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
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
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
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)
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
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
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
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
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
Starling’s Law (Frank-Starling law)
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.
Most common cardiac tumour
Myxoma
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)
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)
Valve anatomy + how many valve leaflets do the heart valves have?
- All have 3 leaflets apart from mitral valve
