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Year 4/5 Revision > Cardio > Flashcards

Cardio Flashcards

1
Q

Stable angina
* Presentation
* Types (3)
* Gold standard imaging
* Special tests (2)
* Initial management

A
  • Substernal chest pain, worsened by exertion, <20mins, relieved by rest/GTN
  • Typical (atherosclerotic), vasospastic (Prinzmeta’s)
  • CTCA
  • Stress Echo or myocardial perfusion scan
  • Treat as ACS: A-E and MONAA
  • GTN spray for acute attacks
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2
Q

Stable angina: managment
Prevention/prophylaxis: All patients should receive (2) in absence of C/I.

  1. First-line options for monotherapy (2) - example
  2. Second-line options (2)
  3. Additional drugs if on monotherapy (4)

Other
In what scenario could a third drug be added (2)
Why non-dihydropurines?
Beta-blockers cannot be prescribed concurrently with which drug and why?
How can nitrate tolerance be avoided?

A

Angina managment
1. CCB/BB
(Dilatiazem/Verapamil or Propanolol etc)
2. Try alternative or combination therapy
3. Montherapy + either:
Isosorbide mononitrate/dinitrate - long-acting nitrate
Ivabradine - HCN channel blocker
Nicorandil - K+ channel activator
Ranolazine - anti-anginal (U/k MOA)

Other
- waiting for PCI or CABG
- nonDHP have primary action on heart, DHP relax vascular smooth msucle
- Verapamil due to risk of CHB
- iof taking standard release isosorbide mononirate - asymmetric dosing interval, daily nitrate-free time of 10-14hrs

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3
Q

ACS: STEMI/NSTEMI
Define (in terms of troponin & ECG changes)
* “Raised trop”
* STEMI
* NSTEMI
* Unstable angina

A
  • A 2x rise between 2 samples (3-6hrs apart).
  • Raised trop, ST elevation >1mm in 2+ contiguous leads or new LBBB (or >2mm in limb leads).
  • Rasied trop, No ST elevation (ST changes - ST dep/T wave inv).
  • Normal trop, no ST elevation (may have ST dep/T wave inv)
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4
Q

ACS Mx
Treatment for ACS assumes that patient is not already on an anticoagulant.
If patient is already taking one, what should be given instead of Praugrel or Ticagrelor?
Or if patient is high bleeding risk?

A

Clopidogrel
* because it is a reversible antiplatelet, unlike Ticagrelor
* basically ticagrelor’s blood thinning actions are much stronger/last longer so patients who are at risk of bleeds or already have thin blood don’t need something this intesne

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5
Q
  • Initial assessment - ACS
  • NSTEMI: initial + mx dependent on GRACE score
  • STEMI: if patient presents within 2 hours. between 2-12 hours (or after 12 hours)
A

For all =
A-E, ECG,MONA.
NSTEMI
- Add an Anticoagulant (LMWH) - if no immediate PCI planned
+ GRACE Score:
* if less than3% = conservative; give Ticagrelor (anti-coag) - DAPT
* If greater than 3% - PCI (immediate if unstable; or delayed w/in 72hrs) + Ticagrelor (anti-coag) - DAPT
STEMI
* Antiplatelet (Ticagrelor/Prasugrel) - part of DAPT + PCI (<2hrs) or
* thrombolysis (antithrombin during, anticoagulant after); if PCI not possible within >2hrs
* (consider PCI if patient presents after 12 hours with evidence of ongoing ischemia)

morphine, o2, nitrates, aspirin 300mg.
GRACE score - 6 month mortality. determines high/low risk pt.
DAPT - dual antiplatelt therapy: aspirin + anticoagulant

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6
Q

For patients undergoing thrombolysis when should they be reconsidered for PCI?

A
  • After a subsequent ECG 1hr later
  • As thrombolysis may not be effective
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7
Q

Complications of MI (DREAAD)
& of Inferior MI (leads II, III, avF - ST elevation in leads V5 and V6 and recriprocal changes in V1-V4?)

A
  • Death
  • Rupture of heart septum or of papillary muscles
  • Arrythmias
  • Pulmonary edema (HF)
  • Aneurysm
  • Dressler’s (pericarditis, 2wks post MI –> NSAIDs).
  • Inferior –> AV block
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8
Q

Global registry of acute coronary events score - uses age, HR, BP< caridac and renal function, cardiac arrest on presentation, ECG findings, toponin levels.
What does it predict

A
  • risk of future adverse cardiovascular events: low- high
  • 6 month mortality
  • less than 3% = low risk
  • 3-6%: intermediate
  • greater than 6%: high risk
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9
Q

Hypertension
* Causes of 2ndary

A

Renal (CKD, renal artery stenosis), Obesity, Pregnancy related/pre-eclampsia, Endocrine (Cushing’s, phaeochromocytoma, Conn’s, hyperthyroid, hyperparathyroid)

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10
Q

HTN
* Stages 1-3; clinic & subsequent ambulatory readings
* Unless stage 3 or >, offer what to aid diagnosis?
* Treatment targets: if >80 and <80
* Mx: Lifestyle +/- medical to Stage 1; medical to Stage 2 to all.
* When would medical treatment be offered to Stage 1 (2)?
* Explain the 3 steps; and options for resistant htn.
* Mx for diabetics, regardless of age - think of what other benefit the antihypertensive can give them

A

Stages
* 1: 140/90, 135/85
* 2: 160/100, 150/95
* 3: 180/120

–> ABPM or HBPM: ambulatory or home blood pressure monitoring

Targets
* >80= 150/90
* <80 = 140/90

Management - antihypertensives

  • A –> A+C –> A+C+D. ACE-I/ARB –> CCB, Thiazide diuretic.
  • >55, or African/American - C –> C+A –> C+A+D. CCB, ARB, Diuretic.

Indications for medical treatment at stage 1
- Under 80 yrs AND comorbidity
- e.g. organ damaage, CVD, renal disease, diabetes, QRISK >10%
Resistant
- Spironalactone if K+ less than 4.5, alpha or beta blocker if K+ greater than 4.5
Specialist review
if BP not well controlled on 4 drugs.
Diabetics - ARBs/ACE-I (renoprotective effect)

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11
Q

Cardiovascular disease
Define QRISK score
Primary prevention mx
Secondary prevention

A
  • % risk of cardiovascular event (stroke or mi) in next 10 years
  • Atorvastatin 80mg
  • for isolated hypercholesterolaemia - 20mg
  • Statin, DAPT (aspirin + antiplt), Beta-blocker, ACE-inhibitor
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12
Q

ECG: Normal durations
* PR interval
* QRS interval
* QT interval
ECG: axis deviation
* Left
* Right
Causes of axis deviation
- general - both (4)
- right; specific (4)

A
  • <200ms, <5 small squares
  • <120, <3 s.s
  • <1/2 R-R interval (& dependent on HR)
  • Left axis = Lead 1 +ve, AVF -ve (II -ve)
  • Right axis = Lead 1 -ve, AVF +ve (II +ve)
  • Both = BBB, ventricular hypertrophy, ventricular ectopy, WPW syndrome, ASD
  • Left specific = ostium primum
  • Right specific = normal in <1, and thin adults; lung disease- cor pulmonale, ostium secundum
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13
Q

Sites of infarction
* Inferior leads: II, III, avF (supply inferior walls)
* Lateral/L side V5, V6, I, avF (supply lateral wall)
* Anterior/septal V1-V4 (anterior wall LV, septum)
* Posterior changes in V1-V3, confirmed with posterior leads V7-9 - ST depression, Tall R waves, upright Q waves, dominant R wave in V2

A
  • RCA in 80% of people (via the PDA branch), LCx in 20%
  • LCx
  • LAD
  • RCA (or LCx)
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14
Q

Infective endocarditis
* RIsk factors
* Most common valve affected
* “ if IVDU
* Presentation (2)
* Risk factor groups (3)
* Signs - immunological & infective phenomena (FROM JANE)
* Major criteria dx requires (2) - Duke’s
* Minor criteria includes - if micro evidence doesn’t fit major critieria, and (3)
* Investigations
* Mx - medical or surgical?

A
  • Previous endocarditis, rheumatic heart disease, prosthetic valves, congenital defects, IVDU
  • Mitral valve
  • Tricuspid
  • Fever, chest pain, new murmur
  • IVDU, post dental surgery, prosthetic valves, immunocompromised
  • FROM JANE - fever, roth spots, osler nodes, murmur (mitral regurg), janeway lesions, anaemia, nail bed haemorrhage, Emboli
    Major
  • Blood cultures (x2 unless one +ve for coxiella burnetti and other atypicals), positive signs on ECHO (regurgitation/valve dehiscence)
    Minor
  • 1 positive blood culture (micro evidence not enough for major)
  • Predisposition - IVDU/existing heart disease
  • FROM JANE signs: vascular
  • FROM JANE signs: immunological
  • Fever >38

investigations
Blood cultures x2
TOE - transoesophageal echocardiogram
Specialist if prosthetic valves

Management
* IV ABx or surgery (if abscess, heart failure, non abx responding infections)

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15
Q

Infective endocarditis organisms
staph aureus - most common
Strep viridens (mitis/sanguis)
staph epidermidis
strep bovis (includes gallolyticus)
Culture negative organisms
Non infective (x2)

A
  • General, acute presentation/IVDU
  • Dental surgery
  • Post-prosthetic valve surgery / indewelling lines
  • colorectal cancer
  • culture negative: HACEK, Coxiella burnetti, Bartonella/Brucella, prior abx therapy
  • noninfective: SLE - Libman Sacks; or malignancy
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16
Q

Myocarditis & pericarditis
* Key Ix (3)
* Examination findings
* ECG findings (myo, peri)
* Mx - general
* For cardiac tamponade?
* For cardiac effusions?
* If trop is raised in pericarditis what would you suspect?

A
  • ECG, Echo (transthoracic), Bloods (trop/FBC/BNP/CRP raised)
  • Myo - coryzal –> chest pain - relieved by leaing forwards; SOB, palpitations.
  • Myo - S3+S4 gallops. Peri - pericardial rub “squeaky leather”.
  • Myo: ST changes, tachy, new carrythmias. Peri: Saddle shaped ST elevation
  • Myo - cons, treat underlying cause.
  • Peri - analgesia & colchicine. Admit if fever >38 or raised trop.
  • Pericardiocentesis
  • myopericarditis (trop is indicator of cardiac muscle damage/inflammation)
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17
Q

Valvular disease - murmurs
Systolic = aortic stenosis/mitral regurg
Diastolic = aortic regurg, mitral stenosis
Common features of stenosis/regurgitation

A

Stenosis =
* hypertrophy (of preceding chamber)
* age-related** calcification**, rheumatic heart disease, congenital
Regurgitation =
- dilatation (of subsequent chamber)
- idiopathic weakening, CTD

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18
Q

Complications of acute pericarditis
* Constrictive pericarditis
* Pericardial Effusion
* Cardiac tamponade (Beck’s triad and ECG finding)

Management
- effusion
- tamponade

Main difference between constrictive pericarditis and tamponade

A
  • pericardium becomes rigid - reduces CO: signs of heart failure (SoB, S3 gallop, raised JVP)
  • pericardium fills with fluid - muffled heart sounds
  • raised JVP, muffled heart sounds AND HYPOTENSION. ECG: “swinging heart” within fluid: electrical alternans (alternating amplitude of QRS complexes)
    Mx
  • Diuretic
  • Pericardiocentesis

Difference
- cardiac tamponade: pulsus paradoxus: fall in BP by 10mmHg during inspiration
- constrictive pericarditis shows calcification on CXR

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19
Q

Extra heart sounds: what they signify?
S3
S4
Which is always abnormal?

A
  • S3After S2 = diastole; rapid ventricular filling (e.g. normal in 15-40 or HF in old- twanging of of chordae tendinae)
  • S4 Before S1 = diastole, turbulent atrial filling against stiffened ventricle. ALWAYS ABNORMAL
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20
Q

Listening to murmurs
MTAP –> Erb’s point: where ii that?
Grading I -VI

A

3rd ICC, left sternal border, best place for heart sounds S1 and S2
Difficult –> can be heard with stetho off the chest

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21
Q

SYSTOLIC MURMURS -

AS/MR - affect valves of L side of heart that pumps blood from lungs, to body

  1. Aortic stenosis - most common valvular disease to require prosthetic valves
    * Features of murmur
    * Other CVS examination findings (2)
    * Px (Beck’s triad)
  2. Mitral regurgitation
    * Features
    * Other CVs exam findings & ECG
    * Px
A

AS
* Ejection systolic, high-pitched, radiates to carotids
* Narrow pulse pressure(<30mmHg) & slow rising pulse
* Exertional syncope, SoB & chest pain
MR
* Pansytolic, high pitched, radiates to axilla
* Signs of HF (back flow into pulmonary veins), p mitrale (broad p wave, sign of atrial enlargement)
* SoB/fatigue

22
Q

DIASTOLIC MURMURS -
1. Aortic regurgitation
* Features of murmur
* Additional murmur heard at apex
* Other CVS examination findings (2 main + 3 uncommon ones)
* Px (acute/chronic)
2. Mitral stenosis
* Features of murmur
* Additional murmur heard at apex
* Other CVs exam findings (1)
* ECG findings
* Px

A

AR
* Early diastolic, high pitched, ++leaning forward & on expiration
* Austin Flint
* Wide pulse pressure (>60mmHg), collapsing pulse - waterhammer
* +Corrigan’s (carotid pulsations)
* De Musset’s (head bobbing)
* Quinke’s (nail pulsations)
* Mullers (uvula)
* Duroziez’s (diastolic femoral bruit)
* Traube’s (pistol shot femorals)
* Rosenbach’s (pulsatile liver - seen in tricuspid regurg)
* Gedraht’s (enlarged spleen)
* acute- endocarditis/aortic dissection –CVS collapse
* chronic - asymptomatic until LVF

MS
* Mid-Late diastolic, low pitched rumbling, ++ rolled on L side & with bell
* Tapping apex beat
* Malar flush
* P mitrale (enlarged, bifid p wave) - atrial enlargement
* SoB/fatigue

23
Q

Valvular disease Mx
Aortic stenosis
* Medical
* Surgical -
* indications for TAVI (transcatheter aortic valve replacement)
* vs S_VR

Mitral regurg
- medical
- surgical

A

AS
* Manage sx, AF, HF- no definitive medical management
* TAVI >75 yrs, high risk pt (comorbidities)
* S_VR: <75 yrs, low risk pt
MR
* symptomatic management - e.g heart fialure
* surgery if acute, severe regurg

24
Q

Other systolic murmurs:
Tricuspid regurg
- type of murmur
- typical patient
- finding on ECG
- finding on abdominal exam
Pulmonary stenosis
- type of murmur
- heard best during inspiration or expiration?

A

Tricuspid regurg
* back flow -signs of right heart failure - ascites, raised JVP
* pansystolic
* younger pt/post MI
* v waves (ECG)
* pulsatile liver
Pulmonary stenosis
* systolic murmur
* loudest in inspiration

RILE - ride sided (T,P) - best on inspiration
left sided (M,A) - expiration -aka most common ones accentuaed by expiration

25
Q

Bradycardia, <60bpm
1. Sinus brachycardia
2. Sick sinus syndrome –> bradytachy, AF
3. AV Blocks (1-3rd degrees)
- AV block 1st degree - ?
- 2nd degree - ?
- 3rd degree - ?

A
  • 1st: PR interval >200ms (>5ss)
  • 2nd: Mobitz Type 1 - progressively increasing PR interval until missed beat.
  • Mobitz Type 2 - 2:1 or 3:1 or 4:1 p:QRS, occasional or in pattern. Risk of progression to CHB.
  • 3rd: CHB. No relation between p:QRS - AV node completely blocked.
26
Q

Summarise the management/ monitoring of valvular disease

A

Valvular disease is often seen in conjunction with other cardiac problems, rarely in isolation.
Management involves:
* Medical - optimise HF/AF mx
* Surgical - except for aortic stenosis (where definitive treatment is TAVI or AVR) surgical options generally if symptomatic, severe, acute presentations, reduced ejection fraction, prolapsed valve (MV)
* Surgery = balloon valvotomy or valve replacement
* Monitoring with ECHOs to see degree of valvular problem

27
Q

Valvular disease mx
Aortic regurg
- medical
- surgery indications
Mitral stenosis
- medical
- surgery indications

A

AR
* manage heart failure
* if symptomatic with severe AR or asymptomatic with LV systolic dysfunction (ECHO)
MS
* manage AF (anticoag - Warfarin)
* ifsymptomatic - mitral balloon valvotomy
* or mitral valve surgery (commuissurotomy/MVR)
*

28
Q

Bradycardia - mx if unstable
* Initial (1) –> further options (3)
* For pts at high risk of asystole (e.g. CHB, Mobitz Type II, previous asystole, broad QRS)

A

A-E approach
* Atropine 500mcg
If necessary-
* Further Atropine (every 5 mins) until max 3mg: seek expert help
* Transcutaenous pacing
* Adrenaline/isoprenaline infusion
High risk pt -
* Transvenouspacing

29
Q

Tachyarrythmia (>100bpm) = narrow or broad complex.
Narrow =
1. sinus tachy
2. Atrial fibrillation
3. Atrial flutter
4. Paroxysmal SVT = AVRT (WPW) and AVNRT (AV WPW is not this one)

Mx of narrow complex tachy:
1. Stable
2. Unstable

General Management for unstable tachycardia

A

A-E –> Unstable/life-threatening signs? –>
1. Synchronised DCCV
2. + Amiodarone 300mg/20mins
3. Repeat shock
Max 3 attempts

30
Q

Stable tachycardia
Narrow complex
Mx for irregular vs regular rhythm

A
  • Irregular (e.g. AF) - rate control (BB) –> Digoxin; if onset within 48hr electrical or chemical cardioversion
  • Regular (e.g. SVT) - vagal manouvre –> AdenosineIV 6mg –> 12mg –> 18mg –> electrical cardioversion
  • Atrial flutter- treat as AF with rate control

note cant dccv after 48hours due to risk of clot dislodging from atria and causing stroke

31
Q

Periarrest rhythms
If any adverse features? *
Aka shock (hypotension, reduced GCS, confusion, cold clammy), syncope, myocardial ischemia, heart failure?
No adverse features?
Mx for
*Broad complex tachycardia
* Regular (assume VT)
* Irregular (VF, AF w/LBBB, polymoprhic VT)

A

Adverse features
DCCV up to 3 shocks
If no adverse features: depends on regular/irregular
1. Regular broad complex tachycardia
* Assume VT
* IV Amiodarone (loading dose followed by 24hr infusion)
2. Irregular broad complex tachycardia
* if VF will be unstable so DCCV.
* Otherwise: if stable: most likely cause is AF with LBBB - treat as AF with rate control.
* Or if - Polymorphic VT (Torsades de Pointes) –> Mg.

32
Q

Supraventricular tachycardias: WPW syndrome - AVRT
genetic conduction disorder or interruption to conduction tissue near/within the AV node
* ECG findings (3)
* Acute mx (3) before DCCV if they fail
* Examples of vagal manouvres (3) to stimulate parasympathetic nervous system
* Definitive treatment
- side effects of adenosine

management is based on “obliterating the accessory circuit” - hence treatment cannot be curative for AVNRT as it would involve obliterating the whole node

A
  • Abnormal circuit within the AV node or not through AV node
  • AVRT - uses accessory pathway - such as Wolf Parkinson White

ECG
* Delta wave (slurred upstroke of QRS)
* short PR interval (<120ms)
* Narrrow complex
* ST segmenta and T wave discordant changes

Mx
1. Vagal manouvre
2. Adenosine
3. Verapamil/CCB -
4. DCCV

  • Valsava (increase intrathoracic pressure), carotid sinus massage, diving test (submerge in cold water)
  • Radiofrequency ablation of accessory pathway
  • chest pain, feeling of impending dooom

can use fleicanide

33
Q
A
34
Q

Atrial fibrillation -
* Example causes (SMITH; common surname for a common condition) + alcohol/caffeine
* Ix - ECG; state findings (3) +/- ECHO.
* Define paroxysmal AF and ix (2)

Note - if asymptomatic, e.g. picked up incidentally, and rate is controlled (7-10) and CHADSVASC 0 there is no treatment required.

  • Mx = rate or rythm control & anticogulation. NICE recommend rate control first line. Which pts may be offered rhtyhm control? (4)
  • Further mx options if above not tolerated / high risk of stroke? (2)
A
  • Sepsis, mitral valve S/R, IHD, thyrotoxicosis, HTN
  • spontaneous episodes that reoccur and then resolve back to rinus rhythm. 24hr ambulatory ECG (Holter) or cardiac event recorder / BARDY/ZIO
    indications for ryhtm control - *put back into normal rhythm, but doesn’t change underlying pathology. *
    1. reversible cause
    2. new onset <48hrs
    3. secondary HF
    4. symptoms despite rate control
  • radiofrequency ablation (left atrial ablation)
  • left atrial appendage occlusion (LAAO) - high stroke risk
35
Q

Assessing need for anticoagulation in paients with AF
CHA2DS2VaSc Score - factors?
0=? 1=? 2=?

A

CHD, HTN, Age (65+ = 1, 75+ = 2), Diabetes, Stroke/TIA/VTE (=2) Vascular disease, Sex (female =1)
0 = none
1 = consider anticoagulation (in men)
2 = offer anticoagulation

36
Q

Risk of stroke without anticoagulation in pts with AF is 5% –> adding it will bring it down to 1-2%.
ORBIT Score - assessing risk of bleeding in patients on anticoagulants with AF(similar to HASBLED)

A
  • Older age >75
  • Renal impairment (GFR<60), Bleeding hx (GI/intracranial)
  • Iron (low Hb)
  • Taking antiplatelet
37
Q

Options for rhythm control in AF - rarely done.Types of cardioversion: medical vs electrical.
What would “long term rhythm contro” consist of?

A

Cardioversion:
* Medical - Fleicanide (younger/normal structure) or Amiodarone (older/sedentary)
* Electrical - DCCV

Long-term rhythm control:
* Betablockers
* Dronedarone (2ndline post cardioversion)
* Amiodarone (e.g. if HF)

38
Q

Acute left ventricular failure
* Px
* Signs - SI + S2 +
* Immediate management
* Monitoring
* Complications (4)

A

sudden failure of heart to maintain cardiac output; failure of LV to pump –> build up in pulmnary veins
Pulmonary oedema
rapid onset SoB, ankle swelling, cough (w. pink frothy sputum)
* S3 gallop (rapid ventricular overfilling)
* A-E –> MON - morphine, O2, nitrates, loop diuretic (Furosemide)’ monitor fluid balance, U&Es, BP.
* Electrolyte abnormalities – > arrythmias.
* AKI (poor perfusion).
* VTE (low cardiac output).
* Impaired liver function (poor perfusion).

39
Q

Chronic heart failure
Caused by either impaired systolic function or diastolic function resulting in chronic back pressure of blood
- Presentation (3)
- Potential findings on ECG (2)
- New York Heart Association grading (I -> IV)
- Findings on CXR (abcde)
- Bloods - nt-pro BNP, affects speed of referral: >2000? or 400-2000?
- ECHO - ejection fraction- define reduced and preserved ejection fraction

A
  • SoB, orthopnoea, PND- also fatigue, muscle weakness etc
  • AF (in 1/4) & LBBB (1/3)
  • 1 = no limittion on activity, 4= sx at rest.
  • CXR findings = cardiomegaly (width is >1/2 of thorax), Kurley B lines, alevolar oedema, diversion of vessels, effusions.
    • > 2000 urgent cardiology referral 2w, >400 - 6 weeks.
  • EJ<40% = reduced.
  • EJ>40% with raised BNP = HF with preserved EJ.
40
Q

Chronic heart failure
1st line
2nd line
3rd line options (specialist) x4
Surgical interventions (2)
- what needs to be monitored (SE ACE-Inhb/Aldosterone antagonist)
- what should also be offered routinely

A

Medical
1. Beta-blocker and ACE-inhibitor
2. Add an aldosterone antagonist Spironalactone/Epleronone
3.Specialist management:
Ivrabradine(HCN blocker)
Hydralazine with nitrate(vasodilator);
Sacubitrol Valsartan = neprilysin inhibitor + ARB
Digoxin= cardiac glycoside, Na+/K+/ATPase inhib.
Interventional:
- Cardiac resynch. therapy
- Implantable defib
Monitoring
- potassium (drugs cause raised K+)

Vaccines
- one off pneumococcal
- annual influenza

Neprilysin breaks down natriretic peptides —> inhibitors reduce breakdown of natruietic peptides –> increased vasodilation

41
Q

Cardiomyopathies
Primary vs secondary (e.g. DM, Friedrich’s ataxis, SLE, amyloid, sarcoidosis).
Inherited, acquired, mixed.
Inherited: HOCUM/ALVC
Distinguish HOCUM from arrythmogenic LV cardiomyopathy (genes, ECG/echo findings).

A
  • HOCUM - mutation in gene encoding myosincause of sudden death in young athletes. Echo - LV hypertrophy (>30mm), mitral valve invovement (SAM, MR).
  • ALVC - mutation in gene encoding desmosome. ECG - epsilon (upstroke after QRS).
42
Q

Cardiomyopathies
Acquired
- peripartum?
- takotsubo?
Causes of restrictive (3)
Causes of dilated (3)

A
  • last month –> 5 mo postpartum
  • stress induced e.g. death of family member; transient apical balooning –> supportive
  • restrictive= amyloidosis, post-radiox, endocarditis (Loeffler’s)
  • dilated = alcohol, Coxsackie B, wet beri beri - thiamine deficiency, Doxorubicin (toxicity bear)
43
Q

Anti-dysrythmics
* Na+ channel blockers (2)
* Ca2+ channel blockers: non-dihydropurines (primary action on heart muscle), - compared with dihydropurines (vascularsmooth muscle)
* K+ channel blockers (2)
* Beta adrenoreceptor blockers (1)

A
  • Lidocaine, Fleicanide.
  • NDHP - primary action on heart muscle: Verapamil, Dilatiazem - DHP -vascular smooth muscle: Amlodipine
  • Amiodarone, Sotalol.
  • Propanolol.
44
Q

Hypokalaemia ECG findings
HTN, hypokalaemia and hypernatreamia is a sign of?

A

inverse t waves
u waves
prolonged QT interval

  • primary hyperaldosteronism (Conn’s) - excess aldosterone. 1st line test is aldosterone:renin ratio, then CT abdomen.
45
Q

Reverse tick (inverted T wave)

A

Digoxin effect

46
Q

Boerhaave syndrome triad

A

Vomiting
Chest pain
Sub cut emphysema (abdominal crepitus)

Typical / middle aged man with alcohol abuse hx

47
Q

When should Ivabradine be considered as third line therapy in heart failure?

A

. Ivabradine should be considered in heart failure if the patient has sinus rhythm > 75/min and a LVEF < 35 (reduced)

48
Q

infective endocarditis
Causative organisms - typical:
IVDU
dental procedure
Previous prosthetic valve surgery
Colorectal cancer
Farmer/animal worker

A

Staph aureus
Step Viridens
Staph epidermis
Strep bovis
Coxiella burnetti

49
Q

Hypocalcaemia on ECG

A

elongated QTc segment
less calcium –> reduced cardiac muscle contraction –> longer phase for ventricular contraction
note post thyroidectomy surgery (damage to parathyroid glands) - perioral and peripheral paraesthesia and cramps

50
Q

ECG findings of myocardial ischemia - from acute to long term

A
  1. Hyperacute t waves = broad based, symmetric, not pointed
  2. ST elevation
  3. Inverted t waves - may be seen with ongoing ischemia - ST elevation - and post ischemic
  4. Pathological q waves
51
Q

Long QTc syndrome
inherited condition causing delayed repolarisation of the ventricles
may lead to VT/TdP –> risk of collapse/sudden death.
greater than 470 ms
Causes can be congenital, drug related or other.
- List some drug causes
- Others

Mx - avoid precipitant drugs, beta-blockers, implantable Cardioverted debrib in high risk

A

Drugs
* Amiodarone, Sotalol
* Tricyclic antidepressants, SSRI
* Methadone
* Chloroquine
* Erythromycin
* Haloperidol, Odansetron

Others
- Electrolytes: low ca, low mg, low K+
- MI, myocardiits
- SAH
- hypothermia

Year 4/5 Revision (21 decks)

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