Cardiology Conditions Flashcards
What is acute coronary syndrome
Refers to three states of myocardial ischaemia:
- Unstable angina
- ST elevation myocardial infarction (STEMI)
- Non-ST elevation myocardial infarction (NSTEMI)
Myocardial infarction, AKA heart attack, refers to death of cardiac tissue (ie myocardial necrosis)
Defined as evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischaemia. Requires the detection of a cardiac biomarker, for diagnosis, (eg troponin) to show a rise and/or fall with at least one value above the upper limit for normal. There should also be at least one of:
- Symptoms of MI
- New or presumed new ECG changes
- Development of pathological Q waves
- Imaging evidence of infarction (loss of viable myocardium or new motion abnormality)
- Angiography or autopsy evidence of thrombus
What is myocardial infarction vs myocardial injury
Myocardial infarction: myocardial necrosis, seen as a rise in toponin, with evidence of acute myocardial ischaemia
Myocardial injury: myocardial necrosis, seen as a rise in troponin, without evidence of acute myocardial ischaemia
What causes acute coronary syndrome
Atherosclerosis is the predominant cause
It leads to narrowing of the coronary vessels which supply the heart
Narrowing secondary to atherosclerosis is known as coronary artery disease or ischaemic heart disease
CAD/IHD can lead to angina which refers to typical chest pain from myocardial ischaemia when there is an increase in the O2 supply/demand (eg on exertion), which quickly improves on rest
If an atheromatous plaque ruptures, it leads to thrombus formation and acute occlusion that causes ACS
What are the risk factors for ACS
Modifiable: High cholesterol Hypertension Smoking Diabetes Obesity
Non-modifiable: Age Family history Male Premature menopause
How does ACS present
Chest pain> 15 minutes (central crushing or pressing pain ± radiation to neck or arm SOB Sweating Nausea and vomiting Palpitations Pale Clammy Tachycardia Cardiac failure
Severe complications:
Cardiac arrest
Life-threatening arrhythmia
Acute heart failure
What are the differentials in ACS
Aortic dissection PE Peptic ulcer disease Acute pericarditis Oesophageal spasm Costochondritis Panic attack Stable ischaemic heart disease Myocardial Acute cholecystitis Boerhaave syndrome Bruga syndrome Acute stress cardiomyopathy Pneumothorax Pneumonia Pericarditis Myocarditis GORD
What is AF
Irregularly irregular heart rhythm
AF is where the contraction of the atria is uncoordinated, rapid and irregular
What causes AF
Normally the sinoatrial node produces organised electrical activity that coordinates the contraction of the atria of the heart
AF is due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node.
The disorganised electrical activity of the atria also leads to irregualr conduction of electrical impulses to the ventricles
Most common causes of AF (mrs SMITH) S-epsis M-itral valve pathology (stenosis or regurgitation) I-schaemic heart disease T-hyrotoxicosis H-ypertension
What are the risk factors for AF
Hypertension Underlying heart disease Drinking alcohol FHx Sleep apnoea Chronic conditions (e.g., diabetes, hyperthyroidism, asthmas)
How does AF present
Presenting symptoms can be:
- Palpitations
- SOB
- Syncope (dizziness or fainting)
- Symptoms of associated conditions (eg. stroke, sepsis, thyrotoxicosis)
Signs:
An ECG will show an abscence of p waves which reflects the lack of coordinate atrial electrical activity
Irregularly irregular ventricular contractions
Tachycardia
Heart failure due to poor filling of the ventricles during diastole
Risk of stroke
What are the differentials for irregularly irregular pulse
- Atrial fibrillation
- Ventricular ectopics
Can be differentiated using an ECG
ECG should be performed on everyone with an irregularly irregular pulse
Ventricular ectopics disappear when the heart rate gets over a certain threshold, therefore a regular heart rate during exercise suggests a diagnosis of ventricular ectopics
What are the differentials in suspected AF
Atrial flutter — characterised by a saw-tooth pattern of regular atrial activation on the electrocardiogram.
Atrial extrasystoles — common and may cause an irregular pulse.
Ventricular ectopic beats.
Sinus tachycardia — sinus rhythm with more than 100 beats per minute.
Supraventricular tachycardias, including atrial tachycardia, atrioventricular nodal re-entry tachycardia, and Wolff-Parkinson-White syndrome.
Multifocal atrial tachycardia — often seen in people with severe pulmonary disease.
Sinus rhythm with premature atrial or ventricular contractions.
How does AF present on ECG
- Absent P waves
- Narrow QRS complex tachycardia
- Irregularly irregular ventricular rhythm
What is the CHA2DS2-VASc Score
Measure of thromboembolism risk in AF, and therefore whether to start on anticoagulants
C-congestive heart failure (1) H-hypertension (1) A-age >75 (2) D-diabetes (1) S-stroke/TIA/thromboembolism (2) V-vascular disease (1) A-age >65-74 (1) S-sex category female (1)
Low risk – 0 (if a woman has no other risk factors gender is no longer significant)
Intermediate risk – 1
High risk > 2 – anticoagulation
What is the HAS-BLED score
Helps the identification of those at risk of significant bleeding on anticoagulation therapy.
H-hypertension A-abnormal liver or renal function (1 point for each) S-stroke B-bleed (prior major/ predisposition) L-labile INR E-elderly >65 D-drugs or alcohol (1 point for each)
How is AF treated
There are two principles to treating atrial fibrilation:
- Rate or rhythm control
- Anticoagulation to prevent stroke
Rate:
In AF the atrial contractions are not coordinated so the ventricles have to fill up by suction and gravity, which is less efficient.
The higher the heart rate, the less time available for the ventricles to fill with blood, reducing the cardiac output.
Aim is to decrease heart rate to below 100, to extend the time during diastole when the ventricles can fill with blood
Treatment options:
-Beta blocker is first line
-Calcium channel blocker (not in hear failure)
-Digoxin (only in sedentary people, needs monitoring and risk of toxicity)
Rhythm:
Aim is to return the patient to normal sinus rhythm
Can be achieved by a single cardioversion event that outs the patient back in to sinus rhythm or long term medical rhythm control that sustains a normal rhythm
Two options are:
-Pharmacological cardioversion (flecanide or amiodarone)
-Electrical cardioversion (involves sedation or a general anaesthetic and using a cardiac defibrillator to deliver controlled shocks in an attempt to restore sinus rhythm)
Long term medical rhythm control:
-Beta blockers (first line)
-Dronedarone (secondline where have had successful cardioversion)
-Amiodarone (useful in patients with heart failure or left ventricular dysfunction)
The uncontrolled and unorganised movement of the atria leads to blood stagnating in the left arium, particularly in the atrial appendage.
This can lead to a thrombus which can become an embolus and travel from the atria to the ventricle, to the aorta then up in the carotid arteries to the brain, it can then lodge in the cerebral arteries and cause on ischaemic stroke.
Options:
-Warfarin
-NOACs (Apixaban, dabigatran and rivaroxaban)
What is angina
A narrowing of the coronary arteries reduces blood flow to the myocardium (heart muscle). During times of high demand such as exercise there is insufficient supply of blood to meet demand. This causes symptoms the symptoms of angina, typically constricting chest pain with or without radiation to jaw or arms.
Angina is “stable” when symptoms are always relieved by rest or glyceryl trinitrate (GTN).
It is “unstable” when the symptoms come on randomly whilst at rest, and this is considered as an Acute Coronary Syndrome.
How is angina investigated
CT Coronary Angiography is the Gold Standard diagnostic investigation. This involves injecting contrast and taking CT images timed with the heart beat to give a detailed view of the coronary arteries, highlighting any narrowing.
All patients should have to following as baseline investigations:
- Physical Examination (heart sounds, signs of heart failure, BMI)
- ECG
- FBC (check for anaemia)
- U&Es (prior to ACEi and other meds)
- LFTs (prior to statins)
- Lipid profile
- Thyroid function tests (check for hypo / hyper thyroid)
- HbA1C and fasting glucose (for diabetes)
How is angina managed
There are four principles to management (RAMP):
R – Refer to cardiology (urgently if unstable)
A – Advise them about the diagnosis, management and when to call an ambulance
M – Medical treatment
P – Procedural or surgical interventions
How is angina medically managed
There are three aims to medical management:
- Immediate Symptomatic Relief
- Long Term Symptomatic Relief
- Secondary prevention of cardiovascular disease
Immediate Symptomatic Relief:
Their GTN spray is used required. It causes vasodilation and helps relieves the symptoms.
Take GTN, then repeat after 5 minutes. If there is still pain 5 minutes after the repeat dose – call an ambulance.
Long Term Symptomatic Relief is with either (or used in combination if symptoms are not controlled on one):
-Beta blocker (e.g. bisoprolol 5mg once daily) or;
-Calcium channel blocker (e.g. amlodipine 5mg once daily)
Other options (not first line):
-Long acting nitrates (e.g. isosorbide mononitrate)
-Ivabradine
-Nicorandil
-Ranolazine
Secondary Prevention:
- Aspirin (i.e. 75mg once daily)
- Atorvastatin 80mg once daily
- ACE inhibitor
- Already on a beta-blocker for symptomatic relief.
How is angina surgically managed
Percutaneous Coronary Intervention (PCI) with coronary angioplasty (dilating the blood vessel with a balloon and/or inserting a stent) is offered to patients with “proximal or extensive disease” on CT coronary angiography. This involves putting a catheter into the patient’s brachial or femoral artery, feeding that up to the coronary arteries under xray guidance and injecting contrast so that the coronary arteries and any areas of stenosis are highlighted on the xray images. This can then be treated with balloon dilatation followed by insertion of a stent.
Coronary Artery Bypass Graft (CABG) surgery may be offered to patients with severe stenosis. This involves opening the chest along the sternum (causing a midline sternotomy scar), taking a graft vein from the patient’s leg (usually the great saphenous vein) and sewing it on to the affected coronary artery to bypass the stenosis. The recovery is slower and the complication rate is higher than PCI.
What are the PCI scars
Brachial artery access
Femoral artery access
What are the CABG scars
Midline sternotomy
Great saphenous vein harvesting
How is angina graded
The severity of angina can be graded according to the Canadian Cardiovascular Society.
- Grade I: angina with strenuous activity (e.g. limitation on strenuous or prolonged ordinary activity).
- Grade II: angina with moderate activity (e.g. slight limitation if normal activities performed rapidly).
- Grade III: angina with mild exertion (e.g. difficulty climbing one flight of stairs at normal pace).
- Grade IV: angina at rest (e.g. no exertion needed to trigger).
How common is angina
An estimated 2 million people in England have, or have experienced, angina.
Who is affected by angina
Smokers
Obese / DM / hypertensive patients
Those with a FHx of premature CAD
What is atherosclerosis
Atherosclerosis is an inflammatory process which predisposes individuals to angina and ACS.
Involves lipids, macrophages and smooth muscle.
Leads to the formation of an atheroma, which may contain plaque on its surface.
The presence of atherosclerosis within coronary vessels is termed coronary artery disease (CAD) or ischaemic heart disease (IHD) and it may be obstructive (i.e. >50% of the vessel lumen) or non-obstructive (<50% of the vessel lumen).
What are the risk factors for angina
Modifiable risk factors: • High cholesterol • Hypertension • Smoking • Diabetes • Obesity
Non-modifiable risk factors: • Age • Family history • Male sex • Premature menopause
What are the signs and symptoms of angina
The three classic features of angina include:
- Constricting pain experienced in the chest +/- typical radiation to the arm/neck/jaw
- Precipitated by physical exertion.
- Relieved by rest or GTN within 5 minutes
Based on these classical features, angina can be differentiated into three types:
Typical: all three of the above features
Atypical: two of the above features
Non-anginal: ≤1 of the above features
Concerning chest pain
Chest pain lasts > 10 minutes
Chest pain not relived by two doses of GTN taken 5 minutes apart
Significant worsening/ deterioration in angina (e.g. increased frequency, severity or occurring at rest)
The above features may be suggestive of ACS and patients need immediate medical attention.
Cardiovascular examination
- Heart sounds
- Signs of heart failure
Dyspnoea
Palpitations
-Angina may be precipitated by tachyarrhythmias (e.g., AF). These increase the oxygen supply/demand mismatch and reduce filling time of the coronary vessels during diastole.
Syncope:
-May be suggestive of dangerous valvular or cardiac muscle disease causing angina, particularly if it occurs on exertion.
What are the differentials in suspected angina
- Myocarditis
- Pericarditis
- Pleuritis
- PE
- Aortic dissection
- CHF
- MI
- GORD
What are potential complications of angina
Cardiovascular complications of angina, caused by coronary artery disease, include: -Stroke. -Myocardial infarction. -Unstable angina. Sudden cardiac death. Other complications include: -Anxiety, and depression. -Reduced quality of life.
What is the prognosis of angina
The prognosis of stable angina is variable. Important indicators of long-term prognosis are the extent and severity of coronary artery disease, left ventricular function, exercise duration or effort tolerance, and comorbidities.
The prognosis depends on the time point at which the person is seen. For example, new-onset angina has a worse prognosis than established angina which has remained stable for some time.
What is hypertension
Hypertension is the term used to describe high blood pressure, meaning a clinical bp measurement of 140/90 or an ambulatory/home reading of 135/85
Essential hypertension is also known as primary hypertension
Essentially means that the hypertension has developed on its own and does not have a secondary cause
How common is essential hypertension
Essential hypertension accounts for 95% of hypertension
What causes hypertension
Essential hypertension develops on ots own and does not have a secondary cause
Secondary causes of hypertension can be remembered by mneumonic ROPE:
R-enal disease
O-besity
P-regnancy induced hypertension/ pre-eclampsia
E-ndocrine (most endocrine conditions can cause hypertension but primarily hyperaldosteronism)
What are the risk factors for hypertension
Obesity Aerobic exercise <3 times per week Moderate to high alcohol intake Metabolic syndrome Diabetes Black ancestry Age >60 years old Family history of hypertension or coronary artery disease Sleep apnoea Poor diet (high sodium, low fruit and veg) Dyslipidaemia
How does hypertension present
Signs and symptoms: Often asymptomatic and detected through routine checks Retinopathy BP ≥140/90 mmHg Headache Visual changes Dyspnoea Chest pain Sensory or motor deficit
