Cardiology Flashcards
how would you manage a patient with mitral regurgitation?
asymptomatic
- monitoring with serial echocardiography
managing AF
- rate control: digoxin, beta blockers, calcium channel blockers
- rhythm control: amiodarone, sotalol or flecanide
- anticoagulation: DOAC or warfarin
managing heart failure
- aldosterone antagonist, beta blocker and ACE-I/ARB
- diuretics for symptom control
- if symptomatic on optimum medical therapy then consider mitral valve replacement
what are the common complications of prosthetic heart valves?
- thromboembolism
- valve dysfunction (leakage, obstruction or dehiscence)
- haemolysis (jaundice)
- bleeding from anticoagulation
- endocarditis
what are the causes of aortic stenosis?
common
- degenerative calcification (old age)
- bicuspid aortic valve
- rheumatic heart disease
- rare
- infective endocarditis
- paget’s disease of the bone
how do you describe the pulse of aortic stenosis?
low volume and slow-rising character (carotid)
NB: do not say this if the patient also has AF because you will be lying.
‘the pulse is of variable but diminished volume’
how do you treat mitral stenosis?
medical
AF = rate control and anticoagulation
LHF = diuretics to relieve preload and pulmonary venous congestion
surgical
closed/open valvuloplasty
closed - inflate baloon between leaflets
open - push finger through valve
closed/open valve replacement
what is the main differentiating factor between aortic sclerosis and degenerative calcification leading to aortic stenosis?
stenosis = aortic outflow obstruction
signs = low volume, slow-rising pulse, LVH etc…
which valvular disease gives a malar flush?
what does this signify?
mitral stenosis
represents a low cardiac output state with pulmonary hypertension
what are roughly the indications for an aortic valve replacement in aortic stenosis?
- symptomatic
- asymptomatic, and
- having heart surgery for another reason
- severe AS with LVF
- severe AS with small valve area
- severe AS with arrythmia
- severe AS with haemodynamic compromise
what are the complications of mitral stenosis?
left atrium
- dilation
- thrombus formation
- atrial fibrillation
- ortner’s syndrome (hoarseness)
elevated left atrial pressure
- pulmonary hypertension, congestion and oedema
- right heart failure
what are the causes of mitral stenosis?
rheumatic heart disease
others (all very rare)
- carcinoid
- SLE
- rheumatoid arthritis
- mucopolysaccaridoses
how do you describe the apex beat in mitral regurgitation ?
thrusting and displaced apex beat
mitral regurg leads to left ventricular overload and subsequent cardiac remodelling, increase in ventricular dimension, which is appreciated as a displaced apex beat
what are the causes of mitral regurgitation?
-
structural
- mitral valve prolapse
- functional mitral regurgitation (LV dilitation)
- chordae tendinae rupture (post-MI)
- papillary muscle dysfucntion (post-MI)
-
infective
- rheumatic heart disease
- infective endocarditis
-
rheumatological
- SLE/Libman-Sachs disease
- connective tissue disorder (ED, Marfan)
what are the causes of chronic aortic regurgitation?
bicuspid aortic valve
hypertension
rheumatic heart disease
aortitis (takayasu, syphilitic)
connective tissue (Marfan, Ehlers-Danlos, Osteogenesis Imperfecta)
what are the causes of acute aortic regurgitation?
infective endocarditis
aortic dissection
what investigations do you want for a patient with suspected aortic stenosis?
-
ECG
- for information on conduction and structure
-
Echo
- for information on structure and function
-
CXR
- post-stenotic dilatation of the aorta
- valvular calcification
- sternal notching (seen in coarctation of the aorta, which is associated with bicuspid aortic valve)
-
coronary angiography
- to rule out atherosclerosis or narrowing as the cause of anginal symptoms
what are the factors that influence the choise of bioprosthetic valve versus mechanical valve?
- patient life expectancy is shorter than the expectancy of the valve
- recipient age >70 usually increases the life expectancy of the valve (less wear and tear)
- anticoagulation would be inappropriate for the patient
how do you describe the apex beat in aortic stenosis?
undisplaced, heaving character
what happens to the pulse pressure typically in aortic stenosis?
narrow pulse pressure in severe cases
what is the differential diagnosis for pansystolic murmur ?
- mitral regurgitation
- tricuspid regurgitation
- ventricular septal defect
what does a apex beat presystolic impulse indicate?
what other sign would be associated with this?
impulse of atrial contraction at the end of diastole against a stiffened, hypertrophied left ventricle shortly before ventricular contraction
is essentially the same thing as an S4, so always mention these together
what are the differential diagnoses for ejection systolic murmur
- aortic stenosis
- aortic sclerosis
- aortic valve replacement
- HOCM
*
what are the complications of aortic stenosis?
progressively…
- arrhythmia (AF and heart block)
- haemolysis
- left venticular failure
- pulmonary hypertension & RHF
- sudden cardiac death (if symptomatic)
what are the options for pharmacological cardioversion for new onset AF?
whne do you use which drug?
class 1c drugs (flecanide) or amiodarone
without structural abnormality/IHD = class 1c
with structural abnormality (mitral valve disease) or history of ischaemic heart disease = amiodarone
acute-onset with WPW = flecanide
what is the mechanism of action and the most common side effect of ivabradine?
when is this drug used?
MoA = inhibition of If channels at the SAN, increasing time to depolarisation and decreasing heart rate
side effects = act off-target on the If channels in the eye, giving the transient luminous phenomenon in up to 15% of patients
use = alternative therapy following aldosterone antagonists in patients with heart failure, HR >75 bpm and LVEF <35%
what medication should all patients with angina be on?
what are the following steps in managing symptoms of angina
- aspirin and statin for prevention if tolerated
- GTN for early rescue of anginal attacks
either beta-blocker or cardioselective CCB, then both as tolerated
other medication to use when either BB/CCB are not tolerated:
- isosorbide mononitrate (and other long-acting nitrates)
- ivabradine
- nicorandil
- ranolizine
how do you treat angina?
conservative
exercise, stop smoking, improve diet and diabetic control
medical
- b-blockers -atenolol or bisoprolol
- CCB - diltiazem or verapamil
-
long-acting nitrates - ISMN, GTN skin patch
- SEs - headache, hypotension and tolerance
-
alternatives
- ranolazine
- nicorandil
- ivabradine
surgical (revascularisation)
- percuteaneous coronary intervention (stenting)
- CABG
what is the difference between an MI and unstable angina?
infarction = cell death & release of cardiac enzymes
troponin rise = myocardial infarction
how do you diagnose myocardial infarction?
rise in cardiac biomarkers and any of:
- history consistent with ACS
- ECG changes consistent with infarction
- regional wall motion abnormalities on echocardiography
what blood tests should you send in ACS?
FBC
U&E
lipids, glucose and HbA1c
cardiac biomarkers
how long does dual anti-platelet therapy continue for following an MI?
at least 12 months
consider adding a PPI for gastroprotection
what medication should all patients be on following an MI?
dual antiplatelet
beta-blocker
statin
ACE-I
send for echo to assess LV, if LVEF <40% then eplerinone has proven outcome benefit long-term
what are the complications of MI?
-
immediate (<4 hours)
- tachyarrythmia
- cardiogenic shock
- exacerbation of CCF
-
early (<7 days)
- brady/tachy arrythmia
- fibrinous pericarditis (post-MI)
-
early-late (<4weeks)
- ventricular free wall rupture/tamponade
- ventricular septal defect
- mitral regurgitation (papillary muscles)
-
late (>1 month)
- dressler’s syndrome
- ventricular wall aneurysm
- systemic embolus (LA/LV mural thrombus)
what are the indications for CABG?
to improve survival
- left main stem disease
- multi-vessel (>2) disease
to improve symptoms
- angina unresponsive to medical therapy
- unstable angina
- failed PCI
what is a major and common complication of CABG?
stenosis of the graft
reduce the incidence with life-long anti-platelet
reduce the incidence with internal mammary artery graft (SE: pectoral numbness)
what is the atrial rate roughly in AF?
300-600 bpm
when can you get away without anticoagulating in AF?
acute! less than 48 hours since the onset of AF
immediate electrical cardioversion is being planned
low-risk for embolus formation.
risk factors are
- past CVA, TIA or embolus
- >75 years old
- HTN, DM
- CAD or PVD
- valvule disease or heart failure
what are some causes of AF?
cardiac - CCF, IHD, HTN, mitral valve disease
non-cardiac - electrolytes (low K+, low Mg+), alcohol, caffeine, hyperthroidism, PE and pneumonia
what are the cardioversion options for acute AF (<48 hours onset)?
- DC cardioversion
- flecanide (CI: structural heart disease or IHD)
- amiodarone
what are roughly the heart rate targets for patients on rate-control for AF?
using beta-blockers/CCB or digoxin…
<90 bpm at rest and [200 - patient age (yrs)] bpm on exertion
what are some indication for permanent pacemaker insertion?
- HEART BLOCK
- Complete AV block (Stokes–Adams attacks, asymptomatic, congenital).
- Mobitz type II AV block
- Persistent AV block after anterior MI.
- Arrhythmia
- Symptomatic bradycardias
- drug-resistant tacharrhythmia
- Heart failure (‘cardiac resynchronization therapy’)
what is the indication for cardiac resynchronisation therapy?
heart failure
LVEF <35%
broad QRS, duration >120 ms
… heart failure with the chambers firing at the wrong time. pacing them together improves overall cardiac output and reduced mortality
how do you describe the heart sounds of mitral regurgitation?
auscultation reveales a soft S1 with splitting of the second heart sound and a loud P2 (indicating pulmonary hypertension).
there was a pan-systolic murmur heard loudest over the mitral area that radiates to the axilla, heard loudest on held expiration in the left lateral position
comment on the P wave.
what is the underlying pathology?
this is P-mitrale, as evidenced by the increased duration (> 120 ms) of the P wave in lead II
this indicates left atrial enlargement, commonly due to mitral valve stenosis
comment on the P wave.
what is the underlying pathology?
this is P-pulmonale, as evidenced by the increased P-wave amplitude (>2.5 mm) in lead II
indicates right atrial enlargement, commonly due to pulmonary valve stenosis or pulmonary hypertension
what is the Austin Flint murmur and how is it different from the other murmur expected in this pathology?
Austin Flint - mid-diastolic rumble caused by mitral valve leaflets fluttering because of the regurgitant flow in AR
normal AR murmur is early diastolic as the regurgitant flow passes across the aortic valve
what is the management of aortic regurgitation?
conservative
echocardiography for monitoring every 6-12 months
medical
reduce systolic hypertension (e.g. ACE-I)
surgical
aortic valve +/- root repair, aim to prevent significant LV dysfunction
indications:
- enlarged aortic root
- enlarging LV (echo)
- worsening LV function (echo)
- worsening symptoms of CCF
what are the ECG findings of hypokalaemia?
prolonged PR
ST segment depression
prolonged QT
small/absent T waves
U waves
what are the ECG findings of hyperkalaemia?
what is the rhythm that these patients are predisposed to?
- absent P waves
- wide QRS
- tall, tended T waves
they are at danger of developing heart block, slow AF, sinusoidal pattern (pre-terminal).
eventually asystole or VF
what is the ‘new’ heart failure medication?
remember the BASICS!
always should be on
- beta-blockers
-
ACE-I/ARB
- 2nd line - hydralazine and ISMN, if cannot tolerate/comorbid renal disease
-
aldosterone antagonist (eplerenone)
- only with reduced ejection fraction
symptomatic relief
- diuretics
- loop/thiazides/loop + thiazide
extra… if you get there
-
Entresto (sacubitril/valsartan)
- angiotensin-receptor/neprilysin inhibior (ARNI)
- approved july 2015
- use instead of ACE-I
- use in NYHA II-IV
- proven morbidity/mortality/rehospitalisation rates
which medication should be avoided in heart failure?
-
NSAIDs
- cause retention of salt and water
- attenuate the effect of ACE-I and increase their likelihood to cause toxicity
-
non-vasoselective CCBs
- worsen heart failure and increase the risk of adverse events
-
antiarrhythmic drugs (apart from amiodarone)
- cardiodepressant effects
- increases the chance of arrhythmia
- worsens survivial
