Cardiology - Valvular Disease Flashcards
Where are most valve disease found
L side
What can go wrong with valves
Stenosis - doesn’t fully open
Regurgitation - doesn’t close properly
What is valve disease caused by
Disease of valve leaflets OR
Stretching of the structure that the valve is attached to
Congenital causes of valve disease
Bicuspid aortic valve
Acquired causes of common valve disease
Degenerative
Rheumatic
Endocarditis
Secondary/ functional regurgitation
Stretching of structure the valve is attached to causing leakage
How do valves work in a normal ventricle
Valve cusps meet –> valve closes
How do valves work in a dilated ventricle
In a stretched valve ring, cusps don’t meet –> valve doesn’t close (leaking valve)
Causes of 2’ regurgitation
Dilated LV
Dilated aortic root
Causes of dilated L ventricle
IHD
Dilated cardiomyopathy
HTN
What type of regurgitation can be caused by dilated LV
MR
What can cause dilated aortic root
Cystic medial necrosis
Bicuspid AV
Aortic dissection
Cystic medial necrosis
Medial layer undergoes necrosis of connective tissue –> weakening
When does cystic medial necrosis happen
Aging
CTD e.g Marfan’s, EDS
Accelerated by hTN
What type of regurgitation can be caused by dilated aortic root
AR
What can high LA pressure cause
Pulmonary oedema
What can high RA pressure cause
Increased JVP
Ascites
Peripheral oedema
What is rheumatic fever
An infl condn involving heart, skin and connective tissue usually affecting children (occasionally young adults)
When does rheumatic fever develop
3 weeks after sore throat from group A strep
What % of rheumatic fever pts have cardiac involvement
50%
Usually occurs after recurrent episodes (fibrosis)
How can rheumatic fever cause valve damage
Abnormal immune response to Group A Strep
How can rheumatic fever be prevented
Penicillin after sore throat
Also treated w/ penicillin
Rheumatic heart disease
Long-term consequence of rhematic fever
Primordial prevention of RHD
Improved living condn
Access to medical care
Primary prevention of RHD
Penicillin for confirmed strep pharyngitis
Secondary prevention of RHD
Extended abx (yrs - lifelong)
Epidemiology of rheumatic disease causing valve disease
Commonest cause in developing world but rare in developed world
How does valve disease present
Incidental finding - hearing murmur or in ECG
Heart failure symptoms - fatigue, breathlessness on exertion, swollen legs
What is mitral valve disease often associated with
AF
What can aortic valve disease be associated with
Angina
Dizziness
Sudden death
Normal valve function in systole
Mitral valve closed
Aortic valve open
Normal valve function in diastole
Mitral valve open
Aortic valve closed
What can cause MS
Thickening of leaflets that fuse at commisures
Repeated infl also causes valve damage
Where do valve leaflets meet
Commisures
What can cause MR
Damage to any part of MV structures LV dilatation (2' MR)
Pathophysiology of MR
Blood leaks back from LV into low pressure LA during systole
What can be heard during MR
Pan-systolic murmur radiating to axilla
Displaced apex beat
Which pts with MR will have surgery
Severe symptomatic MR
Asymptomatic with LV impairment
Most pts are asymptomatic
Mitral valve prolapse
Displacement of some part of one/both mitral valve leaflets into LA during systole
Commonest cause of c/c MR
Mitral valve prolapse
Auscultation of mitral valve prolapse
Mid-systolic click with a late systolic murmur
Mitral valve repair
Removal of extra tissue
Leaflet edges closed with sutures
Annuloplasty ring tightens valve
Normal mitral valve area
4 - 6 cm2
Area of mitral valve when stenosed
<2 cm2
Mitral valve stenosis pathophysiology
Problem of diastole - blood unable to be pushed from LA to LV
Reduced filling of LV –> reduced SV and CO
High pressure of LA transmitted back to pulmonary circulation –> pulmonary oedema
Increases risk of AF
Mitral faces
Rosy cheeks - malar rash
Rest of face has bluish tinge due to cyanosis
Listening for MS
Left lateral position
Place bell lightly over apex
Low frequency rumbling sound beginning in mid-diastole
Auscultation of MS
Loud S1
Opening snap - sudden tensing of chords
Mid-diastolic murmur (+presystolic accentuation)
Treatment of mitral stenosis
Balloon valvotomy
Catheter passed into femoral vein into RA then into MV
Balloon rapidly inflated to crack open commissures
Aortic stenosis
Thickening of aortic leaflets causes obstruction to outflow
Issue of systole
How many aortic leaflets are there
3
Common causes of aortic stenosis
Calcific disease (older pt) Bicuspid valve (younger pt) Rheumatic heart disease
Effects of aortic stenosis on heart structure
LV is pressure loaded because of obstruction to flow and hypertrophies
Symptoms of aortic stenosis
Exertional dyspnoea
Angina-like chest pain
Light-headedness and syncope
Sudden death caused by arrhythmias
What causes exertional dyspnoea
Raised LVEDP
Why is there reduced myocardial oxygen supply in aortic stenosis
Coronary Perfusion Pressure = aortic diastolic pressure - LVEDP
In severe AS, the stiff, hypertrophied LV has a high LVEDP –> reduced CPP
Survival in aortic stenosis
Short lifespan after onset of severe symptoms
Mortality majorly increased by valve replacement surgery
Commonest congenital heart defect
Bicuspid aortic valves - screen 1st degree relatives
Main risks with bicuspid aortic valves
Aortic stenosis and/or regurgitation
Associated aortopathy
IE
Aortopathy
Dilatation of any part or all of the proximal aorta forth aortic root to aortic arch
What condns are bicuspid aortic valves associated with
Coarctation of action (BAV in 50%) Turner Syndrome (BAV in 30%)
Mx of bicuspid aortic valve
All pts must have lifelong surveillance and will require surgery on valve and/or aorta in their lifetime
Is aortic regurgitation a problem of diastole or systole
Diastole - leaflets of aortic valve don’t meet properly allowing blood to leak back into LV
What causes aortic regurgitation
Disease of leaflets
Dilatation of aortic root
Clinical features of aortic regurgitation
Angina-like chest pain (decreased perfusion pressure and compensatory hypertrophy)
Dilated LV –> displaced apex
Collapsing pulse
Wide pulse pressure
Collapsing pulse
High systolic pressure
Low diastolic pressure
Corrigan’s sign
Prominent carotid pulsation
Why is there reduced myocardial oxygen supply in AR
CPP = Aortic Diastolic Pressure - LVEDP
In severe, ar, the aortic diastolic pressure is low –> reduced CPP
Listening for aortic regurgitation
Ask pt to: Sit up Lean forward Exhale completely Hold breath in full expiration
Hold diaphragm firmly at LSE
Early diastolic murmur - decrescendo
Cause of significant tricuspid regurgitation
RV enlargement
Usually functional
Signs of tricuspid regurgitation
Distended JVP w/ prominent v wave
Enlarged and pulsatile liver
Systolic murmur at LSE
Treatment of tricuspid regurgitation
Of the cause of RV enlargement (occasionally surgery is needed)
How common is tricuspid stenosis
Rare
Cause of tricuspid stenosis
Rheumatic heart disease
How common is pulmonary stenosis
Rare
Usual cause of pulmonary stenosis
Congenital
Pulmonary regurgitation as a functional issue
Due to dilated pulmonary artery caused by pulmonary HTN
Epidemiology of CVD
1 in 4 deaths in England
Modifiable risk factors for CHD
HTN DM High cholesterol Smoking Obesity Diet Alcohol Stress Sedentery lifestyle
Non modifiable risk factors for CHD
Fhx
Gender
Ethnicity
Age
Risk calculator for primary prevention of CVD
QRISK2/3
2’ prevention of CHD
Antipltelts (Asp, clop, prasugrel, ticagrelor) Beta-blockers/ ivabridine Statin ACEi Lifestyle modification Cardiac rehab
BP recommendations for pts at risk of CHD
Lower BP to <140/90mmHg
Systolic 120-130 in pts 18 to 69 years old
By how much does medication affect BP
Reduces bp by 10/6 mmHg
Doubling dose results in only further 20% drop
Lifestyle modification for HTN
Wt loss Mediterranean diet Reduced Salt intake (2.4Na/day) Physical activity (30mins aerobic/ day) Mod alcohol
When does cholesterol level become worrying
> 5.2mmol/l
Contributes to 46% of CHD deaths
Where do HDLs carry cholesterol
Away from arteries and back to liver, then excreted from body
What do LDLs do
Build up in walls of the arteries to form thick, hard deposits that narrow the arteries and make them less flexible
Main storage form of LDL
Triglycerides
Treatment of hypercholesterolaemia
Statins first line therapy for all pts with CVD and T2DM
Atorvastatin 80mg OD
Treatment for dysglyceamia
Diet, aerobic exercise and resistance training
Improves lipid profile, alters glucose metabolism and tightens glycemic control
1st line therapy for DM
Metformin
Issues associated with obesity
Raised BP Raised LDL & triglycerides Low HDL Impaired glucose tolerance Increased insulin resistance
What % of pts have depression post-MI
15-20%
Cardiac rehab
Comprehensive, long-term program involving prescribed exercise, risk-factor modification, education and counselling
What does CVD incl
CHD
CVA
PAD
What types of fat should we be eating
MUFA/PUFAs
Mediterrenean-style diet
More bread, fruit, vegetable and fish
Less meat and replace butter/cheese with products based on plant oils
How does HR affect myocardial demand
The higher the HR, the higher the demand
How does force of contraction affect myocardial O2 demand
The stronger the force of contraction, the higher the demand
Types of drugs for CAD
Reduce cardiac workload
Coronary vasodilators
Drugs that reduce cardiac workload
Beta-blockers
Ca channel blockers
Other channel inhibitors - ivabradine, ranolazine
Coronary vasodilators
Nitrates
K channel opener - Nicorandil
Block L-type Ca channels present in
Arterial smooth muscle
Cardiac muscle
Cardiac pacemaking tissue
What does blocking Ca channels in arterial smooth muscle do
Causes vasodilation
What does blocking Ca channels in cardiac muscle do
Reduces force of cardiac muscle contraction
What does blocking Ca channels in cardiac pacemaking tissue do
Reduce HR
Blocks AVN
Types of Ca channel blockers
Non-dihydropyridine (-ve inotropic)
Dihydropyridine (non-inotropic)
Examples of non-dihydropyridine Ca channel blockers
Verapamil - mainly cardiac effects
Diltiazem - both cardiac and vascular
Uses of non-dihydropyridine Ca channel blockers
Angina
Arrhythmias
(Some effect on BP)
Examples of dihydropyridine Ca channel blockers
Amlodipine
Nifedipine (decreases arterial resistance)
Uses of dihydropyridine Ca channel blockers
Acts mainly on vascular smooth muscle to reduce BP
Little to no cardiac effect
Widely used for HTN
Known adverse effects of Ca channel blockers - cardiac
Slow HR
Reduced contraction - may worsen heart failure
Known adverse effects of Ca channel blockers - vascular
Headache (hypotension) Peripheral oedema Reflex tachycardia (may be harmful to those with CAD) Rash Constipation
How do you choose Ca channel blockers
Whether you want arterial or cardiac effects
Types of beta-adrenoceptors
Beta-1 in the heart
Beta-2 in the airways
What do beta-adrenoceptors bind to
Circulating adrenaline and noradrenaline released by sympathetic system
Example of non-selective beta-blocker
Propanolol
Examples of cardio selective beta-blockers
Atenolol
Bisoprolol
Metoprolol
Examples of beta-blockers with vasodilator activity
Carvedilol
Labetalol
Adverse effects of beta-blockers - cardiac
Bradycardia Initially worsens heart failure Bronchoconstriction Fatigue Cold extremities Erectile dysfunction
Adverse effects of beta-blockers - sympathetic blockade
Bronchostriction (blockade of beta2-adrenoceptors)
Tiredness, feel cold
Nitrates MOA
Increases conc of endothelium NO –> vascular smooth muscle relaxation
Effects of nitrates
Arterial dilation
Venous dilation that reduces blood return to heart
Effects of arterial dilation - nitrates
Improve coronary supply
Reduce afterload by lowering BP
Effects of venous dilation - nitrates
Decreased preload and stretching of heart
Decreased pressure in the ventricles (esp diastolic wall pressure)
Commonly used nitrates
GTN/ NTG
Isosorbide mononitrate
Administration of GTN/ NTG
s/l, spray, buccal
For a/c use
Administration of isosorbide mononitrate
po OD
Nitrates and IHD
Symptomatic relief of ischaemic pain
NOT shown to have major impact on mortality
Adverse effects of nitrates
Hypotension
Reflex tachycardia
Headache
Flushing
Who prescribes specialist drugs for angina
Experienced drs for 3rd to 4th line treatment
Examples of specialist drugs for angina
Nicorandil
Ranolazine
Ivabradine
Nicorandil
Has nitrate action
Opens K channel
Ranolazine
Late Na current inhibitor
Ivabradine
Spp sinus node inhibitor
Blocks cardiac conduction
Similar to BB
How does cardiac output affect MAP
Slower and less vigorous pumps lowers MAP
How does vascular resistance affect MAP
Wider arteries, lower MAP
Types of drugs for HTN
Reducing intravascular volume
Reduce sympathetic tone
Relax peripheral arteries
Block neuroendocrine mediators of bp
What drugs reduce intravascular volume
Diuretics - thiazides
Which antihypertensives reduce sympathetic tone
Alpha and BB; central acting agents
Which antihypertensives relax peripheral arteries
Ca-channel blockers
Which antihypertensives block neuroendocrine mediators of bp
ACEi
ARBs
Renin inhibitors
Examples of ACEi
Captopril
Enalapril
Ramipril
What does aldosterone release cause
Salt and water retention
Increasing intravascular volume
When to use ACEi
1st line HTN except for selected pt (<55 or African descent)
1st line in pervious heart failure or cardiac damage
Safety and suitability of ACEi
Drops BP (first dose) Worsens renal function Retains K
Mitigating ACEi dropping BP
Give small test dose
Check pt not too volume depleted
ACEi and renal function
Check U&E’s before and one week after
ACEi and K retention
Stops K supplement or K-sparing diuretic
Mechanism of ACEi
Inhibits angiotensin converting enzyme
Reducing generation of angiotensin II and thus aldosterone –> Na and water aren’t reabsorbed as much
ARBs
Angiotensin II receptor blockers
Similar to ACEi
What happens when AT1 receptors bind to angiotensin II
Vasoconstriction
Increased sympathetic stimulation
Increased ADH secretion
Examples of ARBs
Losartan
Irbesartan
Which pts take ARBs
Pts who can’t tolerate ACEi
Types of diuretics
Loop
Thiazides
Thiazides-like
K sparing
What are Loop diuretics v efficient for
Heart failure
Examples of loop diuretics
Furosemide
Bumetanide
Na excretion in loop diuretics
Up to 25% Na load excreted, can be used in renal impairment
How long do loop diuretics take to work
30 mins (IV) to 1 hr (rapid action)
Administration of loop diuretics
po OD in the morning
Can be used orally for long-term control
Thiziade diuretiucs
Bendroflumethiazide for HTN
Thiazide-like diuretics and Na excretion
5-10% Na load excreted
Ineffective if eGFR is <30 and should be avoided
Example of a thiazide-like diuretic
Indapamide
K sparing diuretics and Na excretion
<5% Na load excreted
Used together with more effective diuretics
Example of K sparing diuretics
Spironolactone - blocks aldosterone for heart failure and HTN
Diuretics safety
Hypovalemia, dehydration and hypotension
Electrolyte imbalance
Electrolyte imbalance on diuretics
Low K, Na
High urea - due to dehydration
Check electrolytes regularly if on high dose
Monitoring for diuretics
BP, urine output or body wt
4th line drugs for resistant HTN
BB Alpha-blockers Renin inhibitors Central sympathetic outflow K channel opener
Renin inhibitors - reistant HTN
Aliskiren
Central sympathetic outflow - resistant HTN
Clonidine
Methyldopa
K channel opener - resistant HTN
Minoxidil
Antihypertensive algorithm
Aged <55 yrs - start w/ ACEi/ARB
Aged >55yrs or Afro/carribean - CCB
ACEi/ARB + CCB
ACEi/ARB + CCB + thiazide-like diuretic
4th line drugs
What is the early part of P wave due to
RA depolarisation
What is middle part of p wave due to
RA and LA depolarisation
What is late part of p wave due to
LA depolarisation
Normal height of p wave
<2.5mm (squares) tall
What can cause tall p waves
RA abnormality - RA is overloaded, usually associated with enlargement of RA
In which leads can you see RA abnormalities in best
Tall, peaked P waves, normal duration
Inferior leads - II, III, aVF
In which condns do we see tall p waves
Pulmonary disease
Congenital heart disease
Normal width of p wave
<3mm wide
What can cause broad p waves
LA abnormality
In which leads can you see LA abnormality best in
Limb leads
In what condns do we see broad p waves
Valvular heart disease - left side
Hypertensive heart disease
Cardiomyopathies
CAD
When might p waves be intermittently absent
Sinus arrest
SA exit block
Sinus arrest
SAN fails to generate impulse
SA exit block
Impulse fails to leave SAN
What can cause a short PR interval
Low atrial pacemaker
Accessory pathway
Why would a low atrial pacemaker cause a short PR interval
Lies closer to AVN so distance is shorter
Why would an accessory pathway cause a short PR interval
The extra connection may conduct more quickly than AVN e.g. Wolf-Parkinson-White
What can cause a long PR interval
AV block
Can be 1st, 2nd or 3rd degree
1st degree AV block
Prolonged PR interval as impulses travel slower from atria
2nd degree AV block
Leads to intermittent failure off the atrial impulse to conduct to ventricles (some impulses make it through AVN)
3rd degree AV block
None of the atrial impulses travel to ventricles
Possible abnormalities of QRS complex
Too wide
Too big (hypertrophy)
Pathological Q waves (after MI)
Supraventricular origin of wide QRS complex
Aberrant conduction: Bundle branch block Brugada pattern 'Toxic' conduction delay Preexcitation
Ventricular origin of wide QRS complex
Ventricular ectopic beat
Ventricular paced beat
Wolf-Parkinson-White on an ECG
Short PR interval
Wide QRS complex
Delta wave
Normal ventricular depolarisation
Phase 1 - septum depolarises L –> R
Phase 2 - both ventricles depolarise simultaneously (but LV is electrically predominant)
Why is LV electrically predominant
LV has more muscle mass so depolarisation move sin that direction (causes -ve deflection in V1 and +ve in V6)
As depolarisation continues, deflections get more pronounced until both ventricles are fully depolarised and everything goes back to baseline
Features of bundle branch block on ECG
Broad QRS complex
Unique QRS shape - 3mm or more
Repolarisation abnormalities in leads over affected area
Repolarisation abnormalities seen on ECG
ST depression
T wave inversion
Causes of bundle branch block
CAD HTN Valve disease Cardiomyopathy Post cardiac surgery
Ventricular depolarisation in RBBB
Phase 1 - septum depolarises normally
Phase 2 - ventricles depolarise sequentially, RV is delayed
RBBB appearance on ECG
MaRRoW
M in V1
W in V6
Why is RBBB more common than LBBB
R bundle is easier to become damaged
Ventricular depolarisation in LBBB
Phase 1 - septum depolarises abnormally (R –> L)
Phase 2 - ventricles depolarise sequentially, LV is delayed
LBBB appearance on ECG
WiLLiaM
W in V1
M in V6
Brugada pattern
RBBB-like in appearance in R precordial leads (V1 - 3) w/ coved ST elevation (shark fin)
What is Brugada pattern caused by
Abnormal RV depolarisation
Epidemiology of Brugada pattern
Rare
Inherited
M > F
How might pts with Brugada syndrome present
With life threatening ventricular arrhythmias —> syncope, seizures & cardiac arrest
ECG changes in hyperkaleamia
T waves become tall and peaks
PR interval prolongs and P wave becomes smaller (may disappear)
QRS complexes progressively widen –> sinusoidal appearance –> asystole
How does hypertrophy affect QRS complex
Produces bigger complexes - simply more +ve and more -ve charges
Depolarisation in RV hypertrophy
Opposite to normal depolarisation
Commonest cause of RV hypertrophy
Pulmonary HTN
Congenital heart disease e.g. pulmonary stenosis
Chronic lung diseases
What is RV hypertrophy associated with
R axis deviation and repolarisation abnormalities in leads V1 - V4
RV hypertrophy appearance on ECG
Large R waves in V1, V2
Deep S waves in V5, V6
Depolarisation in LV hypertrophy
Exaggeration of normal depolarisation
LV hypertrophy appearance on ECG
Axis is usually normal but can be L
Abnormally deep S wave in V1
Abnormally tall R wave in V6
May also see depolarisation abnormalities
Normal Q wave appearance
Short (1mm max) and small (<25% of total QRS height)
Pathologic Q waves appearance
Wide and/or deep
What can cause ST elevation
STEMI - regional ST elevation (V1 - V4) Pericarditis - widespread ST elevation BBB High take off LV aneurysms
Causes of ST depression
Ischaemia
Posterior MI
Repolarisation abnormalities
In which leads would you see an inferior MI
II
III
aVF
In which leads would you see a lateral MI
I
aVL
V5
V6
In which leads would you see an anterior MI
V1 - V6
ECG dx of STEMI
ST elevation >1mm in >2 related leads
However, LBBB can hide ST changes in MI and certain areas aren’t seen well by standard ECG
ECG appearance in unstable angina/ NSTEMI
A/c changes - T wave inversion, ST depression
Normal T wave size
<50% size of preceding QRS
In which leads are T wave normally inverted in
aVR
V1
Causes of a tall T wave
ACS - hyperacute stage of MI
Hyperkalaemia
Causes of inverted T wave
May be normal Myocardial disease (ischaemia, infarction, cardiomyopathy) Ventricular hypertrophy BBB CVA
Normal range for QT interval
0.33 to 0.44 seconds (up to 0.45 in women)
What are both long and short QT intervals associated with
Increased risk of ventricular arrhythmias —> syncope and sudden death
How do people get long or short QT intervals
Inherited
Acquired due to drugs (esp antiarrhythmic) or electrolyte disturbance e.g. K, mg, Ca
Adjusting QT interval for HR
QTc = QT/ square root of RR interval
Easy way to check for prolonged QT interval
Look at where T wave ends - if its beyond halfway point of RR interval then it is prolonged
Systematic ECG checklist
Basics - name, pt identifier, date, speed, calibration Rate Rhythm Axis Waves Intervals
Determining sinus rhythm from rhythm strip
Ask:
Regular or irregular?
P wave before QRS?
Clinical evaluation for valve disease pt
Severity of stenosis Degree of regurgitation Ventricular size and function Atrial size Estimated pulmonary artery pressure
Key ix for valve disease
ECG
Symptoms of valve disease
SOB and HF
Fatigue
Palpitations/AF - spp mitral valve disease
Spp symptoms seen in aortic stenosis
Angina
Syncope (particularly on exercise)
Principles of valve disease mx
Limited benefit from meds
Surgery is usually indicated in severe disease
Medical therapy for AF
Prevent embolism - anticoagulants w/ vit K anatag or DOAC
Rate control - BB and digoxin
Do DOACs work in pts with prosthetic valves
No
Surgical/ interventional options for valve disease
Valvotomy
Repair valve surgically
Valve replacement
How can a valvotomy be done
Surgical
Percutaneous w/ a balloon
Different valves used in valve replacement
Mechanical valves
Tissue valve - heterograft, homograft
TAVI
TAVI
Transcatheter aortic valve implantation
Using mechanical valves as replacement
Durable but anticoags needed
Using tissue valves as replacement
Last less time (15 yrs approx) and less in the young
No anticoags needed unless AF
Repairing valves
Best if it can be done - only mitral
Long lasting, no anticoags, better function
Factors influencing risk of valve surgery
Age
General physical state and comorbidities
Damage already done to heart - particularly LV in c/c cases
Renal function
Cerebral and carotid arteries - risk of CVA
What are the best valves to repair
Those with leaflet prolapse and chordal rupture
Surgeons can repair chord that support valve and repair valve cusps
Use of TAVI
Safe
Suitable for elderly pts w/ contraindications to surgery
Durability unknown
Avoid long-term anticoagulant
Infective endocarditis
Infection of inner lining of heart
Usually affects valves
Why is IE difficult to dx
Masquerades as many other condns
Rare but 100% fatal w/out abx
Examples of organisms causing IE
Staph A - very a/c onset
Strep Viridans - slow onset
Strep faecalalis (enterococcus)
Sites attacked in IE
Prosthetic valves
Previously abnormal valves e.g. MR, AR, AS
High virulence bacteria e.g. staph A attack normal valves
Vegetation
Collection of organisms and thrombus
Embolisation risk
IE clinical px
Very variable and diff to dx
Depends of organisms/ underlying cardiac defect
Signs and symptoms of IE
Fever, night sweats
Roth spots
Osler nodes
Murmur
Janeway lesions
Anaemia
Nail-bed (splinter) haemorrhage
Emboli
Symptoms seen in c/c IE
Enlarged spleen
Clubbing
Pigmentation
Glomerulonephritis
Major complications of IE
Systemic embolisation - vegetation breaking off
Heart failure - damage to valve
Cerebrovascular complications of IE
Embolism
Infected aneurysm - mycotic aneurysm
(May rupture and cause major cerebral damage)
Diagnosing endocarditis
Clinical suspicion Blood cultures - do before abx High infl markers Low grade anaemia and mildly raised WBC Echo to image vegetations, valve damage, abcess
Types of echocardiogram
Transthoracic
Transoesophageal - better views for IE, detects accesses, vegetations and valve damage
Mycotic aneurysm
Dilation of artery wall due to damage to vessel wall following infection
Why is endocarditis so deadly
Antibody antigen complexes damage small blood vessels
Direct damage to heart/ valves due top vegetations or abcesses
Prosthetic endocarditis
V serious complication
May affect any intracardiac device
Makes valves come lose/ detach
Nearly always needs replacement
Mx of endocarditis
Abx - usually IV for 4-6 wks (50% need surgery as well)
MDT approach - cardiology/ microbiology/ cardiac surgery
When should surgery be considered urgently in endocarditis pts
Haemodynamic deterioration due to damage caused by infection
Infection not responding to abx
Abcesses seen on echo
PND
Paroxysmal nocturnal dyspnoea
Waking up gasping for air after 1-2 hrs of sleep
Orthopnoea
Breathlessness lying down
Seen in heart failure
Determining whether murmur is systolic or diastolic
Feel radial pulse while listening - pulse syncs with 1st heart sound
Examples of systolic murmurs
AS
MR
Pulmonary stenosis
Examples of diastolic murmurs
AR
MS
Tricuspid stenosis
Pulmonary regurgitation
Auscultatory areas of heart
Aortic - 2nd IC space (R)
Pulmonary - 2nd IC space (L)
Tricuspid - 4th IC space (L)
Mitral - 5th IC space (L)
Differentiating between AS and MR murmurs
AS radiates to neck and MR radiates to axilla
AS is pan systolic murmur
MR is crescendo-decrescendo
Divisions of left bundle
Anterior fascicle
Posterior facsicle
In which leads can we see the L anterior fascicle
I
aVL
In which leads can we see L posterior fascicle
II
III
aVF
Px of a/c symptomatic MR pts
Severe dyspnoea
Pulmonary oedema
Hypotension
Contraindications of nitrates
Aortic or mitral stenosis
Pericarditis
HCM
Hypotensive condns
Contraindications for BB
Asthmatics
Hypotension
Unstable cardiac failure
Contraindications for CCB
A/c anginal attacks
Cardiogenic shock
Significant aortic stenosis
UA within 1/12 of MI
Interacts w/ BB
Adverse effects of ACEi
Cough - increase in bradykinin Hypotension Angiodema Diarrhoea Muscle pains, skin reactions
Contraindications of ARBs
Pregnancy
Severe renal stenosis
Aortic stenosis
Adverse effects of ARBs
Cough - not as common Hypotension Hyperkalemia Nausea, vomiting Angiodema
Contraindications of loop diuretics
Severe renal impairment
Treatment with cardiac glycoside
Contraindications of thiazides
Electrolytic disturbances
Cardiac glycosides
Contraindications of K sparing diuretics
ACEi
How may pts with tricuspid stenosis present
Hepatomegaly and distended abdomen due to passive vein congestion
Initial ix for heart murmurs
Echo
CXR
ECG
Qualities of benign murmurs
Soft Humming Position-dependent Usually systolic Pt otherwise healthy
Janeway lesions
Painless spots on palms/soles of feet
Oslers nodes
Painful nodules in pulp of fingers/ toes
What is a low volume pulse usually caused by
Low output state (dehydration, heart failure)
Aortic stenosis
When is upstroke delayed
Aortic stenosis
What physiological reasons cause a high volume pulse
Advanced age
High output states (exercise, pregnancy)
What pathological reasons cause high volume pulse
HTN
Aortic regurgitation
High output states (fever, anaemia, thyrotoxicosis)
Chest lead placement for ECG
V1 - 4th intercostal space at LSE
V2 - 4th intercostal space at RSE
V3 - Midway between V2 & V4
V4 - 5th IC space in mid clavicular line
V5 - same level at V4 but more left (—> axillary)
V6 - Mid axillary line (same level as V4 & V5)
Limb lead placement
Red - ulnar styloid process of R arm
Yellow - ulnar styloid process of L arm
Green - malleolus of L leg
Black - malleolus of R leg
Which murmur is best heard in expiration with th eats rolled onto their left
Mitral stenosis
Which type of echo is best
Transoesphageal
Conventional echo
Transthroacic
Why might pts get pan systolic murmurs post-MI
Damage to papillary muscles causes MR
May have ventricular septal defect
Myxoma
Benign tumour usually found in atria
Main ix for AS
Cardiac echo
Coronary angio
What is usually seen in severe AS
LV hypertrophy
CXR in AS
May still appear normal in severe cases as LV is hypertrophied rather than dilated
Causes of increased JVP
Congestive or R heart failure
Tricuspid regurg
Iatrogenic volume overload
Waveforms of JVP
a wave - atrial contraction
v wave - ventricular contraction
JVP vs carotid pulse
2 peaks vs 1 peak
JVP falls on inspiration
JVP rises with hepatojugular reflux
What could high CRT be a sign of
Low CO
When is the volume of the carotid pulse high
Regurgitation
When is the volume of the carotid pulse reduce
Those with low CO
Conditions changing the character of carotid pulse
AS - slow to rise
AR - rapid upstroke and downstroke
Which murmurs are heard best with the pt lying on their left side
Mitral or triscupid murmurs
In which positions are aortic murmurs heard best
Sitting up
Which murmurs are louder in inspiration
Right sided - M or P
Which murmurs are louder on expiration
Left sided murmurs - A or T
Describing heart murmurs
Timing - sys or diastole
Location
Radiation
Manoeuvres
Pitch
Intensity
What is the main trigger for RAAS
Decreased blood flow to renal arteries
Can be initiated in a/c haemorrhage
