Cardiology Flashcards
What are the three types of acute coronary syndrome?
Unstable angina
ST-elevation myocardial infarction (STEMI)
Non-ST-elevation myocardial infarction (NSTEMI)
What is the primary cause of Acute Coronary Syndrome (ACS)?
ACS is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery.
Why are antiplatelet medications important in the treatment of ACS?
Thrombus formation in a fast-flowing artery is primarily made of platelets, making antiplatelet medications like aspirin, clopidogrel, and ticagrelor essential in treatment.
What are the two main coronary arteries branching from the root of the aorta?
Right coronary artery (RCA)
Left coronary artery (LCA)
What areas does the right coronary artery (RCA) supply?
Right atrium
Right ventricle
Inferior aspect of the left ventricle
Posterior septal area
What does the left coronary artery (LCA) become?
The LCA branches into the circumflex artery and the left anterior descending (LAD) artery.
What areas does the circumflex artery supply?
Left atrium
Posterior aspect of the left ventricle
What areas does the left anterior descending (LAD) artery supply?
Anterior aspect of the left ventricle
Anterior aspect of the septum
What is the typical presentation of Acute Coronary Syndrome (ACS)?
Central, constricting chest pain
Pain radiating to the jaw or arms
Nausea and vomiting
Sweating and clamminess
A feeling of impending doom
Shortness of breath
Palpitations
Symptoms typically last more than 15 minutes at rest
Silent myocardial infarction: absence of typical chest pain, especially in patients with diabetes
What are the ECG changes associated with STEMI?
ST-segment elevation
New left bundle branch block
What are the ECG changes associated with NSTEMI?
ST segment depression
T wave inversion
What do pathological Q waves indicate in an ECG?
Suggest a deep infarction (transmural)
Typically appear 6 or more hours after onset of symptoms
Which ECG leads correspond to the left coronary artery?
Heart Area: Anterolateral
ECG Leads: I, aVL, V3-6
Which ECG leads correspond to the left anterior descending artery?
Heart Area: Anterior
ECG Leads: V1-4
Which ECG leads correspond to the circumflex artery?
Heart Area: Lateral
ECG Leads: I, aVL, V5-6
Which ECG leads correspond to the right coronary artery?
Heart Area: Inferior
ECG Leads: II, III, aVF
How are troponin results used in diagnosing ACS?
Troponin is used to diagnose an NSTEMI.
It is not required to diagnose a STEMI (diagnosed based on clinical presentation and ECG).
What does a high or rising troponin indicate in suspected ACS?
A high or rising troponin in repeat tests indicates an NSTEMI.
Name some alternative causes of a raised troponin that are not ACS.
Chronic kidney disease
Sepsis
Myocarditis
Aortic dissection
Pulmonary embolism
What additional investigations are used in suspected or confirmed ACS?
Baseline bloods: FBC, U&E, LFT, lipids, and glucose
Chest x-ray: to investigate pulmonary oedema and other causes of chest pain
Echocardiogram: to assess functional damage to the heart, especially left ventricular function
How is STEMI diagnosed in a patient with acute cardiac-sounding chest pain?
STEMI is diagnosed when the ECG shows:
ST elevation
New left bundle branch block
How is NSTEMI diagnosed in acute coronary syndrome?
NSTEMI is diagnosed when there is a raised troponin with either:
A normal ECG
Other ECG changes (ST depression or T wave inversion)
How is unstable angina diagnosed?
Unstable angina is diagnosed when symptoms suggest ACS, but troponin is normal, with either:
A normal ECG
Other ECG changes (ST depression or T wave inversion)
What should be considered if a patient has chest pain but normal ECG and troponin results?
The diagnosis could be:
Unstable angina
Another cause, such as musculoskeletal chest pain
What is the initial management of acute coronary syndrome?
C – Call an ambulance
P – Perform an ECG
A – Aspirin 300mg
I – Intravenous morphine for pain if required (with an antiemetic, e.g., metoclopramide)
N – Nitrate (GTN)
What should be done when the patient is pain-free but the pain occurred within the past 72 hours?
They should be referred to the hospital for same-day assessment, usually seen by the medical team in the Ambulatory Care Unit. Emergency admission is required if there are ECG changes or complications (e.g., heart failure).
How is a STEMI managed if the patient presents within 12 hours of symptom onset?
–> Primary PCI within 120 minutes of the time thrombolysis could have been given.
–> Thrombolysis if PCI cannot be performed within 120 minutes. If ST elevation persists 90 minutes after thrombolysis, transfer for PCI.
–> Drug therapy during PCI: unfractionated heparin for radial access or bivalirudin for femoral access.
What is percutaneous coronary intervention (PCI) in the management of STEMI?
Inserting a catheter into the radial or femoral artery (radial preferred)
Feeding it to the coronary arteries under x-ray guidance
Injecting contrast to identify blockages (angiography)
Treating blockages with balloons (angioplasty) or devices
Usually inserting a stent to keep the artery open
What is thrombolysis and its associated risks in STEMI management?
Thrombolysis involves injecting a fibrinolytic agent to break down fibrin in blood clots. It carries a significant risk of bleeding.
Examples: Streptokinase, alteplase, tenecteplase
What mnemonic can be used to remember the medical management of NSTEMI?
B: Base decision about angiography and PCI on the GRACE score
A: Aspirin 300mg stat dose
T: Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, or prasugrel if having angiography)
M: Morphine titrated to control pain
A: Antithrombin therapy with fondaparinux (unless high bleeding risk or immediate angiography)
N: Nitrate (GTN)
When should oxygen be administered in the management of an NSTEMI?
Only if oxygen saturation drops below 95% (in someone without COPD).
When should unstable patients with NSTEMI be considered for immediate angiography?
Unstable patients (hypotensive) should be considered for immediate angiography, similar to with a STEMI.
Within 72 hours for GRACE score > 3% or new ischemia post-admission.
What does the GRACE score assess in NSTEMI?
The GRACE score gives a 6-month probability of death after having an NSTEMI.
using factors like age, heart rate, BP, renal function, cardiac arrest on presentation, ECG findings, and troponin levels.
What are the GRACE score risk categories?
3% or less: Low risk
Above 3%: Medium to high risk
What are the drugs used for dual antiplatelet therapy in PCI for NSTEMI/unstable angina?
If not on oral anticoagulants: Prasugrel or Ticagrelor
If on oral anticoagulants: Clopidogrel
When are patients with NSTEMI considered for early angiography with PCI?
Patients at medium or high risk (GRACE score > 3%) are considered for early angiography with PCI within 72 hours.
What are the three key components of ongoing management after the initial management of acute coronary syndrome?
Echocardiogram to assess left ventricular function
Cardiac rehabilitation
Secondary prevention
What is the mnemonic for secondary prevention medications in ACS?
The “6 A’s”:
Aspirin 75mg once daily indefinitely
Another Antiplatelet (e.g., ticagrelor or clopidogrel) for 12 months
Atorvastatin 80mg once daily
ACE inhibitors (e.g., ramipril) titrated as high as tolerated
Atenolol (or another beta-blocker, usually bisoprolol) titrated as high as tolerated
Aldosterone antagonist (e.g., eplerenone) for patients with clinical heart failure
What should be monitored in patients taking ACE inhibitors or aldosterone antagonists?
Renal function and potassium levels (risk of hyperkalaemia).
What safety update did the MHRA issue in 2016 regarding aldosterone antagonists and ACE inhibitors?
Using spironolactone or eplerenone with an ACE inhibitor or angiotensin receptor blocker increases the risk of fatal hyperkalaemia.
What is the mnemonic to remember the complications of a myocardial infarction?
The “DREAD” mnemonic:
D – Death
R – Rupture of the heart septum or papillary muscles
E – “oEdema” (heart failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome
What is Dressler’s Syndrome and how does it present?
Dressler’s Syndrome (post-myocardial infarction syndrome) occurs 2-3 weeks after an MI due to a localised immune response causing pericarditis.
Presentation:
Pleuritic chest pain
Low-grade fever
Pericardial rub on auscultation
Can cause pericardial effusion and rarely, pericardial tamponade
How is Dressler’s Syndrome diagnosed?
ECG: Global ST elevation, T wave inversion
Echocardiogram: Pericardial effusion
Raised inflammatory markers: CRP and ESR
How is Dressler’s Syndrome managed?
NSAIDs: Aspirin or ibuprofen
Steroids (e.g., prednisolone) for severe cases
Pericardiocentesis for significant pericardial effusion
What is a thoracic aortic aneurysm?
A dilation of the thoracic aorta, most commonly affecting the ascending aorta.
What is the normal diameter of the thoracic aorta?
Less than 4.5 cm for the ascending aorta and less than 3.5 cm for the descending aorta.
What is the first sign that a patient may notice with a thoracic aortic aneurysm?
The first sign may be when the aneurysm ruptures, leading to life-threatening bleeding into the mediastinum.
What is the mortality rate of a ruptured thoracic aortic aneurysm?
Extremely high mortality.
What are the three layers of the aorta?
Intima, media, and adventitia.
What is a false aneurysm (or pseudoaneurysm)?
A condition where the inner two layers of the aorta (intima and media) rupture, and the dilation is contained only within the outer (adventitia) layer.
What are common causes of false aneurysms?
Trauma (e.g., road traffic accidents), surgery to the aorta, or infection in the vessel.
What is a true aneurysm?
A condition where all three layers of the aorta (intima, media, and adventitia) remain intact but are dilated
How do thoracic aortic aneurysms typically present?
Thoracic aortic aneurysms are often asymptomatic and may be discovered incidentally on investigations such as chest x-rays, echocardiograms, or CT scans.
What symptoms can a thoracic aortic aneurysm cause due to occupying space in the mediastinum?
Chest or back pain
Cough, shortness of breath, or stridor (from trachea or left bronchus compression)
Hiccups (from phrenic nerve compression)
Dysphagia (difficulty swallowing, from oesophageal compression)
Hoarse voice (from recurrent laryngeal nerve compression)
What are the main investigations used to diagnose and assess a thoracic aortic aneurysm?
Echocardiogram
CT angiogram
MRI angiogram
How can the risk of progression of a thoracic aortic aneurysm be reduced?
By treating modifiable risk factors:
Stop smoking
Healthy diet and exercise
Optimising management of hypertension, diabetes, and hyperlipidaemia
What factors determine management options for thoracic aortic aneurysms?
Individual patient factors and the size of the aneurysm. The larger the aneurysm, the higher the risk of rupture.
What are the management options for a thoracic aortic aneurysm?
Surveillance with regular imaging to monitor size
Thoracic endovascular aortic repair (TEVAR) with a stent graft inserted via the femoral artery
Open surgery (midline sternotomy) to remove the affected section of the aorta and replace it with a synthetic graft
What are the main complications of a thoracic aortic aneurysm?
Aortic dissection
Ruptured aneurysm
Aortic regurgitation (if the aortic valve is affected)
What happens when a thoracic aortic aneurysm ruptures?
Rupture leads to life-threatening bleeding into the mediastinum, with a high risk of mortality
How does the risk of rupture relate to the size of the aneurysm?
The risk of rupture increases with the diameter of the aneurysm.
What are potential sites for bleeding in a ruptured thoracic aortic aneurysm?
Bleeding can occur into:
Oesophagus (causing haematemesis)
Airways or lungs (causing haemoptysis)
Pericardial cavity (causing cardiac tamponade)
What are the key clinical features of a ruptured thoracic aortic aneurysm?
Severe chest or back pain
Haemodynamic instability (hypotension, tachycardia)
Collapse
Death (often before reaching the hospital)
What is the emergency treatment for a ruptured thoracic aortic aneurysm?
Emergency open surgery is required, where the affected section of the aorta is replaced with a synthetic graft.
What is an abdominal aortic aneurysm (AAA)?
AAA refers to the dilation of the abdominal aorta with a diameter of more than 3 cm
When might a patient first become aware of an AAA?
Patients often become aware of an AAA when it ruptures, leading to life-threatening bleeding.
What are the risk factors for developing an abdominal aortic aneurysm (AAA)?
Men are affected significantly more often and at a younger age than women.
Increased age.
Smoking.
Hypertension.
Family history of AAA.
Existing cardiovascular disease.
What is the screening process for abdominal aortic aneurysm (AAA) in England?
Men: All men are offered a screening ultrasound at age 65 to detect asymptomatic AAA. Early detection helps prevent further expansion or rupture.
Women: Screening is not routinely offered due to lower risk. NICE guidelines (2020) suggest considering screening in women over 70 with risk factors such as:
- Cardiovascular disease
- COPD
- Family history
- Hypertension
- Hyperlipidaemia
- Smoking
Referral: If the aortic diameter is over 3 cm, referral to a vascular team is needed, with urgent referral if the diameter exceeds 5.5 cm.
How does an abdominal aortic aneurysm (AAA) typically present?
Most patients are asymptomatic, with AAA often found on routine screening.
Other possible presentations:
Non-specific abdominal pain
Pulsatile and expansile mass in the abdomen (palpated with both hands)
Incidental finding on abdominal x-ray, ultrasound, or CT scan
Rupture may be the first time patients become aware of it, leading to life-threatening bleeding.
What are the key diagnostic investigations for an abdominal aortic aneurysm (AAA)?
Ultrasound: The usual initial investigation to establish the diagnosis.
CT angiogram: Provides a more detailed picture of the aneurysm and helps guide elective surgery for repair.
What are the guidelines for aorta width, interpretation, and corresponding actions in AAA?
< 3 cm: Normal → No further action
3 - 4.4 cm: Small aneurysm → Rescan every 12 months
4.5 - 5.4 cm: Medium aneurysm → Rescan every 3 months
≥ 5.5 cm: Large aneurysm → Refer within 2 weeks to vascular surgery for probable intervention
Prevalence: Found in only 1 per 1,000 screened patients
How can the risk of progression of an AAA be reduced?
–> stop smoking
–> Healthy diet and exercise
–> Optimising the management of hypertension, diabetes, and hyperlipidaemia
What are the NICE (2020) recommendations for elective repair of AAA?
Elective repair is recommended for:
Symptomatic aneurysm
Aneurysm growing more than 1 cm per year
Aneurysm diameter above 5.5 cm
What are the two surgical methods for repairing an AAA?
Open repair via a laparotomy
Endovascular aneurysm repair (EVAR) using a stent inserted via the femoral arteries
What are the driving restrictions for patients with an AAA according to Gov.uk (April 2021)?
Must inform the DVLA if aneurysm is above 6 cm
Stop driving if aneurysm is above 6.5 cm
Stricter rules apply for heavy vehicle drivers
How does the risk of rupture change with the size of the aneurysm?
The risk of rupture increases with the diameter:
5% risk for a 5 cm aneurysm
40% risk for an 8 cm aneurysm
What is the mortality rate for ruptured AAA?
Around 80%.
What are the key clinical features of a ruptured AAA?
–>Severe abdominal pain, possibly radiating to the back or groin
–> Haemodynamic instability (hypotension and tachycardia)
–>Pulsatile and expansile abdominal mass
Collapse
–> Loss of consciousness
What is the initial management of a ruptured AAA?
It is a surgical emergency requiring immediate involvement of vascular surgeons, anaesthetists, and theatre teams.
What is permissive hypotension in the context of ruptured AAA management?
Permissive hypotension refers to the strategy of maintaining lower blood pressure during fluid resuscitation to avoid increasing blood loss.
What should be done for haemodynamically unstable patients with a suspected AAA?
They should be transferred directly to theatre for surgical repair without delaying for imaging.
When is a CT angiogram used in the management of ruptured AAA?
A CT angiogram can be used to diagnose or exclude ruptured AAA in haemodynamically stable patients.
What factors might lead to a discussion about palliative care in a ruptured AAA patient?
If the patient has co-morbidities that make the prognosis with surgery very poor, a discussion about palliative care may be appropriate.
What conditions should prompt consideration of a ruptured AAA in the differential diagnosis?
–> Back pain: In patients over 50 with acute severe back pain, consider an abdominal ultrasound to measure the aortic diameter.
–> Acute pancreatitis: Measure serum amylase/lipase. If normal or mildly raised, perform an abdominal ultrasound to exclude AAA.
–> Renal colic: Even with history of stones and positive urine dip for blood, consider an abdominal ultrasound to rule out AAA.
–> Lower limb ischaemia: Consider abdominal imaging to check for AAA as a cause when evaluating for occlusion.
What is an aortic dissection?
Aortic dissection occurs when a tear forms in the inner layer of the aorta, allowing blood to flow between the intima and media layers. This creates a false lumen full of blood within the aortic wall.
How is aortic dissection classified using the Stanford and DeBakey systems?
Stanford system:
Type A: Affects the ascending aorta, before the brachiocephalic artery.
Type B: Affects the descending aorta, after the left subclavian artery.
DeBakey system:
Type I: Begins in the ascending aorta and involves at least the aortic arch or 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 are the risk factors for aortic dissection?
Shared with peripheral arterial disease:
Age, male sex, smoking, hypertension, poor diet, reduced physical activity, and raised cholesterol.
Hypertension: Major risk factor, can be triggered by events like heavy weightlifting or cocaine use.
Aortic conditions/procedures:
Bicuspid aortic valve
Coarctation of the aorta
Aortic valve replacement
Coronary artery bypass graft (CABG)
Connective tissue disorders:
Ehlers-Danlos Syndrome
Marfan’s Syndrome
What are the key diagnostic features of aortic dissection?
–> Classic symptom: Sudden onset, severe, “ripping” or “tearing” chest pain.
Pain location:
- Anterior chest pain: Ascending aorta affected.
- Back pain: Descending aorta affected.
Pain migration: Pain may change location over time.
Other features:
Hypertension: Present in many cases.
Blood pressure difference: A difference >20mmHg between arms is significant.
Radial pulse deficit: One arm’s radial pulse is decreased/absent compared to the apex beat.
Diastolic murmur: Due to aortic regurgitation.
Neurological signs: Focal deficits, e.g., limb weakness or paraesthesia.
Chest/abdominal pain: Pain in both areas may be present.
Collapse/syncope: Especially as the dissection progresses.
Hypotension: As a late feature or sign of progression.
Signs of organ malperfusion:
Stroke: Carotid artery involvement.
Myocardial infarction: Coronary ostia obstruction.
Paraplegia: Spinal artery compromise.
Mesenteric ischemia: Abdominal pain.
Renal failure: Renal artery occlusion.
Cardiovascular collapse: Sudden death if the ascending aorta ruptures into the pericardium.
What are the key investigations used in diagnosing aortic dissection?
Chest x-ray:
Widened mediastinum may suggest aortic dissection.
CT angiography of the chest, abdomen, and pelvis:
Investigation of choice for stable patients.
Helps with surgical planning.
A false lumen is a key diagnostic finding.
Transoesophageal echocardiography (TOE):
Preferred for unstable patients who cannot be safely moved for a CT scan.
What are the management strategies for Type A and Type B aortic dissection?
Type A (affects the ascending aorta):
Surgical management is required.
Blood pressure control to a target systolic of 100-120 mmHg using IV medications while awaiting surgery.
Type B (affects the descending aorta):
Conservative management:
Bed rest.
Reduce blood pressure with IV labetalol to prevent progression.
What are some key complications of aortic dissection to remember?
Myocardial infarction
Stroke
Paraplegia (motor or sensory impairment in the legs)
Cardiac tamponade
Aortic valve regurgitation
Death
What is Acute Limb Ischaemia (ALI)?
A sudden decrease in arterial blood flow to a limb, threatening its viability, with an incidence of ~1.5 cases per 10,000 per year, primarily affecting the lower limbs.
What are the main causes of acute limb ischaemia?
Thrombosis (80-85%)
Embolism (10-15%)
Trauma (5%)
What are common causes of thrombosis in ALI?
Plaque rupture in atherosclerotic segments
Hypovolaemia
Thrombophilia
Hypotension
Malignancy
What are common sources of embolism in ALI?
Left atrium (atrial fibrillation)
Mural thrombus (myocardial infarction)
Prostheses (heart valves or bypass grafts)
Aneurysms (e.g., popliteal, abdominal aortic)
What are the risk factors for ALI?
Smoking
Diabetes mellitus
Obesity
Hypertension
Hypercholesterolaemia
What are the classical clinical features of ALI?
The six P’s:
Pain
Pallor
Pulselessness
Perishingly cold (poikilothermia)
Paraesthesia
Paralysis
How can you distinguish between embolic and thrombotic ALI?
Embolic ALI: Sudden onset, severe symptoms, normal contralateral pulses
Thrombotic ALI: Gradual onset, less severe symptoms, absent contralateral pulses, history of PAD
What is the Rutherford classification for ALI?
Stage I: Limb viable
Stage IIa: Limb marginally threatened
Stage IIb: Limb immediately threatened
Stage III: Limb irreversibly damaged
What are differential diagnoses for ALI?
Critical limb ischaemia (CLI)
Acute deep vein thrombosis
Peripheral neuropathy
Compartment syndrome
Thromboangiitis obliterans
What are the key investigations for ALI?
Bedside: Duplex ultrasound/Doppler scan, ECG
Laboratory: FBC, U&E, LFTs, coagulation, serum lactate
Imaging: CT/MR angiography, echocardiography
What is the initial management of ALI?
Emergency vascular specialist assessment
Systemic anticoagulation with heparin
Analgesia
What are the surgical management options for ALI?
Thrombotic causes: Thrombolysis, thrombectomy, bypass surgery
Embolic causes: Embolectomy, thrombolysis, bypass surgery
Non-viable limbs: Amputation
What long-term management strategies should be implemented for ALI patients?
Smoking cessation
Lifestyle modifications (diet and exercise)
Statin therapy
Management of diabetes and hypertension
Antiplatelet therapy
What are the complications associated with ALI?
High mortality rate (15-20%)
Reperfusion injury
Compartment syndrome
Peripheral nerve injury
Psychosocial impacts of amputation
What are the common clinical features of symptomatic aortic stenosis?
Chest pain
Dyspnoea
Syncope / presyncope (e.g., exertional dizziness)
Murmur
What type of murmur is classically associated with aortic stenosis?
An ejection systolic murmur (ESM) that radiates to the carotids and is decreased following the Valsalva maneuver.
What are the features of severe aortic stenosis?
Narrow pulse pressure
Slow rising pulse
Delayed ejection systolic murmur (ESM)
Soft or absent S2
S4 gallop
Thrill
Prolonged duration of murmur
Left ventricular hypertrophy or failure
What are the common causes of aortic stenosis?
Degenerative calcification (most common in patients > 65 years)
Bicuspid aortic valve (most common in patients < 65 years)
William’s syndrome (supravalvular aortic stenosis)
Post-rheumatic disease
Subvalvular aortic stenosis (e.g., hypertrophic obstructive cardiomyopathy - HOCM)
What is the management approach for asymptomatic aortic stenosis?
Generally observe the patient.
What should be done for symptomatic aortic stenosis?
Valve replacement is indicated.
When should surgery be considered for asymptomatic patients with aortic stenosis?
If there is a valvular gradient > 40 mmHg and features such as left ventricular systolic dysfunction.
What are the options for aortic valve replacement (AVR)?
–> Surgical AVR: Treatment of choice for young, low/medium operative risk patients; often combined with angiogram due to potential cardiovascular disease.
–> Transcatheter AVR (TAVR): Used for patients with high operative risk.
–> Balloon valvuloplasty: May be used in children without aortic valve calcification and limited to adults with critical aortic stenosis who are not fit for valve replacement.
What is aortic regurgitation (AR)?
AR is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole.
What are the two main categories of causes for aortic regurgitation?
Disease of the aortic valve
Distortion or dilation of the aortic root and ascending aorta
What are the causes of aortic regurgitation due to valve disease?
Chronic: rheumatic fever: the most common cause in the developing world
calcific valve disease
connective tissue diseases e.g. rheumatoid arthritis/SLE
bicuspid aortic valve (affects both the valves and the aortic root)
Acute: Infective endocarditis.
What are the causes of aortic regurgitation due to aortic root disease?
Chronic: bicuspid aortic valve (affects both the valves and the aortic root)
spondylarthropathies (e.g. ankylosing spondylitis)
hypertension
syphilis
Marfan’s, Ehler-Danlos syndrome
Acute: Aortic dissection.
What are the clinical features of aortic regurgitation (AR)?
Early diastolic murmur (increased with handgrip)
Collapsing pulse
Wide pulse pressure
Quincke’s sign (nailbed pulsation)
De Musset’s sign (head bobbing)
Mid-diastolic Austin-Flint murmur in severe AR (due to partial closure of mitral valve)
How is suspected aortic regurgitation investigated?
Suspected AR should be investigated with echocardiography.
What is the management for aortic regurgitation?
Medical management of any associated heart failure
Surgical indications include:
Symptomatic patients with severe AR
Asymptomatic patients with severe AR and LV systolic dysfunction
What are arrhythmias?
Arrhythmias are abnormal heart rhythms caused by interruptions in the normal electrical signals that coordinate heart muscle contractions.
What are the four possible rhythms in a pulseless patient?
Shockable rhythms:
Ventricular tachycardia
Ventricular fibrillation
Non-shockable rhythms:
Pulseless electrical activity (PEA)
Asystole
What distinguishes shockable rhythms from non-shockable rhythms?
Shockable rhythms (VT, VF) may respond to defibrillation, while non-shockable rhythms (PEA, asystole) will not.
What is narrow complex tachycardia?
Narrow complex tachycardia is a fast heart rate characterized by a QRS complex duration of less than 0.12 seconds, fitting within 3 small squares on a standard ECG.
What are the four main differentials for narrow complex tachycardia and how are they normally treated?
Sinus tachycardia (treatment focuses on the underlying cause)
Supraventricular tachycardia (treated with vagal manoeuvres and adenosine)
Atrial fibrillation (treated with rate control or rhythm control)
Atrial flutter (treated with rate control or rhythm control, similar to atrial fibrillation)
How is sinus tachycardia distinguished from other forms of tachycardia?
Sinus tachycardia maintains a normal P wave, QRS complex, and T wave pattern and usually occurs in response to an underlying cause (e.g., sepsis, pain).
What is a key feature of supraventricular tachycardia (SVT) on ECG?
SVT shows a regular rhythm with QRS complexes followed by T waves, but P waves are often buried in the T waves.
How can you differentiate supraventricular tachycardia (SVT) from sinus tachycardia?
SVT has an abrupt onset and a very regular rhythm without variability. In contrast, sinus tachycardia presents with a gradual onset and greater variability in the heart rate. Sinus tachycardia often has identifiable causes (e.g., pain, fever), whereas SVT may occur at rest without an obvious reason.
How can atrial fibrillation be identified on an ECG?
Atrial fibrillation is characterized by absent P waves and an irregularly irregular ventricular rhythm.
What distinguishes atrial flutter on an ECG?
Atrial flutter typically shows a saw-tooth pattern with an atrial rate of around 300 beats per minute, often resulting in a ventricular rate of 150 beats per minute.
What is the typical atrial rate in atrial flutter, and how does it affect the ventricular rate?
The atrial rate in atrial flutter is usually around 300 beats per minute, creating a saw-tooth pattern on the ECG. Due to conduction from the atria, a QRS complex occurs at regular intervals, often resulting in two atrial contractions for every one ventricular contraction, leading to a ventricular rate of approximately 150 beats per minute. 2: conduction
What is the treatment for patients with life-threatening features of narrow complex tachycardia?
Patients with life-threatening features should be treated with synchronized DC cardioversion under sedation or general anesthesia, with intravenous amiodarone if initial shocks are unsuccessful.
What defines broad complex tachycardia, and how is it classified according to resuscitation guidelines?
Broad complex tachycardia is defined as a fast heart rate with a QRS complex duration of more than 0.12 seconds (or 3 small squares) on an ECG. It is classified into:
Ventricular tachycardia or unclear cause (treated with IV amiodarone).
Polymorphic ventricular tachycardia (e.g., torsades de pointes, treated with IV magnesium).
Atrial fibrillation with bundle branch block (treated as AF).
Supraventricular tachycardia with bundle branch block (treated as SVT).
Patients with life-threatening features may require synchronized DC cardioversion and IV amiodarone if shocks are unsuccessful.
What is atrial flutter?
Atrial flutter is caused by a re-entrant rhythm in the atria, where electrical signals circulate in a self-perpetuating loop.
What is the typical atrial rate in atrial flutter?
The atrial rate is usually around 300 beats per minute.
How does atrial flutter appear on an ECG?
Atrial flutter gives a sawtooth appearance on the ECG, with repeated P waves at around 300 per minute and narrow complex tachycardia.
What is the conduction pattern in atrial flutter?
The signal may not enter the ventricles on every lap, often resulting in 2:1 conduction, giving a ventricular rate of about 150 beats per minute.
What are the potential conduction ratios in atrial flutter?
The conduction ratios may also be 3:1, 4:1, or variable.
What is the treatment for atrial flutter?
Treatment includes anticoagulation based on the CHA2DS2-VASc score and radiofrequency ablation of the re-entrant rhythm as a potential permanent solution.
What is the QT interval?
The QT interval is the duration from the start of the QRS complex to the end of the T wave.
What is the corrected QT interval (QTc)?
The QTc estimates the QT interval if the heart rate were 60 beats per minute.
What is considered a prolonged QT interval in men?
More than 440 milliseconds.
What is considered a prolonged QT interval in women?
More than 460 milliseconds.
What does a prolonged QT interval represent?
Prolonged repolarisation of the heart muscle cells (myocytes) after contraction
What are afterdepolarisations and what is this called?
Waiting a long time for repolarisation can result in spontaneous depolarisation in some muscle cells. These abnormal spontaneous depolarisations before repolarisation are known as afterdepolarisations. These afterdepolarisations spread throughout the ventricles, causing a contraction before proper repolarisation. When this leads to recurrent contractions without normal repolarisation, it is called torsades de pointes.
What is torsades de pointes?
A type of polymorphic ventricular tachycardia characterized by a twisting appearance of the QRS complex on ECG.
What causes torsades de pointes?
It can be caused by prolonged QT intervals, leading to recurrent contractions without normal repolarisation.
What are common causes of prolonged QT intervals?
Long QT syndrome, certain medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone and macrolide antibiotics) , and electrolyte imbalances (e.g., hypokalaemia/hypomagnesemia/ hypocalcaemia).
What is the management for a prolonged QT interval?
Stop medications prolonging QT, correct electrolyte disturbances, and consider beta blockers (not sotalol) or devices like pacemakers.
What is the acute management for torsades de pointes?
Correct underlying causes, administer magnesium infusion, and defibrillate if ventricular tachycardia occurs.
What are ventricular ectopics?
Premature ventricular beats caused by random electrical discharges outside the atria, often presenting as extra or missed beats.
In which patients are ventricular ectopics more common?
They are more common in patients with pre-existing heart conditions, such as ischaemic heart disease or heart failure.
common in all ages and in healthy people
How do ventricular ectopics appear on an ECG?
As isolated, random, abnormal, broad QRS complexes on an otherwise normal ECG.
What is bigeminy in the context of ventricular ectopics?
A rhythm where every other beat is a ventricular ectopic, alternating with a normal beat.
What is the management approach for ventricular ectopics in otherwise healthy individuals?
Reassurance and no treatment for infrequent ectopics.
When should specialist advice be sought for ventricular ectopics?
In patients with underlying heart disease, frequent or concerning symptoms, or a family history of heart disease or sudden death.
What medication is sometimes used to manage symptoms of ventricular ectopics?
Beta blockers.
What are the two types of second-degree heart block?
Mobitz type 1 (Wenckebach phenomenon) and Mobitz type 2.
Describe Mobitz type 1 (Wenckebach phenomenon).
The PR interval progressively lengthens until a P wave is not followed by a QRS complex, after which the cycle resets.
How does Mobitz type 2 differ from Mobitz type 1?
Mobitz type 2 has intermittent failure of conduction with absent QRS complexes following P waves, while the PR interval remains normal.
What is a common feature of a 2:1 block?
There are two P waves for each QRS complex, with every other P wave not stimulating a QRS complex., difficult to tell whether this is mobitz type 1 or 2
What is teh common feature of mobitz type 2, 3:1 block
There is usually a set ratio of P waves to QRS complexes, for example, three P waves for each QRS complex (3:1 block).
What is third-degree heart block?
Also known as complete heart block, there is no observable relationship between P waves and QRS complexes, with a significant risk of asystole.
What characterises first-degree heart block?
It is marked by delayed conduction through the atrioventricular node, with every P wave followed by a QRS complex. The PR interval is greater than 0.2 seconds (5 small squares or 1 big square) on ECG.
What is the key feature of second-degree heart block?
In second-degree heart block, some atrial impulses do not reach the ventricles, resulting in P waves that are not followed by QRS complexes.
What is bradycardia?
Bradycardia refers to a slow heart rate, typically less than 60 beats per minute. It can be normal in fit patients without symptoms. Common causes include medications (e.g., beta blockers), heart block, and sick sinus syndrome.
What is sick sinus syndrome?
Sick sinus syndrome is a condition that causes dysfunction in the sinoatrial node, often due to idiopathic degenerative fibrosis. It can result in sinus bradycardia, sinus arrhythmias, and prolonged pauses.
What is asystole?
Asystole refers to the absence of electrical activity in the heart, resulting in cardiac arrest. There is a risk of asystole in conditions like Mobitz type 2, third-degree heart block, previous asystole, and ventricular pauses longer than 3 seconds.
What are the management options for unstable patients at risk of asystole?
Management includes
–> intravenous atropine (first line),
–> inotropes (e.g., isoprenaline or adrenaline)
–> temporary cardiac pacing, and when available
–> permanent implantable pacemaker.
What are the methods for temporary cardiac pacing?
Temporary cardiac pacing can be done via transcutaneous pacing (using pads on the chest) or transvenous pacing (using a catheter to stimulate the heart directly).
How does atropine work and what are its side effects?
Atropine is an antimuscarinic medication that inhibits the parasympathetic nervous system, leading to side effects such as pupil dilation, dry mouth, urinary retention, and constipation.
What is atrial fibrillation (AF)?
AF is a condition where the electrical activity in the atria becomes disorganised, leading to fibrillation (random muscle twitching) of the atria and an irregularly irregular pulse.
What are the effects of atrial fibrillation on the heart?
Irregularly irregular ventricular contractions
Tachycardia (fast heart rate)
Heart failure due to impaired ventricular filling
Increased risk of stroke
What is the normal role of the sinoatrial node in heart contraction?
The sinoatrial node normally produces organised electrical activity that coordinates atrial contraction.
How does atrial fibrillation lead to irregular ventricular contractions?
Chaotic atrial electrical activity overrides the sinoatrial node’s regular impulses, passing to the ventricles and causing irregularly irregular ventricular contraction.
Why is there a risk of stroke in atrial fibrillation?
Uncoordinated atrial activity may cause blood stagnation and thrombus formation in the atria. A thrombus in the left atrium can travel to the brain, causing an ischaemic stroke.
What mnemonic helps remember the common causes of atrial fibrillation?
The mnemonic “SMITH” helps remember common causes of atrial fibrillation:
Sepsis
Mitral valve pathology
Ischaemic heart disease
Thyrotoxicosis
Hypertension.
What lifestyle factors are associated with atrial fibrillation?
Alcohol and caffeine are lifestyle causes of atrial fibrillation.
What is the typical presentation of atrial fibrillation?
Patients may be asymptomatic or present with palpitations, shortness of breath, dizziness, syncope, or symptoms related to associated conditions like stroke, sepsis, or thyrotoxicosis. The key examination finding is an irregularly irregular pulse.
What are the differential diagnoses for an irregularly irregular pulse?
Atrial fibrillation and ventricular ectopics.
How can you distinguish ventricular ectopics from atrial fibrillation?
Ventricular ectopics tend to disappear when the heart rate increases, such as during exercise, unlike atrial fibrillation.
What are the ECG findings in atrial fibrillation?
ECG findings in atrial fibrillation include absent P waves, narrow QRS complex tachycardia, and an irregularly irregular ventricular rhythm.
