Cardiology quickfire Flashcards
JVP
a) Causes of raised JVP
b) Describe the waveforms
a) Right heart failure, fluid overload, constrictive pericarditis (JVP disappears on inspiration - Kussmaul sign), cardiac tamponade, SVC obstruction (non-pulsatile)
b) Waves:
- ‘a’ wave = atrial contraction (atrial systole)
- ‘x’ descent (stage 1) = blood descending from the atria into the ventricles
- ‘c’ waves = ventricular Contraction against Closed tricuspid valve, causing bulging of tricuspid valve into atria and small rise in RA pressure
- ‘x’ descent (phase 2) - ventricles contract further, causing tricuspid valve descent, creating space for the atria to expand, causing a drop in RA pressure
- ‘v’ waves - late Ventricular systole/early diastole, Venous return into RA against closed tricuspid valve causing rise in RA pressure (incompetent tricuspid valve will cause prominent ‘v’ waves)
- ‘y’ descent - atrial emptYing - tricuspid valve opens during diastole and blood descends from RA into RV, causing drop in RA pressure
JVP abnormalities
a) Absent ‘a’ waves
b) Large ‘a’ waves
c) Extra large (Cannon) ‘a’ waves
d) Prominent ‘v’ waves (cv waves) with earlobe involvement
e) Slow ‘y’ descent
f) Steep ‘y’ descent
g) Kussmaul sign
a) AF
b) Any cause of increased resistance to atrial contraction - e.g. tricuspid stenosis, or any cause of RVH (e.g. pulmonary HTN, pulmonic stenosis)
c) AV dissociation - complete heart block, or ventricular tachycardia (Cannon = Complete HB)
d) Tricuspid regurgitation
e) Tricuspid stenosis
f) RV failure, tricuspid regurgitation, constrictive pericarditis*
*May be caused by pericarditis, cardiac surgery (e.g. CABG). May result in heart failure and pulsus paradoxus (fall in SBP >10 during inspiration - may indicating impending tamponade)
g) Paradoxical increase in JVP during inspiration - usual cause is constrictive pericarditis
Long QT
- acquired causes
- management
- Electrolyte disturbances: hypoK/Mg/Ca
- Hypothermia.
- Drugs: class III antiarrhythmics (amiodarone, sotalol), disopyramide, antipsychotics, TCAs, SSRIs, macrolides, quinolones, chloroquine/hydroxychloroquine
- beta-blockers, magnesium (in torsade), pacemakers/ICDs
Aortic stenosis - values to determine severe AS
- Valve area
- Peak velocity
- Mean pressure gradient
- Use of DSE
Valve area <1cm
Peak velocity >4
Mean pressure gradient >40
- If high gradient/velocity, severe AS can be diagnosed provided high output states are excluded
- If low-normal gradient/velocity, if valve area <1cm proceed to DSE (as below)
In patients with normal or high FLOW (i.e. normal - high stroke volume, SV>35), severe AS is unlikely unless there is a condition causing high flow (e.g. anaemia, hyperthyroidism, AV fistulae)
- In patients with low-normal gradient or velocity but valve area <1cm, you should perform DSE to distinguish between pseudo-severe AS and severe AS. This is because low-output states (e.g. severe LVSD) cause reduced valve opening.
- DSE increases CO so should increase valve area in pseudo-severe AS, whereas true severe AS has no increase in valve area during DSE
- Also, DSE shows the LV contractile reserve. If CO increases by 20% or more this indicates good reserve and better outcomes post-surgery
Long QT - genetic causes and genes implicated
Romano-Ward
- Heterozygous mutations in KCNQ1* (a potassium-channel gene) on Ch 11
- Autosomal dominant
*KCNQ1
K (potassium), C (calcium), N (sodium), Q (QT interval), 1
LQTS type 1
- associated with abnormalities in the potassium channel
- arrhythmia triggered by exercise, stress and swimming particularly
LQTS type 2
- reduced activity of potassium ions
- arrhythmia triggered by emotional stress, startling and surprise, also startling noises like alarm clocks and car horns
LQTS type 3
- deficient sodium channels
- arrhythmia tends to occur at rest or during sleep
Jervel and Lange-Nielsen Syndrome
- Autosomal recessive
- Homozygous mutation of KCNQ1 (a potassium-channel gene) on Ch 11
- Congenital bilateral sensorineural deafness and mutism
- Associated with syncope/sudden death
Andersen-Tawil
- Autosomal Dominant
- associated with micrognathia, and fused fingers
Antiarrhythmics - examples and phase of action potential they work on
- Class 1a
- Class 1b
- Class 1c
- Class II
- Class III
- Class IV
Explain the opening/closure of channels through the cardiac action potential
(NaB KiC)
Class 1
- All block sodium channels (reduce slope of phase 0 - depolarisation)
- Class 1a weak, class 1b moderate, class 1c strong
Class Ia
- quinidine, procainamide, disopyramide
Class 1b
- lidocaine, phenytoin
Class 1c
- fleicanide, propafenone
(strong ones used for AF)
Class II
- Beta-blocker - decrease slope of phase 4
Class III
- K-channel blocker (prolong phase 3 - delay repolarisation and increase refractory period)
- e.g. amiodarone, sotalol
- Risk of prolonging QT and inducing TdP
- Avoid in WPW
Class IV
- Ca-channel blocker - prolong the plateau phase (phase 2)
Phase 0 (depolarisation): sodium channels open, rapid influx of Na+
Phase 1 (partial repolarisation): K+ channels open
Phase 2 (“pla-two): Ca+ channels open (K+ still open)
Phase 3 (repolarisation): Ca+ channels close, but K+ remain open
Phase 4 (refractory period): K+ channels close
Endocarditis - causative organisms
a) Most common in native valve
b) Most common in prosthetic valve
c) Most common right sided in IVDU
a) Staph aureus, then strep viridans
b) Staph epidermidis, staph aureus
c) Staph aureus
HCM
- inheritance
- clinical signs
- ECG and ECHO findings (HOCuM)
- management
Autosomal dominant (Ch 14). Most common mutation Cardiac myosin binding protein C
Signs
- Mid systolic murmur in aortic area, worse on standing, relieved by squatting
- Displaced apex beat, loud S4
ECG
- ischaemia signs eg anterior Q waves and deep T waves
- LVH
ECHO (HOCM)
- Hypertrophy of LV 15mm or more
- Outflow obstruction with elevated flow velocity
- Compliance of LV reduced with diastolic dysfunction
- Middle (septal) symmetric hypertrophy
Management
(1) activity restriction with avoidance of volume depletion,
2) control of symptoms - BB, then verapamil, then disopyramide, then PPM, then surgical myectomy (consider if medical therapy ineffective or if LVOT gradient >50 mmHg)
(3) prevention of sudden death - will need ICD if previous cardiac arrest
4) screening of relatives
5) Determine degree of symptoms and LVOT to determine management
Early diastolic murmurs
Aortic regurgitation
Pulmonary regurgitation
LAD stenosis
Late diastolic murmurs
Mitral stenosis*
Tricuspid stenosis
Atrial myxoma
Complete heart block
*Remember ARMS for aortic regurg (early) and mitral stenosis (late)
Late systolic murmurs
MV prolapse
HCM (mid-late)
CoA
3rd line anti-anginals - MOA
- Nicorandil
- Ivabradine
- Ranolazine
- NICOrandil relaxes coronary vascular smooth muscle via K-ATPase channels and NItriC Oxide, causing increasing cyclic GMP (cGMP) levels
- Ivabradine lowers the heart rate via inhibition of the pacemaker current (If, “funny” = If-abradine), sodium-potassium channel controlling the SA node. Used in angina and also HFREF (EF <35%) where HR >70bpm
- Ranolazine blocks late sodium channels, which prevents calcium overload and reduces end-diastolic pressure. It has no effect on HR or BP
AVR
- indications
- alternatives
Indications:
- Severe high-gradient AS with symptoms*
- Asymptomatic severe AS if LVEF <50%
- Severe AS if undergoing other cardiac surgery
- Low flow AS with velocity >4 or gradient >40, if valve area <1 on DSE
*Symptomatic AS has prognosis of 2-3 years
Alternatives:
- Balloon valvuloplasty (may precede TAVI)
- TAVI
- Medical management - diuretics
Endocarditis organisms
- Most common cause of acute NVE
- Most common cause of subacute NVE and associated with dental surgery
- Most common cause of subacute PVE and associated with infected cannulas
- Associated with post GI/GU surgery
- Associated with colorectal cancer
- Associated with poor oral hygiene/dental infections
- Associated with immunosuppression, cardiac surgery or long term IV lines
- Associated with culture negative IE
- staph aureus
- strep viridans
- staph epidermidis
- enterococcus
- strep gallolyticus (bovis) —> colonoscopy
- HÁČEK
- Fungal IE - candida, aspergillus
- Coxiella burnetti (causes Q fever), bartonella (causes cat scratch fever), brucella, non-infective (SLE, malignancy)
S1 heart sound
- Causes of splitting
- Causes of soft S1
- Causes of harsh/loud S1
- Splitting occurs due to physiological early closure of mitral vs tricuspid valve, which is accentuated by inspiration, and best heard (if at all) at the tricuspid area
- Splitting is increased by RBBB
- Soft S1 caused by SEVERE mitral stenosis, obesity or prolonged PR interval (1st degree HB)
- Harsh/loud S1 caused by mild-moderate mitral stenosis, thin build, or high output state (e.g. anaemia, sepsis, thyrotoxicosis)
