Module 2C - Cardiology Flashcards
Name some post-MI complications (ACT RAPID)
What does ST depression in leads V1- V3?
Posterior MI
How should you treat a Pt with LBBB and symptoms of MI?
As if they’re having an MI because their LBBB will hide the ST elevation on the ECG
What is troponin?
Regulatory protein that controls interactions between Actin and Myosin
Acute chest pain differentials
- Pericarditis –> sharp pain, worse on breathing in and lying down due to the myocardium stretching. Presents as wide spread ST elevation
- Aortic Dissection –> sudden and very severe pain (compared to gradual in ACS), pain radiates to the back , can also cause ST elevation
- Respiratory causes –> e.g. Pulmonary embolism, Pneumonia, pneumothorax, Oesophageal rupture
Where does the RCA originate + what node does the RCA supply?
- RCA originates in the right aortic sinus
Where does the LCA originate, how does it divide?
- LCA originates in the left aortic sinus
- LCA then divides into 2 main branches which are the left anterior descending (LAD) artery and the left circumflex artery
Supplies of RCA and LCA
Dominance of coronary arterial system
- Dominance depends on whether right or left coronary artery gives off posterior interventricular branch (PIB)
- 67-85% –> RCA gives off the PIB, this is known as RIGHT dominance –> in this case the RCA and LCA each supply about 50% of the heart supply
- 8-15% –> LCA is dominant and the PIB comes off the left circumflex artery
- 7-18% –> there is codominance, where both the RCA and left circumflex artery give off branches that form the PIB
Collateral circulation of heart
Collateral circulation can occur in all hearts too, typically at the terminal ends of the RCA and LCA in the coronary sulcus
On anterior side of heart, what vein drains areas supplied by the LCA into the coronary sinus?
Great cardiac vein
(heart veins drain into the coronary sinus which then drains into right atrium, some small veins drain directly into the right atrium)
On posterior side of heart, what vein drains areas supplied by the RCA into the coronary sinus?
small cardiac vein (drains from right marginal artery of RCA) and the middle cardiac vein (drains from PIB), these two arteries drain most of the areas supplied by the RCA
Which arteries is coronary angiography usually done via
via radial or femoral artery
- 7 = Right coronary artery
- 8 = right acute marginal artery
- 9 = posterior descending artery
- 1 = Left main coronary artery
- 2 = Left circumflex artery
- 3 = First diagonal artery
- 4 = First septal artery
- 5 = Left aneterior descending (LAD)
- 6 = Left first marginal artery
- 7 = Right coronary artery
- 8 = right acute marginal artery
- 9 = Posterior descending artery
- 10 = Posterior left ventricular artery
Right coronary artery
(looks like the letter ‘C’)
Pathophysiology of 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
Anatomy of coronary arteries
how long should symptoms continue at rest for?
Presentation of acute coronary syndrome
- typically central, constricting chest pain 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 > 15 mins)
ECG changes in ACS
–> STEMi
–> NSTEMI
STEMI:
- ST-segment elevation
- New left bundle branch block
NSTEMI:
- ST segment depression
- T wave inversion
What is PCI (Percutaneous coronary intervention)?
- involves putting a catheter into the patient’s radial or femoral artery (radial is preferred), feeding it up to the coronary arteries under x-ray guidance and injecting contrast to identify the area of blockage (angiography)
- Blockages can be treated using balloons to widen the lumen (angioplasty) or devices to remove or aspirate the blockage
- Usually, a stent is inserted to keep the artery open
Acute management of ACS (STEMI)
MONAT + reperfusion:
- M - Morphine
- O - Oxygen –> if hypoxic
- N - Nitrate (GTN)
- A - Aspirin 300mg
- T/P - Ticagrelor/Prasugrel (if high bleed risk/pt on anticoagulants –> clopidogrel instead)
- PCI –> if < 12hrs onset and can be done within 2hrs
- Thrombolysis –> if PCI not available within 2hrs (alteplase)
Acute management of ACS (NSTEMI)
MANFTA
- M - Morphine
- A - Aspirin 300mg stat
- N - Nitrate (GTN)
- F - Fondaparinux (antithrombin) –> unless high-bleed risk or immediate PCI
- T - Ticagrelor (clopidogrel if high bleed risk or prasugrel if having PCI) –> 180mg stat
- A - Angiography + PCI –> based off GRACE score (if > 3%)
(oxygen given if O2 sats < 95%)
GRACE score
GRACE score gives a 6-month probability of death after having an NSTEMI
- < 3% –> low risk
- > 3% –> medium to high risk
(pts at medium or high risk are considered for early angiography with PCI –> within 72hrs)
After initial management of ACS, what is the ongoing management?
- Echocardiogram –> assess functional damage to heart (left ventricular function)
Secondary prevention:
- Dual Antiplatelet therapy for 12 months (aspirin + ticagrelor/clopidogrel) –> then aspirin 75mg OD lifelong
- ACE-inhibitor –> ramipril
- Atorvastatin 80mg OD
- Beta-blocker –> bisoprolol (or atenolol)
- Heart failure? –> spironolactone (aldosterone-antagonist)
what is it + presentation + management + complciation –> management
What is Dressler’s syndrome (aka. post-MI syndrome)
- when it occurs
- what it is
- ecg changes/diagnosis
- management
- severe condition it can lead to
- usually occurs around 2–3 weeks after an acute MI
- it’s basically severe pericarditis (inflammation of membrane that surrounds heart –> pericardium)
- presents with low-grade fever and pericardial rub on auscultation
- Diagnosis –> ECG (global ST elevation and T wave inversion), ECHO (pericardial effusion), and raised inflammatory markers (CRP and ESR)
- Management –> NSAIDs, steroids
- can cause pericardial tamponade –> severe pericardial effusion which constricts heart and inhibits function
- in this case, pericardiocentesis may be required –> to remove fluid from around the heart
Cardiac rehab advice
- Physical activity
- Lifestyle advice, driving/flying/sex
- Stress management
- Health education
- Lifestyle changes:
- Healthy. Eating
- No more than 14 units a week
- Regular PA
- No smoking
- Maintain a healthy weight
Non-modifiable and modifiable risk factors for cardiovascular disease
Non-modifiable risk factors:
- Older age
- Family history
- Male
Modifiable risk factors:
- Raised cholesterol
- Smoking
- Alcohol consumption
- Poor diet
-Lack of exercise
- Obesity
- Poor sleep
- Stress
when should you offer a statin?
Q-risk score
- estimates the % risk that a patient will have a stroke or MI in the next 10 yrs
- > 10% –> offer a statin (atorvastatin 20mg at night)
When should statins be taken?
- at night –> body makes more cholesterol at night
- studies show an increased reduction in LDH when statins taken at night
Statins MOA
reduce cholesterol production in the liver by inhibiting HMG CoA reductase
Familial hypercholesterolaemia is a genetic condition causing high cholesterol lvls, what inheritance pattern does it have?
Autosomal dominant
Explain what the ECG parts measure:
- p waves
- PR interval
- QRS complex
- ST segment
- T wave
- RR interval
- QT interval
- P waves - represent atrial depolarisation, there should be a p wave preceding every QRS complex
- PR interval - represents the time for electrical activity to move between the atria and the ventricles, begins at start of P wave and ends at beginning of Q wave
- QRS complex - represents depolarisation of the ventricles
- ST segment - an isoelectric line representing the time between depolarisation and repolarisation of the ventricles (ie. ventricular contraction), starts at end of S wave and ends at beginning of T wave
- T wave - represents ventricular repolarisation
- RR interval - represents time between two QRS complexes
- QT interval - represents the time taken for the ventricles to depolarise and then repolarise
How to read ECG paper
- Eachsmall squarerepresents0.04 seconds
- Eachlarge squarerepresents0.2 seconds
- 5 large squares=1 second
- 300 large squares=1 minute
ECG territories and which arteries are affected
- Anteroseptal –> LAD
- Anterolateral –> proximal LAD
- Inferior –> RCA
- Lateral –> left circumflex
- Posterior –> ST depression in V1-V3
Cardiac axis
- most common cause of right axis deviation is right ventricular hypertrophy
- Conduction abnormalities usually cause left-axis deviation
Heart rate
- brady vs tachy
- calculating heart rate from ECG
- Normal range: 60-100bpm (<60bpm is bradycardia, >60bpm is tachycardia)
- Regular heart rhythm –> count the no. large squares within one R-R interval, divide 300 by this number
- Irregular heart rhythm –> count no. QRS complexes on rhythm strip (10 secs long), multiply this number by 6 to give heart rate (bpm)
P waves absent and irregularly irregular rhythm
Atrial fibrillation
Fixed prolonged PR interval
First-degree heart block (AV block)
Progressive prolongation of PR interval until eventually QRS complex dropped
Second-degree heart block (Mobitz type 1 or Wenckebach)
Consistent PR interval duration with intermittently dropped QRS complexes due to a failure of contraction
Second-degree heart block (Mobitz type 2)
where do narrow and broad escape rhythms originate from + values for QRS
Presence of P waves and QRS complexes that have no association with each other
Third-degree heart block (complete heart block)
- Narrow-complex escape rhythms(QRS complexes of <0.12 seconds duration) originateabove the bifurcationof thebundle of His.
- Broad-complex escape rhythms(QRS complexes >0.12 seconds duration) originate frombelow the bifurcation of the bundle of His.
Where does first-degree AV block occur?
Occurs between the SA node and the AV node (i.e. within the atrium)
Where does second-degree AV block occur?
- Mobitz I AV block (Wenckebach) –> occurs in the AV node (this is the only piece of conductive tissue in the heart which exhibits the ability to conduct at different speeds)
- Mobitz II AV block –> occurs AFTER the AV node in the bundle of His or Purkinje fibres
Where does third-degree (complete) AV block occur?
Occurs at or after the AV node resulting in a complete blockade of distal conduction
Delta wave + tachyarrhythmia?
Wolff-Parkinson-White syndrome
LBBB vs RBBB
Broad QRS complexes –> WilliaM MarroW –> look at V1 and V6
Atrial fibrillation –> what is it?
- AF is the commonest cardiac arrhythmia
- Atrial fibrillation (AF) is a supraventricular tachyarrhythmia
- uncoordinated, rapid, and irregular atrial contractions
- irregular and frequently fast heart rate
irregular, no p waves, tachycardia
Paroxysmal AF vs persistent AF vs long-standing AF vs perminent AF
- Paroxysmal –> self-terminating, usually within 48hrs, can last up to 7 days
- Persistent –> lasts longer than 7 days (including episodes terminated by cardioversion)
- Long-standing –> AF lasting for > 1 yr (rhythm control strategy)
- Perminent –> AF accepted by pt and physician, no rhythm control pursued
+ scale used for grading symptoms
Symptoms of AF
- Palpitations
- Dyspnoea
- Chest tightness
- Fatigue/lethargy
- Sleeping disturbance
- Psychological effects
Management of AF
- principles
- if pt haemodynamically unstable
- if pt stable –>
- further management if initial does not work
- Principles are rate or rhythm control + anticoagulation (to prevent strokes)
- If pt haemodynamically unstable –> Electrical cardioversion
-If pt stable –> rate or rhythm control:
Rate control…
- Beta-blocker (first line) –> bisoprolol
- Ca-channel blocker –> diltiazem or verapamil (not for heart failure pts)
- Digoxin –> only in sedentary pts with persistent AF
Rhythm control…
- Pharmacological cardioversion –> flecainide, amiodarone (used for structural heart disease)
- Electrical cardioversion –> controlled shocks to put heart back into sinus rhythm (immediate if pt unstable, or delayed if AF been present for > 48hrs)
Anticoagulation:
- DOACs first line
- Warfarin –> if mechanical heart valves or severe mitral stenosis
Further management if rate or rhythm control inadequate…
- AV node ablation and permanent pacemaker
(gets rid of source of arrhythmia –> but need pacemaker to pace the heart as AV node gone!)
Management of paroxysmal AF
Flecainide –> pill in the pocket
(note: still anticoagulated based off CHADVASC score)
How can AF cause an ischaemic stroke?
- 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
Warfarin target INR for AF + consequences of INR being too high or too low
2.0-3.0
- INR too high –> increased risk of bleeding
- INR too low –> increased risk of stroke (clot formation)
Metabolism of Warfarin involves what… in the liver??
cytochrome P450
CHA2DS2VASc –> why is it used + criteria
- CHA2DS2VASc used for assessing whether pt with AF should start anticoagulation
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)
0 – no anticoagulation
1 – consider anticoagulation in men (women automatically score 1)
2 or more – offer anticoagulation
ORBIT score
- assesses the risk of major bleeding in patients with atrial fibrillation taking anticoagulation
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 Hb 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)
most common cause of mitral stenosis?
Murmurs (turbulent blood flow), name the 4 murmurs
- Mitral stenosis –> mid-diastolic rumble - Rheumatic heart disease is most common cause
- Mitral regurgitation –> pansystolic
- Aortic stenosis –> ejection systolic - ‘crescendo-decrescendo’ (slow-rising pulse with narrow pulse pressure)
- Aortic regurgitation –> early diastolic murmur, wide pulse pressure - ”blowing, decrescendo”
Which valvular heart diseases/murmurs can cause AF?
- Mitral stenosis –> LA struggles to push blood through the stenotic valve causing strain –> increased pressure over time causes LA dilation and ‘atrial kick’ lost –> results in electrical disruption and fibrillation
- Mitral regurgitation –> incompetent mitral valve allows blood to flow back from LV to LA –> overtime can cause dilation of LA which in turn affects RA and causes AF
2 causes of mitral stenosis
- rheumatic heart disease
- infective endocarditis
Risk factors for infective endocarditis
- IV drug use
- Valve disease or prosthetic valves
- over 60yrs
- poor dental health
- implanted heart device
- long-term catheter
Most common causative organism of infective endocarditis
Staphylococcus aureus
Infective endocarditis symptoms and examination fndings
- symptoms are non-specific for infection –> fever, fatigue, night sweats, muscle aches
O/E:
- new or changing heart murmur
- splinter hemorrhages
- Petechiae
- Janeway lesions
- Osler’s nodes
- Roth spots –> hemorrhages on retina seen during fundoscopy
- clubbing (long-standing disease)
Management of infective endocarditis –> + how does treatment differ for normal heart valves vs prosthetic heart valves
- Broad-spectrum antibx (given after blood cultures taken) –> amoxicillin and gentamicin
- 4-week course –> normal heart valves
- 6-week course –> prosthetic heart valves
Antiarrhythmic drug classes
- Class I –> sodium channel blockers (flecainide –> class Ic)
- Class II –> beta-blockers (bisoprolol, propranolol)
- Class III –> potassium channel blockers (amiodarone, sotalol)
- Class IV –> Ca-channel blockers (virapamil, diltiazem)
- Adenosine and Digoxin
- Atropine
Indications for pacemaker
- Symptomatic bradycardias (e.g., due to sick sinus syndrome)
- Mobitz type 2 heart block
- Third-degree heart block
- Atrioventricular node ablation for atrial fibrillation
- Severe heart failure (biventricular pacemakers/CRT)
SA node issue vs AV node issue
Single chamber pacemakers
- Right atrium if SA node issue –> stimulate depolarisation in RA, electrical activity passes to LA and ventricles
- Right ventricle if AV node issue –> stimulate ventricles directly
Dual-chamber pacemakers
- Dual-chamber pacemakers have leads in both the right atrium and right ventricle
- The pacemaker coordinates the contraction of the atria and ventricles
Indications?
Biventricular (Triple-Chamber) Pacemaker –> also known as cardiac resynchronisation therapy
- Have leads in the right atrium, right ventricle and left ventricle
- Usually in pts with severe heart failure
- They coordinate the contraction of these chambers to optimise heart function
- This is referred to as cardiac resynchronisation therapy (CRT).
Implantable cardioverter defibrillators (ICDs) –> what are they + indications
- ICDs continually monitor the heart and apply a defibrillator shock if they identify ventricular tachycardia or ventricular fibrillation
Indications;
- Previous cardiac arrest
- HOCM
- Long QT syndrome
4 main differentials of a narrow complex tachycardia
- Sinus tachycardia –> treatment focuses on the underlying cause (sepsis or pain)
- 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
Sinus tachycardia –> most common causes
- normal P wave, QRS complex and T wave pattern
- Sinus tachycardia is not an arrhythmia and is usually a response to an underlying cause, such as sepsis or pain
Narrow-complex supraventricular tachycardia
- QRS <0.12 secs (3 small squares)
- SVT is similar to sinus tachy, but has a more sudden random onset –> whereas sinus tachy has a more gradual onset and a cause (sepsis or pain…)
- SVT can appear at rest with no apparent cause
Atrial fibrillation
+ definitive management
Atrial flutter and management
- gives a saw-tooth pattern on the ECG
- fast rate with narrow QRS complexes
- atrial flutter is caused by a re-entrant rhythm
- management –> same as AF, but permanent solution is radiofrequency ablation of the re-entrant rhythm
How are narrow-complex tachycardias and broad-complex tachycardias treated
+ with life-threatening features –> syncope, chest pain (muscle ischaemia), shock, or severe heart failure
VS stable
Unstable:
- synchronised DC cardioversion
- IV amiodarone added if initial DC shocks are unsuccessful
Stable:
- vagal manouvres –> valsalva, carotid sinus massage
- then beta-blockers or Ca-channel blockers
4 causes of broad complex tachycardias + managements
- Ventricular tachycardia or unclear cause –> treated with IV amiodarone
- Polymorphic VT (torsades de pointes) –> treated with IV magnesium
- Atrial fibrillation with bundle branch block –> treated as AF
- SVT with bundle branch block –> treated as SVT
Potentially life-threatening condition + what condition can lead to this?
Torsades de Pointes –> Long QT syndrome (inherited condition) can lead to TDP
What does this ecg pattern show, and what is the serious arrhythmia which it can lead to?
Prolonged QT –> can lead to TDP
Causes:
- Long QT syndrome –> an inherited condition
- Medications –> antipsychotics, citalopram, flecainide, sotalol, amiodarone, and macrolide antibiotics
- Electrolyte imbalances –> hypokalaemia, hypomagnesaemia and hypocalcaemia
Management of prolonged QT interval + management of torsades de pointes?
Prolonged QT interval:
- Stopping and avoiding medications that prolong the QT interval
- Correcting electrolyte disturbances
- Beta-blockers
- Pacemakers or ICDs
TDP:
- Correcting the underlying cause –> e.g., electrolyte disturbances or medications
- Magnesium infusion (even if they have normal serum magnesium)
- Defibrillation if VT occurs
What is a ventricular ectopic and what is the management?
- premature ventricular beats caused by random electrical discharges outside the atria –> relatively common (appear as isolated, random, broad QRS complexes on an otherwise normal ECG)
Management:
- Reassurance and no treatment in otherwise healthy people with infrequent ectopics
- Specialist advice in patients with underlying heart disease, frequent or concerning symptoms (e.g., chest pain or syncope), or a family hx of heart disease or sudden death
- Beta-blockers are sometimes used to manage symptoms
Wolff-Parkinson-White syndrome
- WPW –> atrio-ventricular re-entrant tachycardia
- involves an accessory pathway between atria and ventricles, rather than the AV node
- delta wave on ECG –> slurred upstroke of QRS complex due to early ventricular excitation
Causes of bradycardia
- Medications –> e.g., beta-blockers
- Heart block
- Sick sinus syndrome –> dysfunction of SA node (idiopathic degenerative fibrosis)
- High-performance athlete
Management of unstable pts with bradycardia (and those at risk of asystole)
- IV atropine –> first line
- Inotropes –> e.g., isoprenaline or adrenaline
- Temporary cardiac pacing –> transcutaneous (pads on chest) or transvenous (catheter through venous system to stimulate heart directly)
- Permanent implantable pacemaker, when available
Atropine MOA
- antimuscarinic medication and works by inhibiting the parasympathetic nervous system
- used for acute bradycardia and heart block
Management of stable angina (including secondary prevention)
- GTN –> for immediate relief of symptoms
- Beta-blocker (bisoprolol) + Ca channel blocker (diltiazem or verapamil)
(Note: Ca channel blockers avoided in heart failure pts)
Secondary prevention:
- Aspirin 75mg OD
- Atorvastatin 80mg OD
- ACEi –> if diabetes, htn, CKD, or heart failure are also present
Name some causes of pericarditis
- Idiopathic
- Infection –> eg. TB, HIV, coxsackievirus, EBV, and other viruses
- Autoimmune and inflammatory conditions –> eg. SLE, RA
- Injury to the pericardium –> eg. post-MI, open heart surgery or trauma
Investigations for pericarditis include bloods and an ECG, what are the findings? + diagnostic test for pericardial effusion
- Bloods –> raised inflammatory markers (CRP, ESR, WBC if infection)
- ECG –> saddle-shaped ST elevation (widespread) and PR depression
- Echocardiogram can be used to diagnose pericardial effusion
2 key presenting features of pericarditis and typical auscultation finding
- Chest pain and low-grade fever –> think pericarditis
- Auscultation –> pericardial rub
Management of pericarditis
- NSAIDs –> aspirin or ibuprofen
- Colchicine –> longer-term (3 months) to reduce risk of reoccurrence
- Steroids –> second-line
Pericardial effusion and cardiac tamponade + management
- Pericardial effusion –> when the potential space of the pericardial cavity fills with fluid –> this creates an inward pressure on the heart, making it more difficult to expand during diastole (filling of the heart)
- Cardiac tamponade –> severe pericardial effusion which causes increased pressure –> squeezes the heart and affects its ability to function –> reduces heart filling during diastole, decreasing cardiac output during systole
- Management –> emergency drainage of pericardial effusion to relieve pressure (pericardiocentesis)
Cardiac arrest –> 2 shockable rhythms + what is your management
- Pulseless VT
- VF
- deliver shock –> 2 min cycles of CPR and shock –> after 3rd shock give amiodarone 300mg
(give adrenaline 1mg every 3-5mins)
Cardiac arrest –> 2 non-shockable rhythms + what is your management and when would you stop CPR
- Pulseless electrical activity (PEA)
- Asystole
- administer 1mg adrenaline and continue CPR for 2 min cycle –> repeat this process
- Stop if –> return of spontaneous circulation, there is a shockable rhythm, resus team have decided to stop CPR
In cardiac arrest scenario, what is given after the 3rd shock?
- Amiodarone 300mg IV
- Adrenaline 1mg IV, then repeat every 3-5 mins
Reversible causes of cardiac arrest –> 4Hs and 4Ts
- Hypoxia - reduced oxygen levels, give oxygen, consider intubation
- Hypovolaemia - internal bleeds, dehydration, severe burns, sepsis –> give IV fluids
- Hypo/Hyperkalaemia - Digoxin toxicity (give potassium), insulin infusion or dextrose for hyperkalaemia)
- Hypothermia - *pt not dead until warm and dead –> give warm fluids *
- Thrombosis (coronary or pulmonary) - eg. PE, MI, Stroke –> thrombolysis
- Tension pneumothorax - venous return to the heart is compromised –> needle decompression with large bore cannula in 2nd ICS mid-clavicular
- Tamponade (cardiac) - cardiac USS to assess –> pericardiocentesis
- Toxins - eg. opioids, cyanide, CO –> attempt to reverse drugs
Post-resuscitation care
What is HOCM (hypertrophic obstructive cardiomyopathy)?
- HOCM is a genetic condition –> autosomal dominant
- Results from a defect in the genes for sarcomere proteins
- Left ventricle becomes hypertrophic (thickening of muscle) –> this obstructs the blood flow out of the left ventricle (LVOT obstruction)
- HOCM can lead to heart failure, MI, arrhythmias, and sudden cardiac death
Management of HOCM
Depends on severity and symptoms:
- Beta-blockers
- Surgical myectomy –> removing part of the heart muscle to relieve the obstruction
- Alcohol septal ablation –> a catheter-based, minimally invasive procedure to shrink the obstructive tissue
- ICD –> for those at risk of sudden cardiac death or ventricular arrhythmias
- Heart transplant
- advise to avoid intense exercise, heavy lifting, and dehydration
- genetic counseling offered and relatives may be tested
Other types of cardiomyopathy
- Dilated cardiomyopathy –> heart muscle becomes thin and dilated. It may be genetic or secondary to other conditions (e..g, myocarditis, long-term alcohol use)
- Restrictive cardiomyopathy –> heart becomes rigid and stiff, causing impaired ventricular filling during diastole
- Arrhythmogenic cardiomyopathy –> genetic condition where the heart muscle is progressively replaced with fibrofatty tissue (it becomes prone to ventricular arrhythmias) –> it is a notable cause of sudden cardiac death in young people, including high-performing athletes
- Takotsubo cardiomyopathy –> rapid onset of left ventricular dysfunction and weakness. This often follows severe emotional stress, for example, the death of a long-term partner. For this reason, it is known as broken heart syndrome. It tends to resolve spontaneously with time
Cardiac output, stroke volume and the equation linking them
- Cardiac output = volume of blood ejected by the heart per minute
- Stroke volume = volume of blood ejected during each beat
- Cardiac output = stroke volume x heart rate
Why does heart failure cause reduced gas exchange?
- When blood cannot flow efficiently through the left side of the heart, there is a backlog of blood waiting in the left atrium, pulmonary veins and lungs
- As these areas experience an increased volume and pressure of blood, they start to leak fluid and cannot reabsorb excess fluid from the surrounding tissues, resulting in pulmonary oedema
- The lung tissue and alveoli are filled with interstitial fluid –> this interferes with normal gas exchange in the lungs, causing SOB and reduced O2 sats
Symptoms of acute left ventricular heart failure
- acute SOB –> exacerbated by lying flat and improves on sitting up
- cough with frothy white or pink sputum
- O/E –> increased resp. rate, reduced O2 sats, tachycardia, bibasal crepitations
Patient has raised JVp and peripehral oedema in ankles, legs, and sacrum –> diagnosis?
Right-sided heart failure
What is BNP (B-type natriuretic peptide)?
- BNP = a hormone released from the heart ventricles when the cardiac muscle (myocardium) is stretched beyond the normal range –> relaxes the smooth muscle in blood vessels –> reduces systemic vascular resistance, making it easier for the heart to pump blood through the system
- A raised BNP blood result indicates the heart is overloaded beyond its normal capacity to pump effectively –> heart failure
- BNP also acts on the kidneys as a diuretic to promote water excretion in the urine –> this reduces the circulating volume, helping to improve the function of the heart in someone that is fluid-overloaded
An echocardiogram is helpful in assessing function of the left ventricle and structural abnormalities in the heart, what ejection fraction is considered normal?
> 55%
- ejection fraction = % of blood in the left ventricle that is squeezed out with each ventricular contraction
Chest x-ray findings in heart failure
- Pulmonary oedema –> bilateral pleural effusions
- Cardiomegaly
- Kerley B lines –> fluid in septal lines
Management of acute left ventricular failure (heart failure)
S – Sit up –> helps to oxygenate the lungs
O – Oxygen –> if O2 sats < 94%
D – Diuretics –> IV furosemide (reduces volume of blood in circulation that heart has to pump)
I – IV fluids should be stopped
U – Underlying causes need to be identified and treated (e.g., MI)
M – Monitor fluid balance
- Positive inotropes (digoxin) –> increase contractility of heart and increase CO and MAP
- Vasopressors (noradrenaline) - improves blood pressure and tissue perfusion
3 mechanisms of PND (paroxysmal nocturnal dyspnoea)
- Fluid settles across a large SA of the lungs as they lie flat to sleep, causing breathlessness –> as they stand up, the fluid sinks to the lung bases, and the upper lung areas function more effectively
- During sleep, the respiratory centre in the brain becomes less responsive, so the resp rate and effort do not increase in response to reduced oxygen saturation like they would when awake –> this allows the person to develop more significant pulmonary congestion and hypoxia before they wake up feeling very unwell
- There is less adrenaline circulating during sleep –> less adrenalin means the myocardium is more relaxed, reducing cardiac output
New York Heart Association Classification (NYHA)
Used to grade the severity of symptoms related to heart failure:
- 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
Referral criteria for speicalist assessment of chronic heart failure patients depends on the NT-proBNP result, what are these 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
Management of chronic heart failure
A – ACE inhibitor (e.g., ramipril)
B – Beta blocker (e.g., bisoprolol)
A – Aldosterone antagonist when symptoms are not controlled with A and B (e.g., spironolactone)
L – Loop diuretics (e.g., furosemide)
(if ACEi not tolerated –> ARB (eg. candesartan) can be used instead)
(SGLT2 inhibitor can be considered –> dapagliflozin)
- Surgical: valve replacement (underlying cause), ICD, CRT, heart transplant
What should be monitored in a patient taking diuertics, ACE inhibitors, and aldosterone antagonists?
- U&Es –> all three medications can cause electrolyte disturbances (hyperkalaemia)
Essentail hypertension accounts for 90% of hypertension, secondary accounts for the other 10% –> what is the most common cause of secondary hypertension?
Renal artery stenosis
Stages of hypertension
Management of hypertension
- ACEi –> ramipril
- Ca-channel blocker –> amlodipine
- Diuretics (thiazide-like) –> indapamide
- ARB –> cadesartan
- Beta-blocker –> bisoprolol
Hypertension treatment targets for under 80yrs and over 80yrs
Hypertensive emergency –> what is it and management
- Malignant hypertension –> BP >180/120 + retinal haemorrhages or papilloedema
Given IV:
- Labetalol
- GTN
What are the 3 fetal shunts and why are they a thing?
- Blood needs to go to placenta and back for oxygen and nutrients –> no role for lungs/liver, shunts allow blood to bypass these areas
- Ductus venosus –> connects the umbilical vein to the inferior vena cava and allows blood to bypass the liver
- Foramen ovale –> connects the right atrium with the left atrium and allows blood to bypass the right ventricle and pulmonary circulation
- Ductus arteriosus –> connects the pulmonary artery with the aorta and allows blood to bypass the pulmonary circulation
Patent ductus arteriosus –> what is it + management
- PDA = when ductus arteriosus fails to close –> prematurity and rubella increase risk of this
- Causes pulmonary hypertension (left to right shunt) –> right-sided heart strain –> right-sided hypertrophy and secondary left-sided hypertrophy
- Management –> monitor with echos until 1yrs old, then if not closed –> surgical closure
Atrial septal defect –> what causes it + what is it a risk factor for + management
- Foramen ovale (hole in septum secondum) doesn’t close –> ostium secondum/patent foramen ovale
- Blood moves from LA to RA because LA has higher pressure than RA –> leads to pulmonary hypertension and right-sided heart failure (due to right-sided overload)
- risk factor for stroke
- Management –> referral to paediatric cardiologist + anticaogulation
Differentials for a pansystolic murmur
- Ventricular septal defect
- Mitral regurgitation
- Tricuspid regurgitiation
and what conditions associated with?
Ventricular septal defect –> what is it and management
- congenital hole in ventricle septum
- Commonly associated with Down’s syndrome and Turner’s syndrome
- Management –> usually spontaneously close –> if not then surgery
In a younger patient with an ischaemic stroke, what congenital heart condition should you suspect?
Atrial septal defect (ASD) –> DVT embolus would usually go to lungs and cause PE but can go through hole and into brain to cause a stroke
Eisenmeiger syndrome –> 3 causes + what it is + management
3 causes:
- Atrial septal defect
- Ventricular septal defect
- Patent ductus arteriosus
- When pulmonary pressure exceeds systemic pressure –> blood flows from right side of heart to left side of heart –> right to left shunt –> it becomes easier for heart to pump blood through the hole instead of pumping blood into lungs –> deoxygenated blood bypasses lungs and enters body –> causes cyanosis
- Management –> only definitive treatment is heart-lung transplant –> high mortality
Coarctation of the aorta –> what is it
- narrowing of the aortic arch, usually around the ductus arteriosus
- often associated with Turner’s syndrome
- reduces blood flow to arteries distal to the narrowing and increases pressure in areas proximal to the narrowing –> heart and first 3 branches of aorta
Tetralogy of Fallot
4 co-existing congenital conditions
- Ventricular septal defect (VSD)
- Overriding aorta
- Pulmonary valve stenosis
- Right ventricular hypertrophy
What can be given to keep the ductus arteriosus open if waiting for surgery for example
Prostaglandin (E) infusion
Transposition of the great arteries
- a condition where the attachments of the aorta and the pulmonary trunk to the heart are swapped (“transposed”)
- there are two circulations that don’t mix –> baby will be cyanosed
- open heart surgery needed –> infusion of prostaglandin can keep ductus arteriosus open whilst waiting for surgery
Starling’s Law (Frank-Starling law)
Renin Angiotensin Aldosterone System
Dr Matt and Dr Mike video:
https://www.youtube.com/watch?v=ibjodC7Ft7U
Cardiac conducting system
Dr Matt and Dr Mike video:
https://www.youtube.com/watch?v=NR8GvLBfABw
Parts of the heart
Dr Matt and Dr Mike:
https://www.youtube.com/watch?v=uKrgEv7-rVM
Cardiac output –> Preload and Afterload
Dr Matt and Dr Mike:
https://www.youtube.com/watch?v=WuGMqezV3eo
ACS DVLA guidelines
- Resume driving after 1 week if PCI is successful, no other disabling condition
- If not treated with PCI- resume driving after 4 weeks
- CABG –> resume driving after 4 weeks
Splinter haemorrhages
Corneal arcus
Finger clubbing
Xanthelasma
Central cyanosis –> inadequate oxygenation of the blood
What is this + what is the condition associated with it associated with (heart problems)
High arch palate –> feature of Marfan’s syndrome (associated with mitral/aortic valve prolapse and aortic dissection)
Which valve disease is this feature associated with?
Malar flush –> plum-red discolouration of the cheeks associated with mitral stenosis.
Coronary arteries
Dr Matt and Dr Mike video:
https://www.youtube.com/watch?v=F51Tg_KNrKY
Beta-blockers –> MOA, categories, clinical indications, and adverse effects
Dr Matt and Dr Mike video:
https://www.youtube.com/watch?v=xKIpZ3bGUro&t=10s
Cardiac action potentials video
Dr Matt and Dr Mike video:
https://www.youtube.com/watch?v=xqmyODnxVhU
Heart attack vs heart failure video
Dr Matt and Dr Mike video:
https://www.youtube.com/watch?v=JV60tPRJMXQ
Atherosclerosis video
Dr Matt and Dr Mike video:
https://www.youtube.com/watch?v=jwL4lkSlvSA
Myocardial infarction in 2 mins video
Dr Matt and Dr Mike video:
https://www.youtube.com/watch?v=44ez25Hp8lc
Angina pectoris in 2 mins video
Dr Matt and Dr Mike video:
https://www.youtube.com/watch?v=f7EAVI8Vc_k
Blood pressure video
Dr Matt and Dr Mike video:
https://www.youtube.com/watch?v=k-BWyBePu8Q
Heart failure with reduced ejection fraction (HFrEF) –> value + most common cause
- < 40% ejection fraction = heart failure
- Coronary artery disease (CAD)/post-MI is most common cause
HOCM genetics –> most common mutation + pathophysiology
- MYH7
- left ventricle hypertrophy → decreased compliance → decreased cardiac output
Pericarditis management
NSAIDs + colchicine is first-line
Infective endocarditis –> blood cultures
at least 3 samples from different sies over 30-60 mins –> need this before starting antibx
Infective endocarditis –> first-line investigation
- Transthoracic echocardiogram (TTE) is usually the first investigation, but…
- (Transoesophageal (TOE) has higher sensitivity than TTE so is preferred as first-line if available)
Most common heart valve involved in infective endocarditis in IV drug users?
Tricuspid valve
Most common heart valve involved in infective endocarditis?
Mitral valve
Echo findings in mitral stenosis
- Thickening of mitral valve cusps
- Enlargement of left atrium
Most common cardiac tumour
Myxoma
Ramipril MOA
inhibit action of angiotensin-converting enzyme (ACE) –> reducing conversion of angiotensin I to angiotensin II
(angiotensin II is a vasoconstrictor and stimulates aldosterone secretion)
Pulse pressure is the difference between systolic and diastolic blood pressure –> what is considered a low pulse pressure + cause
- usually < 40 mmHg –> occurs when heart isn’t pumping enough blood –> heart failure is most common cause
Wolff-Parkinson-White management
- First-line –> radio-frequency ablation (ablate the accessory pathway)
- Next –> Beta-blockers and Ca-channel blockers
- Then –> Flecainide and sotalol
How are muscle fibers different in HOCM compared to normal?
what makes the murmur louder?
What is heard on auscultation of a Pt with Left Ventricular Outflow Tract Obstruction Hypertrophic cardiomyopathy?
- Systolic murmur –> best heard at the left lower sternal edge
- Due to part of the septum deviating into the left ventricle → turbulent blood flow in the outflow tract during ejection
- Murmur increases/louder –> with a decrease in preload (Valsalva, standing, diuretics)
- Murmur decreases/quieter –> with an increase in preload (squatting)
Which part of the cardiac cycle does coronary perfusion occur?
Early diastole
Cardiac cycle video
Ninja nerd video:
https://www.youtube.com/watch?v=xamYVlNF5Zo
4 phases:
1. Mid-to-late ventricular diastole
2. Isovolumetric contraction
3. Mid-to-late ventricular systole
4. Isovolumetric relaxation
- “lub” or S1 –> AV valves closing (due to ventricular pressure becoming greater than atrial pressure)
- “dub” or S2 –> Semilunar valves closing (due to aterial pressure > ventricular pressure)
What is end-systolic volume + what condition is this value increased?
- Volume of blood left in ventricles after ventricular contraction
- Heart failure –> this increases due to weaker ventricular contractions
Common valve condition which often leads to aortic stenosis
Bicuspid aortic valve
Valve anatomy + how many valve leaflets do the heart valves have?
- All have 3 leaflets apart from mitral valve
When should CABG be considered?
- When there is severe blockage of one or more coronary arteries and PCI has been unsuccessful
Why are Ca-channel blockers contraindicated in heart failure patients?
- Ca-channel blockers decrease contractility of the heart (-ve inotropes)
- heart failure patients already have reduced contractility so it is contraindicated
Which types of heart block require a permanent pacemaker?
- Mobitz type II and complete heart block
- less severe heart blocks may require pacemaker if symptomatic
A collapsing pulse and wide pulse pressure is a sign of which valve disease?
Aortic regurgitation
Head bobbing with heartbeat is a sign of which valve disease?
Aortic regurgititation
Pulmonary stenosis murmur
Ejection systolic –> louder on inspiration
Radio-femoral delay is associated with?
Coarctation of the aorta –> Turner;s syndrome
A 60-year-old man undergoes percutaneous coronary intervention for an ST-elevation myocardial infarction.
After 12 hours he becomes pale, clammy, and bradycardic. The ECG shows complete disassociation between the atria and ventricles.
What coronary artery is most likely to have been affected?
RCA –> cause of complete heart block post-MI as RCA supplies AV node
ECG electrode placement
- V1: 4th intercostal space at the right sternal edge
- V2: 4th intercostal space at the left sternal edge
- V3: midway between the V2 and V4 electrodes
- V4: 5th intercostal space in the midclavicular line
- V5: same horizontal level as V4 in the left anterior axillary line
- V6: same horizontal level as V4 and V5 in the left mid-axillary line
Which drug used in the management of hypertension is associated with hyperkalemia?
Spironolactone (aldosterone antagonist)
Management of broad complex tachycardia with no adverse features vs SVT with narrow QRS complexes (less than 0.12 secs) with no adverse features
- Broad QRS –> IV amiodarone
- Narrow QRS –> IV adenosine
ECG finding associated with hypercalcaemia
Short QT
Acute chest pain which is worse on inspiration, and reclining back worsens symptoms, but sitting upright provides relief for symptoms
Pericarditis
Slow-rising pulse –> which murmur
Aortic stenosis
Jerky pulse –> which murmur
HOCM
Atrial septal defect murmur –>
Ejection systolic –> murmur louder on inspiration
What type of drug should not be given with erythromycin/clarithromycin?
Statins
Orthostatic hypotension
Drop in standing blood pressure of > 20mmHg systolic after 3 mins standing
What drug (used in the treatment of hypertension) can cause hypokalemia, U waves are seen on ECG
Thiazide-like diuretics
Statins –> monitoring
LFTs at baseline, 3 months, and 12 months
(a fasting lipid profile can also be checked during monitoring to assess response to treatment)
What class of antibiotics can cause TDP?
Macrolides
What drug type (used in management of hypertension) is contraindicated in pregnant women?
ACE-inhibitors
Tricuspid regurgitation and mitral regurgitation both have a pansystolic murmur, which is louder on inspiration?
Tricuspid regurgitation
Causative organism of rheumatic fever
Strep A –> can do throat culture to confirm diagnosis
Most common viral cause of myocarditis
Coxsackie virus B
Where is serum BNP secreted from?
Cardiac ventricles
Duke criteria for infective endocarditis
- Major criteria –> Blood culture +ve for typical microorganism (eg. staph A), Echocardiogram showing vavlular vegetation
. - Minor criteria –> predisposing cardic lesion, IV drug use, temp. > 38, embolic phenomena, +ve blood culture not meeting above criteria
. - Definite IE –> 2 major OR 1 major + 3 minor
- Possible IE –> 1 major + 1 minor OR 3 minor
