Cardiology Flashcards
JVP - a wave Cause? Absent? Large? Cannon?
Cause = Atrial contraction Absent = AF Large = TS, R heart failure, pulmonary HTN Cannon = AV dissociation (atrial flutter/tachycardia, complete heart block, VT)
JVP - v wave
Cause?
Giant?
Cause = passive atrial filling against closed tricuspid Giant = TR
JVP - x descent
Cause?
Steep?
Cause = Downward heart movement with ventricular contraction --> atrial stretch Steep = constriction (steep x & y) or tamponade (steep x only)
JVP - y descent
Cause?
Steep?
Slow?
Cause = Tricuspid opening --> passive blood movement into ventricle Steep = Cardiac constriction Slow = TS
Raised JVP
Normal waveform?
Raise on inspiration & drop on expiration?
Loss of normal pulsation?
Normal = HF, overload, severe bradycardia Kussmaul's = Failure of R heart to inc. in size for venous return (constriction, pericardial effusion, tamponade) Loss = SVC syndrome
Causes of loud S1
Open mitral leaflets at end of ventricular diastole which are shut forcefully on systole. Occurs when:
- rapid flow at end of diastole e.g. MR, short diastole with tachycardia, L to R shunt
- Short PR = open valve at time of ventricular contraction
Causes: AF, tachycardia, MS, premature atrial beat
Mitral stenosis Definition? Causes? Features (auscultation, CXR)? Associated rhythm? Management?
Valve area under 2cm^2 (severe <1cm) on echo
Causes: RHEUMATIC FEVER. Also: mucopolysaccharidosis, carcinoid, SLE
Auscultation: mid-late diastolic murmur, opening snap, loud S1
CXR: LA/RV enlargement, subcarinal angle >90 degrees
Associated = AF
Mx = balloon valvuloplasty in suitable cases
Mitral Regurgitation
Causes?
Signs?
COMPLETE THIS CARD
Causes = prolapse, myxomatous degeneration, ischaemic papillary muscle rupture, congenital, rheumatic HD, enddocarditis
Functional (caused by annulus stretch secondary to dilation)
Signs
- Pansystolic murmur
- Soft S1 (incomplete valve closure)
Cardioversion in AF Types? When? AF onset <48h? AF onset >48h?
Electrical - DC cardioversion timed to the R wave
pharmacology - amiodarone if structural heart disease, flecainide/amiodarone without structural heart disease
When:
- Electrical as an emergency when haemodynamically unstable
- Electrical or pharmacological as an elective when rhythm control preferred
<48h
may electrical cardiovert. heparinise before. stroke risk factors = lifelong anticoagulation. Following electrical if onset definitely <48h then anticoagulation can be stopped
> 48h
Electrical preferred
Anticoagulation for at least 3/52 before OR perform TOE to exclude thrombus is L atrial appendage (they can then be heparinised and cardioverted)
High failure risk = 4/52 amiodarone/sotalol prior
Following cardioversion, anticoagulate for at least 4 weeks
Infective endocarditis aetiology
1) Most common?
2) Associated with poor dental hygiene/post procedure?
3) Most common following prosthetic valve surgery?
4) Associated with colorectal cancer?
5) culture negative?
1) Stapylococcus aureus
2) Stapylococcus mitis/sanguinis
3) Coagulase-negative Stapylococci e.g. epidermidis
4) Stapylococcus bovis
5) Prev Abx, Bartonella, Brucell, Coxiella burnetti, HACEK
Hypertension management Step 1? Step 2? Step 3? Step 4?
1:
<55/T2DM = ACE-I/ARB
>55 + no T2DM/african ethnicity = Ca blocker
2:
Add in other step 1 or thiazide diuretic
3:
ACE-I/ARB + Ca blocker + thiazide diuretic
4:
K <4.5 = add spiro
K >4.5 = add alpha/beta blocker
Uncontrolled with 4 drugs = specialist review
Tricuspid regurgitation
Signs?
COMPLETE
Signs: pan-systolic murmur, prominent V wave, pulsatile hepatomegaly, L parasternal heave
Prolonged PR interval
Definition?
Causes?
Duration >200ms
Causes: MILD RASH Myotica dystrophica IHD Lyme Digoxin toxicity Rheumatic fever Aortic abscess Sarcoidosis Hypokalemia
VTE treatment
Agent of choice? In renal impairment?
Length of anticoagulation?
1st line = apixaban/rivaroxaban
2nd = LMWH followed by dabigatran/edoxaban/wafarin
Severe renal impairment = LMWH/heparin followed by warfarin
NB antiphospholipid syndrome = LMWH followed by warfarin
Length
- All Pts at least 3 months
- Cancer Pts = 3-6 months
- Provoked VTE = ?stop after 3 months
- Unprovoked = ?continue for 6 months
Statins
Indications & recommended doses?
Mechanism?
Adverse effects?
Indications
- Established CVD
- 10-year cardiovascular risk >= 10% (inc. Pts with T2DM)
- T1DM diagnosed > 10 years ago/aged > 40/have established nephropathy
Primary prevention = 20mg atorvastatin
Secondary prevention = 80mg atorvastatin
Inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis.
Adverse
- Myopathy (Risk factors: thin old diabetic lady)
- Deranged LFTs. Stop if persistently >3x upper limit
- ?inc. risk of intracerebral haemorrhage. Avoid in Pts with Hx of of intracerebral haemorrhage
MI Complications?
- Cardiac arrest
- Cardiogenic shock
- Chronic HF
- Tachyarrythmia
- Bradyarrythmia - AV block more common following inferior infarction
- Pericarditis - Common in 48h following transmural MI. Dressler’s syndrome tends to occur 2-6/52 after ?due to autoimmune reaction to antigens as myocardium recovers
- LV aneurysm - tends to be associated with persistent ST elevation + LV failure. Thrombus may form in aneurysm
- LV rupture - tends to occur after 1-2/52. Presents with acute failure + tamponade
- VSD - usually occurs in the first week. Features: acute heart failure associated with a pan-systolic murmur. mitral regurgitation presents in a similar way. Urgent surgery needed.
- Acute MR - More common with infero-posterior infarction, may be due to ischaemia/rupture of papillary muscle. Acute hypotension + pulmonary oedema may occur. Early-to-mid systolic murmur typically heard. Treated with vasodilator therapy, often require emergency surgical repair.
ECG coronary territories
V1-V4?
II, III, aVF?
I, aVL +/- V5-6?
V1-V4 = anteroseptal = LAD
II, III, aVF = inferior = R coronary
I, aVL +/- V5-6 = lateral = left circumflex
Components of CHA2DS2-VASc?
C - Congestive HF H - HTN A2 - age >75 (2), age 65-75 (1) D - DM S2 - prev. stroke V - vascular disease S - sex
Ventricular tachycardia
Main types?
Management?
Monomorphic - commonly caused by MI
Polymorphic - Includes torsades de pointes (caused by prolonged QT)
Management
- Adverse signs (BP<90, chest pain, HF) = electrical cardioversion. Otherwise drugs
- Drugs: amiodarone, lidocaine (caution in severe LV impairmen), procainamide.
- DO NOT use verapamil (acts only on nodal tissue, inc. risk of VF)
Causes of prolonged QT
GENRALLY RELATED TO BLOCKAGE/LOSS OF K CHANNEL FUNCTION
Congenital
- Jerval-Lange-Nielson syndrome (associated with deafness. Cause = K channel defect)
- Romano-Ward syndrome
Drugs
- Amiodarone, TCAs, fluoxetine, chloroquine, erythromycin
Electrolyte abnormalities
- Hypo K/Ca/Mg
Other
- Hypothermia, MI, myocarditis, subarach haemorrhage
Pulmonary HTN management
Which test to perform?
Drug therapy?
Test = Acute vasodilator testing
+ve vasodilator response = Ca channel blockers
- ve vasodilator response:
- Prostacycline analogues (e.g. iloprost)
- Endothelin receptor antagonists (e.g. bosentan, ambrisentan)
- Phosphodiesterase inhibitors (e.g. sildefanil)
Indications for implantable cardiac defibrillator?
Long QT HOCM Prev. arrest due to VT/VF Brugada syndrome previous myocardial infarction with non-sustained VT on 24 hr monitoring, inducible VT on electrophysiology testing and ejection fraction < 35%
LBBB
Causes?
Causes: MI, HTN, AS, cardiomyopathy, idiopathic fibrosis, digoxin toxicity, hyperkalaemia
ECG changes in hypokalaemia?
U waves small or absent T waves (occasionally inversion) prolong PR interval ST depression long QT
U have no Pot and no T, but a long PR and a long QT
Patent ductus arteriosus
Definition?
Features?
Treatment?
Connection usually between pulmonary trunk and descending aorta
Features
- Cont. machinery like murmur
- L subclavian thrill
- large volume, bounding, collapsing pulse
- wide pulse pressure
- heaving apex beat
- Late: cyanosis in lower extremities
Mx
indomethacin/ibuprofen (inhibits prostaglandin synthesis)
if associated with another congenital defect amenable to surgery then prostaglandin E1 to keep the duct open until after repair
Multifocal atrial tachycardia
Definition?
Management?
Irregular rhythm arising from at least three atrial sites (morphologically distinct P waves)
Management
- Correct hypoxia/electrolyte disturbance
- 1st line = rate limiting Ca blockers (e.g. verapamil)
- Not useful: cardioversion, digoxin
Peri-arrest: Bradycardia
Adverse signs?
Management?
Asystole risk factors?
Shock, syncope, myocardial ischaemia, HF
Mx
- 1st line: Atropine 500mcg IV, repeated up to 6x
- Transcutaneous pacing
- Adrenaline infusion
- ?transvenous pacing if no response to above or risk factors for asystole
Asystole RFs
- Complete block with broad QRS
- Recent asystole
- Mobitz type II AV block
- Ventricular pause >3s
Ebstein’s anomaly
Definition?
Associations?
Features?
Congenital. Low tricuspid insertion –> large atrium, small ventricle
Associations: WPW, PFO/ASD
Features: Tricuspid regurg, prominent ‘a’ wave, hepatomegaly, RBBB
Ventricular septal defect
Aetiology?
Complications?
Aetiology - chromosomal disorders 9e.g. Down’s), congenital infections, acquired (e.g. post MI)
Complications
- AR (poorly supported R coronary cusp –> prolapse)
- IE
- R heart failure
- Pulmonary HTN
- Eisenmenger’s complex (prolonged pulm HTN from L to R shunt –> R vent hypertrophy + inc pressure –> exceeding LV pressure causing reversal of flow –> cyanosis)
Brugada syndrome Definition? Cause? Criteria? Management?
ECG abnormality with high incidence of sudden cardiac death in structurally normal hearts
Cause: mutation in cardiac Na gene. Tends to be autosomal dominant
Criteria for type 1 (BOTH ECG & CLINICAL)
- ECG: coved ST elevation >2mm in >1 V1-3 followed by -ve T wave
- Clinical: VF/polymorphic VT, coved ECG in family, FHx sudden cardiac death, syncope, nocturnal agonal respiration, inducible VT
Mx = ICD
Atrial fibrillation: rate & rhythm control
- When to not offer rate control?
- Medication choice for rate?
- Medication choice for rhythm?
- Catheter ablation: anticoagulation, complications?
- Reversible cause, HF caused by AF, onset <48h, flutter suitable for ablation
- 1st line = beta-blocker.
Digoxin if limited physical exercise (limited rate control during exercise) or other options ruled out
Avoid Ca blockers in HFrEF due to -ve inotropic effect - beta-blockers, dronedarone, amiodarone (esp. if co-existing HF), flecainide
- Anticoag: 4/52 before. Ablation does not reduce stroke risk even in sinus so Pts require anticoag based on CHADVASC score (0 = 2/12, >1 = longterm)
Complications: cardiac tamponade, stroke, pulmonary vein stenosis
Angina medical management
Prophylaxis?
Avoiding nitrate tolerance?
All Pts on aspirin & statin
SL GTN to abort attacks
Prophylaxis (improve perfusion/reduce metabolic demand)
1st line: beta blockers, Ca antagonists
CA antag monotherapy = verapamil/diltiazem (rate limiting)
If used with BB then long-acting dihydropyridine
NB: beta blocker + verapamil = complete heart block risk
2nd line: long-acting nitrate, ivabradine, nicorandil, ranolazine
? 3 drugs If uncontrolled with 2 drugs + awaiting revascularisation/revasc not appropriate
Nitrate tolerance = asymmetric ISMN dosing interval to maintain nitrate free period
Broad complex tachycardia
Features suggestive of VT rather than SVT with abnormal conduction?
Suggestive of VT:
- Absence of LBBB/RBBB
- Extreme axis deviation
- Very borad complex (>160ms)
- AV dissociation
- Capture beat (SAN “captures” ventricles in the midst of AV dissociation –> normal QRS)
- Fusion beat (when a sinus and ventricular beat coincide to produce a hybrid complex)
- Positive/negative concordance in precordial leads
- Clinical: IHD, structural heart disease, Hx MI, FHx sudden cardiac death
- marked L axis deviation
- Hx of IHD
- QRS > 160ms
- AV dissociation
Use Brugada algorithm Suggestive of VT: - Absent RS in precordial leads - RS interval >100ms in 1 lead - AV dissociation
High INR
- Major bleeding
- INR >8 minor bleeding
- INR >8 no bleeding
- INR 5-8 minor bleeding
- INR 5-8 no bleeding
- Stop warfarin, IV vit K 5mg, PCC (FFP if unavailable)
- Stop warfarin, IV vit K 1-3mg. Start warfarin when INR <5
- Stop warfarin, PO vit K 1-5mg. Start warfarin when INR <5
- Stop warfarin, IV vit K 1-3mg. Start warfarin when INR <5
- Withhold 1/2 doses. Reduce maintenance dose
Wolf-Parkinson-White Definition? ECG features? Management? Drugs to avoid?
Accessory pathway between atria/ventricles –> AV re-entry tachy
ECG: short PR, wide QRS with slurred upstroke (delta wave), R axis deviation (L side pathway), L axis deviation (R side pathway)
Mx
- Definitive: ablation
- Medical: sotalol (UNLESS AF: prolonging AV refractory –> inc. accessory pathway transmission –> inc. ventricular rate –> VF), amiodarone, flecainide
AVOID: verapamil, digoxin. May precipitate VF/VT
MI secondary prevention
Drugs?
Another drug if signs of HF?
Drugs: DAPT, ACE-I, beta blocker, statin
Aldosterone antagonist e.g. eplerenone
Arrythmogenic right ventricular cardiomyopathy
Definition?
Investigations?
Management?
Inherited (autosomal dominant, variable expression), RV myocardium replaced with fatty & fibrofatty tissue
Ix:
- ECG: V1-3 TWI, epsilon wave (notch in QRS)
- Echo: RV enlarged, hypokinetic/thin wall
- MRI
Mx
- Drugs: sotalol
- Catheter ablation
- ICD
Infective endocarditis
Indications for surgery?
ECG change to monitor?
Severe CHF
Overwhelming sepsis/Recurrent emboli despite Abx
Aortic abscess
Pregnancy
ECG: PR prolongation, indicated aortic abscess
4th heart sound
Cause?
Seen in which conditions?
Atrial contraction against a stiff ventricle. Occurs in late diastole. Coincides with P wave on ECG (PS4)
AS, HOCM, HTN
Atrial septal defect
Features generally?
Ostium primum features?
Ostium secundum features?
Ejection systolic murmur, fixed split S2
Primum
associated with abnormal AV valves
ECG: RBBB with LAD, prolonged PR interval
Secundum
associated with Holt-Oram syndrome (tri-phalangeal thumbs)
ECG: RBBB with RAD
“something not RIGHT with the thumb”
Therapy required after insertion of a drug-eluting stent?
12 months of DAPT
Dilated cardiomyopathy
Associated valve abnormality?
Mitral regurg
Exercise tolerance test
Indications to stop?
23 rule
2mm ST elevation 3mm ST depression SBP >230 SBP fall by >20 HR >20% of starting
Investigations of stable anginal chest pain?
1st line: CT coronary angiography
2nd line: non-invasive functional imaging (?reversible myocardial ischaemia)
3rd line: Invasive coronary angiography
Second heart sound Loud? Soft? Fixed split? Reversed split?
Loud = HTN
Soft = AS
Fixed split = ASD
Reversed split = LBBB
Pregnancy and hypertension
BP changes during pregnancy?
Gestational hypertension definition?
pre-eclampsia definition?
BP falls in first half of pregnancy before rising to pro-pregnancy levels before term
Gestational HTN
- HTN in second half of pregnancy (>20/40)
- SBP >140/DBP>90 or rise of SBP>30/DBP>15
Pre-eclampsia
- Pregnancy induced HTN + proteinuria
- Occurs after 20 weeks
ECG changes in hypothermia?
J wave (hump at end of ORS)
Irregular rhythm (long QT, arrythmias)
Bradycardia
First/other degree heart blocks
“Jesus, It’s Bloody Freezing”
Pulmonary embolism: indication for thrombolysis?
Massive PE + haemodynamic instability
Cyanotic congenital heart disease causes?
5Ts: Tetralogy of Fallot Transposition of great arteries Trunctus arteriosus Total anomalous pulmonary venous return Tricuspid valve abnormalities & hypoplastic R heart syndrome
Ivabradine
Indications?
Mechanism?
Common side effect?
Indications: symptomatic angina relief (HR >70), CHF (HR >75)
Mechanism
If channel inhibition (funny channel), found in SAN, triggered by hyperpolarisation, responsible for spontaneous myocyte activity.
Inhibition –> delayed depolarisation –> selectively slowed HR.
SE: visual disturbance e.g. bright spots
Valve replacement
Types & who they are given to?
Disadvantages?
Anticoagulation?
Bioprosthetic - older Pts (>65/70) due to deterioration over time
Mechanical
Bio - degrade over time
Mech - Inc. thrombosis risk
Bio - Long term anticoag not usually needed ?3/12 warfarin depending on patient factor
Mech - Long term. Warfarin > DOAC. INR 3 for aortic, 3.5 for mitral
Adult advanced life support Reversible causes? Defibrillation principles? Adrenaline principles? Amiodarone principles?
4 ‘H’s - Hypoxia, Hypovolaemia, Hypokalaemia/calcaemia/glycaemia (other metabolic causes), Hypothermia
4 ‘T’s - Thrombosis, Tension pneumothorax, Tamponade, Toxins
Defibrilation
- SIngle shock for VF/VT then 2 mins CPR
- If on monitored Pt, can give up to 3 shocks then CPR
Adrenaine
- 1mg ASAP for non-shockable
- VT/VF arrest: 1mg after 3rd shock then repeat every 3-5 mins
Amiodarone
- VT/VF: 300mg after 3 shocks. Further 150mg after 5 shocks
- Lidocaine as an alternative
