace affected valves
What antibiotics are used to treat infective endocarditis?
1) Empirical:
- Native - amoxicillin +/- gentamicin
- Prosthetic - vancomycin + gentamicin and rifampicin
2) Staphylococci
- Native - flucloxacillin
- Prosthetic - flucloxacillin + rifampicin + gentamicin
3) Staphylococci (MRSA)
- Native - vancomycin + rifampicin
- Prosthetic - vancomycin + gentamicin and rifampicin
4) Streptococci
- Native - benzylpenicillin +/- gentamicin
What is the function of the pericardium?
It restrains filling of the heart
Define pericarditis
The pericardium is formed of the parietal and visceral layers, innervated by the phrenic nerve.
Pericarditis is the inflammation of the pericardium - pericardial effusion can develop, which can lead to cardiac tamponade
What is the aetiology of pericarditis?
1) 80 - 90% are idiopathic
2) Viral (common) e.g. coxsackievirus - most common viral cause
What are the risk factors for developing pericarditis?
- Male gender
- 20-50 years of age
- Previous myocardial infarction
- Viral or bacterial infection
- Systemic autoimmune disorders
What are the symptoms of pericarditis?
- Chest pain! Described as severe, sharp and pleuritic. Rapid onset. Pain can radiate to the arm. Relieved by leaning forward.
- Prodromal viral illness: e.g. upper respiratory tract infection
- Fever and myalgia
- Shortness of breath
- Peripheral oedema - suggestive of RHF secondary to pericarditis
What are the signs of pericarditis?
- Pericardial rub - squeaky sound heard at the left sternal edge as the patient leans forward
- Tachycardia
- Tachypnoea
What investigations and tests are used to diagnose pericarditis?
1) ECG: widespread saddle-shaped ST-elevation and PR depression
2) Chest X-ray: pericardial effusion; “water-bottle heart”
3) Transthoracic echocardiogram: exclude a pericardial effusion or tamponade
4) ESR and CRP: raised indicates inflammation
What is a DDx for acute pericarditis?
Myocardial infarction, rule out ASAP!
What is the management plan for acute pericarditis?
1) Acute idiopathic or viral pericarditis:
- 1st line: NSAIDs and colchicine
- 2nd line: NSAIDs, colchicine and low-dose prednisolone
2) Bacterial pericarditis
- IV antibiotics and pericardiocentesis with washout, culture and sensitivities
3) Cardiac tamponade:
- Urgent therapeutic pericardiocentesis
4) Refractory pericarditis:
- Pericardectomy
Why does chronic pericarditis hardly cause cardiac tamponade?
The parietal pericardium is able to adapt when effusions accumulate slowly and so tamponade is prevented.
What can cause myocarditis?
Viral infection.
Name 3 cardiomyopathies
1) Hypertrophic (HCM)
2) Dilated (DCM)
3) Arrhythmogenic right/left ventricular (ARVC/ALVC).
What can cause HCM?
Sarcomeric gene mutations e.g. beta myosin, troponin T mutations. About 1 in 500 people are affected.
What can cause DCM?
- Autosomal dominant familial - cytoskeleton gene mutation
- IHD
- Alcohol
- Haemochromatosis
What can cause RCM?
- Granulomatous disease (sarcoidosis, amyloidosis)
- Idiotipathic
- Post-MI fibrosis
What is the usual inheritence pattern for cardiomyopathies?
Autosomal dominant -Ventricular dilation and dysfunction = poor contractility. offspring have 50% chance of inheriting the disease
What is the pathophysiology of HCM?
Systole is normal but diastole is affected; the heart is unable to relax properly due to thickening of the ventricular walls.
What is the pathophysiology of DCM?
Ventricular dilation and dysfunction = poor contractility.
What is the pathophysiology of RCM?
Ridgid fibrotic myocardium, which restricts filling during diastole and contracts poorly.
Give 3 symptoms of HCM
- Angina.
- Dyspnoea.
- Syncope.
SUDDEN DEATH IS POSSIBLE!
Give 3 symptoms of DCM
DCM usually presents with symptoms similar to those seen in heart failure:
- Breathlessness
- Fatigue
- Oedema
What are the signs and symptoms of RCM?
- Severe dyspnoea
- Oedema
- S3 and S4 heart sounds
- Congestive heart failure
- Narrow pulse pressure (105/95 mmHg)
How is HCM diagnosed?
- ECG - large QRS complexes, large inverted T waves.
- Echo (definitive)
- Genetic testing
How is DCM diagnosed?
ECG and echo (definitive)
How is RCM diagnosed?
ECG, echo, cardiac catheterisation (definitive)
What is the management plan for HCM?
1) Asymptomatic:
- At risk of sudden death - implantable cardioverter-defibrillator
- Not at risk of sudden death - observation
2) Symptomatic:
- Negative inotropic and chronotropic agents
What is the treatment/management plan for DCM?
- Pacemaker –monitor and pace your heart rhythm by delivering electrical impulses if your heart misses a beat or is beating too slowly
- Implantable cardioverter defibrillator (ICD) – to monitor your heart rhythm and deliver an electrical shock to restore your heart’s normal rhythm if your rhythm becomes dangerous
What is the management plan for RCM?
None, consider heart transplant
Patients usually die within a year of diagnosis
What is aortic stenosis?
The pathological narrowing of the aortic valve orifice results in obstruction of blood flow.
- Progressive disease, with decades of preclinical period
- Often preceded by aortic sclerose, the thickening + stiffening of the valve leaflets without narrowing of the orifice.
What is the aetiology of aortic stenosis?
- Calcification and fibrosis of aortic valve - 80%
- Congenital bicuspid valves - valve leaflets are subject to abnormal mechanical stress predisposing them to degeneration and calcification
- Rheumatic fever - developing countries and rare
What are the risk factors for developing aortic stenosis?
1) Advancing age: increase in calcification
2) Congenital bicuspid valve: presents 20+ years earlier than patients with trileaflet valves
3) Turner syndrome and coarctation of the aorta - higher incidences of bicuspid valves
4) Rheumatic fever
5) Chronic kidney disease: abnormal calcium homeostasis
6) Hypertension, smoking, high LDL cholesterol: increase risk of aortic sclerosis
What is the pathophysiology of aortic stenosis?
- The aortic orifice is restricted e.g. by calcific deposits and so there is a pressure gradient between the LV and the aorta.
- LV function is initially maintained due to compensatory hypertrophy.
- Overtime this becomes exhausted = LV failure.
What are the symptoms of aortic stenosis?
- Exertional syncope.
- Angina.
- Exertional dyspnoea.
- Onset of symptoms is associated with poor prognosis.
What are the signs of aortic stenosis?
- Slow rising carotid pulse and decreased pulse amplitude.
- Soft or absent heart sounds.
- Ejection systolic murmur over aortic area
What investigations/tests are used to diagnose aortic stenosis?
1) ECG: features of left ventricular hypertrophy
2) Transthroacic echocardiography: abnormal
- Aortic valve area: reduced
- Mean aortic pressure gradient: increased
- LVEF: this may be reduced if there is heart failure
What is the management plan for aortic stenosis?
- Ensure good dental hygiene.
- Consider IE prophylaxis.
- Aortic valve replacement or Transcatheter aortic valve implantation (TAVI)
Aortic stenosis: which patients should be offered an aortic valve replacement?
1) Symptomatic patients with aortic stenosis.
2) Any patient with decreasing ejection fraction.
3) Any patient undergoing CABG with moderate/severe aortic stenosis.
What is mitral regurgitation?
The inability of the mitral valve to close properly, allowing backflow of blood from the LV to the LA during systole.
Describe the aetiology of mitral regurgitation/risk factors for mitral regurgitation
1) Myxomatous degeneration (prolapse of mitral valve).
2) Ischaemic mitral regurgitation.
3) Rheumatic heart disease.
4) IE.
What are the signs and symptoms of mitral valve regurgitation?
- Dyspnoea on exertion.
- Evidence of heart failure - peripheral oedema etc.
- Pansystolic murmur (always there).
- Soft 1st heart sound.
- 3rd heart sound.
- In chronic MR the intensity of the murmur correlates with disease severity.
What investigations might you do in someone who you suspect to have mitral regurgitation?
- ECG.
- Transthoracic echocardiogram: estimates LA/LV size and function
What is the management plan for mitral regurgitation?
- Rate control for AF e.g. beta blockers.
- Anticoagulation for AF.
- Diuretics for fluid overload.
- IE prophylaxis i.e. Abx
- If symptomatic = surgery
What is aortic regurgitation?
A regurgitant aortic valve means blood leaks back into the LV during diastole due to ineffective aortic cusps.
What is the aetiology of aortic regurgitation?
- Bicuspid aortic valve.
- Rheumatic fever
- Infective endocarditis
What is the pathophysiology of aortic regurgitation?
Pressure and volume overload in the LV due to backflow of blood from aorta.
LV dilatation and hypertrophy to compensate
Progressive dilatation leads to HF eventually
What signs and symptoms are present in aortic regurgitation?
Symptoms:
- Dyspnoea on exertion.
- Orthopnea.
- Palpitations.
- Paroxysmal nocturnal dyspnea (waking up at night with episods of breathlessness and wheezing)
Signs:
- Wide pulse pressure (difference between systolic and diastolic)
- Diastolic blowing murmur.
- Systolic ejection murmur.
What investigations might you do in someone who you suspect to have aortic regurgitation?
- Echocardiogram - confirms the diagnosis and detects the origin of the regurgitant jet
- CXR - cardiomegaly possible
- ECG - ST-T waves changes, conduction abnormalities
What is the management plan for someone with aortic regurgitation?
Acute:
- Inotropes
- Urgent aortic valve replacement/repair
- Vasodilators e.g. ACEi.
Ongoing:
- Surgery if symptomatic - aortic valve surgery
- Regular echoes to monitor progression.
- IE prophylaxis
What is mitral stenosis?
Narrowing of the mitral valve that causes obstruction of blood flow from LA to LV, which prevents proper filling during diastole.
Give 3 causes of mitral stenosis.
1) Rheumatic heart disease.
2) IE.
3) Calcification.
Describe the pathophysiology of mitral stenosis.
Narrowing of mitral valve orifice has two main pathological consequences:
1) LA pressure higher than LV -> pulmonary congestion (oedema)
- Pulmonary venous hypertension causes RHF symptoms.
2) Limits filling of the left ventricle, so limiting cardiac output.
What are the signs and symptoms of mitral stenosis?
Symptoms:
- Dyspnoea.
- Haemoptysis.
- RHF symptoms.
Signs:
- ‘a’ wave in jugular venous pulsations.
- Signs of RHF (see RHF flashcard).
- Pink patches on cheeks due to vasoconstriction.
- Low pitched diastolic murmur.
- Loud opening 1st heart sound snap.
What investigations might you do in someone who you suspect to have mitral stenosis?
1) ECG - AF, LA enlargement, RV hypertrophy
2) CXR - enlarged left atrium
3) transthoracic echocardiogram is the gold standard - hockey stick-shaped mitral deformity
What is the management plan for mitral stenosis?
- If AF rate control, then beta-blockers/CCB.
- Anticoagulation if AF.
- Balloon valvuloplasty or valve replacement.
- IE prophylaxis.
Why does medication not work for mitral and aortic stenosis?
The problem is mechanical and so medical therapy does not prevent progression.
DDx for stable angina (stable IHD)
- Aortic dissection
- Pericarditis
- Pulmonary embolism
DDx for unstable angina
- Stable angina
- Non-ST elevation myocardial infarction
- ST-elevation myocardial infarction
DDx for non-STEMI
- STEMI
- Unstable angina
- Aortic dissection
For STEMI, the DDx are the same (swap for non-STEMI)
DDx for acute heart failure
- Pneumonia
- Pulmonary embolism
- Asthma
DDx for chronic heart failure
- Aging
- COPD
- Pneumonia
DDx for mitral regurgitation
- Acute coronary syndrome
- Infective endocarditis
- Mitral stenosis
DDx for aortic regurgitation
- Mitral regurgitation
- Mitral stenosis
- Aortic stenosis
DDx for aortic stenosis
- Aortic sclerosis (stiffening)
- Ischaemic heart disease
- Hypertrophic cardiomyopathy (HCM)
DDx for mitral stenosis
- Unexplained AF
DDx for hypertrophic cardiomyopathy
- Athlete’s heart
- LVH due to hypertension
DDx for tetralogy of Fallot
- Pulmonary valve stenosis
- Ventricular septal defect
DDx for aortic coarctation
- Aortic stenosis
DDx for acute AF
- Atrial flutter
- Wolff-Parkinson-White syndrome
DDx for chronic AF
Atrial flutter with variable atrioventricular (AV) conduction
DDx for AV block
- Supraventricular tachycardia
- AF
DDx for essential hypertension
- Drug-induced hypertension
- CKD
DDx for DVT
- Cellulitis
- Calf muscle tear
DDx for PE
- Unstable angina
- Non-STEMI
- STEMI
DDx for peripheral vascular disease
- Spinal stenosis
- Arthritis
DDx for shock
- Simple hypotension
- Syncope or pre-syncope
