BLOCK 13 WEEK 3 Flashcards
Heart Failure
Heart failure (HF), also known as congestive heart failure (CHF) and congestive cardiac failure (CCF), is defined as the failure of the heart to generate sufficient cardiac output to meet the metabolic demands of the body.
The prognosis for HF varies, but approximately 50% of those diagnosed are alive at 5 years.
Epidemiology of heart failure
HF is common: the prevalence in the UK is estimated at 1-2%.
HF primarily affects the elderly population: the average age of diagnosis is 75 years old. The incidence of HF has been increasing with the ageing population.
HF pathophysiology:
The pathophysiology for HF is diverse and depends on the aetiology of the HF.
How can HF be classified?
HF can be classified in different ways.
It can be classified as being:
- low output vs. high output HF
- predominantly systolic or diastolic dysfunction
- whether the process has been acute or chronic
- or by the severity of symptoms (and consideration for predominantly left or right ventricle features).
low output vs. high output HF
Low-output HF is much more common than high-output HF.
Low-output HF occurs: when cardiac output is reduced due to a primary problem with the heart and the heart is unable to meet the body’s needs.
High-output HF: refers to a heart that has a normal cardiac output, but there is an increase in peripheral metabolic demands that the heart is unable to meet.
Common causes of high output heart failure
The common causes of low-output HF wll be further discussed below. Common causes of high-output HF include:
Anaemia
Arteriovenous malformation
Paget’s disease
Pregnancy
Thyrotoxicosis
Thiamine deficiency (wet Beri-Beri)
Systolic vs Diastolic HF
Systolic dysfunction refers to an impairment of ventricular contraction.
The ventricles are able to fill well, but the heart is unable to pump the blood sufficiently out of the ventricle due to impaired myocardial contraction during systole (reduced ejection fraction).
Common causes include: ischaemic heart disease, dilated cardiomyopathy, myocarditis or infiltration (haemochromatosis or sarcoidosis).
Diastolic dysfunction refers to the inability of the ventricles to relax and fill normally, hence the heart is still able to pump well but pumps out less blood per contraction due to reduced diastolic filling (preserved ejection fraction).
Common causes include: uncontrolled chronic hypertension (significant left ventricular hypertrophy reduces filling of the left ventricle), hypetrophic cardiomyopathy, cardiac tamponade, and constrictive pericarditis.
Acute vs Chronic HF
HF can also be classified according to time of onset. Acute HF occurs with new-onset of HF symptoms (acute mitral regurgitation following an MI) or an acute deterioration in a patient with known, chronic HF.
In comparison, chronic HF progresses more slowly and may take many years to develop.
The clinical features of left heart failure
LHF, or left ventricular failure (LVF), causes pulmonary congestion (pressure builds up on the LHS of the heart and there is backpressure to the lungs) and there is systemic hypoperfusion.
Hypoperfusion: means low blood flow and occurs because of circulatory failure caused by the failing of the heart’s pumping action
Symptoms:
-Shortness of breath on exertion
-Orthopnoea: shortness of breath that occurs while lying flat and is relieved by sitting or standing
-Paroxysmal nocturnal dyspnoea
-Nocturnal cough (± pink frothy sputum)
-Fatigue
Signs:
Tachypnoea
Bibasal fine crackles on auscultation of the lungs
Cyanosis
Prolonged capillary refill time
Hypotension
Less common signs: pulsus alternans (alternating strong and weak pulse), S3 gallop rhythm (produced by large amounts of blood striking compliant left ventricle), features of functional mitral regurgitation.
The clinical features of right heart failure
Right heart failure causes venous congestion (pressure builds up behind the right heart) and pulmonary hypoperfusion (reduced right heart output).
Symptoms:
- Ankle swelling
- Weight gain
- Abdominal swelling and discomfort
- Anorexia and nausea
Signs:
-Raised JVP
-Pitting peripheral oedema (ankle to thighs to sacrum)
-Tender smooth hepatomegaly
-Ascites
-Transudative pleural effusions (typically bilaterally)
Congestive Cardiac Heart Failure
Sometimes left sided heart failure can lead to pulmonary congestion which in turn also pushes the right ventricle into failure. In these cases signs and symptoms of both left and right sided heart failure may be present. This is congestive cardiac failu
Ejection Fraction
Chronic heart failure symptoms
Signs on examination include:
- Tachycardia (raised heart rate)
- Tachypnoea (raised respiratory rate)
- Hypertension
- Murmurs on auscultation indicating valvular heart disease
- 3rd heart sound on auscultation
- Bilateral basal crackles (sounding “wet”) on auscultation of the lungs, indicating pulmonary oedema
- Raised jugular venous pressure (JVP), caused by a backlog on the right side of the heart, leading to an engorged internal jugular vein in the neck
- Peripheral oedema of the ankles, legs and sacrum
Location
Investigating Heart Failure
- Clinical assessment (history and examination)
- N-terminal pro-B-type natriuretic peptide (NT‑proBNP) blood test
- ECG:
ECG may be normal or hint at underlying aetiology (ischaemic changes or arrhythmias). - Echocardiogram
-Transthoracic echocardiogram (TTE)
Echocardiogram will confirm the presence and degree of ventricular dysfunction.
Other investigations include:
-Bloods for anaemia, renal function, thyroid function, liver function, lipids and diabetes
-Chest x-ray and lung function tests to exclude lung pathology
New York Heart Association Classification
The New York Heart Association (NYHA) classification system is used to grade the severity of symptoms related to heart failure. Here is a simplified summary:
Class I: No limitation on activity
Class II: Comfortable at rest but symptomatic with ordinary activities
Class III: Comfortable at rest but symptomatic with any activity
Class IV: Symptomatic at rest
MANAGEMENT OF HEART FAILURE
There are five principles of management. You can remember this with the “RAMPS” mnemonic:
R – Refer to cardiology
A – Advise them about the condition
M – Medical treatment
P – Procedural or surgical interventions
S – Specialist heart failure MDT input, such as the heart failure specialist nurses, for advice and support
The urgency of the referral and specialist assessment depends on the NT-proBNP result. According to the NICE guidelines:
From 400 – 2000 ng/litre should be seen and have an echocardiogram within 6 weeks
Above 2000 ng/litre should be seen and have an echocardiogram within 2 weeks
Medical Treatment of Heart Failure
The first-line medical treatment of chronic heart failure can be remembered with the “ABAL” mnemonic:
A – ACE inhibitor (e.g., ramipril) titrated as high as tolerated
B – Beta blocker (e.g., bisoprolol) titrated as high as tolerated
A – Aldosterone antagonist when symptoms are not controlled with A and B (e.g., spironolactone or eplerenone)
L – Loop diuretics (e.g., furosemide or bumetanide)
An angiotensin receptor blocker (ARB) (e.g., candesartan) can be used instead of an ACE inhibitor if not tolerated. Avoid ACE inhibitors in patients with valvular heart disease until initiated by a specialist.
Aldosterone antagonists are used when there is a reduced ejection fraction and symptoms are not controlled with an ACEi and beta blocker.
Patients should have their U&Es closely monitored whilst taking diuretics, ACE inhibitors and aldosterone antagonists, as all three medications can cause electrolyte disturbances. It is particularly essential to closely monitor the renal function in patients taking ACE inhibitors and aldosterone antagonists. Both can cause hyperkalaemia (raised potassium), which is potentially fatal.
Additional specialist
Loop diuretics
ACE inhibitors and ARBS
DIGOXIN
Side effects of Beta Blockers
SGLT- 2 Inhibitors
Treatment
Surgical Procedures
Surgical procedures may be used to treat underlying valvular heart disease.
Implantable cardioverter defibrillators continually monitor the heart and apply a defibrillator shock to cardiovert the patient back into sinus rhythm if they identify a shockable arrhythmia. These are used in patients who previously had ventricular tachycardia or ventricular fibrillation
Differential Diagnosis
Valvular Disease
The three types of heart valve diseases are regurgitation, stenosis, and atresia.
The type of heart valve disease you have depends on which valve is affected and in what way.
Heart valve diseases can cause problems in any of the heart’s four valves: the aortic, mitral, pulmonary, and tricuspid valves
CORONARY ARTERIES
- The left anterior descending artery is sometimes called the ANTERIOR INTERVENTICULAR ARTERY
-
Left Marginal Artery
- The left marginal artery goes down (vertical)
- The left circumflex artery goes across (horizontal)
Stroke Volume
Stroke Volume: The volume of blood pumped from the left ventricle per beat
Cardiac Output
Cardiac Output: The volume of blood pumped out of the heart per minute
Ejection Fraction
Is a measurement expressed as a percentage of how much blood the left ventricle pumps out with each contraction
Arteries of Heart
CORONARY VEINS
-drain deoxygenated blood from coronary distribution and return it to the right atrium so it can be reoxygenated.
-A number of cardiac veins run alongside the cardiac arteries
e.g the great cardiac veins runs along the left anterior descending
-All of the cardiac veins drain into the coronary sinus which then takes the blood to the coronary sinus in the right atrium.
-Some veins carry deoxygenated blood back to the right atrium without going through the coronary sinus such as the smallest cardiac vein (thebesian vein) and the anterior cardiac vein
Ligamentum Arteriosum
This small ligamentous attachment runs between the aortic arch and left pulmonary artery.
Conus arteriosus
Space between the right ventricle and the pulmonary trunk
Electrocardiogram
ECG is an electrocardiogram.
its a simple test that can be used to check your hearts rhythm and electrical activity.
Describe atrial fibrillation on an ECG ?
The R waves are irregular
There’s no p waves
There’s no F waves
Atrial Fibrillation
The R waves are irregular
There’s no p waves
There’s no F waves
Why is Digoxin no longer used to treat atrial fibrillation ?
Digoxin is no longer used to treat atrial fibrillation because it can cause arrythmia
Atrial Fibrillation Pathophysiology
Normally, the sinoatrial node produces organised electrical activity that coordinates the contraction of the atria.
Atrial fibrillation occurs when this electrical activity is disorganised, causing the contraction of the atria to become uncoordinated, rapid and irregular.
This chaotic electrical activity overrides the regular, organised activity from the sinoatrial node. It passes through to the ventricles, resulting in irregularly irregular ventricular contraction.
Uncoordinated atrial activity means the blood can stagnate in the atria, forming a blood clot (thrombus).
A thrombus formed in the left atrium may travel to the brain and block a cerebral artery, causing an ischaemic stroke.
The risk of stroke is about 5 times higher than usual in patients with atrial fibrillation (depending on individual factors).
What are the overall effects of atrial fibrillation ?
The overall effects of atrial fibrillation are:
-Irregularly irregular ventricular contractions
-Tachycardia (fast heart rate)
-Heart failure due to impaired filling of the ventricles during diastole
-Increased risk of stroke
What are the most common causes of atrial fibrillation?
The most common causes of atrial fibrillation can be remembered with the “SMITH” mnemonic:
S – Sepsis
M – Mitral valve pathology (stenosis or regurgitation)
I – Ischaemic heart disease
T – Thyrotoxicosis aka hyperthyroidism
H – Hypertension
Alcohol and caffeine are lifestyle causes worth remembering.
How does AF Present?
Presentation
Patients are often asymptomatic, and atrial fibrillation is an incidental finding. It may be diagnosed after a stroke.
Patients may present with:
-Palpitations
-Shortness of breath
-Dizziness or syncope (loss of consciousness)
-Symptoms of associated conditions (e.g., stroke, sepsis or thyrotoxicosis)
The key examination finding is an irregularly irregular pulse. There are two differential diagnoses for an irregularly irregular pulse:
Atrial fibrillation
Ventricular ectopics
Ventricular ectopics disappear when the heart rate gets above a certain threshold. Therefore, a regular heart rate during exercise suggests a diagnosis of ventricular ectopics.
Investigations of AF
Investigations
An ECG is required in all patients with an irregularly irregular pulse. The ECG findings in atrial fibrillation are:
Absent P waves
Narrow QRS complex tachycardia
Irregularly irregular ventricular rhythm
An echocardiogram may be required to investigate further in cases of:
Valvular heart disease
Heart failure
Planned cardioversion
Paroxysmal Atrial Fibrillation
Paroxysmal atrial fibrillation refers to episodes of atrial fibrillation that reoccur and spontaneously resolve back to sinus rhythm. These episodes can last between 30 seconds and 48 hours.
Patients with a normal ECG and suspected paroxysmal atrial fibrillation can have further investigations with:
24-hour ambulatory ECG (Holter monitor)
Cardiac event recorder lasting 1-2 weeks
Valvular atrial fibrillation
Valvular atrial fibrillation is AF with significant mitral stenosis or a mechanical heart valve. The assumption is that the valvular pathology has led to atrial fibrillation. Atrial fibrillation without valve pathology or with other valve pathologies, such as mitral regurgitation or aortic stenosis, is classed as non-valvular AF.
The NICE guidelines (2021) do not reference valvular atrial fibrillation. They recommend patients with valvular heart disease are referred to a cardiologist for further assessment and management.
Principles of management
Management here is based on the NICE guidelines from 2021. Follow local and national guidelines when treating patients.
There are two principles to treating atrial fibrillation:
-Rate or rhythm control
-Anticoagulation to prevent strokes
RATE CONTROL
The function of the atria is to pump blood into the ventricles. In patients with atrial fibrillation, the atrial contractions are not coordinated, so the ventricles must fill by suction and gravity, which is considerably less efficient. The higher the heart rate, the less time is available for the ventricles to fill with blood, reducing the cardiac output. Rate control aims to get the heart rate below 100 and extend the time during diastole for the ventricles to fill with blood.
NICE guidelines (2021) suggest all patients with AF should have rate control as first-line, except with:
A reversible cause for their AF
New onset atrial fibrillation (within the last 48 hours)
Heart failure caused by atrial fibrillation
Symptoms despite being effectively rate controlled
Options for rate control:
Beta blocker first-line (e.g., atenolol or bisoprolol)
Calcium-channel blocker (e.g., diltiazem or verapamil) (not preferable in heart failure)
Digoxin (only in sedentary people with persistent atrial fibrillation, requires monitoring and has a risk of toxicity)
RHYTHM CONTROL
Rhythm control may be offered to patients with:
-A reversible cause for their AF
-New onset atrial fibrillation (within the last 48 hours)
-Heart failure caused by atrial fibrillation
-Symptoms despite being effectively rate controlled
Rhythm control aims to return the patient to normal sinus rhythm. This can be achieved through:
-Cardioversion
-Long-term rhythm control using medications
CARDIOVERSION
Cardioversion is a medical procedure that uses quick, low-energy shocks to restore a regular heart rhythm. It’s a treatment for certain types of irregular heartbeats (arrhythmias), including atrial fibrillation (A-fib)
For cardioversion, there is a choice between:
- Immediate cardioversion
- Delayed cardioversion
Immediate Cardioversion
Immediate cardioversion is used if the atrial fibrillation is either:
-Present for less than 48 hours
-Causing life-threatening haemodynamic instability
There are two options for immediate cardioversion:
-Pharmacological cardioversion
-Electrical cardioversion
Pharmalogical Cardioversion
- Flecainide
- Amiodarone (the drug of choice in patients with structural heart disease)
Electrical Cardioversion
Electrical cardioversion aims to shock the heart back into sinus rhythm. It involves using a cardiac defibrillator machine to deliver controlled shocks. This is usually done with sedation or general anaesthesia.
Delayed Cardioversion
Delayed cardioversion is used if the atrial fibrillation has been present for more than 48 hours and they are stable. Electrical cardioversion is recommended.
Transoesophageal echocardiography‑guided cardioversion is an option where available. Amiodarone may be considered before and after electrical cardioversion to prevent AF from recurring.
The patient should be anticoagulated for at least 3 weeks before delayed cardioversion. During the 48 hours before cardioversion, they may have developed a blood clot in the atria, and reverting them to sinus rhythm carries a high risk of mobilising that clot, causing a stroke. They are rate controlled whilst waiting for cardioversion.
Long term rhythm control
- Beta blockers first-line
- Dronedarone second-line for maintaining normal rhythm where patients have had successful cardioversion
- Amiodarone is useful in patients with heart failure or left ventricular dysfunction
Management of Paroxysmal Atrial Fibrillation
Patients with paroxysmal atrial fibrillation may be appropriate for a “pill-in-the-pocket” approach. They take a pill to terminate their atrial fibrillation only when they feel the symptoms starting. To be suitable for a pill-in-the-pocket approach, they must have infrequent episodes without structural heart disease. They also need to be able to identify the signs of atrial fibrillation and understand when to take the treatment.
Flecainide is the usual treatment for a pill-in-the-pocket approach. There is a risk of flecainide converting the atrial fibrillation into atrial flutter, with 1:1 AV conduction to the ventricles, causing a very fast ventricular rate.
Patients with paroxysmal atrial fibrillation should still be anticoagulated based on their CHA2DS2-VASc score, similar to permanent atrial fibrillation.
ABLATION
Ablation is a procedure to treat atrial fibrillation. It uses small burns or freezes to cause some scarring on the inside of the heart to help break up the electrical signals that cause irregular heartbeats. This can help the heart maintain a normal heart rhythm.
ABLATION
Where drug treatment for rate or rhythm control is not adequate or tolerated, there are two options for ablation:
- Left atrial ablation
- Atrioventricular node ablation and a permanent pacemaker
Left atrial ablation is performed in a catheter laboratory, often called a “cath lab”. It involves a general anaesthetic or sedation. A catheter is inserted into a femoral vein and fed through the venous system under x-ray guidance to the heart. The catheter punctures through the septum into the left atrium. Once in the left atrium, it is placed against different areas to test the electrical signals. The operator attempts to identify the location of any abnormal electrical pathways. Once identified, radiofrequency ablation (heat) is applied to burn the abnormal area of electrical activity. This leaves scar tissue that does not conduct electrical activity. The aim is to remove the source of the arrhythmia and restore normal sinus rhythm.
Atrioventricular node ablation involves destroying the connection between the atria and ventricles (the atrioventricular node). It is a catheter procedure. After the procedure, the irregular electrical activity in the atria cannot pass through to the ventricles. A permanent pacemaker is required to control ventricular contraction (the pacemaker is inserted before the ablation procedure). Anticoagulation is still needed to prevent strokes.
ANTICOAGULATION
Anticoagulation
Uncontrolled and unorganised activity in the atria leads to blood stagnating in the left atrium, particularly in the left atrial appendage. Eventually, this stagnated blood leads to a thrombus (clot). This thrombus then mobilises (becomes an embolus) and travels from the left atrium to the left ventricle, into the aorta and up in the carotid arteries to the brain. It can then lodge in a cerebral artery and cause an ischaemic stroke.
Anticoagulation treatment reduces coagulation (thrombus formation) by interfering with the clotting cascade. Without anticoagulation, patients with atrial fibrillation have around a 5% risk of stroke each year, depending on individual factors. With anticoagulation, patients with atrial fibrillation have around a 1-2% risk of stroke each year, depending on individual factors. Anticoagulation reduces the risk of stroke by about 2/3.
Anticoagulation treatment carries around a 2.5-8% risk of serious bleeding each year, depending on individual factors.
The NICE guidelines (2021) recommend for anticoagulation:
- Direct-acting oral anticoagulants (DOACs) first-line
- Warfarin second-line, if DOACs are contraindicated
DOACs
Direct-Acting Oral Anticoagulants
Direct-acting oral anticoagulants (DOACs) are oral anticoagulants that do not require INR monitoring, unlike warfarin. They are suitable for most patients, including patients with cancer. They have a 6-14 hour half-life.
Apixaban, edoxaban and rivaroxaban are direct factor Xa inhibitors. Dabigatran is a direct thrombin inhibitor.
Apixaban and dabigatran are taken twice daily, and edoxaban and rivaroxaban are taken once daily.
Some of the DOACs have agents available to reverse the effects in uncontrolled or life-threatening bleeding:
Andexanet alfa (apixaban and rivaroxaban)
Idarucizumab (a monoclonal antibody against dabigatran)
DOACs have several advantages compared with warfarin:
No monitoring is required
No issues with time in therapeutic range (provided they have good adherence)
No major interaction problems
Equal or slightly better than warfarin at preventing strokes in atrial fibrillation
Equal or slightly lower risk of bleeding than warfarin
The most common indications for DOACs are:
Stroke prevention in patients with atrial fibrillation
Treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE)
Prophylaxis of venous thromboembolism (DVTs and PEs) after a hip or knee replacement
CHA2DS2-VASc
CHA2DS2-VASc is a tool for assessing whether a patient with atrial fibrillation should start anticoagulation. It is a list of risk factors that increase the likelihood of a stroke. The higher the score, the higher the risk of developing a stroke or TIA.
CHA2DS2-VASc is a mnemonic for the factors that score a point:
C – Congestive heart failure
H – Hypertension
A2 – Age above 75 (scores 2)
D – Diabetes
S2 – Stroke or TIA previously (scores 2)
V – Vascular disease
A – Age 65 – 74
S – Sex (female)
NICE (2021) recommends, based on the CHA2DS2-VASc score:
0 – no anticoagulation
1 – consider anticoagulation in men (women automatically score 1)
2 or more – offer anticoagulation
Aspirin alone is not used for stroke prevention in atrial fibrillation (using aspirin was an option years ago).
BLEEDING RISK
Bleeding Risk
The NICE guidelines recommend using the ORBIT score for assessing the risk of major bleeding in patients with atrial fibrillation taking anticoagulation. The easiest way to calculate the ORBIT score is using an online calculator. The “ORBIT” mnemonic can be used to remember the 5 factors:
O – Older age (age 75 or above)
R – Renal impairment (GFR less than 60)
B – Bleeding previously (history of gastrointestinal or intracranial bleeding)
I – Iron (low haemoglobin or haematocrit)
T – Taking antiplatelet medication
For most patients with atrial fibrillation, the risk of stroke with no anticoagulation will outweigh the risk of bleeding on anticoagulation.
CVD
Cardiovascular disease (CVD) is a general term that describes a disease of the heart or blood vessels.
Blood flow to the heart, brain or body can be reduced because of a: blood clot (thrombosis) build-up of fatty deposits inside an artery, leading to the artery hardening and narrowing (atherosclerosis)
Atherosclerosis
Athero- refers to soft or “porridge-like”, and -sclerosis refers to hardening. Atherosclerosis is a combination of atheromas (fatty deposits in the artery walls) and sclerosis (hardening or stiffening of the blood vessel walls).
Atherosclerosis affects the medium and large arteries.
It is caused by chronic inflammation and activation of the immune system in the artery wall. This causes the deposition of lipids in the artery wall, followed by the development of fibrous atheromatous plaques.
Plaques can cause:
These plaques results in:
-Stiffening
-Stenosis
-Plaque rupture
Stiffening of the artery walls leads to hypertension (raised blood pressure) and strain on the heart as it tries to pump blood against extra resistance.
Stenosis leads to reduced blood flow (e.g. in angina).
Plaque rupture creates a thrombus that can block a distal vessel and cause ischaemia. An example is acute coronary syndrome, where a coronary artery becomes blocked.
Modifiable and Non-Modifiable Risk Factors of CVD
Medical co-morbidities that increase your likeliness of getting CVD
Medical co-morbidities increase the risk of atherosclerosis and should be carefully managed to minimise the risk:
-Diabetes
-Hypertension
-Chronic kidney disease (CKD)
-Inflammatory conditions, such as rheumatoid arthritis
-Atypical antipsychotic medications
End Results of Atherosclerosis
Angina
Myocardial infarction
Transient ischaemic attacks
Strokes
Peripheral arterial disease
Chronic mesenteric ischaemia
Prevention of CVD
Primary prevention of CVD
Medication for primary prevention is based on the QRISK3 score.
The QRISK score estimates the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years. The NICE guidelines (updated February 2023) recommend when the result is above 10%, they should be offered a statin, initially atorvastatin 20mg at night.
Atorvastatin 20mg is offered as primary prevention to all patients with:
-Chronic kidney disease (eGFR less than 60 ml/min/1.73 m2)
- Type 1 diabetes for more than 10 years or are over 40 years
The draft NICE guidelines due for publication in mid-2023 advise that atorvastatin 20mg can be considered for primary prevention in patients with a QRISK3 score below 10%.
STATINS
Statins reduce cholesterol production in the liver by inhibiting HMG CoA reductase.
NICE recommend checking lipids 3 months after starting statins and increasing the dose to aim for a greater than 40% reduction in non-HDL cholesterol. Check adherence (are they taking the medications?) before increasing the dose.
NICE also recommend checking LFTs within 3 months of starting a statin and again at 12 months. Statins can cause a transient and mild rise in ALT and AST in the first few weeks of use. They usually do not need to be stopped if the rise is less than 3 times the upper limit of normal.
Rare and significant side effects of statins include:
-Myopathy (causing muscle weakness and pain)
-Rhabdomyolysis (muscle damage – check the creatine kinase in patients with muscle pain)
-Type 2 diabetes
-Haemorrhagic strokes (very rarely)
Usually, the benefits of statins far outweigh the risks, and newer statins (such as atorvastatin) are well tolerated.
TOM TIP: Several common medications interact with statins. One key interaction to remember is with macrolide antibiotics. Patients being prescribed clarithromycin or erythromycin should be advised to stop taking their statin whilst taking these antibiotics.
Other Cholesterol lowering drugs
Ezetimibe works by inhibiting the absorption of cholesterol in the intestine. It can be used as an alternative when statins are not tolerated or in combination with a statin when statins alone are inadequate.
PCSK9 inhibitors (e.g., evolocumab and alirocumab) are monoclonal antibodies that lower cholesterol. They are highly specialist treatments, given as a subcutaneous injection every 2-4 weeks.
Secondary prevention of CVD
Secondary prevention after developing cardiovascular disease depends on the specific condition. Secondary prevention can be remembered with the “4 As” mnemonic:
A – Antiplatelet medications (e.g., aspirin, clopidogrel and ticagrelor)
A – Atorvastatin 80mg
A – Atenolol (or an alternative beta blocker – commonly bisoprolol) titrated to the maximum tolerated dose
A – ACE inhibitor (commonly ramipril) titrated to the maximum tolerated dose
After myocardial infarction
After a myocardial infarction, patients are offered dual antiplatelet treatment initially, with:
-Aspirin 75mg daily (continued indefinitely)
-Clopidogrel or ticagrelor (generally for 12 months before stopping)
Clopidogrel is the antiplatelet of choice in peripheral arterial disease and following an ischaemic stroke.
Familial Hypercholesterolemia
Familial hypercholesterolaemia is an autosomal dominant genetic condition causing very high cholesterol levels. Several genes have the potential to cause the disorder.
Heterozygous means only one copy of the gene is abnormal. This occurs in about 1 in 250 people.
Homozygous means both copies of the gene are abnormal. This very rare condition causes extremely high cholesterol (over 13 mmol/L) and almost guaranteed early cardiovascular disease.
The Simon Broome criteria or the Dutch Lipid Clinic Network Criteria are used for making a clinical diagnosis. Three important features to remember are:
Family history of premature cardiovascular disease (e.g., myocardial infarction under 60 in a first-degree relative)
Very high cholesterol (e.g., above 7.5 mmol/L in an adult)
Tendon xanthomata (hard nodules in the tendons containing cholesterol, often on the back of the hand and Achilles)
Management of familial hypercholesterolaemia involves:
-Specialist referral for genetic testing and testing of family members
-Statins
HYPERTENSION
The NICE guidelines on hypertension (updated 2022) suggest a diagnosis of hypertension with a blood pressure above 140/90 in the clinical setting, confirmed with ambulatory or home readings above 135/85.
Stages of Hypertension
What does hypertension do not so obvious
Essential Hypertension
Essential / Primary hypertension accounts for 90% of hypertension. This is also known as primary hypertension.
It means a high blood pressure has developed on its own and does not have a secondary cause.
Causes of hypertension
- Essential Hypertension
- Secondary causes of hypertension can be remembered with the “ROPED” mnemonic:
R – Renal disease
O – Obesity
P – Pregnancy-induced hypertension or pre-eclampsia
E – Endocrine
D – Drugs (e.g., alcohol, steroids, NSAIDs, oestrogen and liquorice)
RENAL DISEASE
Renal disease is the most common cause of secondary hypertension. When the blood pressure is very high or does not respond to treatment, consider renal artery stenosis. Renal artery stenosis can be diagnosed with duplex ultrasound or an MR or CT angiogram.
Conns syndrome
Most endocrine conditions can cause hypertension. Hyperaldosteronism (Conn’s syndrome) is an important cause and may be present in 5-10% of patients with hypertension.
Complications due to having high blood pressure
High blood pressure increases the risk of:
-Ischaemic heart disease (angina and acute coronary syndrome)
-Cerebrovascular accident (stroke or intracranial haemorrhage)
-Vascular disease (peripheral arterial disease, aortic dissection and aortic aneurysms)
-Hypertensive retinopathy
-Hypertensive nephropathy
-Vascular dementia
-Left ventricular hypertrophy
-Heart failure
Hypertensive patients may get left ventricular hypertrophy
Patients with hypertension may develop left ventricular hypertrophy.
The left ventricle is straining to pump blood against increased resistance in the arterial system, so the muscle becomes thicker.
On examination, there may be a sustained and forceful apex beat. It can be seen on an ECG using voltage criteria and is best diagnosed with an echocardiogram.
Diagnosing Hypertension
NICE recommend measuring blood pressure every 5 years to screen for hypertension. It should be measured more often in borderline cases and every year in patients with type 2 diabetes.
Patients with a clinic blood pressure between 140/90 mmHg and 180/120 mmHg should have 24-hour ambulatory blood pressure or home readings to confirm the diagnosis
WHITE COAT SYNDROME
Having 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 involves more than a 20/10 mmHg difference in blood pressure between clinic and ambulatory or home readings.
NICE recommend measuring blood pressure in both arms, and if the difference is more than 15 mmHg, using the reading from the arm with the higher pressure.
END ORGAN DAMAGE
NICE recommend all patients with a new diagnosis should have:
-Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage
-Bloods for HbA1c, renal function and lipids
-Fundus examination for hypertensive retinopathy
-ECG for cardiac abnormalities, including left ventricular hypertrophy
NICE recommend calculating the QRISK score, which estimates the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years. When the result is above 10%, they should be offered a statin, initially atorvastatin 20mg at night.
MANAGING HYPERTENSION
Lifestyle advice includes a healthy diet, stopping smoking, reducing alcohol, caffeine and salt intake and taking regular exercise.
Medications used in management are:
A – ACE inhibitor (e.g., ramipril)
B – Beta blocker (e.g., bisoprolol)
C – Calcium channel blocker (e.g., amlodipine)
D – Thiazide-like diuretic (e.g., indapamide)
ARB – Angiotensin II receptor blocker (e.g., candesartan)
Calcium Antagonists
A blockers
Central Agents
Minoxidil
Alternative Medications
Angiotensin receptor blockers (ARBs) are recommended by NICE instead of ACE inhibitors in patients of Black African or African-Caribbean family origin. In the steps below, you can replace A with ARB for these patients.
ARBs are an alternative if the person does not tolerate ACE inhibitors (commonly due to a dry cough). ACE inhibitors and ARBs are not used together.
Thiazide-like diuretics are used as an alternative if the patient does not tolerate calcium channel blockers (commonly due to ankle oedema).
Pottasium Balance
Spironolactone is a potassium-sparing diuretic. It works by blocking the action of aldosterone in the kidneys, resulting in sodium excretion and potassium reabsorption. It can be helpful when thiazide diuretics are causing hypokalaemia.
Using spironolactone increases the risk of hyperkalaemia. ACE inhibitors can also cause hyperkalaemia. Thiazide-like diuretics can also cause electrolyte disturbances. Therefore, it is essential to monitor U+Es regularly with these drugs.
Treatment Targets
HYPERTENSIVE EMERGENCY
Accelerated hypertension, also called malignant hypertension, refers to extremely high blood pressure, above 180/120, with retinal haemorrhages or papilloedema.
The NICE guidelines recommend a same-day referral for patients with accelerated hypertension. Therefore, patients with a blood pressure above 180/120 require a fundoscopy examination to look for these key findings. Additional complications also warrant same-day assessment, such as confusion, heart failure, suspected acute coronary syndrome or acute kidney injury.
Patients admitted with a hypertensive emergency are assessed for secondary causes and end-organ damage. Their blood pressure is closely monitored while medications bring it under control.
Intravenous options in a hypertensive emergency (guided by an experienced specialist) include:
-Sodium nitroprusside
-Labetalol
-Glyceryl trinitrate
-Nicardipine
Secondary Hypertension
ANGINA
-Angina is caused by atherosclerosis affecting the coronary arteries, narrowing the lumen (inside diameter) and reducing blood flow to the myocardium (heart muscle).
-During times of high demand, such as exercise, there is an insufficient supply of blood to meet the demand.
- This causes the symptoms of angina, typically constricting chest pain, with or without radiation to the jaw or arms.
STABLE ANGINA
Angina is “stable” when symptoms only come on with exertion and are always relieved by rest or glyceryl trinitrate (GTN).
UNSTABLE ANGINA
It is “unstable” when the symptoms appear randomly whilst at rest. Unstable angina is a type of acute coronary syndrome (ACS) and requires immediate management.
Investigating Angina
Investigations
All patients with angina should have the following baseline investigations:
-Physical examination (e.g., heart sounds, signs of heart failure, blood pressure and BMI)
-ECG (a normal ECG does not exclude stable angina)
-FBC (anaemia)
-U&Es (required before starting an ACE inhibitor and other medications)
-LFTs (required before starting statins)
-Lipid profile
-Thyroid function tests (hypothyroidism or hyperthyroidism)
-HbA1C and fasting glucose (diabetes)
Cardiac Stress Testing
Cardiac stress testing involves assessing the patient’s heart function during exertion. This can involve having the patient exercise (e.g., walking on a treadmill) or giving medication (e.g., dobutamine) to stress the heart.
The options for assessing cardiac function during stress testing are an ECG, echocardiogram, MRI or a myocardial perfusion scan (nuclear medicine scan).
CT Angiogram
CT coronary angiography involves injecting contrast and taking CT images timed with the heart contractions to give a detailed view of the coronary arteries, highlighting the specific locations of any narrowing.
Invasive Coronary Angiography
Invasive coronary angiography involves an invasive procedure performed in a catheter laboratory (cath lab).
A catheter is inserted into the patient’s brachial or femoral artery, directed through the arterial system to the aorta and the coronary arteries under x-ray guidance, where contrast is injected to visualise the coronary arteries and identify any areas of stenosis using x-ray images.
This is considered the gold standard for determining coronary artery disease.
MANAGEMENT
The management described here is based on NICE clinical knowledge summaries on stable angina (updated August 2022) and chest pain (updated October 2022), and the SIGN guidelines (2018).
There are five principles of management. You can remember this with the “RAMPS” mnemonic:
R – Refer to cardiology
A – Advise them about the diagnosis, management and when to call an ambulance
M – Medical treatment
P – Procedural or surgical interventions
S – Secondary prevention
Referrals are usually sent to the rapid access chest pain clinic (RACPC).
Medical Management
There are three aims of medical management:
-Immediate symptomatic relief during episodes of angina
-Long-term symptomatic relief
-Secondary prevention of cardiovascular disease
Immediate Symptomatic Relief
Immediate symptomatic relief is with sublingual glyceryl trinitrate (GTN) in the form of a spray or tablets. GTN causes vasodilation, improving blood flow to the heart muscle (myocardium). Patients are advised to:
-Take the GTN when the symptoms start
-Take a second dose after 5 minutes if the symptoms remain
-Take a third dose after a further 5 minutes if the symptoms remain
-Call an ambulance after a further 5 minutes if the symptoms remain
Side Effects of GTN
Key side effects of GTN are headaches and dizziness caused by vasodilation.
For long-term symptomatic relief, first-line is with either, or a combination, of:
-Beta blocker (e.g., bisoprolol)
-Calcium-channel blocker (e.g., diltiazem or verapamil – both avoided in heart failure with reduced ejection fraction)
Medications for secondary prevention
Medications for secondary prevention can be remembered with the “four As” mnemonic:
A – Aspirin 75mg once daily
A – Atorvastatin 80mg once daily
A – ACE inhibitor (if diabetes, hypertension, CKD or heart failure are also present)
A – Already on a beta blocker for symptomatic relief
Surgical Interventions
Surgical procedures are generally offered to patients with more severe disease and where medical treatments do not control symptoms. There are two options:
-Percutaneous coronary intervention (PCI)
-Coronary artery bypass graft (CABG)
PCI
Percutaneous coronary intervention (PCI) involves inserting a catheter into the patient’s brachial or femoral artery.
This is fed in, under x-ray guidance, through the arterial system to the coronary arteries.
Then a contrast is injected to visualise the coronary arteries and identify areas of stenosis on the x-ray images.
Areas of stenosis can be treated by dilating a balloon to widen the lumen (angioplasty) and inserting a stent to keep it open.
This can be referred to as coronary angioplasty and stenting.
CABG ( Coronary Artery Bypass Graft)
Coronary artery bypass graft (CABG) surgery may be offered to patients with severe stenosis. This involves opening the chest along the sternum, with a midline sternotomy incision. A graft vessel is attached to the affected coronary artery, bypassing the stenotic area. The three main options for graft vessels are:
-Saphenous vein (harvested from the inner leg)
-Internal thoracic artery, also known as the internal mammary artery
-Radial artery
Difference between PCI and CABG
Generally, short and medium-term outcomes are similar between PCI and CABG. However, PCI has a:
-Faster recovery
-Lower rate of strokes as a complication
-Higher rate of requiring repeat revascularisation (further procedures)
TOM TIP: When examining a patient that you think may have coronary artery disease in your OSCEs, check for a midline sternotomy scar (previous CABG), scars around the brachial and femoral arteries (previous PCI) and along the inner calves (saphenous vein harvesting scar) to see what procedures they may have had done.
Difference between arrhythmia and AF
An arrhythmia is when the heart beats too slowly, too fast, or in an irregular way.
When a person has AFib, the normal beating in the upper chambers of the heart (the two atria) is irregular, and blood doesn’t flow as well as it should from the atria to the lower chambers of the heart (the two ventricles).
Arrhythmias
Arrhythmias are abnormal heart rhythms. They result from an interruption to the normal electrical signals that coordinate the contraction of the heart muscle. There are several types of arrhythmia, each with different causes and management options
Defibrilator
Cardiac Arrest Rhythms
These are the four possible rhythms in a pulseless patient. They are either shockable (meaning defibrillation may be effective) or non-shockable (meaning defibrillation will not be effective).
Shockable rhythms:
Ventricular tachycardia
Ventricular fibrillation
Non-shockable rhythms:
Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
Asystole (no significant electrical activity)
Narrow Complex Tachycardia
Narrow complex tachycardia refers to a fast heart rate with a QRS complex duration of less than 0.12 seconds. On a normal 25 mm/sec ECG, 0.12 seconds equals 3 small squares. Therefore, the QRS complex will fit within 3 small squares in narrow complex tachycardia.
There are four main differentials of a narrow complex tachycardia:
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)
Patients with life-threatening features, such as loss of consciousness (syncope), heart muscle ischaemia (e.g., chest pain), shock or severe heart failure, are treated with synchronised DC cardioversion under sedation or general anaesthesia. Intravenous amiodarone is added if initial DC shocks are unsuccessful
Broad Complex Tachycardia
Broad complex tachycardia refers to a fast heart rate with a QRS complex duration of more than 0.12 seconds or 3 small squares on an ECG.
The resuscitation guidelines break down broad complex tachycardia into:
Ventricular tachycardia or unclear cause (treated with IV amiodarone)
Polymorphic ventricular tachycardia, such as 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, such as loss of consciousness (syncope), heart muscle ischaemia (e.g., chest pain), shock or severe heart failure, are treated with synchronised DC cardioversion under sedation or general anaesthesia. Intravenous amiodarone is added if initial DC shocks are unsuccessful
Atrial Flutter
Normally the electrical signal passes through the atria once, stimulating a contraction, then disappears through the atrioventricular node into the ventricles.
Atrial flutter is caused by a re-entrant rhythm in either atrium. The electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway in the atria. The signal goes round and round the atrium without interruption.
The atrial rate is usually around 300 beats per minute
Atrial Flutter
The signal does not usually enter the ventricles on every lap due to the long refractory period of the atrioventricular node. This often results in two atrial contractions for every one ventricular contraction (2:1 conduction), giving a ventricular rate of 150 beats per minute. There may be 3:1, 4:1 or variable conduction ratios.
Atrial flutter gives a SAWTOOTH appearance on the ECG, with repeated P wave occurring at around 300 per minute, with a narrow complex tachycardia.
Treatment is similar to atrial fibrillation, including anticoagulation based on the CHA2DS2-VASc score. Radiofrequency ablation of the re-entrant rhythm can be a permanent solution
PROLONGED Q-T INTERVAL
The QT interval is from the start of the QRS complex to the end of the T wave. The corrected QT interval (QTc) estimates the QT interval if the heart rate were 60 beats per minute. It is prolonged at:
More than 440 milliseconds in men
More than 460 milliseconds in women
A prolonged QT interval represents prolonged repolarisation of the heart muscle cells (myocytes) after a contraction. Depolarisation is the electrical process that leads to heart contraction. Repolarisation is a recovery period before the muscle cells are ready to depolarise again. 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
Torsades de pointes
Torsades de pointes is a type of polymorphic ventricular tachycardia. It translates from French as “twisting of the spikes”, describing the ECG characteristics. On an ECG, it looks like standard ventricular tachycardia but with the appearance that the QRS complex is twisting around the baseline. The height of the QRS complexes gets progressively smaller, then larger, then smaller, and so on.
Torsades de pointes will terminate spontaneously and revert to sinus rhythm or progress to ventricular tachycardia. Ventricular tachycardia can lead to cardiac ar
Causes of Prolonged Q-T interval
-Long QT syndrome (an inherited condition)
-Medications, such as antipsychotics, citalopram, flecainide, sotalol, amiodarone and
macrolide antibiotics
-Electrolyte imbalances, such as hypokalaemia, hypomagnesaemia and hypocalcaemia
Management of Prolonged Q-T interval
Management of a prolonged QT interval involves:
-Stopping and avoiding medications that prolong the QT interval
-Correcting electrolyte disturbances
-Beta blockers (not sotalol)
- Pacemakers or implantable cardioverter defibrillators
Ventricular Ectopics
Ventricular ectopics are premature ventricular beats caused by random electrical discharges outside the atria. Patients often present complaining of random extra or missed beats. They are relatively common at all ages and in healthy patients. However, they are more common in patients with pre-existing heart conditions (e.g., ischaemic heart disease or heart failure).
Ventricular ectopics appear as isolated, random, abnormal, broad QRS complexes on an otherwise normal ECG.
Bigeminy refers to when every other beat is a ventricular ectopic. The ECG shows a normal beat (with a P wave, QRS complex and T wave), followed immediately by an ectopic beat, then a normal beat, then an ectopic, and so on.
Management involves:
-Reassurance and no treatment in otherwise healthy people with infrequent ectopics
-Seeking specialist advice in patients with underlying heart disease, frequent or concerning symptoms (e.g., chest pain or syncope), or a family history of heart disease or sudden death
-Beta blockers are sometimes sed to manage symptoms
Slide: Ventricular ectopic is a wide QRS complex which is not preceded by a P wave
Heart Block
First-degree heart block occurs where there is delayed conduction through the atrioventricular node. Despite this, every atrial impulse leads to a ventricular contraction, meaning every P wave is followed by a QRS complex. On an ECG, first-degree heart block presents as a PR interval greater than 0.2 seconds (5 small or 1 big square).
Second-degree heart block is where some atrial impulses do not make it through the atrioventricular node to the ventricles. There are instances where P waves are not followed by QRS complexes. There are two types of second-degree heart block:
Mobitz type 1 (Wenckebach phenomenon)
Mobitz type 2
Mobitz type 1 (Wenckebach phenomenon) is where the conduction through the atrioventricular node takes progressively longer until it finally fails, after which it resets, and the cycle restarts. On an ECG, there is an increasing PR interval until a P wave is not followed by a QRS complex. The PR interval then returns to normal, and the cycle repeats itself.
Mobitz type 2 is where there is intermittent failure of conduction through the atrioventricular node, with an absence of QRS complexes following P waves. There is usually a set ratio of P waves to QRS complexes, for example, three P waves for each QRS complex (3:1 block). The PR interval remains normal. There is a risk of asystole with Mobitz type 2.
A 2:1 block is where there are two P waves for each QRS complex. Every other P wave does not stimulate a QRS complex. It can be difficult to tell whether this is caused by Mobitz type 1 or Mobitz type 2.
Third-degree heart block is also called complete heart block. There is no observable relationship between the P waves and QRS complexes. There is a significant risk of asystole with third-degree hart block.
Bradycardias
Bradycardia refers to a slow heart rate, typically less than 60 beats per minute. A heart rate under 60 can be normal in healthy fit patients without causing any symptoms. There is a long list of causes of bradycardia, including:
Medications (e.g., beta blockers)
Heart block
Sick sinus syndrome
Sick sinus syndrome encompasses many conditions that cause dysfunction in the sinoatrial node. It is often caused by idiopathic degenerative fibrosis of the sinoatrial node. It can result in sinus bradycardia, sinus arrhythmias and prolonged pauses.
Asystole refers to the absence of electrical activity in the heart (resulting in cardiac arrest). There is a risk of asystole in:
Mobitz type 2
Third-degree heart block (complete heart block)
Previous asystole
Ventricular pauses longer than 3 seconds
Management of unstable patients and those at risk of asystole involves:
Intravenous atropine (first line)
Inotropes (e.g., isoprenaline or adrenaline)
Temporary cardiac pacing
Permanent implantable pacemaker, when available
Options for temporary cardiac pacing are:
Transcutaneous pacing, using pads on the patient’s chest
Transvenous pacing, using a catheter, fed through the venous system to stimulate the heart directly
Atropine is an antimuscarinic medication and works by inhibiting the parasympathetic nervous system. Inhibiting the parasympathetic nervous system leads to side effects of pupil dilation, dry mouth, urinary retention and constipation.
Acute Coronary Syndrome (ACS)
Acute coronary syndrome (ACS) is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery. When a thrombus forms in a fast-flowing artery, it is formed mainly of platelets.
This is why antiplatelet medications such as aspirin, clopidogrel and ticagrelor are the mainstay of treatment.
ST depression on an ECG
- ST depression on an ECG is subendocardial ischemia
- subendocardial infarction occurs if the coronary artery remains blocked for around 20 minutes, and the subendocardial cells begin to die, resulting in necrosis.
- And with necrosis, the subendocardial cells leak cardiac enzymes, like troponins and CK-MB, into the blood.
- With a subendocardial infarction, there is no ST elevation on the ECG, so this is called a non-ST elevation myocardial infarction, or an NSTEMI for short. Instead, the ECG can show ST depression and T-wave inversion.
ST depression and T-wave inversion
On ECG, both unstable angina and NSTEMI’s may show ST-depression as well as T wave inversions.
The difference is that with an NSTEMI, cardiac enzyme levels in the blood are elevated, whereas with unstable angina, the damage resolves in a short time window, so there is no cardiomyocyte death - and therefore no elevated cardiac enzymes.
Transmural Infarction
-Transmural infarction, which occurs when a coronary artery becomes completely blocked for greater than about 20 minutes, which causes transmural necrosis.
-Within minutes a transmural infarction leads to ECG changes. The most common would be T wave inversions,
-The classic sign of transmural infarction is ST elevation, and when that happens it’s called an ST-elevation myocardial infarction, or STEMI.
- STEMI, the ischemia is so severe that damaged heart cells die - resulting in myocardial necrosis - and leak out certain enzymes like troponin and CK-MB. But ST elevation can also be caused by other conditions like, left ventricular hypertrophy, and pericarditis.
- For example, a 20-year-old physically fit person with a viral illness that gradually develops chest pain and is found to have ST-elevation on ECG is more likely to have pericarditis than an ST-elevation myocardial infarction.
Transmural Infarction
Besides ST elevation and T-wave inversions, a transmural infarction can also cause pathologic Q waves to appear on the ECG.
Normally, depolarization in the ventricle spreads from the endocardium to the epicardium, and most of that ends up pointing toward the positive electrode, which means a positive deflection.
With infarcted tissue, though, it doesn’t conduct electricity, which means that the electrode essentially sees through the infarcted tissue, like it was a hole, to the other ventricular wall, the depolarization wave that moves through the healthy wall on the opposite side of the heart, and since those are mostly moving away from the positive electrode, you end up with this big, negative pathologic q wave.
So pathologic Q waves are those that are longer than .04 seconds or one small box, and over 2mm or 2 small boxes deep.
The location of the transmural infarction can be identified based on the lead that has pathologic Q waves. Septal wall infarctions show changes in leads V1 and V2, whereas anterior wall infarctions show changes in leads V3 and V4.
Anterolateral wall infarctions show up in leads V3 through V6, I, and AVL. Small subendocardial infarctions don’t cause pathologic Q waves because some of the affected wall still conducts electricity.
Also, the aVR lead is oriented in a way that normally produces Q waves, so it’s not a reliable lead to look for pathologic Q waves.
Finally, pathologic Q waves can also result from things other than transmural infarction like a left bundle branch block and Wolff-Parkinson-White syndrome.
ACS
There are three types of acute coronary syndrome:
-Unstable angina
-ST-elevation myocardial infarction (STEMI)
-Non-ST-elevation myocardial infarction (NSTEMI)
Coronary Artery Anatomy
Two coronary arteries branch from the root of the aorta:
-Right coronary artery (RCA)
-Left coronary artery (LCA)
The right coronary artery (RCA) curves around the right side and under the heart and supplies the:
-Right atrium
-Right ventricle
-Inferior aspect of the left ventricle
-Posterior septal area
The left coronary artery becomes the:
-Circumflex artery
-Left anterior descending (LAD)
The circumflex artery curves around the top, left and back of the heart and supplies the:
-Left atrium
-Posterior aspect of the left ventricle
The left anterior descending (LAD) travels down the middle of the heart and supplies the:
-Anterior aspect of the left ventricle
-Anterior aspect of the septum
Presentation ACS
Acute coronary syndrome typically presents with central, constricting chest pain.
The chest pain is often associated with:
-Pain radiating to the jaw or arms
-Nausea and vomiting
-Sweating and clamminess
-A feeling of impending doom
-Shortness of breath
-Palpitations
Symptoms should continue at rest for more than 15 minutes.
A silent myocardial infarction is when someone does not experience typical chest pain during acute coronary syndrome.
Patients with diabetes are particularly at risk of silent MIs.
ECG Changes in Acute Coronary Syndrome
STEMI:
-ST-segment elevation
-New left bundle branch block
Location of Infarction in STEMI
ECG Changes in Acute Coronary Syndrome
NSTEMI:
-ST segment depression
-T wave inversion
ECG Changes in Acute Coronary Syndrome
Pathological Q waves suggest a deep infarction involving the full thickness of the heart muscle (transmural) and typically appear 6 or more hours after the onset of symptoms.
TROPONIN
Troponin is a protein in cardiac muscle (myocardium) and skeletal muscle. The specific type of troponin, normal range and diagnostic criteria vary based on different laboratories, so check the local policy.
A rise in troponin is consistent with myocardial ischaemia, as they are released from the ischaemic muscle tissue.
Troponin NSTEMI
Troponin results are used to diagnose an NSTEMI. They are not required to diagnose a STEMI, as this is diagnosed based on the clinical presentation and ECG findings.
Assessment may involve repeated troponin tests, depending on the local policy (e.g., at baseline and 3 hours after the onset of symptoms).
A high troponin or a rising troponin on repeat tests, in the context of suspected acute coronary syndrome, indicates an NSTEMI.
Troponin is a non-specific marker, meaning that a raised troponin does not automatically imply acute coronary syndrome. The alternative causes of a raised troponin include:
-Chronic kidney disease
-Sepsis
-Myocarditis
-Aortic dissection
-Pulmonary embolism
Other Investigations
Additional investigations in patients with suspected or confirmed acute coronary syndrome are:
-Baseline bloods, including FBC, U&E, LFT, lipids and glucose
-Chest x-ray to investigate for pulmonary oedema and other causes of chest pain
-Echocardiogram once stable to assess the functional damage to the heart, specifically the left ventricular function
Classification
Patients with acute cardiac-sounding chest pain will have an ECG and troponin blood test as part of their workup.
The results of the ECG and troponin will determine the type of acute coronary syndrome.
STEMI is diagnosed when the ECG shows either:
-ST elevation
-New left bundle branch block
NSTEMI is diagnosed when there is a raised troponin, with either:
-A normal ECG
-Other ECG changes (ST depression or T wave inversion)
Unstable angina is diagnosed when there are symptoms suggest ACS, the troponin is normal, and either:
-A normal ECG
-Other ECG changes (ST depression or T wave inversion)
When a patient is presenting with chest pain and the troponin and ECG are normal, the diagnosis is either unstable angina or another cause, such as musculoskeletal chest pain.
Initial Management
In patients presenting with symptoms of acute coronary syndrome, the initial management can be remembered with the “CPAIN” mnemonic:
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)
When the patient is pain-free, but the pain occurred within the past 72 hours, they need to be referred to the hospital for same-day assessment, usually to be seen by the medical team in the Ambulatory Care Unit (depending on local pathways). They may require emergency admission if there are ECG changes or complications (e.g., signs of heart failure).
Result of Myocardial Infarction
