Cardiology Flashcards
What is the definition of, and epidemiology of an AAA?
An Abdominal Aortic Aneurysm (AAA) is a permanent dilation of the abdominal aorta with a diameter >1.5 times the expected diameter for that segment given the patient’s sex and body size. The prevalence of AAAs in men ranges from 1.3% in 45-55 yr olds, to 12.5% in 75-84 year olds (increases with age).
What is the aetiology and [pathophysiology] of an AAA?
Typically, the aneurysm is around 3cm (as normal abdominal aortic diameter is 2cm) 90% of AAAs happen below the renal arteries as there is less collagen around the segment, making it weaker. The aetiology if aortic aneurysms are multifactorial, including atherosclerosis and altered tissue metalloproteinases which diminishes the integrity of the abdominal wall.
What are the risk factors for an AAA?
Risk factors include: • Cigarette smoking • Hereditary/family history • Increasing age • Male sex (prevalence) • Female sex (rupture)
What are the clinical features of an AAA?
Tend to be asymptomatic and picked up only on screening. It is therefore important to know the risk factors. On examination a pulsatile mass may only be felt in slim patients with an AAA >5cm (therefore not a good screening tool).
Ruptured AAA:
• Abdominal, back or groin pain (do not dismiss as renal colic)
• Hypotension
• Pulsatile mass
How can an AAA be investigated?
An abdominal ultrasound is the first test to do, which can show vessel diameter.
Blood tests can show increased CRP/ESR with leukocytosis and positive blood cultures in infective AAA.
CT, MRI and aortography can also be used in investigation.
What is the definition and epidemiology of an Aortic Dissection?
An aortic dissection is where a tear in the aortic intima allows blood to surge into the aortic wall, causing a split between the inner and outer tunica media, and creating a false lumen. It is most common in males between the ages of 40 and 60.
What is the aetiology of an Aortic Dissection?
The aetiology of an aortic dissection causes degenerative changes in the smooth muscle of the aortic media. Causes and predisposing factors are:
• Hypertension
• Aortic atherosclerosis
• Connective tissue disease (e.g. SLE, Marfan’s, Ehlers-Danlos)
• Congenital cardiac abnormalities
• Aortitis (e.g. Takayasu’s aortitis, tertitary syphilis)
• Iatrogenic (e.g. during angiography or angioplasty)
• Trauma
• Crack cocaine
What are the symptoms of an Aortic Dissection?
Patients commonly present with an acute severe central ‘tearing’ chest pain that may radiate to the back (or may mimic an MI). Interscapular pain is a feature of descending aorta dissection.
Up to 20% of patients present with syncope and no pain.
An aortic dissection can also lead to occlusion of the aorta and its branches:
• Carotid obstruction - hemiparesis, dysphasia, blackout.
• Coronary artery obstruction - chest pain (angina or MI)
• Subclavian obstruction - ataxia or loss of consciousness.
• Coeliac obstruction - severe abdominal pain.
• Renal artery obstruction - anuria, renal failure.
What are the examination features of an Aortic Dissection?
- May find a murmur in the back below the left scapula, descending to the abdomen.
- Blood pressure differential between the two arms, as well as a widened pulse pressure
- A pulse differential or deficit between the two legs
- Signs of aortic insufficiency such as collapsing pulse, and early diastolic murmur.
Hypotension is a sign of cardiac tamponade.
There may also be signs of Marfan’s or Ehlers-Danlos syndrome such as tall stature, arachnodactyly, pectus excavatum, hypermobile joints, and narrow face.
What are the complications of an Aortic Dissection?
Complications: Aortic rupture is often fatal. Cardiac tamponade is also very dangerous, and occurs when blood leaks into the pericardium.
Other complications include pulmonary oedema, MI, syncope, and cerebrovascular, renal, mesenteric or spinal ischaemia.
How can an Aortic Dissection be investigated?
An ECG is an important first-line test to look for evidence of myocardial ischaemia, and is often normal. ST depression may occur in acute aortic dissection (inferior MI), but ST elevation is rare.
A CXR is used to exclude pulmonary causes of pain. A widened mediastinum or a localised bulge points to an aortic dissection.
Bloods:
• FBC can show anaemia or is normal
• Cross-match 10 units of blood (in case of surgery)
• Cardiac enzymes are usually negative unless an MI is caused by the dissection. • U&Es to look for renal function.
A CT of the thorax can be used to visualise the false lumen of dissection. A trans-oesophageal echocardiography is a highly specific way to confirm diagnosis.
Define cardiac arrest
Cardiac arrest is the acute cessation of cardiac function.
What are the most common causes of cardiac arrest?
Most cases of cardiac arrest occur secondary to structural heart disease:
• Coronary artery disease (up to 70%): both ACS and stable CAD
• Heart failure
• Cardiomyopathy particularly hypertrophic and arrythmogenic right ventricular sub-types.
What are the classically reversible causes of cardiac arrest?
Hypoxia
Hypothermia
Hypovolemia
Hypo- or hyperkalaemia
Tamponade
Tension pneumothorax
Thromboembolism
Toxins and other metabolic disorders
What are the clinical features of a Cardiac Arrest?
(History obtained from patient’s relatives) Patients may have a family history of sudden cardiac arrest. They may have a history of pulmonary disease, chest pain, palpitations or syncope.
Patient may have had symptoms of main risk factors such as:
• Coronary artery disease
• Left ventricular dysfunction
• Hypertrophic cardiomyopathy (due to disordered myofibrils and scaring)
• Arrythmogenic right ventricular dysplasia
• Long QT syndrome
• Acute medical or surgical emergency (4 H’s and 4T’s)
Patients suffering from cardiac arrest rarely have symptoms prior to arrest, and lose consciousness 10-15 seconds after cerebral hypoxia. Patients can sometimes take gasps (agonal breathing) unconsciously, but often stop breathing all together.
On examination: Patient is unconscious, not breathing and has absent carotid pulses.
How can Cardiac Arrest be investigated?
Cardiac monitor is important as classification of the rhythm directs management. There are four main non-perfusing rhythm abnormalities that occur in cardiac arrest:
• Pulseless Ventricular Tachycardia (shockable)
• Ventricular Fibrillation (shockable)
• Pulseless Electrical Activity (PEA): organised electrical activity on the ECG with no demonstrable pulse or blood pressure.
• Asystole: absence of any electrical or mechanical cardiac activity.
Bloods: ABG, U&E, FBC, cross-match, clotting, toxicology screen, glucose.
What are the complications of Cardiac Arrest?
Irreversible hypoxic brain damage, death.
What is the management of Cardiac Arrest?
DR (Danger, Response) : Ensure there is no danger at the arrest scene, summon help as soon as possible. Check if patient is unconscious
ABC:
• Ensure airway is clear with jaw thrust and chin lift.
• Assess breathing by looking, listening and feeling If not breathing, give 2 breaths immediately
• Assess circulation at carotid pulse for 10s.
Basic Life Support (includes ABC) if carotid pulse is not felt:
- Give 30 chest compressions at a rate of 100 /min.
a. Compressions at lower sternum at least depth of 5cm. Allow sufficient recoil of the chest after each compression. Sub-optimal compression greatly reduces the chance of survival. - Give two breaths using mouth-to-mouth or bag-mask.
- Continue cycles, proceed to advanced life support as soon as possible.
Advanced Life Support:
- Attach cardiac monitor and defibrillator.
- Assess the rhythm.
a. If shockable, defibrillate once. Resume CPR immediately for 2 minutes, re-assess rhythm before shock. Continue CPR and shock cycle until return of spontaneous circulation. Administer adrenaline every 3-5 minutes, and consider amioderone.
If un-shockable, start CPR and administer adrenaline every 3-5 minutes. Re-assess rhythm after two minutes of CPR, and return to step 2.
What is the prognosis of cardiac arrest?
Resuscitation is less successful in the arrests that occur outside hospital. Duration of inadequate effective cardiac output is associated with poor prognosis.
What is the definition and epidemiology of Aortic Regurgitation?
Aortic Regurgitation is the reflux of blood from the aorta into the left ventricle during diastole. AR is also called aortic insufficiency. Chronic AR often begins in the late 50s, documented most frequently in patients >80 years old.
What is the aetiology of Aortic Regurgitation?
Causes are either due to:
• Aortic root dilation which pulls the leaflets apart. This can be secondary to:
○ Systemic hypertension
○ Aortic distention
○ Aortitis (due to syphilis, or Tayakasu’s aortitis)
• Aortic valve abnormalities or damage. This can be secondary to a biscuspid valve, rheumatic fever, infective endocarditis, or trauma.
Acute causes are: infective endocarditis, ascending aorta dissection and chest trauma.
What are the symptoms of Aortic Regurgitation?
Chronic AR can be asymptomatic initially, but later progress to symptoms of heart failure such as exertional dyspnoea, orthopnoea, fatigue and occasionally angina.
In acute AR, the left ventricle is of normal size and unable to compensate, leading to shortness of breath and pulmonary oedema due to backwards transmission of pressure through the pulmonary system.
Sudden cardiovascular collapse can be a symptom of acute AR. Patient may also have symptoms of aetiology such as chest or back pain due to aortic dissection.
What are the examination features of Aortic Regurgitation?
An early diastolic murmur can be heard best with the patient lent forward with breath on expiration and with the stethoscope on the lower left sternal edge. The absence of a diastolic murmur significantly reduces the chances of AR.
You may also hear an Austin Flint mid-diastolic murmur .
A collapsing ‘water-hammer’ pulse and a wide pulse pressure is also a common feature. A displaced apical pulse is also common.
Uncommon signs are those due to a hyperdynamic pulse producing visible pulsations.
How is Aortic Regurgitation investigated?
An echocardiography and Doppler is diagnostic as can visualise the regurgitant jet.
An ECG may show signs of left ventricular hypertrophy (deep S wave in V1–2, tall R wave in V5–6, inverted T waves in I, aVL, V5–6 and left-axis deviation).
A CXR can show cardiomegaly and dilation of the ascending aorta. Signs of pulmonary oedema can also be seen with left heart failure.
A cardiac catheterisation with angiography can also be done.
What is the definition and epidemiology of Aortic Stenosis?
Aortic stenosis is the narrowing of the left ventricular outflow at the level of the aortic valve. It affects 3% of over 75-year-olds, and men more than women. However, those with bicuspid valves may present earlier (as young adults).
What is the aetiology of Aortic Stenosis?
Causes include:
- Stenosis due to rheumatic heart disease (commonest worldwide)
- Calcification of a congenital bicuspid aortic valve
- Calcification/degeneration of a tricuspid valve in the elderly.
What are the clinical features of Aortic Stenosis?
May be asymptomatic initially. Symptoms are due to insufficient oxygen delivery to tissues, common ones include:
• Dyspnoea on exertion
• Angina
• Syncope or dizziness on exercise.
On examination:
• Ejection systolic murmur (crescendo-decrescendo pattern) radiating to the carotids. S2 may be diminished or softened.
• BP: narrow pulse pressure
• Pulse: slow rising
• Palpation: trill in the aortic area (if severe)
How is Aortic Stenosis investigated?
A transthoracic echocardiogram is the best test for the initial diagnosis and subsequent evaluation of AS. The sensitivity and specificity of the test are high. It shows increased aortic pressure gradient.
An ECG can show left ventricular hypertrophy and absent Q waves, AV block, hemiblock, or bundle branch block.
A CXR can show post-stenotic enlargement of the ascending aortic valve area and calcification of the aortic valve.
Cardiac angiography allows differentiation from other causes of angina, and to assess for concomitant coronary artery disease (50% of patients with severe aortic stenosis have significant coronary artery disease).
What is the definition and epidemiology of Atrial Fibrillation?
Atrial fibrillation is an atrial tachyarrhythmia characterised by an irregularly irregular heart rhythm and indiscernible P waves on an ECG. It is the most common atrial tachyarrhythmia seen in 1% of the entire population, and is commonly seen in the elderly. Prevalence increases with age. Male predominance.
What are the subtypes of Atrial Fibrillation?
Often subdivided into:
• Paroxysmal - Self-resolving episode of less than 7 days
• Persistent - Non self-resolving episode of more than 7 days
• Permanent - AF for more than 1 year.
What is the aetiology of Atrial Fibrillation?
There may be no identifiable cause. Secondary causes lead to abnormal electrical pathways that result in AF. These include:
• Systemic causes: Thyrotoxicosis, hypertension, pneumonia and alcohol.
• Heart: Mitral valve disease, ischaemic heart disease, rheumatic heart disease, cardiomyopathy, pericarditis, suck sinus syndrome, atrial myxoma.
• Lung: Bronchial carcinoma, pulmonary embolism.
What are the clinical features of Atrial Fibrillation?
Often patients are asymptomatic. Some patients experience palpitations, dyspnoea on exertion, and syncope/light-headedness.
On examination: Patient has irregularly irregular pulse, with or without pulse deficit. Look for thyroid disease and valvular heart disease.
How is Atrial Fibrillation investigated?
ECG: Uneven baseline (fibrillation) with absent P waves, irregular QRS complexes. If there is a saw-tooth baseline, consider if there is atrial flutter.
Bloods:
• Cardiac enzymes to rule out ischaemic causes of symptoms
• TFTs to identify underlying cause
• U&E used to assess for co-morbid conditions, as well as helpful in choosing anti-rhythmic agents.
Electrocardiogram to assess structural causes e.g. mitral valve disease, left atrial dilation or ventricular dysfunction.
CXR can show signs of pneumonia.
What is the GENERAL (just strategy) management outlines for Atrial Fibrillation?
If haemodynamically unstable, then use DC cardioversion immediately.
The AFFIRM and RACE trial have shown similar outcomes (in both mortality benefit and stroke risk) with either rate or rhythm control. As a general rule of thumb:
• Asymptomatic or mildly symptomatic patients above the age of 65, consider rate control.
• Symptomatic patients under 65, or concomitant heart failure, consider rhythm control.
Symptomatic patients given heparin before cardioverted.
Assess stroke risk and anticoaugulate if needed.
How do you elicit rate control in an patient with atrial fibrillation?
In symptomatic patients:
Rate control is indicated as first-line option unless there is a reversible cause, or if AF is secondary to heart failure, or if new-onset AF.
1. Beta-blockers (esmolol, atenolol, propranlol, metoprolol) or calcium-channel blockers (diltiazem or verapamil). (Unless patient has heart failure, in which case use digoxin) 2. Add Digoxin if need to, or if patient has heart failure.
How do you assess and manage stroke risk in a patient with Atrial Fibrillation?
Assess stroke risk with CHA2DS2-VASc score.
• No anticoagulation for patient with a CHA2DS2-VASc score of 0-1 and has not got heart failure.
• Anticoagulate patients with a score of ≥2 and/or with heart failure.
○ Once sinus rhythm is restored, add warfarin to heparin. In select patients warfarin may be replaced by direct oral anticoagulants such as dabigatran (direct thrombin inhibitor), or rivaroxaban or apixaban (direct factor Xa inhibitor).
What is the definition and epidemiology of Atrial Flutter?
Atrial flutter is an atrial tachyarrhythmia which is characterised by a regular, rapid atrial rate. It is less common than atrial fibrillation and the prevalence ratio in males to females is 5:2. Incidence increases with age.
What is the aetiology of Atrial Flutter?
Common causes include (all cause macro re-entrant circuit):
- Right atrial dilatation - due to pulmonary embolus, mitral and/or tricuspid pathologies, congestive heart failure.
- Ischaemic heart disease
- Idiopathic - no underlying hear disease
- Normal variant - tall males
- Patients with a history of endurance sports (causing atrial enlargement).
Other causes include drugs, metabolic disturbances, and iatrogenic (catheter ablation, cardiac surgery).
What are the clinical features of Atrial Flutter?
Patients commonly present with breathlessness and palpitations. Syncope and severe dyspnoea (at very rapid rates), can also present with chest pain.
How can Atrial Flutter be investigated?
ECG shows narrow-complex tachycardia with characteristic regular sawtooth pattern of flutter waves.
Classically has an atrial rate of 300bmp and a ventricular rate of 150bmp. Has fixed conduction ratio (2:1, 3:1, etc.).
Sometimes the ECG does not show flutter waves, as they are buryed by the QRS complexes. Only tend to show flutter waves on injection of adenosine?? In general, a narrow complex tachycardia that has a division of 300bmp e.g 150 bmp or 200bmp is likely to be atrial flitter.
How is Atrial Flutter managed?
Managed similar to AF, however achieving rate control is more difficult.
Radiofrequency ablation is highly recommended in patients with chronic atrial flutter as therapy can induce high rates of remission (90%).
Define cardiomyopathy, and what are the three main types?
Cardiomyopathy is disease of the myocardium (heart muscle).
There are several types with the majority of causes being idiopathic for each type. The three main types of cardiomyopathy and non-idiopathic causes include:
- Dilated cardiomyopathy (heart is dilated and has impaired function) - post-viral myocarditits, alcohol, drugs, familial (25% of idiopathic causes), thyrotoxicosis, haemochromatosis, peripartum.
- Hypertrophic cardiomyopathy - up to 50% are genetic.
- Restrictive cardiomyopathy - amyloidosis, sarcoidosis, haemochromatosis.
What are the clinical features of dilated cardiomyopathy?
- Patients present with symptoms of heart failure, dyspnoea, chest discomfort, paliptations, and syncope.
- Patient may also have arrythmias, thromboembolisms, and a family history of sudden death.
- On examination, they may have a raised JVP, displaced apex beat, functional mitral and tricuspid regurgitations and a third heart sound (made by blood hitting thin wall).
What are the clinical features of hypertrophic cardiomyopathy?
- Patients are usually asymptomatic.
- May also complain of syncope, angina, arrhythmias, and have a family history of sudden cardiac death.
- On examination may have a jerky carotid pulse, double apex beat, and an ejection systolic murmur.
What are the clinical features of restrictive cardiomyopathy?
- Patients present dyspnoea, fatigue, arrhythmias, and ankle or abdominal swelling.
- On examination, patients have an increased JVP, palpable apex beat, third heart sound, ascites, ankle oedema and hepatomegaly.
How is cardiomyopathy investigated?
CXR may show cardiomegaly and signs of heart failure.
ECG may show non-specific ST changes, conduction defects and arrhythmias for all types.
• In hypertrophic cardiomyopathy, may also note left axis deviation, and signs of left ventricular hypertrophy. Q waves in inferior and lateral leads.
• In restrictive cardiomyopathy ECG shows low-voltage complexes.
Echocardiography may show:
• Dilated: dilated ventricles with global hypokinesia.
• Hypertrophic: Ventricular hypertrophy
• Restrictive: non-dilated non-hypertrophic ventricles. Atrial enlargement, preserved systolic function, diastolic dysfunction, granular or ‘sparkling’ appearance of myocardium in amyloidosis.
Cardiac cathertisation and endocardial biopsy may be helpful.
What is the definition and epidemiology of cardiac failure?
Cardiac failure is the inability of the cardiac output to meet the body’s demands despite normal venous pressures. Heart failure is common, affecting 10% of > 65-year-olds.
How can cardiac failure be classified by function?
Low output causes of heart failure can be divided into systolic (low ejection fraction) or diastolic heart failure (preserved ejection fraction, but reduced ventricular filling).
High output heart failure is due to increased demand from the body. This is usually rare, and sometimes seen in thyrotoxicosis, beriberi, severe anaemia, pregnancy, and AV malformation.
What are the common causes of heart failure (classified anatomically)?
Alternatively, they can be divided anatomically:
- Left heart failure: Commonly caused by ischaemic heart disease, hypertension, valvular disease and cardiomyopathy.
- Right heart failure: Commonly secondary to left heart failure, infarction, cardiomyopathy, pulmonary hypertension/embolus/valve disease (cor pulmonale/pulmonary heart disease), chronic lung disease, tricuspid regurgitation, constrictive pericarditis/pericardial tamponade.
- Biventricular failure: Caused by arrhythmia, cardiomyopathy (dilated or restrictive), myocarditis, drug toxicity.
[What are the mechanical and neurohumoral adaptation of cardiac failure/]
Mechanical adaptations:
• Frank-Starling Law states that as myocardial contractility declines, stroke volume reduces as a consequence. This results in an increased end diastolic volume due to incomplete emptying, and this increases stroke volume in the following contraction. Eventually, this process results in ventricular remodelling, increased wall stress and reduced cardiac output as this mechanism fails.
Neurohumoral adaptations:
• Activation of the sympathetic nervous system. As cardiac output declines, there is early activation of the SNS. This causes tachycardia, increased sodium and fluid reabsorption by the kidneys and increased peripheral vascular resistance.
• Activation of the renin-angiotensin-aldosterone system (RAAS). In heart failure, activation of the RAAS is a late compensatory mechanism. This is mediated primarily by angiotensin II, and causes increased preload and afterload. As the heart tries to cope with this increased workload, further activation of the RAAS leads to a vicious cycle of fluid overload and worsening wall stress.
What are the clinical features of Chronic Left-sided Heart Failure?
Left-sided heart failure: As blood is not adequately pushed out from the left ventricle, blood gets backed up to the lungs via the pulmonary veins. This is called pulmonary congestion. Symptoms are primarily due to this pulmonary oedema (fluid inside the lungs), but also can be due to a pulmonary effusion. These symptoms include:
• Dyspnoea due to the pulmonary oedema causing impaired gas exchange.
• Orthopnoea - as lying down allows blood from legs and abdomen to return to the heart leading to more fluid in lungs.
• Paroxysmal nocturnal dyspnoea
• Nocturnal cough and chest discomfort
• Fatigue.
On examination: Note tachycardia, tachypnoea, displaced apex beat, bilateral basal crackles (due to pulmonary oedema), third heart sound (due to rapid ventricular filling), and a pan-systolic murmur (functional mitral regurgitation).
What are the clinical features of Right-sided Heart Failure?
Right-sided heart failure is usually a result of left-sided heart failure, and so symptoms of LVF are commonly also present: In right-sided heart failure, blood backs up to the rest of the systemic venous circulation. Symptoms include: • Swollen ankles • Fatigue • Increased weight (due to oedema) • Decreased exercise tolerance
On examination: Note increased JVP, hepatosplenomegaly, ascites, ankle/sacral pitting oedema and signs of functional tricuspid regurgitation.
What are the clinical features of ACUTE Left-sided Heart Failure?
Acute LVF is characterised by dyspnoea, wheeze, cough and pink frothy sputum. On examination, patient would have tachypnoea, cyanosis, tachycardia, peripheral shutdown, pulsus alternans, gallop rhythm, wheeze and fine crackles throughout lung.
How can Cardiac Failure be investigated?
Bloods:
• FBC, U&Es, LFTs, CRP, glucose, lipids and TFTs are roitinely performed.
• In acute: ABG, troponin, BNP (brain natriuretic peptide) - high BNP suggests cardiac failure, low plasma BNP rules out cardiac failure.
CXR is used to exclude other causes of dyspnoea and support a diagnosis of heart failure. CXR appearance includes:
• A: Alveolar Oedema
• B: Kerley B lines (sign of interstitial oedema)
• C: Cardiomegaly
• D: Diversion of upper lobes, resulting in prominent upper lobe vessels secondary to increased pulmonary pressures.
• E: Pleural Effusion.
ECG may show ischaemic changes, arrhythmia, left ventricular hypertrophy or may be normal.
Echocardiogram can be used to assess ventricular contraction.
Swan-Ganz catheter allows measurements of right atrial, right ventricular, pulmonary artery, pulmonary wedge and left ventricular end-diastolic pressures.
What are the non-pharmacologic/surgical treatments for Cardiac Failure?
Lifestyle modifications are necessary. Notably: • Salt and fluid retention • Weight reduction • Smoking cessation • Alcohol reduction • Low intensity aerobic exercise.
What are the pharmacological treatments for Cardiac Failure?
First-line:
• ACE-inhibitors such as Ramipril, Captopril, decrease mortality and morbidity associated with heart failure.
○ Angiotensin-II receptor blockers such as Valsartan should replace ACEi if not well tolerated.
• Beta-blockers such as Bisoprolol and Carvediol also improve mortality and morbidity and should be prescribed with ACEi.
• Diuretics should also be prescribed to patients with previous evidence of fluid retention. First line are loop diuretics (e.g. frusemide), then thiazide-like diuretics (e.g. metolazone).
Second-line:
• Aldosterone antagonists such as spironolactone should be prescribed to patients with moderate-severe LVF (but also beneficial to people with mild LVF). Improves mortality. Monitor K+ as can cause hyperkalaemia.
• Vasodilators such as hydralazine may be added to patients (particularly in Afro-Caribbeans) with persistent symptoms.
• Digoxin is a positive inotrope. Decreases hospitalisation, but not mortality.
