Cardiology Diseases Flashcards
Left axis deviation?
Lead 1+ve and lead avf -ve
Right axis deviation?
Lead 1-ve and lead avf +ve
Normal axis deviation?
both lead 1 and avf +ve
Atherosclerosis - define
Atherosclerosis is a progressive disease and is a combination of atheroma’s (fatty deposits in the artery walls e.g. fatty substances, cholesterol, cellular waste, calcium and fibrin) and sclerosis (the process of hardening or stiffening of the blood vessel walls).
Pathology of atherosclerosis
- Endothelial damage
- Protective response
- chronic inflammation and immune activation
- macrophages take up oxidised LDL-C causing lipid depositing in artery walls (foam cells)
- fatty streak - fibrous atheromatous plaques
- stiff artery walls - hypertension
- stenosis - reduced blood flow (angina)
- plaque rupture - thrombus - ischaemia
atherosclerotic plaque exposes what when it ruptures?
collagen and vWF - initiate thrombus formation (platelet adherence)
risk factors for atherosclerotic plaque
Non-Modifiable Risk Factors
o Older age
o Family and personal history
o Gender: male
Modifiable Risk Factors o Smoking o Alcohol o Poor diet (high sugar and trans-fat and reduced fruit and vegetables and omega 3 consumption) o Low exercise o Obesity o Poor sleep o Stress
End Results of Atherosclerosis
- Angina
- Myocardial Infarction
- Transient Ischaemic Attacks
- Strokes
- Peripheral Vascular Disease
- Chronic Mesenteric Ischaemia
Primary prevention of CVD?
QRisk > 10%, CKD or type I diabetes for > 10 years : start atorvastatin 20mg
Statin - mechanism and side effects
HMG-CoA Reductase inhibitor check LFTs (AST/ALT) and myopathy (CK)
Secondary prevention of CVD (patients that have had angina, myocardial infarction, TIA, stroke or peripheral vascular disease)?
A – Aspirin (plus a second antiplatelet such as clopidogrel for 12 months)
A – Atorvastatin 80mg
A – Atenolol (or other beta blocker – commonly bisoprolol) titrated to maximum tolerated dose
A – ACE inhibitor (commonly ramipril) titrated to maximum tolerated dose
hypertension?
140/90 in clinic or 135/85 with ambulatory or home readings.
causes of hypertension?
essential hypertension - developed on its own e.g. salt, genetics
secondary hypertension
- Renal (e.g. stenosis, disease or infection)
- Obesity
- Pregnancy induced hypertension
- Endocrine e.g. conns syndrome
- Aortic disease - coarctation
- Drugs - steroids
Benign hypertension vs malignant (accelerated) hypertension
Benign hypertension – usually insidious (gradual) disease and asymptomatic and eventually causes LVH, CCF, atheroma, aneurysm and berry rupture
Malignant (accelerated) hypertension: serious life threatening
o Diastolic pressure >130-140
o Can develop from either benign primary or secondary hypertension (‘accelerated’ hypertension), or arise de-novo
o Urgent treatment due to causing cerebral oedema (papilloedema), acute renal failure/heart failure, Headache and cerebral haemorrhage,
diagnosis of hypertension
o ABPM: at least two measurements per hour during the person’s usual waking hours (usually 14/day).
o HBPM: two consecutive seated measurements, 1 minute apart. BP is recorded twice a day for at least 4 days and preferably for 7 days. measurements on the first day are discarded – average value of all remaining is used.
white coat syndrome?
more than a 20/10 mmHg difference in blood pressure between clinic and ambulatory or home readings
Stages of hypertension
• Stage 1
o Clinic: >140/90
o Ambulatory/home reading: >135/85
• Stage 2
o Clinic: >160/100
o Ambulatory/home reading: >150/95
• Stage 3
o Clinic: >180/120essential hypertension management?
Step 1: A or C
o Aged less than 55 and non-black use ACE inhibitor (A) e.g. ramipril 1.25mg up to 10mg
o Aged over 55 or black of African or African-Caribbean descent use Calcium channel blocker (C) e.g. amlodipine 5mg up to 10mg once daily
o ACEi & ARB: not used in young women due to fertility therefore Beta-blockers (B)
Step 2: A + C
o Alternatively A + thiazide diuretic (D) e.g. indapamide 2.5mg once daily
o C + D. If black then use an ARB instead of A.
Step 3: A + C + D
Step 4: A + C + D + additional (see below)
For step 4, if t potassium < 4.5 mmol/l consider a potassium sparing diuretic such as spironolactone. If the potassium > 4.5 mmol/l consider an alpha blocker (e.g. doxazosin) or a beta blocker (e.g. atenolol/bisoprolol 5mg up to 20mg once daily).`
Spironolactone mechanism
“potassium-sparing diuretic” that works by blocking the action of aldosterone in the kidneys, resulting in sodium excretion and potassium reabsorption.
drugs that cause hyperkalaemia
ACEi, spironolactone
True Resistant hypertension
blood pressure that remains above goal despite concurrent use of three antihypertensive agents of different classes, one of which should be a diuretic. Spironolactone needs to be tried
secondary hypertension management
treat underlying causes
stable angina - define
A narrowing of the coronary arteries reduces blood flow to the myocardium (heart muscle).
Visceral pain from myocardial hypoxia
stable angina - immediate management
• GTN Spray: 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.
Stable angina - long term management
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):
o Long acting nitrates (e.g. isosorbide mononitrate)
o Ivabradine: reduces HR with minimal impact on BP: Must be in sinus rhythm. 5mg or 2.5mg in elderly
o Nicorandil: K+ channel activator: start 5-10mg BD
o Ranolazine: inhibits late Na current.
Secondary prevention of angina
Aspirin (i.e. 75mg once daily): anti-platelet
Atorvastatin 80mg once daily: Reduce cholesterol
ACE inhibitor: reduce BP
Already on a beta-blocker for symptomatic relief: slow HR and reduce O2 demand
Define - ACS
Acute Coronary Syndrome is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery.
Types of ACS
Unstable Angina
ST Elevation Myocardial Infarction (STEMI)
Non-ST Elevation Myocardial Infarction (NSTEMI)
signs/symptoms of ACS
Severe central, constricting chest pain associated with:
o Nausea and vomiting
o Sweating and clamminess
o Feeling of impending doom
o Shortness of breath
o Palpitations
o Pain radiating to jaw or arms (left side more)
Symptoms should continue at rest for more than 20 minutes (similar to angina but prolonged)
ECG: STEMI
> 1mm ST elevation in 2 adjacent limb leads
> 2mm ST elevation in at least 2 contiguous precordial leads
New LBBB
ECG NSTEMI
ST segment depression in a region
Deep T Wave Inversion
Pathological Q Waves (suggesting a deep infarct – a late sign)
Evolving ECG MI traces
o Evolving changes of acute MI:
ST elevation –first few hours
Q wave formation and T wave inversion – first day – becomes enlarged
“Old MI” – Q waves +/- inverted T waves
Left Coronary Artery - ECG and distribution
anterolateral ECG: I, aVL, V3-6
LAD - ECG and distribution
anterior ECG: V1-V4
Circumflex - ECG and distribution
lateral ECG: I, aVL, V5-6
Right coronary Artery - ECG and distribution
inferior ECG: II, III, aVF
troponins?
I and T
STEMI treatment
MONA +C/T - Early treatment
Analgesia - diamorphine iv + Anti-emetic – IV – against vomiting and nausea
Oxygen - if hypoxic
Nitrates: GTN - if BP > 90 mmHg
Aspirin 300 mg and Clopidogrel 300 mg (ADP receptor antagonist)/ Ticagrelor (P2Y12 ADP-receptor to prevent signal transduction and platelet activation)
Definitive treatment
o Primary PCI or CABG (if available within 2 hours of presentation)
o Thrombolysis (if PCI not available within 2 hours): paramedics can give
NSTEMI Mx
BATMAN
• B – Beta blockers unless contraindicated
• A – Aspirin 300mg stat dose
• T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative)
• M – Morphine titrated to control pain
• A – Anticoagulant: Low Molecular Weight Heparin (LMWH) at treatment dose (e.g. enoxaparin 1mg/kg twice daily for 2-8 days)
• N – Nitrates (e.g. GTN) to relieve coronary artery spasm
• Give oxygen only if their oxygen saturations are dropping (i.e. <95%).
• In addition to long term aspirin, clopidogrel therapy should be continued for three months in patients with no-ST elevation acute coronary syndromes
GRACE SCORE: FOR PCI
o <5% Low Risk
o 5-10% Medium Risk
o >10% High Risk
• High risk: angiography within 24 hours and considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.
• Intermediate risk: angiography within 3 days and considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.
• Low risk: non-invasive testing`
Secondary prevention of ACS
6As
• Aspirin 75mg once daily
• Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
• Atorvastatin 80mg once daily
• ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily)
• Atenolol (or other beta blocker titrated as high as tolerated)
• Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)
• Anti-coagulate until discharge e.g. fondaparinux
Types of MI
- Type 1: Traditional MI due to an acute coronary event
- Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)
- Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
- Type 4: MI associated with PCI / coronary stunting / CABG
What is Dressler’s syndrome?
It usually occurs around 2-3 weeks after an MI. It is caused by a localised immune response and causes pericarditis (inflammation of the pericardium around the heart)
symptoms of Dressler’s syndrome?
- Pleuritic chest pain
- Low grade fever
- Pericardial rub on auscultation.
- It can cause a pericardial effusion
- rarely a pericardial tamponade (where the fluid constricts the heart and prevents function).
dressler diagnosis?
- ECG (global ST elevation and T wave inversion)
- Echocardiogram (pericardial effusion)
- Raised inflammatory markers (CRP and ESR).
Management of dresslers?
NSAIDs
severe: prednisolone
pericardiocentesis: remove fluid around heart
symptoms/signs of cardiac arrest
non-responsive, not breathing and no pulse
VF - define?
bizarre irregular waveform
1. No recognisable QRS complexes and random frequency and amplitude
VF management
CPR and Defib: shock
Adrenaline 1 mg IV after 3rd shock then every 3 – 5 min thereafter (every 2 cycles/alternate shock)
amiodarone (300mg) after 3 shocks
Chronic: ICD and anti-arrythmias
Monomorphic vs polymorphic VT?
Monomorphic VT: Broad complex rhythm, rapid rate & constant QRS morphology
Polymorphic VT: Torsade de pointes: This arrhythmia may cease spontaneously or degenerate into ventricular fibrillation (forth road bridge)
pulseless VT management
Defib: shock with haemodynamic compromise
Adrenaline 1mg IV after 3rd shock and then 3-5 mins thereafter (2 cycles)
Amiodarone 300mg after 3rd shock
Asystole
- Absent ventricular (QRS) activity (check electrodes)
- Atrial activity (P waves) may persist
- Rarely a straight line trace
asystole management
• Adrenaline 1 mg IV as soon as possible. Then every 3 – 5 min thereafter (every 2 cycles)
Pulseless electrical activity (PEA)
Electricity is working, but the mechanics and plumbing are not.
The absence of a palpable pulse and absence of myocardial muscle activity with presence of organized electrical activity on the cardiac monitor
PEA management
treat reversible causes
adrenaline 1mg (3rd shock - then 3-5 mins then after)
Amiodarone (300mg) after 3 shocks
Normal Sinus Arrhythmia?
Variation in heart rate, due to reflex changes in vagal tone during the respiratory cycle e.g. inspiration reduces vagal tone and increase heart rate
Sinus bradycardia causes?
physiological, drugs (e.g.beta blocker) and ischaemia (inferior STEMI)
Sinus bradycardia management
atropine
pacing if haemodynamic compromise
Sinus tachycardia causes?
Physiological (Anxiety, fever, hypotension, anaemia)
Inappropriate (drugs, etc)
sinus tachycardia management
Treat underlying cause
B-adrrenergic blockers
sinus pause (sick sinus syndrome)
A sinus pause or arrest is defined as the transient absence of sinus P waves that last from 2 seconds to several minutes.
abnormal firing of SA node
sinus pause management
Only treated if symptomatic:
Atropine
Pacemaker
Atrial ectopic beat - define?
A PAC is not a rhythm, it is an ectopic beat that originates from the atria. Normal beat just occurs early!
Atrial ectopic beat - ECG findings?
P wave morphology can differ, but the rest is regular!
can have varying PR and RR intervals
Atrial ectopic management
Generally None
- Beta adrenergic blockers
- avoid stimulants
Junctional rhythm?
originates in the AV node. Impulse travels simultaneously to atria and ventricles
Junctional rhythm ECG?
inverted P waves just after the QRS complex
AF - define
The contraction of the atria is uncoordinated, rapid and irregularly due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node.
AF - ECG?
absence of p waves, irregular irregular ventricular QRS (narrow: >300bpm) and ragged baseline
Paroxysmal vs persistent vs permanent
Paroxysmal: Lasting less than 48 hours and often recurrent
Persistent: Episode of AF lasting greater than 48 hours, which can still be cardioverted to NSR. Unlikely to spontaneously revert to NSR
Permanent: Inability of pharmacologic or non-pharmacologic methods to restore NSR
Lone (Idiopathic): Absence of any heart disease and no evidence of ventricular dysfunction
CHA2DS2-VASc SCORE?
o C – Congestive heart failure
o H – Hypertension
o A2 – Age >75 (Scores 2)
o D – Diabetes
o S2 – Stroke or TIA previously (Scores 2)
o V – Vascular disease
o A – Age 65-74
o S – Sex (female)
0: no anticoagulation, 1: consider, 1> offer anticoagulation
Rate or rhythm control 1st?
Rate!
Rate control: first line unless?
There is reversible cause for their AF
Their AF is of new onset (within the last 48 hours)
Their AF is causing heart failure
They remain symptomatic despite being effectively rate controlled
Rate control management?
Beta blocker is first line (e.g. atenolol 50-100mg once daily)
Calcium-channel blocker (e.g. diltiazem or verapamil) (not preferable in heart failure)
Digoxin (only in sedentary people, needs monitoring and risk of toxicity)
o Acts on brain and increases vagal tone to AV node
Rhythm control: Immediate vs delayed cardioversion for AF?
Immediate cardioversion if the AF has been present for less than 48 hours or they are severely haemodynamically unstable.
Delayed cardioversion if the AF has been present for more than 48 hours and they are stable (Anti-coagulated for min of 3 weeks)
Cardioversion options for AF?
Pharmacological cardioversion: 1st line is Flecanide (1c) and amiodarone (III) for patients with structural heart disease (others being sotalol)
Electrical cardioversion: shock back into sinus rhythm. Sedation or GA and using cardiac defibrillator to deliver controlled shocks to restore sinus rhythm
Maintenance rhythm control for AF?
- Beta-blockers
- Dronedarone: after successful cardioversion
- Amiodarone: heart failure or LVD
- Catheter ablation of atrial focus/pulmonary veins
- Surgery - Maze procedure (ablate AV node and pace heart)
Paroxysmal AF? Other options?
• Flecainide is the usual treatment for a “pill in the pocket” approach.
