Cardio Flashcards
What is angina?
Explain what it is and what causes it.
Explain the difference between unstable and stable 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.
Angina is “stable” when symptoms only come on with exertion and are always relieved by rest or glyceryl trinitrate (GTN).
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.
For angina what is the immediate symptomatic relief, Long-term symptomatic relief, and Secondary prevention of cardiovascular disease
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).
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).
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)
What condition could this be? :
crushing chest pain
Pain radiating to the jaw or arms
Nausea and vomiting
Sweating and clamminess
A feeling of impending doom
Shortness of breath
Palpitations
ACS (acute coronary syndrome)
what is 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.
There are three types of acute coronary syndrome:
Unstable angina
ST-elevation myocardial infarction (STEMI)
Non-ST-elevation myocardial infarction (NSTEMI)
Which ECG leads indicate which heart areas and arteries?
Left coronary artery:
Anterolateral
I, aVL, V3-6
Left anterior descending:
Anterior
V1-4
Circumflex:
Lateral
I, aVL, V5-6
Right coronary artery:
Inferior
II, III, aVF
What classifies STEMI, NSTEMI, and unstable angina?
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)
What is initial and normal management of a STEMI?
Initial management:
Call an ambulance
Perform an ECG
Aspirin 300mg
Intravenous morphine for pain if required (with an antiemetic, e.g., metoclopramide)
Nitrate (GTN)
Management after:
PCI
Thrombolysis (if PCI is unavailable)
What is the management for an NSTEMI?
B – Base the 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)
What is Dressler syndrome, how does it present and how is it diagnosed and managed.
Dressler’s syndrome is also called post-myocardial infarction syndrome. It usually occurs around 2 – 3 weeks after an acute myocardial infarction. It is caused by a localised immune response that results in inflammation of the pericardium, the membrane that surrounds the heart (pericarditis). It has become less common as the management of acute coronary syndrome has advanced.
It presents with pleuritic chest pain, low-grade fever and a pericardial rub on auscultation. A pericardial rub is a rubbing, scratching sound that occurs alongside the heart sounds. It can cause a pericardial effusion and rarely a pericardial tamponade (where the fluid constricts the heart and inhibits function).
A diagnosis can be made with an ECG (global ST elevation and T wave inversion), echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).
Management is with NSAIDs (e.g., aspirin or ibuprofen) and, in more severe cases, steroids (e.g., prednisolone). Pericardiocentesis may be required to remove fluid from around the heart, if there is a significant pericardial effusion.
What is pericarditis, what are the key examination findings and presentation factors.
Pericarditis is inflammation of the pericardium, the membrane surrounding the heart. The most common causes are idiopathic (no underlying cause) and viral. It presents with chest pain and fever. Chest pain is worse when lying down and better when sitting forward.
ECG changes include:
Saddle-shaped ST-elevation
PR depression
Management involves:
Non-steroidal anti-inflammatory drugs (NSAIDs) are the mainstay of treatment (e.g., aspirin or ibuprofen)
Colchicine (taken longer-term, e.g., 3 months, to reduce the risk of recurrence).
What is endocarditis? How does it present? What investigations would you do? What is the management plan?
Infective endocarditis refers to infection of the endothelium (the inner surface) of the heart. Most commonly, it affects the heart valves. The most common cause is Staphylococcus aureus.
The presenting symptoms are non-specific for an infection:
Fever
Fatigue
Night sweats
Muscle aches
Anorexia (loss of appetite)
Blood cultures are essential before starting antibiotics. Three blood culture samples are recommended, usually separated by at least 6 hours and taken from different sites. The gap between repeated sets may have to be shorter if antibiotics are required more urgently (e.g., sepsis).
Echocardiography is the usual imaging investigation.
Intravenous broad-spectrum antibiotics (e.g., amoxicillin and optional gentamicin) are the mainstay of treatment. The choice of antibiotic may be more specific once the causative organism is identified on cultures. Antibiotics are typically continued for at least: 4 weeks for with native heart valves
6 weeks for patients with prosthetic heart valves
What is the management for hypertension?
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)
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).
The NICE recommendations vary for patients under 55 or over 55, type 2 diabetics and patients of Black African or African-Caribbean family origin:
Step 1: Aged under 55 or type 2 diabetic of any age or family origin, use A. Aged over 55 or Black African use C.
Step 2: A + C. Alternatively, A + D or C + D.
Step 3: A + C + D
Step 4: A + C + D + fourth agent (see below)
Step 4 depends on the serum potassium level:
Less than or equal to 4.5 mmol/L consider a potassium-sparing diuretic, such as spironolactone
More than 4.5 mmol/L consider an alpha blocker (e.g., doxazosin) or a beta blocker (e.g., atenolol)
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
what are some complications of hypertension?
What investigations would you do for these?
What is malignant hypertension?
Ischaemic heart disease (angina and acute coronary syndrome) - ECG
Cerebrovascular accident (stroke or intracranial haemorrhage)
Vascular disease (peripheral arterial disease, aortic dissection and aortic aneurysms) - CT angiograph
Hypertensive retinopathy- fundoscopy
Hypertensive nephropathy- alubumin creatinine ratio and urine dipstick
Heart failure- x-ray /echo
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
What is 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 gives a sawtooth appearance on the ECG, with repeated P wave occurring at around 300 per minute, with a narrow complex tachycardia.
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.
What is atrial fibrillation?
What are the most common causes?
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).
Common causes:
Sepsis
Mitral valve pathology (stenosis or regurgitation)
Ischaemic heart disease
Thyrotoxicosis
Hypertension
