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.
Anticoagulation for AF?
Warfarin (INR 2-3)
NOACs/DOACs: apixaban (Xa), dabigatran (IIa: direct thrombin inhibitor), rivaroxaban (Xa)
Atrial flutter - define?
Atrial flutter is caused by a macro “re-entrant rhythm” in either atrium.
This is where the electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway. The signal goes round and round the atrium without interruption.
The signal makes its way into the ventricles every second lap due to the long refractory period to the AV node, causing 150 bpm ventricular contraction.
Atrial Flutter - ECG?
Sawtooth appearance on ECG with P wave after P wave
Atrial: 300bpm
Ventricular:150bpm
Management of Atrial Flutter?
Rate/rhythm control with beta blockers (rate) or cardioversion (rhythm)
Anti-arrhymics such as procainamide to convert the flutter
Pharmacologic therapy
Slow the ventricular rate e.g. beta blocker, verapamil, digitalis
Restore and maintain sinus rhythm once converted
Treat the reversible underlying condition (e.g. hypertension or thyrotoxicosis)
Radiofrequency ablation of the re-entrant rhythm
Anticoagulation based on CHA2DS2VASc score e.g. warfarin for prevention of thromboembolism
SVTs define?
electrical signal re-entering the atria from the ventricles.
Once the signal is back in the atria it travels back through the AV node and causes another ventricular contraction.
This causes a self-perpetuating electrical loop without an end point and results in fast narrow complex tachycardia (QRS < 0.12).
Types of SVT?
AVNRT “Atrioventricular nodal re-entrant tachycardia” is when the re-entry point is back through the AV node.
Dual AV node (micro-re-entry)
AVRT “Atrioventricular re-entrant tachycardia” is when the re-entry point is an accessory pathway (Wolff-Parkinson-White syndrome).
Macro-re-entry
“Ectopic Atrial tachycardia” is where the electrical signal originates in the atria somewhere other than the sinoatrial node. This is not caused by a signal re-entering from the ventricles but instead from abnormally generated electrical activity in the atria. This ectopic electrical activity causes an atrial rate of >100bpm.
SVT ECG?
Narrow QRS, T wave repeat
No clear P waves
SVT acute management?
- Valsalva manoeuvre
- Carotid Sinus massage
- IV adenosine
- alternative: verapamil - Direct current cardioversion
SVT long term management?
Avoid stimulants
Medication (beta blockers, calcium channel blockers or amiodarone)
Electrophysiological studies and radiofrequency ablation
Wolff-Parkinson White Syndrome?
Caused by an extra electrical pathway connecting the atria and ventricles (BUNDLE OF KENT). Premature beat - back up accessory pathway
WPWS ECG?
Short PR interval (< 0.12 seconds), Wide QRS complex (> 0.12 seconds) and “Delta wave” which is a slurred upstroke on the QRS complex
WPWs management
• Radiofrequency ablation of the accessory pathway.
1st degree heart block?
ECG?
Management
First degree heart block occurs where there is delayed atrioventricular conduction through the AV node.
PR interval >0.20secs
Observe stables
2nd degree heart block?
• Second degree heart block is where some of the atrial impulses do not make it through the AV node to the ventricles (dropped beats)
Mobitz type I
ECG?
This is where the atrial imputes becomes gradually weaker until it does not pass through the AV node.
After failing to stimulate a ventricular contraction the atrial impulse returns to being strong. This cycle then repeats.
PR interval lengthens until it drops a QRS complex
Mobitz type II
ECG?
This is where there is intermitted failure or interruption of AV conduction.
Usually 2:1, or 3:1, but may be variable
2 P waves for each QRS complex. Every second p wave is not a strong enough atrial impulse to stimulate a QRS complex.
3rd degree block?
ECGs?
referred complete heart block. No action potentials from the SA node/atria get through the A-V node
This is no observable relationship between P waves and QRS complexes. There is a significant risk of asystole with third degree heart block.
Mobitz type II and 3rd degree block management
Unstable or risk of asystole (i.e. Mobitz Type 2, complete heart block or previous asystole)
First line: Atropine 500mcg IV and isoprenaline (β-adrenergic receptors)
No improvement:
Atropine 500mcg IV repeated (up to 6 doses for a total to 3mg)
Other inotropes (such as noradrenalin)
Transcutaneous cardiac pacing (using a defibrillator)
In patients with high risk of asystole (i.e. Mobitz Type 2, complete heart block or previous asystole):
Temporary transvenous cardiac pacing using an electrode on the end of a wire that is inserted into a vein and fed through the venous system to the right atrium or ventricle to stimulate them directly
Permanent implantable pacemaker when available
Ventricular ectopic
premature ventricular beats caused by random electrical discharges from outside the atria. Not a rhythm
Ventricular ectopic ECG AND management
individual random, abnormal, broad QRS complexes on a background of a normal ECG.
- betablockers
- Lidocaine
- Ablation of focus
Idioventricular rhythm
Idioventricular arrhythmia is also termed ventricular escape rhythm. It is considered a last-ditch effort of the ventricles to try to prevent cardiac standstill (SA/AV node have failed)
20-40bpm
ECG idioventricular rhythm and management
slow, no P wave, and bizarre QRS
atropine, pacing, dopamine and CPR
Accelerated idioventricular rhythm
last-ditch effort of the ventricles to try to prevent cardiac standstill. The SA node and AV node have failed
Rate usually between 40 to 100 beats per minute (bpm)
Agonal rhythm
Idioventricular rhythm is 20 beats or less per minute.
CPR and Defib
Long QT syndrome - LT management
Avoid medications that prolong the QT interval
Correct electrolyte disturbances
Beta blockers (not sotalol)
Pacemaker or implantable defibrillator
Inherited Long QT syndrome QT: times
440ms in males
450ms in females
Management: inherited long QT syndrome
Beta- blockers: Nadolol (appears to be the most effective at preventing ventricular arrhythmia compared to other BBs,
Avoid QT prolonging drugs
Diet: potassium rich foods such as bananas
Correction of electrolyte abnormalities
Avoidance of triggers
Try not to do high dynamic sport
strenuous swimming o Breath holding o Loud sudden noises o Diarrhoea, vomiting: special hydration • Pacemaker and ICD
Brugada syndrome - define
autosomal dominant (8x male adults) sodium channelopathy
ECG brugada syndrome
ST elevation (Doming of ST segment) and RBBB in V1-V3
might only been seen with flecainide (blocks sodium channel)
Brugada syndrome triggers
o Usually rest or sleep o Fever and medications Anti-arrhythmic drugs, Psychotropics, Analgesics & Anaesthetics o Electrolyte imbalances and ischaemia o Excessive alcohol and large meals
Brugada management
Correction of electrolyte abnormalities and avoid certain medications
Avoidance of triggers (reduce developing a fast heartbeat) e.g. strenuous swimming, Breath holding, Loud sudden noises and a high temperature – if you develop a high temperature, take painkillers such as paracetamol to bring it down; get medical advice as soon as possible if this does not help, alcohol and dehydration
Implanted defibrillator
left bundle branch splits into
anterior hemi-bundle
posterior hemi-bundle
right bundle branch block is stimulated by
impulse from left ventricle
RBBB: ECG
QRS >0.12s
M QRS in V1 (rSR)
W QRS in VS
positive in V1 and V2
LBBB: left ventricle is activated from the
right bundle
LBBB: ECG
Negative V1 and V2: W in V1
M in V6
symptoms/signs of acute LVF
SOB
Pink frothy cough/sputum
reduced o2 sats
bilateral basal crackles
Acute LVH investigations
- examine
- ECG
- ABGs
- CXR: Cardiomegaly, bilateral pleural effusions, kerley B lines and fluid interlubular fissures
- Bloods: troponin, BNP, kidney function
- Echo
BNP actions
BNP: hormone released from heart ventricles when myocardium is stretching beyond normal range
reduces the systemic vascular resistance making it easier for the heart to pump blood through the system.
BNP also acts on the kidneys as a diuretic to promote the excretion of more water in the urine. This reduces the circulating volume helping to improve the function of the heart.
Acute LVF management
- stop IV fluids and sit up
- Oxygen
- Prescribe loop diuretic (frusemide)
severe
- IV opiates (e.g. morphine - act as vasodilator)
- CPAP
- Inotropes
Chronic heart failure types
Impaired left ventricular contraction (“systolic heart failure”)
Left ventricular relaxation (“diastolic heart failure”).
o
symptoms/signs of chronic heart failure
breathlessness, orthoponea, cough, paroxysmal nocturnal dypnoea
Peripheral oedema
Reduced exercise tolerance, fatigue and tiredness
Elevated JVP, bibasal crackles on lungs, 3rd and 4th heart sounds (galloping rhythm)
CHF Investigations
- BNP blood test
- ECG
- Echo
- CXR
- Bloods: Hb, U&E, TFT and ferritin
CHF Medical management
- ACEi
- Beta - blockers
- MRA - spinolactrone if A and B not working
- Vasodilators if they can’t tolerate ACEI/ARBs): hydralazine
- Sinus node blocker e.g. ivabradine
- Remove ACEi, allow 36 hours and add in entresto
- Iron therapy (trial)
Improve symptoms
- Loop: furosemide
- Add thiazide e.g. bendroflumethiazide
- Digoxin
Refractory to medical treatment CHF
- CRT
- ICD
- IABP
- ECMO
- lvad
- Cardiac transplantation
Cor Pulmonale
right sided heart failure - respiratory disease
3rd heart sound
0.1 after S2
4th heart sound timing
before S1
SCRIPT - Murmurs
Site character radiation intensity pitch time
mitral stenosis causes
- rheumatic
- infective endocarditis
- congenital
mitral stenosis murmur
a mid-diastolic, low pitched “rumbling” murmur (descredeno-cresendo)
MS symptoms/signs
Malar flush
AF
Tapping Apex
breathlessness, fatigue and palpitations
MS management
- Diuretics (reduce preload & pulmonary congestion)
- Ventricular rate control with digoxin, beta-blockers or calcium antagonists
- treat AF (anticoagulated if AF)
- Surgery: Valve replacement and Balloon Valvuloplasty
MR causes
Leaflets: Prolapse, rheumatic, connective tissue disorders (Ehlers Danlos syndrome or Marfan syndrome) myxomatous (floppy) and endocarditis
Chordae rupture (degenerative): Prolapse/flail leaflet
Papillary muscles rupture: Ischaemic heart disease
Annular dilatation: Functional
MR signs/symptoms
pan-systolic, high pitched “whistling” murmur
murmur radiates to left axilla
peripheral oedema, fatigue and breathlessness
MR management
Medication: Diuretics and heart failure (ACE inhibitors/ARB: vasodilators to reduce afterload)
Anticoagulated and potentially digoxin if AF
Surgical
o Repair – prolapse
o Replacement - degenerative
Aortic stenosis causes
- calcified
- congenital
- rheumatic heart disease
AS signs/symptoms
crescendo-decrescendo character
radiates to carotids
Slow rising pulse and narrow pulse pressure
Breathlessness, chest pain and dizziness/syncope
AS Management
Conventional valve replacement
Mechanical (longevity, lifelong warfarin, younger patients)
o Bio-prosthetic (no warfarin, 10 years and older patients)
Trans catheter aortic valve replacement (TAVI)
Balloon Aortic valvotomy (BAV)
AR causes
Causes: Idiopathic age related weakness
Leaflets
o Endocarditis, Connective tissue diseases (Ehlers Danlos syndrome or Marfan syndrome) and rheumatic
Annulus
o Marfans and Aortic dissection
signs/symptoms AR
early diastolic, soft murmur
collapsing pulse
wide pulse pressure and displaced apex
AR management
Medication: ACE inhibitors – control systolic BP
Surgery: Valve replacement. Symptoms and LV dilatation
Organisms causing endocarditis native valve
Staphylococcus aureus (38%)
Viridans group streptococci (31%) e.g. strep mitis (normally live in mouth)
Enterococcus sp (8%)
Staphylococcus epidermidis
Empirical therapy for endocarditis
Native valve indolent (Subacute): Amoxicillin IV 2g 4 hourly + Gentamicin 1mg/kg bd
Native valve severe sepsis (Acute): Flucloxacillin IV 2g 6 hourly (4 hourly if >85kg)
Suspected MRSA: Vancomycin IV + Gentamicin IV 1mg/kg bd (use actual body weight - max 120mg/dose + when therapeutic vancomycin levels reached add Rifampicin PO 600mg bd (always check for interactions)
Drug user endocarditis (MSSA): Flucloxacillin IV
Endocarditis: specific Mx after blood cultures
Staphylococcus aureus (not MSSA): Flucloxacillin IV
MRSA: Vancomycin IV + Gentamicin IV 1mg/kg bd + when therapeutic vancomycin levels reached add Rifampicin PO 600mg bd (always check for interactions)
Viridans streptococci: Benzylpenicillin iv & gentamicin iv (synergistic)
Enterococcus sp.: Amoxicillin/vancomycin & gentamicin IV
Staphylococcus epidermidis: Vancomycin & gentamicin IV & rifampicin PO
4-6 weeks
atrial myxoma
Most common benign cardiac tumour (but still very rare)
dilated cardiomyopathy and management
• Big heart: 2 or 3 times normal (normal 350g)
Diuretics, ACEi
Anticoagulation
ICDs, LVADs and transplantation
Hypertrophic Cardiomyopathy
Left ventricle outflow tract obstruction from the asymmetric septal hypertrophy (Loss of cavity and increase in thickening)
Diastolic dysfunction (not systolic as contraction is fine) therefore heart cannot relax. Outflow obstruction
Hypertrophic cardiomyopathy ecg and echo
• ECG: LVH, progressive T wave inversion, deep Q waves, AF, WPW syndrome, VT, ventricular ectopic
Echo: asymmetric septal hypertrophy, small LV cavity with hypercontractile posterior wall, mid-systolic wall closure of the aortic valve
Hypertrophic cardiomyopathy management
Β-blockers or verapamil for symptoms (to reduce ventricular contractibility)
Amiodarone: for VF or VT
Anticoagulated for AF
Septal myomectomy for severe symptoms: surgical or chemical (alcohol) to reduce LV outflow tract gradient
ICD
Restrictive Cardiomyopathy
lack of compliance therefore diastolic dysfunction
Arrhythmogenic Right Ventricular Dysplasia/cardiomyopathy (ARVD)
Genetic: autosomal dominant with low penetrance.
Right ventricle becomes largely replaced by Fibro-fatty replacement of cardiomyocytes.
Arrhythmogenic Right Ventricular Dysplasia/cardiomyopathy (ARVD) Mx
- ACEi
- Anti-arrhythmic medication
- Anti-coagulants
- Beta-blockers
- diruetics
- Pacemaker, ICD
- Catheter ablation
Myocarditis causes
infectious: enteroviruses (coxsackie A&B), echovirus, chagas disease, lymes and HIV
non-infectious disease :
Immune mediated hypersensitivity reactions
Hypersensitivity to infection – Rheumatic fever after strep sore throat
Hypersensitivity to drugs – Eosinophilic myocarditis
Systemic Lupus Erythematosus (SLE)
rheumatic fever core symptoms
fever, joint pain and rash (erythema marginatum)
JONES CRITERIA J - oint athririts O - rgan inflammation N - odules E -rythema marginatum rash S - ydenham chorea
Rheumatic fever management
phenoxymethylpenicillin (10 days)
o NSAIDs (e.g. ibuprofen) are helpful for treating joint pain
o Aspirin and steroids are used to treat carditis
o Prophylactic antibiotics (oral or intramuscular penicillin) are used to prevent further streptococcal infections and recurrence of the rheumatic fever. These are continued into adulthood.
pericarditis - signs
Central chest pain worse on inspiration or lying flat with relief when sitting forward
Pericardial friction rub
Pericardial effusion or cardiac tamponade
pericarditis - investigations
ECG: saddle shaped (concave) ST segment elevation and PR depression
Blood tests: FBC, ESR, U&E, cardiac enzymes (troponin),
CXR: Cardiomegaly: indicate pericardial effusion
CMR and CT: Localised inflammation
echo: effusion
Management of pericarditis
NSAIDs or aspirin with gastric protection for 1-2 weeks
Add colchicine 500mg OD or BD for 3 months to reduce risk of reoccurrence
Rest until symptoms resolve
Treat the cause
If not improving or autoimmune considers steroids or other immunosuppressive
pericardial effusion management
treat causes and pericardiocentesis
constrictive pericarditis
Heart is encased in rigid pericardium
Unknown cause, TB elsewhere
investigations for constrictive pericarditis
- CXR: small heart ± pericardial calcification
- CT/MRI: distinguish from constrictive cardiomyopathy
- Echo
- Cardiac catheterisation
management for constrictive pericarditis
surgical excision
cardiac tamponade
• Pericardial effusion that raises intraperitoneal pressure reducing ventricular filling and dropping cardiac output leading to cardiac arrest
signs/symptoms of cardiac tamponade?
tachycardia, hypotension, pulsus paradoxus, raised JVP, muffled S1 and S2
Investigations and management of cardiac tamponade?
Becks triad: Falling BP, rising JVP, muffled heart sounds
pericardiocentesis
Aortic dissection
A break in the lumen causes blood to flow between the layers of the wall of the aorta
This creates a false lumen in the aorta (a space where blood is contained within the wall of the aorta
aortic dissection signs/symptoms
Tearing chest pain of sudden onset: intracapsular
Radiating to the back
hypertension > hypotension (severe)
AAA
dilated abdominal aorta (increased circumference): dilation of a vessel by more than 50% of its normal diameter
Normal is 1.2-2.0cm. Anything >3cm
risk factors for AAA
Male and older age (>65 years) and Family history
Smoking and alcohol consumption
Poor diet (i.e. high trans-fat and reduced fruit and vegetables and omega 3 consumption)
Low exercise
Obesity
Diabetes
Hypertension, raised cholesterol
AAA investigations
ultrasound - one and there AP diameter
CT/MRI angiography - shape, size and iliac involvement
AAA management
monitor size
surgical intervention when:
o e.g. pain, trashing and rupture
o asymptomatic e.g. size >5.5cm diameter or expansion of >0.5cm/6months or >1cm/year
endovascular stenting or laparoscopic repair
AAA ruptured signs/symptoms
severe abdominal pain
pulsatile mass
hypotension, tachycardia
chronic lower limb ischaemia
Peripheral Arterial Disease results from atherosclerosis and narrowing of the arteries supplying the limbs and periphery
Critical Limb Ischaemia is the end stage of peripheral arterial disease, where there is inadequate supply of blood to a limb to allow it to function normally at rest.
Intermittent Claudication is the symptom of having ischaemia in a limb during exertion that is relieved by rest. It is typically a crampy, achy pain in the calf muscles associated with muscle fatigue when walking beyond a certain intensity.
6 Ps of critical limb ischaemia
Pain, Pallor, Pulseless, Paralysis, Paraesthesia and Perishing cold
ABPI results
> 0.9-1.2 is normal
0.4 – 0.85: claudication
0-0.45 is severe disease
<0.3 is critical ischaemic
Intermittent claudication management
improve walking distance
medical treatment
- atorvastatin
- clopidogrel
- Naftidrofuryl oxalate
surgical:
angioplasty and stenting
endarterectomy: remove atheromatous plaque
bypass surgery
Critical limb ischaemia management
Analgesia
Urgent revascularisation by
Angioplasty and stenting
Surgical reconstruction / amputation
Acute Limb Threat
sudden loss of blood supply to limb e.g. embolism, atheroembolism, arterial dissection, trauma or extrinsic compression
Acute Limb Threat Management
ABC – resuscitate and investigate FBC, U/Es, CK, Coag +/- Troponin ECG – MI, dysrhythmia CXR – underlying malignancy Anticoagulated: Stops propagation of thrombus, May improve perfusion
If limb is salvageable
o Yes: embolectomy ± fasciotomies ± thrombolysis
o No: Palliation or amputation
diabetic foot sepsis?
Combination of infection, neuropathy and ischaemia that contribute to the sequence of tissue ulceration, necrosis and gangrene which eventually may lead to amputation
diabetic foot sepsis management
antibiotics
rapid surgical debridement of infection tissue and leave open to drain
Virkows triad
endothelial injury
circulatory stasis
hypercoagulable state
DVT management
Treatment dose LMWH e.g. enoxaparin
long term: warfarin, NOAC or LMWH (cancer or pregnancy)
PE (high risk)
thrombolysis then oral anticoagulation
PE anticoagulation duration
o Provoked VTE with reversible factor = 3-6 months treatment
o Provoked VTE with irreversible factor = 3-6 months or lifelong depending on patient factors
o Indefinitely if cause unclear / underlying irreversible cause (e.g. cancer) / recurrent VTE
VTE prevention
If no contraindications, this should be 40mg of enoxaparin
If eGFR <30, 20mg enoxaparin
varicose veins
When the valves are incompetent in these perforators, blood flows from the deep veins back into the superficial veins and overloads them
causes: deep vein obstruction and deep valve incompetence
Primary vs secondary varicose veins
Primary: Out of the blue – one valve breaks allowing the back flow of blood
Secondary: previous DVT, usually increase in pressure from blockage that breaks the valves the wrong way
haemosiderin
• The haemoglobin in this blood breaks down to “haemosiderin”, which is deposited around the shins. This gives a brown discolouration to the lower legs. Can cause varicose eczema due to drug and inflamed skin
lipodermatosclerosis
• The skin and soft tissue become fibrotic causing tight, narrowed lower legs. This is called “lipodermatosclerosis”
varicose veins management
mobilsing
graduated compression
surgery:
- endothermal ablation
- sclerotherapy
- stripping
chylomicrons
snythesised in gut and transport fat from gut to sites of use
VLDL
produced in liver and main carriers of endogenous fat and choletsrol to sites of use
IDL
formed during the breakdown of VLDL and chylomicrons
LDL
in carriers of cholesterol, accounting for 60–70% of plasma cholesterol. They comprise four main subtypes: LDL I, II, III and IV, of which LDL-III is the most atherogenic subclass.
HDL
return about 20–30% of cholesterol in the blood to the liver from peripheral tissue for excretion
