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RACP Written Exam 2015 > Cardiology > Flashcards

Cardiology Flashcards

0
Q

Which leads are affected if there is a STEMI of:

  1. Posterior descending artery
  2. RCA
  3. left main stem
  4. LAD
A
  1. Posterior descending artery
    Posterior MI
    = ST depression in V1-4 with a dominant R wave in V1
    (Supplies the posterior LV)
  2. RCA
    Inferior
    II, III aVF
  3. left main stem
    Occlusion of LCx (I aVL V5 V6) PLUS LAD simultaneously
    = ST elevation across ALL chest leads, I aVL.
  4. LAD STEMI
    ST elevation V1-4
    RECIPROCAL changes (ST depression) Inferior leads
    these changes correspond to “watershed” ISCHAEMIA in territories supplied by the LAD
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1
Q

What are the absolute contraindications for Thrombolysis in a STEMI patient? (7)

A

Active bleeding

RECENT (IN LAST 3 MONTHS)

    • ISCHAEMIC STROKE
    • HEAD OR FACIAL TRAUMA

ANY

  • ICH
  • Arteriovenous malformations / cerebrovascular lesions
  • Brain malignancy (primary or met)

Suspected aortic dissection

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2
Q 
In deciding antiplatelet and antithrombosis drugs for use in an acute MIA, which of the following factors is associated with a higher bleeding risk?
A. Diabetes
B. Low body weight
C. Obesity
D. PPI use
E. Younger age
A 
Risk factors for bleeding are:
OLDER AGE
Renal impairment
UNDERWEIGHT
Known bleeding problems
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3
Q

In CCF management, what are the agents that provide a mortality benefit?

A

ACEI
Beta-blocker
Spironolactone
Ivabradine

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4
Q

What are the ECG findings in Brugada syndrome?

A

Baseline ECG without symptoms: 2 leads in V1-V3 with an elevated (>2 mm) ST segment that descends with an UPWARD CONVEXITY to an inverted T wave

Note - FLEICANIDE CHALLENGE ELICITS BRUGADA

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5
Q

What are the conditions associated with:

  • beta MHC (beta myosin heavy chain)
  • LMNA
  • SCN5A loss of function
  • SCN5A gain of function
  • KCNQ1
  • KCNQ2
A
  • beta MHC (beta myosin heavy chain) = HOCM
  • LMNA = Dilated CM (Lamin A or C genes)
  • SCN5A loss of function of Na channels = Brugada
  • SCN5A gain of function of Na channels = LQT3
  • KCNQ1 = Long QT 1
  • KCNQ2 = Long QT 2
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6
Q

Signs of severity of Aortic Stenosis.

A

(I am “APaLLD” that you don’t know the signs of severity in AS!)

A2 absent
"Pressure loaded" Apex beat
LATE peaking murmur - ***most important sign! ***
Length of murmur
Delayed carotid upstroke
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7
Q

What is the treatment for symptomatic AS?

A

Surgery: TAVI or AV replacement (no difference in mortality)

Try for AVR first. Use AVR if patient is not a high risk candidate for surgical complications.

TAVI (is like a stent for the Aortic valve) is indicated for severe, symptomatic AS in patients NOT SUITABLE. Eg. High risk surgical candidate. Life exp should be >1 year.

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8
Q

What is the mode of action of Flecainide?

A

Class 1c antiarrythmic
Blocks Na channels –> reduces excitability

The antiarrhythmic actions of Flecainide are mediated through effects on sodium channels in Purkinje fibers. Flecainide is a sodium channel blocker, binding to voltage gated sodium channels. It stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses. Ventricular excitability is depressed and the stimulation threshold of the ventricle is increased during diastole.

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9
Q

What are the indications for surgery for infective endocarditis?

A 
decompensated heart failure
overwhelming sepsis, despite conventional antibiotic therapy
perivalvular abscess
intracardiac fistulae
valve perforation
recurrent embolic episodes despite antibiotic therapy
prosthetic valve endocarditis
fungal endocarditis
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10
Q

What is Heyde’s Syndrome?

A

Bleeding from Angiodysplasia in patients with AS has been termed Heyde’s Syndrome.

This is a combination of Aortic Stenosis, Angiodysplasia & GI bleed due to Acquired Von Willebrand’s disease.

Bleeding IMPROVES AFTER AORTIC VALVE REPLACEMENT.

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11
Q

What are the indications for Cardiac Resynchronisation therapy (Biventricular pacing)?

A

Class III or IV CCF
QRS > 120ms
LBBB (** DOES NOT work in RBBB!! **)
Sinus rhythm

--> (outcomes of trials) :
CRT reduces mortality
CRT+AICD reduces mortality
60% of patients improve
Benefit is maintained for at least 2 years

***** Differs slightly from RPA Prep Course Notes!!
“CURRENT RECOMMENDATIONS in BiVPacing +/- AICD in HEART FAILURE AHA 2012”
Criteria for Cardiac Resynchronisation Therapy:
- ** HF Class II (TWO) to IV
- Dilated HF with LVEF 150ms and LBBB
- Sinus rhythm

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12
Q

What is the earliest event in atherosclerosis?

A

Earliest event = Endothelial dysfunction. Due to unbalanced endothelin.

Then..
Monocytes adhere to endothelial cells via adhesion molecules.
Monocytes migrate into endothelial cell wall.
Modified LDL is taken up by macrophages –> become FOAM CELLS.
Smooth muscle proliferation.

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13
Q

What are the criteria for metabolic syndrome?

A

Any 3 of:

  • Waist circumference (M >94 and F >80cm)
  • BP > 130/85
  • TRIGLYCERIDES > 1.7
  • Low HDL: less than 1.0 In males, less than 1.29 in females
  • Impaired Fasting Glucose (Fasting BSL > 5.6) OR IGT (2hr post OGTT BSL 7.8-11.1) OR T2DM (Fasting BSL greater than 7, 2hr p/prandial greater than 11.1)

metabolic syndrome DOUBLES the risk of CAD over 5-10yrs
5x increased risk of diabetes

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14
Q

After an AMI, in addition to Aspirin, which of these has shown to be beneficial as an adjunctive therapy?

Clopidogrel
Oral nitrate
Mg
ACEI 
Beta blocker
Insulin
Bone Marrow Cell therapy
A

Clopidogrel - significant benefit
Oral nitrate - no benefit
Mg - no benefit
ACEI - benefit
Beta blocker - benefit (but now being questioned)
Insulin - yes for diabetics
Bone Marrow Cell therapy - small benefit!!! Decreased all-cause mortality by OR 0.3, improved LVEF

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15
Q

Signs of severity of Mitral stenosis.

A

Mitral stenosis just “PLODS” along until patient goes into Failure!!

“PLODS”

  • Pulmonary HTN
  • Long murmur
  • Opening snap! (Indicates LA pressure&raquo_space; LV)
  • Diastolic rumble/thrill
  • Small pulse pressure

MS
–> higher LA pressures –> back pressure into pulmonary vasculature –> results in Pulm HTN, APO.
Symptoms made worse by high CO states such as pregnancy, sepsis, tachycardia

16
Q

What are the current criteria/recommendations for ICD Implantation in heart failure? (4)

A

Consider AICD in patients with ANY 1 of the following:

  1. Survived cardiac arrest resulting from VF/VT (that was not due to a transient or reversible cause)
  2. Spontaneous, Sustained VT in association with structural CAD
  3. LVEF < 35% with Class II-III HF and 40 days after AMI
  4. LVEF < 30% with prior AMI, Class I/asymptomatic
    * Assuming patients are on chronic, optimal medical therapy and have a reasonable expectation of survival with good functional status for more than 1 year
17
Q

AF. What are the antiarrythmic drugs proven beneficial for treatment AND prophylaxis of AF?

A

Sotalol
Flecainide
Amiodarone

(Then AF ablation-PV isolation)

Note Digoxin does NOT prevent attacks of AF, does NOT terminate AF, does not control rate during acute attacks. Often inadequate for rate control in active people.

18
Q

Hereditary long QT.

What is the mainstay of treatment for Long QT syndrome?

A

The mainstay of treatment is beta-blockers PROPRANOLOL and NADOLOL (new- proven better)

Then AICD if cardiac arrest or drug failure.

Note the longer the QT the greater the risk of SCD. Any QT >280 is abnormal (cut offs for male > 440, female > 460)

19
Q

What are the causes of prolonged QT?

A 
NON-DRUG CAUSES:
HypoCALCAEMIA
Hypo Mg, K
Hypothyroid
Hypothermia

DRUG CAUSES: beware the pneumonia patient on antibiotics!
** Ciprifloxacin / Moxifloxacin (FQ’s) **
Erythromycin / Clarithromycin / Azithro (Macrolides)
Fluconazole/ Voricomazole (Triazole Antifungals)
Pentamidine (for PCP)
ARSENIC
SSRIs
* Methadone
Tricyclics antidepressants

20
Q

TAVI versus Aortic Valve replacement in AS.

Which one would you choose & reasons why.

A

TAVI vs AVR
- TAVI and AVR have equivalent reduction in mortality and symptom control
But
- TAVI has increased frequency of paravalvular regurgitation

hence opt for AVR if possible.
If patient is a high-risk surgical candidate (and life exp >1yr) opt for TAVI

21
Q

What are the best ARBs to use in heart failure?

A

Best evidence for CANDESARTAN or VALSARTAN in Class II-III heart failure.

  • lower risk of cardiovascular death
  • lower hospitalisation rates
22
Q

HOCM. What is the gene involved and what is the mode of inheritance.
How do you diagnose HOCM?

A

BMHC - beta Myosin Heavy Chain.
This is a disease of the SARCOMERE.

Auto dominant inheritance with INCOMPLETE PENETRANCE.
Commonest cause of SCD.

ECG is the most sensitive test (according to deltamed 2013).. deep TWI inferolaterally with high voltages.
Need to do an Echo.

Mx with beta blockers for everyone, and AICD for high-risk individuals. (LV thickness >35mm, previous cardiac arrest)

23
Q

What are the genes involved in Dilated Cardiomyopathy?

A

Lamin A or C genes.
SCN5A.

This is a disease of the CYTOSKELETON

24
Q

Patient presents with ankle swelling and fatigue. She has a past history of panic attacks and has hot flushes with alcohol, recent Abdo discomfort and diarrhoea. Her JVP is elevated with a pulsation in her earlobes.
What is the diagnosis?

A

Carcinoid Syndrome

Rarel neuroendo tumour
Mostly GI origin
Arise from Enterochromaffin cells
Suspect if any FLUSHING and DIARRHOEA

25
Q

Which valvular lesion is most likely to be associated with foetal or maternal complications in pregnancy?

A

Mitral stenosis

26
Q

Mode of action of Ivabradine

A

Reduces Heart rate by acting on the “If” channel in the SA node.

Primary mode of action is to increase the duration of diastole.

No negative effect on LV function.
Used for stable angina in sinus rhythm, in patients who are unable to tolerate beta blockers.

27
Q

Perhexiline has been used in the treatment of CCF and stable angina. How does it work?
What are the side effects of treatment?

A

Modifies myocardial substrate from fatty acids to carbohydrates, which is energetically more efficient –> reduces myocardial oxygen consumption.
No mortality benefit, but reduces symptoms.

S/E:
Hepatotoxicity 
(metabolised by Cyp 2D6 -->
** 7-10 % of patients are SLOW METABOLISERS / have Cyp 2D6 mutations **
--> careful drug monitoring!!)

Hypoglycaemia
Peripheral neuropathy

28
Q

Rheumatic fever.
How does it present?
What tests would you order?
What are the main principles of management and screening contacts?

A

Sore throat, fevers, coryzal Sx, arthralgias, Sydenham chorea (self limiting), Indigenous population.

Must confirm diagnosis with TWO Streptococcal antibody titres:

  1. Plasma anti-streptolysin O test
    - -> picks up 75-80% of Group A strep throat

PLUS

  1. Anti-DNAse B titres
    - -> increases the sensitivity of testing

(Only less than 5% is picked up on throat swab in Aboriginals, less than 10% picked up in white population - hence need BOTH ASOT and anti-DNAse B)

DRUG OF CHOICE For Streptococcal pharyngitis is ORAL PENICILLIN V BD DOSING .
** START TREATMENT WITHIN 9 DAYS of symptom onset! ** to prevent Rheumatic fever.

Treatment for arthralgias = ASPIRIN first line

Treatment for Sydenham chorea = None, because self-limiting & benign, and anti-chorea meds are toxic.

Screening of asymptomatic family members is NOT NECESSARY as Group A Strep is only responsible for 5% of pharyngitis in adults.

29
Q

When does Anthracycline Cardiotoxicity generally present?
What are the risk factors for developing chronic Anthracycline cardiotoxicity?
What agent can REDUCE THE RISK of toxicity?

A

Generally presents within 1 year of finishing chemotherapy, with the peak time for the appearance of symptoms about 3 months after last dose.

RISK FACTORS:

  • cumulative dose (strongest risk factor)
  • IV administration
  • concurrent Cardiotoxic agents particularly PACLITAXEL, CTX And TRASTUZUMAB
  • concurrent or prior chest radiation
  • preexisting CV disease (debatable)

** DEXRAZONANE significantly reduces risk of chronic Cardiotoxicity when given with anthracyclines **
It is an EDTA Chelator.
Used in patients who are receiving high cumulative chemo doses.

30
Q

When is the use of CTCA most appropriate?

A 
CTCA
Highly sensitive (98%) and moderately specific (88%) for CAD

Excellent for ruling out significant disease in patients with LOW TO INTERMEDIATE pre-test probability of CAD.

Current data does NOT support the use in asymptomatic patients.

Not used in patients with previous stents because stents are likely to cause artefact.

Need to rule out any allergy to CONTRAST.
Need to rule out renal impairment.

Patients need to:

  • be in sinus rhythm with no tachycardia
  • be able to hold breath for 10sec
  • be able to tolerate beta blockers and nitrates (nitrates given to dilate coronary vessels during procedure)
  • able to hold arms above head
31
Q

What are the ECG findings in:

  1. LAHB
  2. Bifascicular block
  3. Trifascicular block
A
  1. LAHB
    - LAD + tall R waves in left sided leads I and aVL + deep S waves in inferior leads II III aVF
  2. Bifascicular block
    - RBBB plus LAHB (eg RBBB plus LAD) usually
  3. Trifascicular block
    - 1st deg HB + LAD + RBBB (usually - this is incomplete Trifascicular block)
    Or
    - 3rd deg HB + LAD + RBBB (complete Trifascicular block)
32
Q

What are the clinical and lab findings in Cholesterol Embolisation Syndrome?

A

CLINICAL:
(Always suspect in patient who has recently undergone a vascular procedure eg. Angiogram)
- renal failure
- bowel ischaemia
- skin: blue toe syndrome (“Trash foot”), livedo reticularis
- FEVER, Weight loss, Myalgias, Fatigue
(CONSTITUTIONAL Sx as cholesterol crystals trigger an Inflammatory response when they lodge in the small arteries of target organ)

LAB FINDINGS:
High inflam markers - WCC, CRP
Low/consumed C3/4
HIGH EOSINOPHILS for first few days (in 80%!) (mechanism unknown)
May have anaemia / thrombocytopaenia
33
Q 
Following an orthotopic heart transplant, what is the best way to monitor for post-transplant coronary artery disease?
A. Clinical history
B. Coronary Angiography
C. ECG
D. Myocardial contrast echocardiography
E. Intravascular Ultrasound
A

B. Coronary Angiography for diagnosis and monitoring of TCAD.

Transplant coronary artery disease (TCAD):

  • the most significant cause of mortality / morbidity post transplant
  • largely an IMMUNOLOGICAL process –> inflammation –> fibromuscular and smooth cell proliferation –> coronary artery obstruction
34
Q

Rise in JVP with inspiration. What does this suggest?

A

Suggests either restrictive or constrictive cardiomyopathy.

35
Q

How do you differentiate a restrictive vs constrictive cardiomyopathy?

A

Difficult clinically! Differentiate using an Echo.

If Echo shows STIFF VENTRICLES and NO pericardial effusion - most likely Restrictive CM rather than Constrictive.

Restrictive cardiomyopathy:
- increased STIFFNESS OF VENTRICLES leading to POOR DIASTOLIC FILLING with PRESERVED LV FUNCTION

  • occurs with infiltrative (sarcoid, amyloid, myeloma, lymphoma, irradiation, CT disease) or storage diseases (Haemochromatosis, Fabry), or inflammation (endomyocardial fibrosis, Loffler CM)

Echo findings in restrictive CM

  • no effusion
  • stiff ventricles
  • increased early diastolic filling to atrial filling ratio (E:R ratio)
  • decreased E-deceleration time
  • decreased isovolumetric relaxation time (40 ms)
36
Q

What are the hallmarks of an Atrial Septal Defect murmur?

A

FIXED SPLITTING OF 2nd heart sound, PLUS ESM in PULMONIC AREA.

Most common ASD is “Ostium Secundum ASD” (75%) and occurs in the region of the Fossa Ovalis

ECG may show RAD and RBBB.

Patients typically present with NO symptoms, but may have SVTs, right heart failure, paradoxical emboli or recurrent chest infections.

RACP Written Exam 2015 (14 decks)

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