Cardio

Question 1

In the PALLAS trial, researchers studied dronedarone in patients with permanent atrial fibrillation (AF) of 6 months’ duration. Which of the following best describes an outcome that occurred in more than twice as many patients in the dronedarone group as in the placebo group?

A. stroke

B. cardiovascular death

C. myocardial infarction

D. all of the above

Answer 1

D. all of the above

Question 2

Which of the following statements does not accurately describe a finding from a study of functional mitral regurgitation (MR) in patients with normal leaflet motion and left ventricular ejection fractions 50% who underwent ablation for AF?

A. Patients with recurrent AF after ablation had significantly less MR than those in sinus rhythm.

B. Large mitral annular dimension was the patient characteristic most strongly associated with MR.

C. The mean left atrial volume index was significantly smaller in patients in sinus rhythm after ablation than in those with recurrent AF.

D. The mean annular dimension tended to be larger in patients with recurrent AF after ablation than in those in sinus rhythm.

Answer 2

A. Patients with recurrent AF after ablation had significantly less MR than those in sinus rhythm.

Question 3

Which of the following is designated a Class I recommendation in the 2011 focused update of the 2006 American College of Cardiology/American Heart Association guidelines for the management of AF?

View Summary

A. a target resting heart rate of <80 beats per minute

B. catheter ablation in patients with symptomatic paroxysmal AF who have not responded to antiarrhythmic medications

C. the use of dronedarone in patients with NYHA class IV heart failure

D. the combination of aspirin and clopidogrel in patients who are poor candidates for warfarin

Answer 3

B. catheter ablation in patients with symptomatic paroxysmal AF who have not responded to antiarrhythmic medications

Question 4

Which of the following statements accurately describes a finding from a trial comparing a strict target resting heart rate with a lenient one (<80 and <110 beats/minute, respectively) in patients with AF managed with rate control alone?

View Summary

A. At the end of the dose-titration phase, the resting heart rate did not differ significantly between the strict-control and lenient-control groups.

B. In the lenient-control group, the resting heart rate at 1 year was significantly higher than it was at the end of the dose-titration phase.

C. At 3 years, the composite rate of death and major cardiovascular events did not differ significantly between the strict-control and lenient-control groups.

D. The rate of adverse drug effects during follow-up was significantly higher in the strict-control group than in the lenient-control group.

Answer 4

C. At 3 years, the composite rate of death and major cardiovascular events did not differ significantly between the strict-control and lenient-control groups.

Question 5

Using data from the Women’s Health Study, researchers evaluated the association between smoking and peripheral arterial disease (PAD) in women. Which of the following best describes the researchers’ findings?

A. Smoking was not associated with excess risk for PAD, when age is considered.

B. PAD risk associated with smoking was highest among women who also used hormone replacement therapy.

C. Twenty years after smoking cessation, PAD risk in former smokers approached that of nonsmokers.

D. At 13 years, former smokers who smoked 15 cigarettes daily were at similar PAD risk as current smokers.

Answer 5

C. Twenty years after smoking cessation, PAD risk in former smokers approached that of nonsmokers.

Question 6

In a controlled trial, patients with peripheral arterial disease were randomized to either aspirin or aspirin plus warfarin and were followed for 3 years. The researchers found that, with regard to the combined primary endpoint of cardiovascular death, myocardial infarction, stroke, and arterial ischemia:

A. aspirin was superior to aspirin plus warfarin.

B. aspirin was equivalent to aspirin plus warfarin.

C. aspirin was inferior to aspirin plus warfarin.

D. aspirin alone was not effective.

Answer 6

B. aspirin was equivalent to aspirin plus warfarin.

Question 7

This analysis of the 1999–2004 National Health and Nutrition Examination Survey (NHANES) data demonstrated an inverse relation between bilirubin and peripheral arterial disease. This association is strongest for patients with which characteristic?

A. black race

B. male sex

C. older age

D. history of diabetes

Answer 7

B. male sex

Question 8

The APPRAISE-2 trial of the factor Xa inhibitor apixaban as an adjunct to antiplatelet therapy for prevention of recurrent ischemia in patients with acute coronary syndromes was halted early. The rate of which of the following outcomes was significantly higher in the apixaban group than in the placebo group?

A. mortality

B. recurrent myocardial infarction (MI)

C. major bleeding

D. the composite of cardiovascular death, MI, and ischemic stroke

Answer 8

C. major bleeding

Question 9

Which of the following statements accurately describes a finding from the ROCKET AF study of rivaroxaban versus warfarin in moderate-to-high-risk patients with atrial fibrillation (AF)?

A. The primary event rate was higher in the rivaroxaban group than in the warfarin group.

B. The international normalized ratio of warfarin recipients was in the therapeutic range about 50% of the time.

C. The rate of systemic embolism was higher in the warfarin group than in the rivaroxaban group.

D. Intracranial and fatal bleeding were more common in rivaroxaban recipients than in warfarin recipients.

Answer 9

B. The international normalized ratio of warfarin recipients was in the therapeutic range about 50% of the time.

Question 10

Which of the following statements accurately describes a finding from a study of apixaban versus aspirin in patients with AF and 1 risk factor for stroke who were not considered appropriate candidates for warfarin treatment?

A. The rate of the primary outcome was more than twice as high in the aspirin group as in the apixaban group.

B. The rate of major bleeding was significantly higher in the apixaban group than in the aspirin group.

C. The rate of cerebrovascular events or MI was lower in the aspirin group than in the apixaban group.

D. Treatment-related adverse events were more common in the apixaban group than in the aspirin group.

Answer 10

A. The rate of the primary outcome was more than twice as high in the aspirin group as in the apixaban group.

Question 11

In a large, manufacturer-funded trial, patients with AF were randomized to receive warfarin or twice-daily doses of either 110 mg or 150 mg of dabigatran. Compared with warfarin, both doses of dabigatran were associated with a significant improvement in which of the following outcomes?

A. study-drug discontinuation

B. hemorrhagic stroke

C. stroke or systemic embolism

D. major bleeding

Answer 11

B. hemorrhagic stroke

Question 12

Name the types of atrial septal defects

Answer 12

Ostium secundum (70% of ASDs)

associated with Holt-Oram syndrome (tri-phalangeal thumbs)

ECG: RBBB with RAD

Ostium primum

present earlier than ostium secundum defects

associated with abnormal AV valves

ECG: RBBB with LAD, prolonged PR interval

Question 13

Describe the heart sound S4

Answer 13

S4 (fourth heart sound)

may be heard in aortic stenosis, HOCM, hypertension

caused by atrial contraction against a stiff ventricle

in HOCM a double apical impulse may be felt as a result of a palpable S4

Question 14

Which drug will cause complete heart block if combined with a beta-blocker?

Answer 14

Verapamil

Question 15

What are the features of Ivrabadine?

Answer 15

Ivabradine

a new class of anti-anginal drug which works by reducing the heart rate

acts on the If (‘funny’) ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activity

adverse effects: visual effects, particular luminous phenomena, are common. Bradycardia, due to the mechanism of action, may also be seen

there is no evidence currently of superiority over existing treatments of stable angina

Question 16

What is the acute mx of SVT?

Answer 16

Acute management

vagal manoeuvres: e.g. Valsalva manoeuvre

intravenous adenosine 6mg → 12mg → 12mg: contraindicated in asthmatics - verapamil is a preferable option

electrical cardioversion

Question 17

Describe the modified Duke criteria

Answer 17

pathological criteria positive, or

2 major criteria, or

1 major and 3 minor criteria, or

5 minor criteria

Pathological criteria

Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)

Major criteria

Positive blood cultures

two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, or

persistent bacteraemia from two blood cultures taken > 12 hours apart or three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis, or

positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci, or

positive molecular assays for specific gene targets

Evidence of endocardial involvement

positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves), or

new valvular regurgitation

Minor criteria

predisposing heart condition or intravenous drug use

microbiological evidence does not meet major criteria

fever > 38ºC

vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura

immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots

Question 18

Criteria for AVR

Answer 18

Symptomatic patients with severe aortic stenosis (<1cm)

Patients with severe aortic stenosis undergoing coronary artery bypass surgery

Patients with severe aortic stenosis undergoing surgery on the aorta or other heart valves

Patients with severe aortic stenosis and LV systolic dysfunction (ejection fraction < 0.50)

Question 19

What is the classification of critical and severe AS?

Answer 19

Always done with TTE

Mean gradient (mmHg) >70 is critical, >40 is severe

Valve area <0.6 is critical, <1.0cm is severe

Question 20

What are the lines of drug therapy in long term maintenance of AF in terms of ventricular control?

Answer 20

B- blocker first line

Then diltiazem

then verapamil

Question 21

When would you consider Digoxin in the control of rapid AF?

Answer 21

Useful in the elderly

Useful in both AF and heart failure as other drugs may be contraindicated or needed to be introduced slowly (i.e. beta blockers)

Not that useful in younger and more active patients

IV dosing has little therapeutic advantage so just give oral

Question 22

Rate or rhythm control for AF?

Answer 22

AFFIRM trial

• no difference in mortality or QOL
• no imperative for cardioversion
• only that QOL may be improved by being in sinus rhythm

Always try to have an ax of LV function and any coronary disease when starting rhythm and rate control drug as they may depress the myocardium or have proarrhythmic potential.

Question 23

What is atrial ‘stunning’? Why is it important?

Answer 23

Risk of atrial ‘stunning’ following cardioversion (electrical, pharmacological or spontaneous).

• unpredictable failure of the atria to contract.
• more common after longer attacks and may persist for hours to days.
• fresh thrombus can form in the hypocontractile atria, and this constitutes an embolic risk even if a TOE an hour or two earlier was clear.

Question 24

What is post -cardioversion maintenance therapy?

Answer 24

Not required if AF was associated with a transient condition.

Anticoagulate for 6-12 months

Long-term antiarrhythmics - flecainide, sotalol, amiodarone

Consider ablation if poorly controlled on antiarrhythmic therapy

If using sotalol, watch out for prolonged QTc (>500ms or >20% from baseline, avoid in renal impairment)

Question 25

What consideration do you need to make in Warfarinising an elderly person?

Answer 25

There is a high risk of bleeding in the first year after starting warfarin in patients aged more than 80 years, and the decision whether to start oral anticoagulation or not is often a difficult one, especially as patients at higher risk of thromboembolism also tend to be those with a higher risk of bleeding.

Question 26

Epidemiology of atrial myxoma

Answer 26

Most common primary cardiac tumor in adults

Mean presentation around 50 (but can be any age)

Women

Associated with MEN (can have myxomas elsewhere too)

Question 27

What are the clinical features of atrial myxoma?

Answer 27

1. valvular obstruction

left sided: dyspnoea, orthopnoea, pulmonary oedema

right sided: symptoms of right heart failure

2. embolic event

distribution will depend on location of tumour

most are left sided, and therefore most are systemic (brain or extremities)

3. constitutional symptoms

weight loss, fatigue, weakness

may resemble infective endocarditis (fever, arthralgia, lethargy)

Question 28

What is the characteristic heart sound of someone with an atrial myxoma?

Answer 28

On auscultation a cardiac murmur is usually present. A characteristic finding in patients with pedunculated and prolapsing myxoma is the so called “tumour plop”

In up to 20% of patients

Question 29

What is the histopath of atrial myxoma?

Answer 29

Benign, often haemoorhagic

Usually pedunculated and over variable size

Usually in the LA attached to the interatrial septum in the fossa ovale region

Question 30

What does an atrial myxoma look like on CT?

Answer 30

Myxomas, as is the case with other cardiac tumours, appear as intra-cardiac masses, most often in the left atrium and attached to the interatrial septum. They are usually heterogeneously low attenuating (approximately 2/3 of cases). Due to repeated episodes of haemorrhage, dystrophic calcification is common.

If the mass is pedunculated, the motion within the heart can be demonstrated, including prolapse through the mitral valve.

Question 31

What is this?

Answer 31

Metastatic pericardial disease

Question 32

What complication does papillary muscle rupture or dysfunction lead to?

Answer 32

Mitral valve prolapse

Question 33

What is cor triatriatum?

Answer 33

Cor triatriatum (or triatrial heart) is a congenital heart defect where the left atrium (cor triatriatum sinistrum) or right atrium (cor triatriatum dextrum) is subdivided by a thin membrane, resulting in three atrial chambers (hence the name). Cor triatriatum represents 0.1% of all congenital cardiac malformations.

Question 34

What is this a picture of?

Answer 34

Cardiac mechanical prosthesis (St Jude)

Question 35

What is the natural history of a VSD?

Answer 35

Blood from higher pressure LV leaks into RV

Reenters the left ventricle after recirculating

Volume overload of left ventricle

Back leakage into RV due to volume overload

Elevated RVP and volume –> pulmonary hypertension

Eventually PAP = systemic pressure (really bad)

Shunt reverses and goes L-R –> cyanosis

Question 36

What is the clinical finding of a VSD

Answer 36

Holosystolic (pan systolic) murmur over lower left sternal edge +/- palpable thrill or heave

Smaller = louder + more palpable thrill

Displaced apex if big enough

Normal HS

Question 37

Three points about VSD

Answer 37

• most common heart defect in children
• most commonly membranous
• most common cause of Eisenmengers syndrome (due to severe overload)

Question 38

What is the purpose of stress ECG testing?

Answer 38

Stress exercise ECG test indirectly assesses adequacy of supply in periods of increased demand

Other modalities are more sensitive because you can see these abnormalities

Question 39

What are the factors predicting an adverse outcome in CHD?

Answer 39

Poor exercise capacity < 5METS

Exercise induced angina (esp if exercise limiting or occurs at low workload)

Abnormal low peak systolic BP (<130mmHg) or fall in systolic BP below baseline

Chronotropic incompetence

Question 40

What are the stress ECG findings that predict an increased risk of adverse outcome?

Answer 40

≥ 1mm down slopping or flat ST depression

≥ 2mm ischaemic ST depression at low workload (stage 2 or less or ≤130bpm)

Early onset (stage 1) or prolonged duration (>5min) ST depression

Multi leads (>5) with ST depression

Ventricular couplets or tachycardia at low workload or in recovery

SR/HR slope (6microV/beat per min)

Question 41

What is the significance of early and late onset ST depression in stress testing?

Answer 41

Normally seen in prolonged exercise probably due to atrial repolarisation extending into the QRS.

Much more significant is early onset ST depression in predicting severe coronary artery disease

Question 42

What is the significance of PVCs in stress testing?

Answer 42

PVC’s occur in about 7-20% of people having exercise testing.

It is not proven to have an association with CAD but potentially be an indicator of ventricular arrhythmia development risk and is an independent predictor of mortality.

Question 43

What does this CXR show?

Answer 43

Severe pulm HT

• markedly prominent main pulm artery (MPA)
• RPA enlarged
• prominent right atrial contour (RA dilation due to RVH)

Question 44

What is pulmonary hypertension?

Answer 44

Resting mean PAP of 25mmHg or more on right heart cath (less than 20 is normal)

Arterial-only hypertension

• high precapillary resistance and normal pulmonary venous pressure (wedge pressure of 15mmHg or less)

Question 45

What is the clinical presentation of pulmonary hypertension

Answer 45

Combination of:

Dyspnoea - esp with exercise

Right heart failure including peripheral oedema and abdominal distension

ECG - RV strain and hypertrophy

Question 46

Name the causes of pulmonary hypertension caused by pulmonary vein and left heart pathology

Answer 46

• chronic left heart failure
• mitral valve stenosis
• hypoplastic left heart syndrome

Question 47

Name the cause of pulmonary hypertension caused by pulmonary capillary and parenchymal pathology

Answer 47

Emphysema of any kind

Asthma

Bronchiectasis of any kind

Lymphangiomyomatosis

Langerhans cell histiocytosis

Pulmonary fibrosis (any cause ie scleroderma, dermatomyositis, rheumatoid, SLE)

Pneumoconiosis

Question 48

Name the cause of pulmonary hypertension caused by pulmonary artery pathology

Answer 48

Chronic pulmonary emboli

Arteritis - PAN, SLE, Takayau, Wegeners

Pulmonary artery stenosis

Question 49

Name the causes of pulmonary hypertension caused by right heart pathology

Answer 49

Eisenmenger phenomenon (inc ASD, VSD, PDA)

Question 50

What are the extra-cardiad findings on CT in pulmonary hypertension?

Answer 50

enlarged pulmonary trunk (pulmonary trunk enlargement is a poor predictor of PH in patients with interstitial lung disease (specificity ~40%)

pulmonary trunk diameter larger than the adjacent ascending aorta

enlarged pulmonary arteries

mural calcification in central pulmonary arteries most frequently seen in patients with Eisenmenger phenomenon

evidence of previous pulmonary emboli

a segmental artery–to-bronchial diameter ratio of 1:1 or more in three or four lobes in the presence of a dilated (29 mm or more) main pulmonary artery-has a specificity of 100% for the presence of pulmonary hypertension

Question 51

What are the medical options in pulmonary hypertension?

Answer 51

calcium channel antagonists

nitric oxide

prostanoids, e.g. epoprostenol, treprostinil, iloporst

endothelin antagonists e.g. bosentan, sitaxsentan, ambrisentan

phosphodiesterase inhibitors

Question 52

What are the causes of a split S2?

Answer 52

Normal - splits a little on inspiration, normal on expiration

Wide split and fixed –> ASD

Wide split and varies with inspiration –> Pulmonary stenosis, RBBB

Paradoxical splitting (pulm first instead of a) –> HOCM

Question 53

3 points about the second heart sound

Answer 53

Splitting of S2 is best heard over the 2nd left intercostal space

The normal P2 is often softer than A2 and rarely audible at apex

Differential Diagnosis of P2 audible at apex- Significant pulmonary hypertension

-Atrial septal defect

(Findings should be present in both upright and supine positions: normal subjects may have expiratory splitting when recumbent that disappears when upright.)

Question 54

What are the causes of a loud first heart sound?

Answer 54

Hyperdynamic (fever, exercise)

Mitral stenosis

Atrial myxoma (rare)

Question 55

What are the causes of a soft first heart sound?

Answer 55

Soft First Sound

Low cardiac output (rest, heart failure)

Tachycardia

Severe mitral reflux (caused by destruction of valve)

Question 56

What are the causes of variable intensity first heart sound?

Answer 56

Variable Intensity of First Sound

Atrial fibrillation

Complete heart block

Question 57

How do you define a split heart sound?

Answer 57

Audible expiratory splitting means > 30 msec difference in the timing of the aortic (A2) and pulmonic (P2) components of the second heart sound.

Question 58

What is the significance of a 3rd heart sound?

Answer 58

Low frequency sound in early diastole

Increased atrial pressure –> increased flow rate

CHF is the most common cause but may be normal in people under 40

Question 59

What is the significance of a 4th heart sound?

Answer 59

Presystolic portion of diastole

Stiff left ventricle - i.e. hypertension, AS, ischemic or HOCM

If the patient has MR, may be due to acute regurgitation following chorda tendinae rupture

Question 60

What’s the best way to hear the 3rd and fourth heart sounds?

Answer 60

Both sounds are low frequency and thus best heard with the bell of the stethoscope.

Location:

If originating from LV

Usually best heard over apex with patient in the left lateral position

Softer during inspiration

If originating from RV

Usually best heard over left lower sternal border

Louder during inspiration

Question 61

What is definition of HOCM and it’s prevalence?

Answer 61

LVH in absence of other loading conditions

Prevalence 0.2% or 1 in 500!

Question 62

Epidemiology of HOCM?

Answer 62

AD with variable penetrance

Offspring of affected = 50%

Can be benign

Commonest cause of sudden cardiac death <35 years

Can have angina, signs of pulm congestion (PND, orthopnoea), syncope, and palpitations

Question 63

What are the clinical examination features of HOCM?

Answer 63

Jerky rapidly rising pulse

Prominent LV impulse

Apical systolic murmur that increases with valsalva (related to dynamic obstruction)

Fourth heart sound

Question 64

What are the ECG findings in HOCM?

Answer 64

LVH

TWI

Q waves

Question 65

What are the causative genes of HOCM?

Answer 65

Primarily encode sarcomere or sarcomere related proteins

Cardiac β-myosin heavy chain (β MHC) (45%)

Myosin binding protein C (MyBPC) (35%)

Also:

Cardiac troponin T, tropomyosin, cardiac

troponin I, essential and regulatory myosin light c

hain, and more recently, titin and actinin-2 genes

Question 66

What is the role of genetic testing in HOCM?

Answer 66

Identifies at-risk earlier

Avoids unecessary screening of non-carriers

Can distinguish between other causes of LVH

Pick up rate of 50-50%

Question 67

When does sudden death in HOCM most frequently occur?

Answer 67

Sudden death occurs most commonly in HCM either during or immediately after exercise, although death can also occur at rest

Question 68

Who should be screened for HOCM and how often?

Answer 68

All first-degree relatives of an affected individual be clinically screened for HCM. As a minimum, this involves a physical examination by a cardiologist, an ECG and a transthoracic echocardiogram.

>31 - every 3-5 years

21-30 - every 2-3 years

11-20 - every 1-1.5 years

Question 69

When should the physician report someone to the RTA?

Answer 69

The health professional should consider

reporting directly to the driver licensing authority in situations where the patient is either:

•

unable to appreciate the impact of their condition, or

•

unable to take notice of the health professional’s recommendations due to cognitive impairment, or

•

continues driving despite appropriate advice and is likely to endanger the public

Question 70

What are the driving rules for:

Elective PCI

MI

CABG

Arrest

Answer 70

Elective PCI - 2 days
MI - 2 weeks
CABG - 4 weeks

Arrest - 6 months

Question 71

What are the driving rules for:

DVT

Cardiogenic syncope

PE

Answer 71

DVT - 2 weeks

Cardiogenic syncope - 4 weeks

PE - 6 weeks

Question 72

What is the driving license rule with regard to heart failure?

Answer 72

Sx on moderate exertion = no licence

Question 73

What are the driving rules for seizures?

Answer 73

First seizure - six months

First treatment - on treatment for six months and compliant, even if they had a seizure within those six months.

Otherwise - 12 months

Question 74

How long after a stroke can you drive?

Answer 74

4 weeks - 2 if TIA

SAH - 3 months

Question 75

How do you differentiate between chronic hypertension and pre-eclampsia?

Answer 75

Chronic hypertension

• hypertension before 20 weeks gestation, often diastolic
• no or stable proteinuria

(if after 20 weeks gestation and no proteinuria –> gestational hypertension)

Question 76

What does the a-wave of JVP mean?

Answer 76

‘a’ wave = atrial contraction

large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension

absent if in atrial fibrillation

coincides with first heart sound

Question 77

What is a cannon a-wave?

Answer 77

Cannon ‘a’ waves

caused by atrial contractions against a closed tricuspid valve

are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular pacing

Question 78

What is the v wave of the JVP?

Answer 78

‘v’ wave

due to passive filling of blood into the atrium against a closed tricuspid valve

giant v waves in tricuspid regurgitation - very reliable sign

Question 79

What does the S1 of the heart sound refer to? Pathology?

Answer 79

S1

closure of mitral and tricuspid valves

soft if long PR or mitral regurgitation

loud in mitral stenosis

Question 80

What does the S2 of the heart sound refer to? Pathology?

Answer 80

S2

closure of aortic and pulmonary valves

soft in aortic stenosis

splitting during inspiration is normal

Question 81

What is the significance of an ASD?

Answer 81

• most likely congenital heart defect to be found in adulthood. They carry a significant mortality, with 50% of patients being dead at 50 years.

DVTs can cross the circulation and embolise to the brain.

Question 82

What are the features of an ASD?

Answer 82

ejection systolic murmur

fixed splitting of S2

embolism may pass from venous system to left side of heart causing a stroke

Question 83

How do you calculate stroke volume?

Answer 83

Stroke Volume = End Diastolic Volume– End Systolic Volume

Question 84

How do you calculate cardiac output?

Answer 84

Cardiac Output = Heart Rate x Stroke Volume

Question 85

What is VO2 max?

Answer 85

VO2 max (also maximal oxygen consumption, maximal oxygen uptake, peak oxygen uptake or maximal aerobic capacity) is the maximum rate of oxygen consumption as measured during incremental exercise

Question 86

Why is it useful to measure the mixed venous oxygen concentration?

Answer 86

It can be used as a marker of how well O2 is being delivered to the peripheral tissues by extrapolation (if SvO2 low and patient in multiorgan failure then we can add a inotrope to help increase cardiac output ie. in severe sepsis)

High

increased O2 delivery (increased FiO2, hyperoxia, hyperbaric oxygen)

decreased O2 demand (hypothermia, anaesthesia, neuromuscular blockade)

high flow states: sepsis, hyperthyroidism, severe liver disease

Low

decreased O2 delivery:

1. decreased Hb (anaemia, haemorrhage, dilution)
2. decreased SaO2 (hypoxaemia)
3. decreased Q (any form of shock, arrhythmia)

increased O2 demand (hyperthermia, shivering, pain, seizures)

Question 87

How do you calculate venous oxygen content?

Answer 87

Venous Oxygen content = Arterial Oxygen content - Oxygen consumption / Cardiac output.

Therefore, mixed venous O2 content is directly related to arterial oxygen content (therefore related to hemoglobin concentration and partial pressure of Oxygen) and cardiac output (therefore it will increase in cases of low cardiac output) and oxygen consumption which means tissue perfusion (therefore you have increased mixed venous O2 content in shock and in any case of impaired tissue perfusion).

Question 88

What is Fick’s principle?

Answer 88

CO = VO2 (oxygen consumption) / arteriovenous oxygen difference (Ca-Cv)

Question 89

How do you measure VO2?

Answer 89

VO2, oxygen consumption in ml of pure gaseous oxygen per minute. This may be measured using a spirometer within a closed rebreathing circuit incorporating a CO2 absorber

Question 90

What happens to the heart in old people?

Answer 90

Heart rate decreases (really affects max CO)

Stroke volume declines (major factor for the decline lower cardiac output in submax exercise)

LV contractility declines

Decreased vascular capacity and local blood flow autoregulation

Poor O2 delivery

Poor muscle oxidative capacity

Increased TPR

Question 91

In which cardiac patients is antibiotic prophylaxis recommended if undergoing dental surgery?

Answer 91

• prosthetic valve or material used for valve repair
• previous IE
• Congenital heart disease but only if
• unrepaired cyanotic defects (inc pal shunts and conduits)
• completely repaired with material or device either by surgery or cath and it’s during the first 6 months afterward
• repaired defects with resiudal defects at or adjacent to the site of a patch or device (which inhibit endothelialisation
• cardiac transplant with subsequent development of valvulopathy
• RHD in in aboriginals only

Question 92

For which dental procedures is antibiotic phrophylaxis always required in at-risk cardiac patients?

Answer 92

• extraction
• periodontal procedures inc surgery, subgingival scaling and root planing
• replanting avulsed teeth
• other surgical procedures ie implants

(Cleaning, braces, - only if repeated)

No need if just having anaesthetic, intracanal procedure, removal of sutures

Question 93

What is the standard antibiotic prophylaxis for IE in at-risk patients undergoing dental procedures?

Answer 93

Amoxicillin 2g 1 hour before procedure

If hypersensitive/already on long-term/or in last month

Clindamycin 600mg 1 hour beforehand

Question 94

Which respiratory tract procedures require endocarditis prophylaxis in those at-risk?

Answer 94

Anything involving incision or bx of resp mucosa

• tonsillectomy/adenoidectomy
• bronch PLUS incision or bx

Any surgery inc bronchial sinus, nasal or middle ear mucosa including tympanosomty tube insertion

Question 95

For which GI and GUT procedures is antibiotic prophylaxis required in at-risk cardiac patients?

Answer 95

Lithotripsy

Any GU procedure in the prsence of a GU infection (unless already treating enterococci) - get an MSU beforehand!

Ditto GIT

Do NOT need for catheters, vaginal deliveries, TOE, endoscopy/colonoscopy +/- bx, perc gastrostomy

Question 96

Name the points on the JVP

Answer 96

A- wave (S1) - atrial contraction

C-wave - tricuspid valve closure

X-descent - atrial relaxation

V-wave (S2) - atrial filling

Y-descent - rapid ventricular filling

Question 97

What is the definition of a raised JVP?

Answer 97

More than 3cm from the zero point (or 8cm from the right atrium)

The zero point is the sternal angle when the patient is lying at 45 degrees

Question 98

Define the anatomy of the JVP

Answer 98

Internal jugular vein is preferred (although does correlate well with external

This is lateral to the SCM

Question 99

Why is the right sided internal jugular vein preferred for measuring the JVP?

Answer 99

The left sided veins cross from the left side of the chest before entering the right atrium so are less accurate

Question 100

What does the pulmonary artery wedge pressure measure?

Answer 100

• pressure within the pulmonary arterial system when catheter tip ‘wedged’ in the tapering branch of one of the pulmonary arteries
• in most patients this estimates LVEDP thus is an indicator of LVEDV (preload of the left ventricle)
• PCWP >18 mmHg in the context of normal oncotic pressure suggests left heart failure

Question 101

In what situations is the PAWP not equivalent to LVEDP?

Answer 101

(Wedge pressure greater) than LVEDP

Mitral stenosis or MR
Atrial myxoma

Pulmonary venous obstruction (i.e. fibrosis, vasculitis)

L-R shunt

COPD

IPPV

Wedge pressure less than LVEDP

• severe LV failure
• high PEEP
• noncompliant LV (i.e. hocm)
• AR

Question 102

What is the normal distribution of the ECG leads?

Answer 102

Inferior = II, III, aVF

Lateral = I, aVL, V5-6

Anterior = V2-6

Question 103

What does LBBB and RBBB do to the t-wave?

Answer 103

Left bundle branch block produces T-wave inversion in the lateral leads I, aVL and V5-6.

Left bundle branch block produces T-wave inversion in the lateral leads I, aVL and V5-6.

Question 104

How do you interpret a troponin?

Answer 104

A test should be interpreted as positive if level

is

≥

99th centile for reference population OR

there is a change of

≥

50% above an initial base-

line level. A positive finding identifies patients

at increased risk, but does not provide defini-

tive evidence of MI. A positive troponin result

should be followed up by a search for an

alternative plausible diagnosis and/or cardiac

consultation if ACS is suspected in the context

of the clinical presentation.

Question 105

What is the epidemiology of familial hypercholesterolaemia?

Answer 105

AD

Prevalence in offspring of 50%

Mediterraneans

Question 106

What is the clinical presentation of familial hypercholesterolaemia?

Answer 106

1) Severe hypercholesterolaemia that is not explained by secondary causes,
2) A strong personal or family history of premature atherosclerotic cardiovascular disease (CVD),
3) Tendon Xanthomas

Question 107

How do women differ from men with regard to familial hypercholesterolaemia?

Answer 107

Protected prior to menopause

Natural hx delayed by about one decade

But still accelerated b y 2 decades in both women and men

Question 108

What are the specific signs of familial hypercholesterolaemia

Answer 108

Tendon xanthomas (achilles and extensors on dorsum of the hand) –> pathognomonic

Arcus (white ring around around iris - corneal margin) in a young person is suggestive.

Question 109

What are the nonspecific clinical presentations of familial hypercholesterolaemia?

Answer 109

Arcus and xanthelasma

Premature CHD/CVD

Aortic stenosis

Question 110

What are the metabolic features of hypercholesterolaemia?

Answer 110

Increased LDL

Increased remnants including precursor IDL

Question 111

What are the top 3 specific features of familial hypercholesterolaemia?

Answer 111

8 points DNA Mutation, or LDL-C > 8.5

6 points Tendon xanthomas

5 points LDL-C 6.5 – 8.4

4 points Arcus senilis < 45 yrs

3 points LDL 5.0 – 6.4

2 points Xanthomas or premature arcus in 1 st degree relative, childhood LDL > 95th percentile, or premature CHD

1 point 1st deg relative with premature CVD or LDL > 95 th percentile, personal history of LDL 4.0 – 4.9 or premature CVD

Question 112

When should you suspect familial hypercholesterolaemia?

Answer 112

Patients presenting to cardiology and stroke units with premature CVD (aged < 60 yr), and in primary care amongst those with a family history of hypercholesterolaemia and

premature CVD.

Risk factor counting, non-invasive testing for atherosclerosis (carotid ultrasonography, cardiac CT) and documented CVD should be used to stratify patients for routine, enhanced and high intensity treatment.

Question 113

What is the main value of molecular diagnosis of familial hypercholesterolaemia?

Answer 113

The major value in making a molecular diagnosis is its use in predictive testing

of other family members for FH. This is useful in early detection of cases that need intervention to prevent CVD and in re-assuring family members who may not have the condition.

Question 114

What genes are associated with familial hypercholesterolaemia?

Answer 114

LDL receptor (most common)

LDL receptor ligand (apolipoprotein B100) - second most common

Proprotein Convertase Subtilsin Kexin 9 (PCSK-9) - third most common

Question 115

When would you be most likely to find a causative mutation for familial hypercholesterolaemia?

Answer 115

Definite clinical familial hypercholesterolaemia –> causative mutation found 80% of the time.

Question 116

What is the management of predominantly elevated LDL-C?

Answer 116

Statins are first-line therapy for predominant elevation of LDL-C. The efficacy of statins in reducing the risk of cardiovascular events is proven, and there is a low rate of serious adverse effects with long-term use.

Question 117

When is use of a bile acid binding resin inappropriate?

Answer 117

Addition of a bile acid binding resin can enhance LDL-C reduction, but is inappropriate when triglycerides are elevated because hypertriglyceridaemia can be exacerbated.

Question 118

What does doubling the dose of a statin do to the LDL-C?

Answer 118

Each doubling of statin dose is likely to reduce LDL-C by an additional 5% to 10%.

Question 119

What is the next step after maximal statin therapy fails to bring down the LDL-C enough?

Answer 119

The addition of ezetimibe to statin therapy is often synergistic, with the additional lowering of LDL-C ranging from 20% to 25%.

Ezetimibe is well tolerated in about 75% of patients who are unable to tolerate statin therapy, with LDL-C decreasing by 15% to 20%.

Question 120

Under what circumstances are bile acid binding resins used in dyslipidemia?

Answer 120

If LDL-C is still not well controlled, or there are adverse effects from ezetimibe, consider adding a bile acid binding resin. Bile acid binding resins are mainly used in combination with statins, but they can be used alone or in combination with other drugs, including ezetimibe. Resins increase triglyceride levels and are inappropriate in moderate to severe hypertriglyceridaemia.

Question 121

What are the adverse effects of bile acid binding resins?

Answer 121

GI effects limit the max dose and are a common reason for nonadherence - need to take with lots and lots of water to minimise upper GIT disturbance

Constipating

Can interfere with drdug absorption esp anticoagulants, thyroxine, cyclosporin, and digoxin

Question 122

What is third line after a statin plus ezetimibe for dyslipidemia of LDL-C variant?

Answer 122

Bile acid binding resin

Question 123

What is fourth line therapy for dyslipidemia of the LDL-C kind?

Answer 123

Nicotinc acid - rarely used as is poorly tolerated mainly due to flushing (can give with food and prophylactic aspirin)

Can also cause gastric irration, gout and impaired glucose tolerance.

Need to monitor BSL, CK, and liver.

Use with caution with a statin (but can be done)

Question 124

Can you use fibrates with a statin to reduce LDL-C? What do you need to consider?

Answer 124

May lead to 5-10% reduction in LDL-C

Does not increase risk of myopathy beyond the level of statin monotherapy, EXCEPT…

Gemfibrozil - DO NOT DO IT, significantly increases the risk of myositis when given with a statin.

Use fenofibrate instead and monitor CK.

Question 125

How do you treat hypertriglyceridaemia?

Answer 125

Dietary/behaviour/diabetic control are central.

If severe (>10), or >4 and have low HDL-C (<1) or is associated with increased absolute CVD risk:

Fibrate plus fish oil (Two Fs!) - and probably need to max both out.

Nicotinic acid is third line. Statins are inappropriate

Question 126

High CVD risk

Elevated LDL-C

Mild to moderate elevation of TGLs

What is the treatment?

Answer 126

Statins are first line

Question 127

High absolute CVD risk

LDL-C elevated

TGLs >4

What is first line therapy?

Answer 127

Fibrate

Question 128

How safely do you treat mixed hyperlipidaemia that is severe? (Mixed = high cholesterol and TGL)

Answer 128

Statin plus fish oil

Fibrate plus ezetimibe

Statin plus fenofibrate or statin plus nicotinic acid can be done but only with caution.

Question 129

What are the side effects of Ezetimibe?

Answer 129

Steatorrhea

Myalgia and rhabdo have been repeated

Raise ALT/AST

NOT CYP450 so limited drug interactions

Avoid in mod-severe liver impairment (no data)

Question 130

What are the risk factors for developing liver and muscle problems from lipid-modifying therapy?

Answer 130

Risk factors for these adverse effects include pre-existing muscle, liver or kidney disease, high-dose therapy, concomitant interacting drugs, intercurrent illness, frailty and advanced age.

Question 131

How do you monitor lipid modifying therapy?

Answer 131

Basleine LFTS and when you assess response to lipids - 1-2 months post initiation/dose adjustment

No need to routinely monitor CK/LFT if asymptomatic - unless on combination therapy

If asymptomatic CK elevation - avoid exercise for a few days. Continiue if CK is not >5 ULN

Question 132

When should you stop lipid-modifying therapy?

Answer 132

Mild muscle sx - still benefit from max dose, try second daily or twice weekly

Stop lif:

previously normal ALT is persistently more than 3 times ULN

CK is more than 10 times ULN

CK is more than 5 times ULN and patient has muscle symptoms

patient has persistent unexplained muscle pain

patient has persistent unexplained muscle weakness.

Question 133

What do you do if someones muscles or liver enzymes normalise after you stop lipid-modifying therapy?

Answer 133

If the symptoms were mild, drug can be restarted (at a lower dose), if it recurs - change statin or go to alternative lipid modifying drug

Question 134

Which lipid-modifying agents impair glucose metabolism?

Answer 134

High-dose statins may slightly impair glucose metabolism, while nicotinic acid can cause impaired glucose tolerance as well as hyperuricaemia and gout. Check blood glucose before starting therapy, and repeat 1 to 2 months after starting therapy or adjusting the dose.

Question 135

Which lipid modifying drugs affect the CK and ALT respectively?

Answer 135

CK: statin > fibrate > nicotinic acid or ezetimibe

ALT: nicotinic acid > ezetimibe > fibrate > statin

Question 136

What lipid tests are required to calculate absolute CVD risk?

What are the drawbacks of this?

Answer 136

TC (total cholesterol) and HDL-C

TC may overestimate risk of HDL-C is raised

TC may underestimate risk of TGLs are raised

Predictive value is improved by considering LDL-C and HDL-C independently

Question 137

What impact does significantly elevated triglycerides have on the measurement of cholesterol and LDL-C?

Answer 137

LDL composition changes when TGL >2mmol

• in this case, non-HDL-c becomes a better indicator than LDL-c
• LDL-C requires a fasting sample and becomes unreliable if TGLs exceed 4mmol

Question 138

How do statins reduce LDL?

Answer 138

Reduce liver cholesterol synthesis

Increased LDLr and SREBP gene expression

Receptors produced by normal gene (even in familial disease) will reduce LDL cholesterol levels.

Question 139

What are the target lipid levels for patients on lipid-modifying therapy?

Answer 139

total cholesterol (TC) - less than 4.0 mmol/L

low-density lipoprotein cholesterol (LDL-C) - less than 2.0 mmol/L

high-density lipoprotein cholesterol (HDL-C) - more than 1.0 mmol/L

triglycerides -less than 2.0 mmol/L

non–high-density lipoprotein cholesterol (non–HDL-C) - less than 2.5 mmol/L

Question 140

What are the target LDL-C levels in those with familial hypercholesterolaemia?

Answer 140

Target plasma levels for LDL-cholesterol for low, intermediate an d high risk FH are < 4, < 3 and < 2 mmol/L, respectively

Question 141

Which subset of familial hypercholesterolaemia patients benefits the most from statins?

Answer 141

Statin treatment of FH males is one of the most cost-effective medical intervention

s available and several lines of evidence point towards major improvements in CVD event rates and total mortality of FH patients since its introduction. Still evolving for younger patients.

Question 142

What does this ECG show?

Answer 142

Broad QRS >120ms

RSR pattern in V1-V3

Wide slurred S wave in lateral leads (I, AVL, V5-V6)

RBBB

Question 143

What syndrome do you need to be mindful of when diagnosing a RBBB on ECG?

Answer 143

An RSR’ pattern in V1-3 may also be caused by Brugada syndrome – an ECG pattern associated with malignant ventricular arrhythmias.

Question 144

When is treatment stress testing indicated?

Answer 144

Symptoms of known or probably ischaemic heart disease

Stable chest pain

Unstable chest pain stabilised by medical therapy

Post MI

Post revascularisation

Question 145

What are the absolute contraindications to EST?

Answer 145

Acute MI

Unstable angina

Symptomatic uncontrolled cardiac arrhythmia

Severe AS

Acute PE or pulm infarct

Acute myocarditis or pericarditis

Acute aortic dissection

Question 146

What are the most important pre-test predictive parameters of CAD?

Answer 146

Chest pain

Sex

Age

Diagnostic power of EST is maximal when the pretest probability is intermediate (30-70%)

Question 147

What are the indications for PCI?

Answer 147

Clinical indications for PCI include the following:

Acute ST-elevation MI (STEMI)

Non–ST-elevation acute coronary syndrome (NSTE-ACS)

Stable angina

Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)

Asymptomatic or mildly symptomatic patient with objective evidence of a moderate-sized to large area of viable myocardium or moderate to severe ischemia on noninvasive testing

Angiographic indications include hemodynamically significant lesions in vessels serving viable myocardium (vessel diameter >1.5 mm).

Question 148

What is the evidence behind CTCA?

Answer 148

Meta-analyses of over 45 single-centre studies have consistently shown CTCA to have excellent sensitivity (98%) and very good specificity (88%) compared with invasive coronary angiography for significant disease (stenosis > 50%).5,8,9 The negative predictive values (96%–100%) were better than positive predictive values (93%), demonstrating CTCA to be an excellent tool for ruling out significant disease in patients with low-to-intermediate pretest probability of CAD.

Question 149

What are the indications for CTCA in the evaluation of non-acute chest pain?

Answer 149

Evaluation of chest pain with no previous known disease:

able to exercise and no previous tests (intermediate risk)

unable to exercise or ECG uninterpretable (low-to-intermediate risk)

equivocal or uninterpretable stress test results

normal ECG exercise test but ongoing symptoms.

Question 150

What are the indications for CTCA with acute chest pain?

Answer 150

Evaluation of acute chest pain (emergency department):

normal ECG and cardiac enzymes

low-to-intermediate pretest probability of CAD.

Question 151

What are the indications for CTCA outside of chest pain?

Answer 151

Evaluation of suspected coronary anomalies/complex congenital heart disease.

Exclusion of CAD in new-onset heart failure/cardiomyopathy.

Assessment of CABG patency and vascular mapping before repeat CABG surgery.

Exclusion of significant CAD before non-coronary cardiac surgery.

Investigation of left bundle branch block for suspected CAD as an aetiology.

Question 152

What is the most appropriate application of CTCA?

Answer 152

It is used most appropriately in symptomatic patients with low to intermediate pretest probability of CAD.

Question 153

When should CTCA not be used?

Answer 153

It should not be used in asymptomatic subjects, patients with known significant CAD or patients with a high pretest probability of CAD.

Question 154

How does the radiation dose of CTCA compare with invasive coronary angio?

Answer 154

The radiation dose of CTCA was previously two to three times that of invasive coronary angiography but with modern protocols, it is similar or lower.

Question 155

What are the absolute contraindications to thrombolysis?

Answer 155

Any previous history of hemorrhagic stroke

History of stroke, dementia, or central nervous system damage within 1 year

Head trauma or brain surgery within 6 months

Known intracranial neoplasm

Suspected aortic dissection

Internal bleeding within 6 weeks

Active bleeding or known bleeding disorder

Major surgery, trauma, or bleeding within 3 weeks

Traumatic cardiopulmonary resuscitation within 3 weeks

Question 156

What are the indications for digoxin?

Answer 156

CHF (regardless of side) particularly due to chronic overload and supply of energy is not impaired (i.e impaired in hypoxia, thiamine deficiency, thyrotoxicosis

AF - depresses conduction in the AV bundle –> slower ventricular beat. Converts flutter to fibrillation and may restore SR on withdrawal - but not first line.

Not for prevention of paroxysmal AF

Question 157

What does the ECG show?

Answer 157

QRS > 120ms w/ abnormal morphology

Steep R-wave and absent S wave in leads 1 and V6

Deep rapid S wave in V1 (arrow)

Multiple ST segment elevation (mild), and T-wave polarity is opposite to the ventricular complex

LBBB - reversal of interventricular septum activation with delayed impulse to the LV

Question 158

What are the limitations of coronary artery calcium scoring?

Answer 158

Current expert consensus does not recommend CAC measurement in asymptomatic low-risk (a 10-year risk less than 10%) or high-risk (a 10-year risk more than 20%) patients, in those with a documented history of CVD or to establish the presence of obstructive coronary artery disease.

Question 159

What are the indications for coronary calcium scoring?

Answer 159

CAC scoring is only recommended for asymptomatic men aged 45-75 (or women aged 55-75) with an intermediate Framingham score (10-year risk of 10%) in whom a high-risk CAC (more than 100) may prompt a more aggressive approach to risk factor modification. CAC assessment may also be reasonable for assessment of symptomatic patients in the setting of an equivocal treadmill or other functional test.

Question 160

What are the scoring categories of the Framingham Risk Score?

Answer 160

Individuals with low risk have 10% or less CHD risk at 10 years, with intermediate risk 10-20%, and with high risk 20% or more. However it should be remembered that these categorisations are arbitrary.

Question 161

Give a scenario where a coronary calcium score would be useful

Answer 161

The type of clinical situation where CAC scoring can be useful is the following: an asymptomatic 45-year-old male smoker with a systolic BP of 120mmHg, no history of diabetes or hypertension, without left ventricular hypertrophy criteria on ECG, and normal cholesterol (eg, total cholesterol 6.0mmol/L, HDL-C 1.0mmol/L) has a 10-year Framingham risk score of 10% (ie, intermediate risk) and lifestyle measures only would be prescribed.

A high CAC score above 100 AU would yield a post-test probability of more than 2% per year for a coronary event and would move the patient into the high-risk category (a 10-year risk above 20%). Such a patient would require the adoption of aggressive secondary (as opposed to primary) prevention strategies.

Goals for blood pressure and lipid levels may be tightened to those of someone known to have coronary artery disease (eg, LDL-cholesterol less than 1.8mmol/L) and medications, along with lifestyle measures, prescribed.

f the CAC score was either very low (less than 10) or zero, the patient’s post-test risk for CHD would be lower than 10% per 10-year period (ie, low risk) and lifestyle-only measurements would be prescribed.

Question 162

What is CHD risk equivalent?

Answer 162

Some patients without known CHD have risk of cardiovascular events that is comparable to that of patients with established CHD. Cardiology professionals refer to such patients as having a CHD risk equivalent. These patients should be managed as patients with known CHD.

CHD risk equivalents are patients with a 10-year risk for MI or coronary death >20%. CHD risk equivalents are primarily other clinical forms of atherosclerotic disease.

The NCEP’s ATP III guidelines also list diabetes as a CHD risk equivalent since it also has a 10-year risk for CHD around 20%. NCEP ATP III CHD risk equivalents are:

clinical coronary heart disease (CHD)

symptomatic carotid artery disease (CAD)

peripheral arterial disease (PAD)

abdominal aortic aneurysm (AAA)

diabetes mellitus

Chronic Kidney Disease

Question 163

What are the ECG changes in LVH?

Answer 163

Increased R wave amplitude in the left-sided ECG leads (I, aVL and V4-6)

Increased S wave depth in the right-sided leads (III, aVR, V1-3).

Question 164

How do you recognise left axis deviation on ECG?

Answer 164

QRS is positive (dominant R wave) in leads I and aVL

QRS is negative (dominant S wave) in leads II and aVF

Question 165

What are the causes of left axis deviation?

Answer 165

LVH

Inferior MI

LBBB

WPW

Question 166

What ECG finding is suggestive of left main coronary artery occlusion?

Answer 166

A pattern of widespread ST depression plus ST elevation in aVR > 1 mm is suggestive of left main coronary artery occlusion.

Question 167

What do you make of ST depression localised to a specific territory on ECG?

Answer 167

ST depression localised to a particular territory (esp. inferior or high lateral leads only) is more likely to represent reciprocal change due to STEMI. The corresponding ST elevation may be subtle and difficult to see, but should be sought.

Question 168

When is T-wave inversion considered to be evidence of myocardial ischemia?

Answer 168

At least 1 mm deep

Present in ≥ 2 continuous leads that have dominant R waves (R/S ratio > 1)

Dynamic — not present on old ECG or changing over time

NB. T wave inversion is only significant if seen in leads with upright QRS complexes (dominant R waves). T wave inversion is a normal variant in leads III, aVR and V1.

Question 169

What is Mobitz II heart block?

Significance?

Answer 169

A-V block

PR of constant interval

Constant PR interval until P waved dropped with P-P interval twice normal

Likely to progress to CHB

Question 170

What does the ECG show?

Answer 170

Constant PR interval until P waved dropped with P-P interval twice normal

This the Mobitz II (the bad one)

Question 171

What is Wenkebach block?

Significance?

Answer 171

Lengthening PR interval until P waved dropped with P-P interval variable. Grouped beats.

Need follow up but less likely to progress to CHB

Question 172

What does this ECG show?

Answer 172

ST elevation primarily localised to leads I and aVL is referred to as a high lateral STEMI.

It is usually associated with reciprocal ST depression and T wave inversion in the inferior leads.

Occlusion of the first diagonal branch (D1) of the left anterior descending artery (LAD) may produce isolated ST elevation in I and aVL

Occlusion of the circumflex artery may cause ST elevation in I, aVL along with leads V5-6.

Question 173

What ECG findings are best used to differentiate PE from ACS?

Answer 173

Negative T waves in both leads III and V1 (Part of an RV strain pattern - can be in other right sided things too)

Question 174

How do you recognise right axis deviation?

Answer 174

QRS is positive (dominant R wave) in leads III and aVF

QRS is negative (dominant S wave) in leads I and aVL

Question 175

What does the ECG show?

Answer 175

QRS is positive (dominant R wave) in leads III and aVF

QRS is negative (dominant S wave) in leads I and aVL

Right axis deviation

Question 176

How is the cardiac axis defined?

Answer 176

RA is negative

LA is positive

A depolarization wave is always positive on ECG when it is heading toward the left.

V1 and V2 are always negative for this reason and reflect the septum

Leads II and II are the feet leads and are always positive

Question 177

Name the different infarct patterns on ECG

Answer 177

The different infarct patterns are named according to the leads with maximal ST elevation:

Septal = V1-2

Anterior = V2-5

Anteroseptal = V1-4

Anterolateral = V3-6, I + aVL

Extensive anterior / anterolateral = V1-6, I + aVL

Question 178

ECG findings in PE

Answer 178

Sinus tachycardia - the most common abnormality; seen in 44% of patients.

Complete or incomplete RBBB - associated with increased mortality; seen in 18% of patients.

Right ventricular strain pattern – T wave inversions in the right precordial leads (V1-4) ± the inferior leads (II, III, aVF). This pattern is seen in up to 34% of patients and is associated with high pulmonary artery pressures.

Right axis deviation – seen in 16% of patients.

Dominant R wave in V1 - a manifestation of acute right ventricular dilatation.

SI QIII TIII pattern – deep S wave in lead I, Q wave in III, inverted T wave in III. This “classic” finding is neither sensitive nor specific for pulmonary embolism; found in only 20% of patients with PE.

Question 179

What are the causes of acute cor pulmonale (i.e. any disease that causes right ventricular strain / hypertrophy due to hypoxic pulmonary vasoconstriction)?

Answer 179

Severe pneumonia

Exacerbation of COPD / asthma

Pneumothorax

Recent pneumonectomy

Upper airway obstruction

Question 180

How do you define a low-voltage ECG?

Answer 180

Peak-to-peak QRS <5mm in the limb leads or <10mm in the precordial leads

Question 181

What causes a low voltage ECG?

Answer 181

Obesity

COPD

Pericardial effusion

Severe hypothyroidism

Massive damage

Infiltrative/restrictive disease ie amyloid

Question 182

When using a right heart catheter to measure drug response in pulmonary hypertension, which two values are you looking at?

Answer 182

• mean PAP - looking for reduction as this measures response
• pulm vascular resistance - this measures prognosis (high is bad)

So an agent that changes the mean PAP the most, and reduces the PVR is a good one.

Question 183

What are the biomarkers used in pulm hypertension?

Answer 183

Pro-BNP – correlated with degree of RV dysfunction

Uric acid: sign of tissue hypoperfusion

Troponin

Also (not a biomarker but)

Key prognostic measure is pulmonary vascular resistance – higher is a worse prognosis

Question 184

What is the evidence for CCB’s in PHT?

Answer 184

Increase 5 year survival

Question 185

What is the evidence for prostacyclin (Epoprostenol) in PHT?

What about an endothelin receptor antagonist (Bosentan)?

Answer 185

Decrease PAP

Decrease PVR

Increase survival

Increase six minute walk

Bosentan is the same but also increases cardiac output

Question 186

What’s the evidence for a PDE5 inhibitor (Sildenafil) in PHT?

Answer 186

Decreases PAP

Decreases PVR

Increases 6min walk test

Question 187

What’s the evidence for epoprostenol and prostacyclin analogues in PHT?

Answer 187

Both increase 6 minute walk test and decrease symptoms

Question 188

What is the role of atrial septostomy in PHT?

Heart-lung transplant?

Answer 188

Atrial septostomy: creates R -> L shunt to decrease RHF. Last resort

Heart-Lung Transplant for patients with class III-IV symptoms not responsive to medical treatment

Question 189

What are the mitigating factors of CCBs in PHT?

Answer 189

Ca antagonists can cause sustained improvement (use amlodipine or diltiazem – may need high doses – eg 120 – 900 mg diltiazem). Improved survival in responders only. Evidence only idiopathic PAH – no evidence in CTD

Question 190

What is the clinical definition of PHT?

Answer 190

Most commonly used: Mean pulmonary artery pressure > 25 mmHg at rest [Severe = > 50 mmHg]or 30 with exercise (if you exercise people you find more) AND the absence of significant parenchymal lung disease, chronic thromboembolic disease, LH valve or myocardial disease, congential heart disease or systemic connective tissue disease

Alternative threshold: WHO 1998 systolic peak pulmonary pressure > 40 mmHg, corresponds to tricuspid regurgitant velocity on Doppler of 3.0 to 3.5 m/sec

Question 191

Which is more common - primary or secondary PHT?

Answer 191

Secondary (ie disease associated) - much more common

Question 192

What is the epidemiology of idiopathic PHT?

Answer 192

5 year survival 35%

Women of childbearing years

6-10% familial - AD w/ incomplete penetrance - PPH1 gene –> morphogenetic protein receptor II (BMPR2) –> normal protein inhibits muscle proliferation, abnormal protein –> vascular remodelling

Question 193

In which infarct settings is more volume support required?

Answer 193

RV infarct (need high filling Pa to maximize filling of LV)

Venodilatation and hypotension with inferior MI.

Question 194

What is the culprit lesion in an inferior STEMI?

Answer 194

The vast majority (~80%) of inferior STEMIs are due to occlusion of the dominant right coronary artery (RCA).

Question 195

Why will up to 20% of patients with inferior stemi develop heart block?

Answer 195

Ischaemia of the AV node due to impaired blood flow via the AV nodal artery. This artery arises from the RCA 80% of the time, hence its involvement in inferior STEMI due to RCA occlusion.

Bezold-Jarisch reflex = increased vagal tone secondary to ischaemia.

Question 196

What do you do about heart block caused by an inferior MI?

Answer 196

Bradyarrhythmias and AV block in the context of inferior STEMI are usually transient (lasting hours to days), respond well to atropine and do not require permanent pacing.

Question 197

What does the ECG show?

Answer 197

Inferior STEMI with third degree heart block and slow junctional escape rhythm.

Question 198

What are the general features of pericarditis?

Answer 198

Inflammation of the pericardium (e.g. following viral infection) produces characteristic chest pain (retrosternal, pleuritic, worse on lying flat, relieved by sitting forward), tachycardia and dyspnoea.

There may be an associated pericardial friction rub or evidence of a pericardial effusion.

Widespread ST segment changes occur due to involvement of the underlying epicardium (i.e. myopericarditis).

Question 199

How do you recognise pericarditis on ECG?

Answer 199

Widespread concave ST elevation and PR depression throughout most of the limb leads (I, II, III, aVL, aVF) and precordial leads (V2-6).

Reciprocal ST depression and PR elevation in lead aVR (± V1).

Sinus tachycardia is also common in acute pericarditis due to pain and/or pericardial effusion.

Question 200

What are the ECG stages of pericarditis?

Answer 200

Stage 1 – widespread STE and PR depression with reciprocal changes in aVR (occurs during the first two weeks)

Stage 2 – normalization of ST changes; generalized T wave flattening (1 to 3 weeks)

Stage 3– Flattened T waves become inverted (3 to several weeks)

Stage 4 – ECG returns to normal (several weeks onwards)

Question 201

What does the ECG show?

Answer 201

Widespread concave ST elevation and PR depression is present throughout the precordial (V2-6) and limb leads (I, II, aVL, aVF).

There is reciprocal ST depression and PR elevation in aVR.

Question 202

How do you differentiate pericarditis from a STEMI?

Answer 202

Pericarditis can cause localised ST elevation but there should be no reciprocal ST depression (except in AVR and V1).

STEMI, like pericarditis, can also cause concave up ST elevation.

Only STEMI causes convex up or horizontal ST elevation.

ST elevation greater in III than II strongly suggests a STEMI.

PR segment depression is only reliably seen in viral pericarditis, not by other causes. It is often only an early transient phenomenon (lasting only hours). MI can also cause PR segment depression due to atrial infarction (or PR segment elevation in aVR).

You can’t rely on history either — STEMI can also cause positional or pleuritic pain. A pericardial friction rub

Question 203

What is the clinical presentation of aortic dissection in order of frequency of symptom?

Answer 203

Severe or ‘worst ever’ pain 90%

Abrupt (maximal at onset) 84-80%

Sharp or tearing 64%

Down the back 46%

Retrosternal or interscapular pain, migrating (16%)

Question 204

What are the complications of aortic dissection?

Answer 204

Aortic incompetence (32%), cardiac tamponade, myocardial ischaemia (but only 2-5% of ECG’s mimick AMI + incidence of AMI is 800 x that of aortic dissection!).

Different BP >20 mmHg in arms, or missing pulse (15-30%; LR+ 5.7).

Pleural rub or effusion, haemothorax.

Altered consciousness, syncope (13 %), hemiplegia (5%), paraplegia. Any focal neurology (17%; LR+ 6.6-33).

Abdominal pain (43% descending, 22% ascending), intestinal ischaemia, bowel infarct.

Oliguria, haematuria

Question 205

What are the CXR findings in aortic dissection?

Answer 205

Widened mediastinum (56-63%), abnormal aortic contour (48-71%), aortic knuckle double calcium sign >5mm (9-14%), pleural effusion (L>R; 16%), tracheal shift, left apical cap. ‘Normal’ in 11-16%.

Question 206

What is the role of d-dimer in acute aortic dissection?

Answer 206

Limited prospective data suggest D-dimer is useful to risk stratify and ‘rule out’ if negative (< 0.1 µg/mL has NPV 100%; <500 ng/mL NPV 95% / LR- 0.07 in first 24 hours).

Perhaps consider particularly if access to imaging is limited (i.e. in rural / remote areas).

Question 207

What is the role of echo in aortic dissection?

Answer 207

Transthoracic 75% diagnostic Type A (ascending), 40% descending (Type B).

Transoesophageal (TOE). Much higher sensitivity (97-99%) / specificity, though operator-dependent, needs sedation / intubation, and is less available. Useful in ICU / perioperative.

Question 208

What is the role of CT in aortic dissection?

Answer 208

Helical CT

Most useful screen for widened mediastinum etc, with sensitivity 83- >98%. Multiplane/slice scanners may even negate additional need for TOE or aortography to plan operative management.

Question 209

What is the role of MRI/MRA or aortography in acute aortic dissection?

Answer 209

MRI / MRA

Excellent sensitivity and specificity, but limited by availability.

Aortography

Was the traditional ‘gold standard’, delineating aortic incompetence and branch vessel involvement, but in fact lacks sensitivity.

Question 210

What is the management of type A ascending aortic dissection?

Answer 210

Immediate blood pressure control prior to transfer for operation using IV beta blocker (propranolol, esmolol or labetalol) combined with SNP (or GTN) as vasodilators aiming for SBP 100-120 mmHg, and surgery or endovascular stenting.

Question 211

What is the management of type A descending aortic dissection?

Answer 211

Medical control of BP with beta blockers, with surgery or endovascular stent grafting for selected patients with an unfavourable outlook.

Question 212

What are the stats like for out of hospital VF arrest and AEDs?

Answer 212

>25% for survival to hospital admission and survival at one year (inc w/o neurological impairment)

Time in interval between collapse and first shock achieves the highest survival rates.

Question 213

Which drugs decrease preload?

Answer 213

preload reduction: diuretics, opioids, decrease intake, spironolactone

Question 214

Which drugs decrease afterload?

Answer 214

afterload reduction: ACE-I, GTN, IABP

Question 215

Which drugs increase contracitility?

Answer 215

increase contractility: milrinone, dobutamine, adrenaline, VAD

Question 216

Which drugs degrease myocardial work?

Answer 216

decreased myocardial work: beta-blockers, IABP, VAD

Question 217

What increases coronary perfusion and oxygenation?

Answer 217

increased coronary perfusion and oxygenation: O2, Hb, Stents, CABG, IABP

Question 218

What is the role of assisted ventilation in heart failure

Answer 218

ASSISTED VENTILATION

CPAP: favourable effects on intrathoracic and left ventricular transmural pressure

-> significant reduction in mortality and intubation rates

BIPAP: reduction in intubation, trend to reduction in mortality

invasive ventilation: associated with poor prognosis but can produce dramatic improvement

Question 219

What is the role of TTE in heart failure?

Answer 219

All patients with suspected CHF should have an echocardiogram, the single most useful investigation in such patients. The echocardiogram can make the all-important distinction between systolic dysfunction (typically an LV ejection fraction < 40%) and normal resting systolic function, associated with abnormal diastolic filling, while alsexcluding correctable causes of CHF, such as valvular disease.

Question 220

What is the significance of anaemia in CHF?

Answer 220

Mild anaemia may occur in patients with CHF and is associated with an adverse prognosis

Question 221

What happens to serum sodium in heart failure?

Answer 221

dilutional hyponatraemia, exacerbated by high-dose diuretic therapy

Question 222

What happens to serum potassium in heart failure?

Answer 222

elevated plasma potassium in the presence of impaired renal function, or resulting from the use of potassium- sparing diuretics, ACEIs, or angiotensin II receptor antagonists and aldosterone antagonists.

hypokalaemia is more common and is often secondary to

therapy, with thiazide or loop diuretics

Question 223

What happens to serum magnesium in heart failure?

Answer 223

plasma magnesium levels may be reduced due to the

effects of diuretic therapy; magnesium replacement to

normal levels reduces ectopic beats and helps normalise

potassium levels

Question 224

What happens to the LFTs in heart failure?

Answer 224

Congestive hepatomegaly results in abnormal liver function tests (elevated levels of aspartate transaminase (AST), alanine transaminase (ALT) and lactate dehydrogenase (LDH).

Theremay be a rise in serum bilirubin, particularly in severe CHF.

In long-standing CHF, albumin synthesis may be impaired, resulting in hypoalbuminaemia. The latter finding may also indicate cardiac cirrhosis

Question 225

What is an “angina equivalent”?

Answer 225

Dyspnoea on exertion is a frequent manifestation of inducible myocardial ischaemia, sometimes referred to as an ‘angina equivalent’.

Question 226

What is a frequent manifestation of inducible myocardial ischaemia that isn’t pain? How is it assessed?

Answer 226

Dyspnoea on exertion is a frequent manifestation of inducible myocardial ischaemia, sometimes referred to as an ‘angina equivalent’.

Inducible ischaemia can be assessed with numerous stress

protocols, using either technetium-9m-labelled agents or

thallium-201. Many patients have limited physical activity

capacity and therefore pharmacological stress testing—e.g.

using dipyridamole or dobutamine—is more appropriate.

Stress echocardiography is another alternative using either

physical activity or dobutamine

Question 227

What is the role of a right heart cath in heart failure?

Answer 227

heart failure appears refractory to therapy

the diagnosis of CHF is in doubt

diastolic heart failure is recurrent and difficult to confirm by other means

Question 228

What are BNP levels useful for?

Answer 228

BNP levels have been demonstrated to be useful for differentiating dyspnoea caused by CHF from dyspnoea due to other causes.

This reduced both the time to initiation of the most appropriate therapy and the length of hospital stay.

BNP and N-terminal proBNP levels vary with age, gender and renal function.

Question 229

When are BNP levels less useful?

Answer 229

Better for systolic, not diastolic dysfunction.

In particular, BNP levels do not appear to discriminate well between elderly

female patients with diastolic heart failure—the most common patient group with this condition—and healthy age-matched controls. Furthermore, mildly raised levels can be due to other

causes, including corpulmonale and pulmonary embolism.

Question 230

What is the CSANZ recommendation for use of plasma BNP in patitens with recent-onset dyspnoea?

Answer 230

Plasma BNP or N-terminal pro-BNP measurement may be helpful in patients presenting with recent-onset dyspnoea; it has been shown to improve diagnostic accuracy with a high negative predictive value

Question 231

What is the role of plasma BNP in therapy for CHF titration?

Answer 231

Repeated measurement of plasma BNP or N-terminal pro-BNP to monitor and adj ust therapy in CHF should be confined to patients with CHF and systolic dysfunction who are not doing well on conventional management. Further, more definitive trials are required to fully establish the role of hormone level measurement in guiding CHF treatment

Question 232

When would you do an endomyocardial biopsy?

Answer 232

Endomyocardial biopsy may be indicated in patients with cardiomyopathy with recent onset

of symptoms, where CHD has been excluded by angiography, or where an inflammatory or

infiltrative process is suspected.

Question 233

How do you delineate between systolic and diastolic heart failure?

Answer 233

Systolic dysfunction (LVEF < 40%)

Diastolic dysfunction (LVEF > 40%

Question 234

Who are the high risk CHF patients?

Answer 234

age ≥ 65 years

NYHA Class III or IV symptoms

Charlson Index of Comorbidity Score of 2 or more

left ventricular ejection fraction (LVEF) ≤ 30%

living alone or remote from specialist cardiac services

depression

language barrier (e.g. non-English speaking)

lower socioeconomic status (due to poorer compliance, reduced understanding of reasons for medicines, fewer visits to medical practitioners, high-salt diet in ‘take-awayfoods’, reduced ability to afford medicines, higher rates ofcigarette smoking, etc.)

significant renal dysfunction (glomerular filtration rate < 60 mL/min/1.73 m).

Question 235

What type of exercise should be avoided in CHF?

Answer 235

Isometric physical activity with heavy straining should be avoided, as it may increase LV afterload.

Isokinetic muscle-strengthening physical activity has been used safely in patients with CHF.

Question 236

Can patients with heart failure have sex? Why?

Answer 236

Sexual activity is likely to be safe in patients who are able to achieve approximately six metabolic equivalents (MET) of exercise— that is, able to climb two flights of stairs without stopping due to angina, dyspnoea or dizziness.

Question 237

Male patients with CHF frequently experience erectile dysfunction. Would you give them viagra? Why?

Answer 237

Male patients frequently suffer from erectile dysfunction.

Sildenafil is contraindicated in patients receiving nitrate therapy, or those who have hypotension, arrhythmias or angina pectoris

Question 238

How do you manage fluid status in CHF?

Answer 238

Weight diary with daily morning weights

>2kg/ days –> see doctor ASAP, ditto with loss

No more than 2L fluid a day

1.5L / day if fluid retaining

Can self regulate diuretic dose based on weight monitoring and symptoms - can only ever double - drop back when dry weight/symptoms resolve

May need to have a bit more fluid in warmer weather esp if losing weight

Question 239

What do you do about alcohol in CHF?

Answer 239

ETOH related disease –> abstain, can slow disease or even improve LVF

Other patients - 1-2 drinks a day

ETOH is a direct myocardial toxin and impairs contracitlity, also adds to fluid intake

Question 240

What is the role of psychosocial support in heart failure?

Answer 240

LVEF <20% –> depression –> increased mortality

Depression –> impaired functional capacity and CHF sx with no relationship between the 2

CBT reduces depression in cardiac patients as does antidepressents but does not significantly reduce mortality

Question 241

What impact does CHF have on pregnancy?

Answer 241

CHF greatly increases the risk of maternal and neonatal morbidity and mortality

pregnancy and delivery may cause deterioration in women with moderate to severe CHF—pregnancy in mild CHF may be considered for a fully informed patient and her partner

Question 242

Can people with CHF travel?

Answer 242

Increased risk of DVT (need prophylaxis of single injection of LMWH on long-haul flights plus stockings, plus calf stretches. Anticoagulate if higher risk)

Avoid high altitude destinations (relative hypoxia)

Hot climates = dehydration

Question 243

How do youprevent clinical deterioration post-discharge in a CHF visit?

Answer 243

Patient support by a doctor and pre-discharge review and/or home visit by a nurse is recommended to prevent clinical deterioration.

Question 244

Why shouldn’t you initiate beta-blockers in acute decompensated heart failure?

Answer 244

Beta-blockers should not be initiated during a phase of acute decompensation, but only after the patient’s condition has stabilised. Adverse effects of beta-blockade in this setting include symptomatic hypotension, worsening of symptoms due to withdrawal of sympathetic drive and bradycardia.

Question 245

What is the role of nebivolol in heart failure?

Answer 245

More recently, nebivolol (a selective beta-1 receptor

antagonist) has been approved for use in Australia for the treatment of stable CHF. It has been found to be safe and effective in elderly patients with both relatively preserved and impaired ejection fraction.

Question 246

In someone with stable heart failure, which should you start first, a beta-blocker or an ACEI?

Answer 246

A randomised study has suggested that major clinical

outcomes are similar whether a beta-blocker is started first followed by ACEI, or the opposite (conventional) order is followed.

Therefore, the order of commencing these life-saving heart failure drugs may be left to the individual prescribing physician, dependent on clinical circumstances.

Question 247

Why do beta-blockers work in heart failure?

Answer 247

As with ACEIs, beta-blockers inhibit the adverse effects of chronic activation of a key neurohormonal system (the sympathetic nervous system) acting on the myocardium.

Question 248

Which three beta blockers have the best evidence fo CHF and why?

Answer 248

Three beta-blockers—carvedilol (beta-1, beta-2 and alpha-1 antagonist), bisoprolol (beta-1 selective antagonist) and metoprolol extended release (beta-1 selective antagonist) prolong survival in patients with mild to moderate CHF already receiving an ACEI. This survival benefit includes both reductions in sudden death, as well as death due to progressive pump failure.

Question 249

Carvedilol or metoprolol in CHF?

Answer 249

A study demonstrated that carvedilol (25 mg bd) was superior to immediate-release metoprolol (50 mg bd) in prolonging survival in patients with mild to moderate symptoms. It is not clear whether these differences relate to the doses used, or the pharmacological effects of carvedilol beyond blockade of the beta-1 adrenoceptor. This study highlights the importance of aiming to achieve the target doses of beta-blockers as used in the major successful trials.

Carvedilol has also been shown to prolong survival in patients with severe symptoms who did not have overt volume overload or recent acute decompensation

Question 250

What effect does aldosterone have on the heart?

Answer 250

Aldosterone receptors within the heart can mediate fibrosis, hypertrophy and arrhythmogenesis.

Question 251

What is eplenerone indicated for?

Answer 251

A ‘selective’ aldosterone antagonist without antiandrogenic effects, eplerenone, has been found to reduce mortality (and hospitalisation) in the immediate (3–14 days) post-MI period in patients with LV systolic dysfunction and symptoms of heart failure.

This benefit appeared to be additive to those of ACEIs and beta-blockers. Eplerenone is now registered in Australia for this indication; a study of the selective aldosterone antagonist, eplerenone, in patients with systolic heart failure and mild (NYHA Class II) symptoms was recently halted due to overwhelming benefit with regard to the study’s primary composite endpoint of cardiovascular mortality and hospitalisation for heart failure.

Question 252

What is the role of Digoxin in CHF?

Answer 252

Valuable for therapy of AF in CHF patients

Increased mortality of women even in therapeutic range, survival advantage for men.

Question 253

What is the role of ARBs in CHF?

Answer 253

In patients who are ACEI intolerant, angiotensin II receptor antagonists provide morbidity and mortality benefits in comparison to placebo. Therefore, angiotensin II receptor antagonists are recommended as an alternative for patients who experience ACEI mediated adverse effects, such as a cough

Question 254

What is the role of direct sinus node inhibitors in CHF?

Answer 254

Ivrabadine reudces CV mortality and HF hospitalisation in patients who were in sinus rhythm with a rate over 70

Benefit LARGELY contributed to by a reduction in hospitalisation and in addition to patients being on highest tolerated dose of background b-blockade (although they never got past 25% of the target dose).

HR needs to be above 70 for Ivrabadine to have an effect

Question 255

What is the role of CCBs in heart failure?

Answer 255

Non-dihydropyridine calcium-channel blockers that are direct negative inotropes, such as verapamil and diltiazem, are contraindicated in patients with systolic heart failure.

The dihydropyridine calcium-channel blockers, amlodipine and felodipine, have not shown survival benefits in patients with systolic CHF but, as outcomes were not adverse, may be used to treat comorbidities (such as hypertension and CHD) in these patients.

Question 256

Anti-arrhythmics in heart failure?

Answer 256

Avoid unless beta-blockers or amiodarone

Question 257

Psych drugs in heart failure?

Answer 257

Avoid TCAs and Clozapine

Question 258

Diabetic drugs in heart failure?

Answer 258

Avoid thiazolidendiones

Metformin is safe unless concomitant renal impairment

Question 259

TNF-abs and steroids in heart failure?

Answer 259

Avoid

Question 260

Trastuzumab and heart failure?

Answer 260

Trastuzumab has been associated with the development of reduced LVEF and heart failure.

It is contraindicated in patients with symptomatic heart

failure or reduced LVEF (< 45%). Baseline and periodic evaluation of cardiac status including assessment of LVEF should occur

Question 261

Moxonidine in heart failure?

Answer 261

Avoid

Moxonidine has been associated with increased

mortality in patients with heart failure and is

contraindicated in such patients.

Question 262

When are aldosterone receptor antagonists (spironolactone and eplenerone) indicated in heart failure?

Answer 262

Severely symptomatic despite appropraite doses of ACEI’s and diuretics

Question 263

Indication for Ivrabidine in heart failure?

Answer 263

Direct sinus node inhibition with ivabradine should be considered for CHF patients with impaired systolic function and a recent heart failure hospitalisation who are in sinus rhythm where their heart rate remains > 70 bpm despite efforts to maximise dosage of background beta- blockade.

Question 264

First line heart failure drugs in order of prescription are…

Answer 264

ACEIs

Diuretics

Beta-blockers (when still symptomatic)

Aldosterone blockade (spironolactone) (when still symptomatic)

Aldosterone blockade (epleronone)

ARBs (alternative to ACE, can consider dual therapy)

Ivrabadine (if on max b-blockade)

Question 265

What are the second line agents in CHF?

Answer 265

Digoxin - symptom relief and reduction of hospitalisation, AF

Hydralazine + isosorbide dinitrate –> intolerant of ACE/ARBs and no other tx option

Fish oil - symptomatic despite standard therapy

Question 266

What is the general mx of asymptomatic LV dysfunction (NYHA class I)?

Answer 266

• Exercise and RF modification
• ACEI
• B-Blocker
• Disease specific rx (i.e. CHD - aspirin, statin etc)

Question 267

Which class of NYHA heart failure should you give b-blockers

Answer 267

These should be given irrespective of class, just need to not be fluid overloaded.

Question 268

When would you consider cardiac transplant in heart failure?

Answer 268

65

Class IV heart failure and no major comorbidities, refractory or intolerant to beta-blocker therapy

Question 269

How do you decide between spironolactone and eplerenone?

Answer 269

Symptomatic on therapy and LVEF >40 = spironolactone

Symptomatic on therapy and LVEF <40 = eplerenone

Question 270

What are the contraindications to eplerenone?

Answer 270

Eplerenone is contraindicated in patients with hyperkalaemia, severe renal impairment (creatinine Cl less than 30 ml/min), or severe hepatic impairment (Child-Pugh score C). The manufacturer of eplerenone also contraindicates ( relative C.I. ) concomitant treatment with ketoconazole, itraconazole or other potassium-sparing diuretics (though the manufacturer still considers taking these drugs to be absolute C.I.) Potential benefits should be weighted against possible risks.

Question 271

When is Levosimendan used in CHF?

Answer 271

Levosimendan is available in Australia on a compassionate-use basis. It should be reserved for patients who do not respond to dobutamine or in those in whom dobutamine is contraindicated due to arrhythmia or myocardial ischaemia

Question 272

What is the indication for biventricular pacing?

Answer 272

NYHA symptoms Class III/IV despite optimal medical therapy

dilated heart failure with an ejection fraction ≤ 35%

QRS duration ≥ 120 ms

sinus rhythm

Question 273

What is the evidence behind biventricular pacing?

Answer 273

Significant mortality reduction

Symptom reduction

Reduced hospitalisation

Good in asymptomatic patients and in combo with ICD therapy in terms of death reduction and hospitalisation but not cost-effective at this point in time

Question 274

What are the indications for ICD?

Answer 274

ICDs are first-line therapy for patients who have bee n resuscitated from ventricular fibrillation, or from sustained ventricular tachycardia with syncope, or from sustained ventricular tachycardia with haemodynamic compromise and an LVEF of ≤ 40%.

Question 275

What is the evidence behind ICD therapy?

Answer 275

Use of ICDs is associated with a 20–30% relative reduction in mortality at 1 year, which is maintained over 3–5 years of follow-up. Long-term follow-up (mean of 5.6 years) of a subgroup of the ICDs study showed that survival curves continued to diverge.

Absolute mortality of inpatients treated with amiodarone was 5.5% per year versus 2.8% per year in those receiving ICDs.

Question 276

When would you consider ICD plus CRT?

Answer 276

In patients in whom implantation of an ICD is planned to reduce the risk of sudden death, i t is reasonable to also consider CRT to reduce the risk of death and heart failure eve nts if the LVEF is ≤ 30% and the QRS duration is ≥ 150 ms (left bundle branch block morphology), with assoc iated mild symptoms (NYHA Class II) despite optimal medical therapy

Question 277

What are the definite indicators for cardiac transplant?

Answer 277

Persistent NYHA Class IV symptoms

Volume of oxygen consumed per minute at maximal exercise (VO 2 max) < 10 mL/kg/min

Severe ischaemia not amenable to revascularisation

Recurrent uncontrollable ventricular arrhythmias

Question 278

What drug changes can precipitate decompensated CHF?

Answer 278

• starting drugs that predispose to renal function and salt and water retention - ie NSAIDS, COX-2 inhibitors, steroids, thiazolidinediones
• negative inotropes i.e. diltiazem, verapamil, antiarrhythmics, high dose beta blockers

Question 279

What comorbid conditions can precipitate decompensated heart failure?

Answer 279

Infections (particularly pulmonary) due to haemodynamic changes

Renal failure –> fluid overload

Anaemia or pulm emboli impairing oxygen delivery

Thyroid imbalance

Question 280

What is the role of thiazide diuretics in decompensated CHF?

Answer 280

In a CHF patient, diuretic resistance happens due to homeostatic increase in distal tubular reabsorption of sodium.

In the short term, adding a thiazide can block sodium uptake in the distal tubule, evoking a powerful diuretic response.

Question 281

What is the difference between APO and decompensated CHF?

Answer 281

APO is truly acute (hence the term ‘flash pulmonary oedema’) and is typically a condition of wet lungs without extravascular fluid overload (i.e. acute diastolic LV failure).

In decompensated CHF the picture is subacute, extending over more than 6 hours of increasing symptoms with clinical signs of intravascular, pulmonary and peripheral fluid overload

Question 282

Which drug should you avoid in bilateral renal artery stenosis?

Answer 282

ACEIs

Question 283

What is the role of nitrates in decompensated CHF?

Answer 283

Nitrates are predominantly venodilators, but also have the effect of epicardial artery dilatation, and hence they are particularly desirable in the setting of decompensation induced by cardiac ischaemia. Nitrates may also have a role in decompensation through their beneficial haemodynamic effects, particularly in reducing central blood volume and filling pressure (as occurs in APO treatment). This can often relieve symptoms of pulmonary congestion, particularly at night when the heart is exposed to increased filling pressures due to the recumbent position. Evidence from large-scale RCTs of the effect of nitrates alone in decompensated CHF is lacking.

Question 284

In a patient with APO, what constitutes cardiogenic shock and what should you do?

Answer 284

The presence of hypotension (systolic blood pressure < 90 mmHg) with APO constitutes a diagnosis of cardiogenic shock and requires emergency circulatory assistance with inotropes and/or intra-aortic balloon pump insertion.

Question 285

What are some causes of systolic, diastolic, and normal LV function CHF?

Answer 285

Systolic LV dysfunction—CHD, dilated cardiomyopathy, mitral regurgitation

Diastolic LV dysfunction—hypertensive heart disease, hypertrophic cardiomyopathy, aortic stenosis

Normal LV function—mitral stenosis

Question 286

What is the hierarchy of emergency therapy of acute heart failure?

Question 287

3 points about HFPSF (diastolic heart failure)

Answer 287

diagnosis of possible orprobable diastolic heart failure is based on the combination of clinical CHF and preserved LV systolic function.

• symptoms and physical signs of CHF, chest radiological evidence and an LVEF of ≥ 45% on echocardiography, gated blood pool scanning, or direct left ventriculography
• NOT synonymous with diastolic dysfunction

Question 288

What is the epidemiology of HFPSF?

Answer 288

• 30-50% of community patients with CHF have normal or near normal LV systolic function
• women and elderly
• largely hypertensive heart disease, age, and diabetes (after exclusion of coronary and valvular heart disease)
• high mortality rates, low short term mortality than systolic dysfunction

Question 289

What investigations are done for diastolic heart failure and what are their findings?

Answer 289

Echo

• restrictive or pseudonormal mitral inflow filling pattern
• LA enlargement
• reduced septal annular velocity

Angio

• elevated LVEDP
• Prolonged Tau

Question 290

What are the diagnostic criteria for diastolic heart failure (HFPSF?)

Answer 290

• clinical hx of CHF
• exclude myocardial ischaemia, valvular disease
• objective evidence of CHF (i.e. CXR)
• EF >45% (echo, gated, left ventriculography)
• echo or cath evidence of diastolic dysfunction where possible
• NOT plasma BNP

Question 291

Which is superior for patients with LV systolic CHF and drug resistant symptomatic AF - AV node ablation w/ bi-ventricular pacing or pulmonary vein isolation and ablation?

Answer 291

For patients with CHF due to LV systolic

dysfunction associated with drug-resistant symptomatic AF, the study demonstrated the superiority of a rhythm-control strategy based on pulmonary vein isolation compared with a ventricular rate-control strategy based on atrioventricular node ablation with biventricular pacing.

Question 292

In CHF patients, what is the strongest single predictor of suddent cardiac death?

Answer 292

LVEF

Question 293

How is the CHF of severe aortic stenosis managed?

Answer 293

Poorly to medical therapy

Arterial vasodilators including ACEIs are contraindicated due to the risk of coronary hypoperfusion

Appropriate medical therapy = digoxin and diuretics

Question 294

What is the management of angina in CHF?

Answer 294

Revascularise

Avoid nondihydropyridine CCBs in LVEFs <40%

Use betablockers wherever tolerated for angina

Prophylactic nitrates

Severe angina + systolic heart failure + inoperable disease - consider perhexiline (last line, highly toxic)

Question 295

How should you treat decubitus angina? (nocturnal angina associated with orthopnoea)

Answer 295

Treat as CHF

Loop diuretic in the arvo to minimise filling pressures overnight and prophylactic night tiem nitrates

Question 296

What is perhexiline?

Answer 296

Nonselective CCB

Last line for angina

CYP450 - watch out for liver toxicity

Question 297

What is the role of ACEIs in protecting against CHF?

Answer 297

• after acute anterior infarction, ACEIs have been shown to protect against development of CHF independent of baseline renal function and preserve renal function
• in patients with type 2 DM and nephropathy, ARBs protect against the development of CHF

Question 298

What is the role of spironolactone in CHF and renal failure?

Answer 298

Spironolactone carries a significant risk of hyperkalaemia, particularly in patients who are also taking an ACE I or an angiotensin II receptor antagonist and whose creati nine clearance is less than 30 mL/min. It should be used with caution in patients with creatinine clearances between 30–60 mL/min

Question 299

What is the link between chemotherapy and CHF?

Answer 299

Cancer chemotherapy, particularly with anthracycline (the ‘rubicins and mitoxantrone)derivatives, may lead to the development of CHF; the risk is directly related to cumulative anthracycline dosage. Pre- existent impairment of LV systolic function represents a relative contraindication to aggressive chemotherapy with such agents

Question 300

What impact does diabetes have on CHF?

Answer 300

The diagnosis of diabetes is not only an independent risk factor for the development of CHF, but is also associated with an adverse outcome in patients with established disease.

Question 301

In CHF, when should Metformin be avoided?

Answer 301

Severe of decompensated - risk of lactic acidosis

Glitazones should avoided in patients with Class III or IV sx

Question 302

Which group of CHF is most at risk of hyperkalemia from dual ACE/ARB therapy?

Answer 302

Patients with diabetes, in whom hyporeninaemic hypoaldosteronism is common, may be at risk of developing hyperkalaemia when an angiotensin II receptor antagonist is added to ACEI therapy, and vigilant monitoring of serum potassium is recommended.

Question 303

What is the thromboembolism risk of CHF patients?

Answer 303

There is evidence that CHF is associated with an increased risk of thromboembolism (e.g. because of the frequent presence of thrombi within akinetic segments of failing ventricle and an increased propensity to develop AF). The SOLVD trial clearly demonstrated an increase in the incidence of stroke (mainly thromboembolic) with decreasing ventricular function.

However, retrospective analyses of studies of anti- thrombotic therapy in CHF have yielded conflicting results.

Question 304

How is gout managed in CHF?

Answer 304

Plasma urate goes up in CHF and levels have adverse prognostic significance

Can’t have NSAIDs or Cox-2s
Can’t have steroids

Use colchicine

Xanthine oxidase inhibition does not demonstrate benefits on clinical outcomes

Question 305

In what arrhythmias is EPS not indicated?

Answer 305

The value of electrophysiology studies is greatest in patients who are suspected of having a tachyarrhythmia whose mechanism is reentry.

There is no role for electrophysiology studies in the evaluation or management of the long QT syndrome, catecholaminergic polymorphic ventricular tachycardia, or the short QT syndrome.

Question 306

What are the diagnostic indications of EPS?

Answer 306

Syncope plus:

Underlying ischemic or structural heart disease to see if underlying sustained ventricular arrhythmias or congenital tachyrrhtyhmias may be the cause

Inappropriate sinus bradycardia due to suspected sick sinus syndrome (prolonged corrected SA node recovery may predict future syncope recurrence)

Bifascicular, or LBBB/RBBB + hemifasciular block of unknown cause. Induction of infra-Hisian block with bifasci block can predict future adverse cardiovascular events

Following palpitations

Patients with high risk occupations

Unexplained syncope

Sudden cardiac death with no established cause (presumed idiopathic VF)

Wide complex tachyarrythmias of unclear etiology on noninvasive measures

Question 307

What are the risk stratification indications for EPS?

Answer 307

Previous MI with ischemic cardiomyopathy who have LVEF<40% and found to have nonsustained VT/VT on ambulatory monitoring

AV conduction block below the level of the AV node (Mobitz II is infranodal which is bad) - EP is used when you can’t work out the site of block in an asymptomatic individual. If infranodal –> pacemaker.

Asymptomatic young (8-21 years) with ECG manifestations of pre-excitation - risk of sudden cardiac death from atrial arrhythmia progressing to ventricular. Need EST first and if loss of pre-excitation is NOT seen –> EP

Screening test for those with TOF who do not have high risk factors, or in patients with prepared TOF

Controversial in Brugada, can be used for risk stratification with cardiac sarcoid if LVEF <35 despite optimal medical therapy and immunosuppression

Question 308

What are the absolute contraindications to EPS?

Answer 308

Unstable angina

●Bacteremia or septicemia

●Acute decompensated congestive heart failure not caused by the arrhythmia

●Major bleeding diathesis

●Acute lower extremity venous thrombosis if femoral vein cannulation is desired

Question 309

Where is the value of EP studies the greatest?

Answer 309

It would also be important to realize that the value of electrophysiology studies is greatest in patients who are suspected of having a tachyarrhythmia whose mechanism is reentry. There is no role for electrophysiology studies in the evaluation or management of the long QT syndrome, catecholaminergic polymorphic ventricular tachycardia, or the short QT syndrome.

Question 310

In Mobitz II block, when is pacing indicated?

Answer 310

An EP study is indicated if the site of block cannot be determined reliably in an asymptomatic individual with second degree AV block. If the site is infranodal, pacing is indicated

Question 311

What is the risk with young people and pre-excitation syndromes?

Answer 311

Asymptomatic young (8 to 21 years) patients with electrocardiographic manifestations of preexcitation may be at high risk of sudden cardiac death due to atrial fibrillation progressing to ventricular fibrillation. These patients are advised to undergo exercise stress testing. The clear and sudden loss of preexcitation with exercise stress testing predicts a favorable prognosis. If clear loss of preexcitation is not seen or the data are uninterpretable, invasive risk stratification via transesophageal or EP studies is recommended

Question 312

What are the annual risk factors of untreated stroke?

Answer 312

CHADS risk factors are cumulative

< 65 years with no risk factors the untreated annual risk of stroke is about 1%, whereas with one or more risk factors it is about 5%;

65-75 years with no risk factors the annual risk of stroke is about 4%, and with one or more risk factors it is about 6% per year;

>75 years with no risk factors the risk of stroke is about 3%-4%, whereas with one or more risk factors it is about 8%

Question 313

In patients who receive thrombolysis and are later found to have a total occlusion of a vessel on angio - should they get stented?

Answer 313

If asymptomatic - NO, medical therapy has better effect on cardiovascular remodelling than PCI

If symptomatic (i.e. angina or poor stress testing results) then YES

Question 314

How long after thrombolysis should angio be performed?

Answer 314

ASAP but AFTER 2 hours if high risk features: anterior MI, killip class >2, inferior MI w/ RV involvement, BP <100, HR > 100

Not high risk, should be performed within 24 hours

Question 315

What is the difference between primary failure of fibrinolysis and threatened reocclusion?

Answer 315

Primary failure - evidence of continuing or worsening myocardial ischemia

Threatened reocclusion - early recurrent ischemia after apparently successful fibrinolysis

Question 316

In a patient who undergoes fibrinolysis for MI, when would you consider re-thrombolysing?

Answer 316

In patients with both primary failure and threatened reocclusion - PCI is preferable.

In PCI can’t be done within two hours, for threatened reocclusion, thrombolysis with a non-antigenic agents should be done.

For primary failure, if rescue PCI can’t be performed within 12 hours, conservative care wins over thrombolysis

Question 317

Which group of patients should get a bare metal stent?

Answer 317

Patients in whom a DES cannot be implanted for technical reasons

Patients for whom compliance with a recommendation for 12 months of dual antiplatelet therapy is likely to be problematic, including those known to have difficulty with medication compliance.

Those who are scheduled to undergo surgery requiring cessation of dual antiplatelet therapy in the ensuing year

Those known to be at higher risk of bleeding, including individuals taking an oral anticoagulant.

Question 318

How long after PCI should you continue dual antiplatelet therapy for?

Answer 318

For patients treated with either DES or BMS who are not at high bleeding risk and who do not have planned noncardiac surgery within one year, we recommend DAPT for at least 12 months rather than a shorter treatment duration (Grade 1B). Practitioners should evaluate patients after the first 12 months of DAPT to be certain that there has not been major bleeding or other important difficulty related to DAPT. For patients who have had a complication of DAPT, continuation after 12 months may not be appropriate

Question 319

A patient has a DES and completes 12 months of dual antiplatelet therapy with no complications - how long should you continue it for?

Answer 319

For patients who have not had a significant complication with DAPT during the first 12 months, we suggest continuing such therapy for an additional 18 months (Grade 2B).

Question 320

How long should you continue dual antiplatelet for in a high risk patient with a BMS?

Answer 320

For patients treated with BMS at high bleeding risk or who have planned noncardiac surgery within one year, we recommend a minimum of one month of uninterrupted DAPT (Grade 1B). For such patients treated with DES, we recommend uninterrupted DAPT for a minimum of six months

Question 321

When should you use clopidogrel over ticagrelor or prasugrel?

Answer 321

In most randomized trials of stent placement for stable coronary artery disease, clopidogrel was the P2Y12 receptor blocker tested. Thus, we prefer clopidogrel to prasugrel or ticagrelor for most patients requiring dual antiplatelet therapy.

Question 322

When is Prasugrel used?

Answer 322

Prasugrel, co-administered with aspirin, has proven benefit in:

prevention of atherothrombotic events in patients with acute coronary syndromes (unstable angina, non–ST elevation myocardial infarction, ST elevation myocardial infarction) who are to undergo percutaneous coronary intervention.

Question 323

What are the considerations with Ticagrelor and Prasugrel?

Answer 323

A higher risk of bleeding may be seen when prasugrel is used for patients weighing less than 60 kg or aged 75 years or more. It should be avoided or used with extreme caution in these patients.

Ticagrelor should be avoided or used with extreme caution in patients at high risk of bleeding, such as those with low body weight (less than 60 kg), reduced kidney function and of older age (65 years or more).

Question 324

What are the Glycoprotein IIB/IIA inhibitors?

Answer 324

Abciximab, eptifibatide and tirofiban block platelet aggregation by preventing binding of fibrinogen to platelets through blockade of the platelet glycoprotein IIb/IIIa receptor. These drugs should only be used under specialist supervision.

Question 325

How do GPIIb/IIIa inhibitors work?

Answer 325

Inhibit the final common pathway of platelet aggregation, the cross-bridging of platelets secondary to fibrinogen binding to the activated GP IIb/IIIa receptor. The addition of GP IIb/IIIa improves outcomes in some patients with non-ST elevation ACS.

Question 326

What is the most important risk factor for stent thrombosis?

Answer 326

The premature cessation of dual antiplatelet therapy is the most important risk factor for ST.

Question 327

How does stent restenosis present?

Answer 327

Stable coronary sx as opposed to acute and dynamic

Question 328

What is the difference between stent thrombosis and stent restenosis?

Answer 328

Restenosis is a gradual re-narrowing of the stented segment that occurs mostly between 3 to 12 months after stent placement. It usually presents as recurrent angina but can present as acute myocardial infarction in approximately 10 percent of patients. It can usually be managed by repeat percutaneous revascularization.

In contrast, stent thrombosis is an abrupt thrombotic occlusion of a previously widely patent stent. It is a catastrophic complication that presents as sudden death or large myocardial infarction in most patients. Despite successful repeat revascularization, the six-month mortality is high.

Question 329

In what acute MI setting would you use beta-blockers immediately?

Answer 329

Failed thrombolysis with preserved blood pressure and tachycardia - aim is to get HR <70 while maintaining systolic BP >90

Question 330

Why is amitriptyline so cardiotoxic?

Answer 330

As well as being an SNR it is also a sodium channel blocker and an L-type calcium channel blockerr

Question 331

What are the clinical features of TCA overdose?

Answer 331

Sedation and coma

Seizures

Hypotension

Tachycardia

Broad complex dysrhythmias

Anticholinergic syndrome

Question 332

What does this ECG show and what is it consistent with?

Answer 332

Sinus tachycardia with first-degree AV block (P waves hidden in the T waves, best seen in V1-2).

Broad QRS complexes.

Positive R’ wave in aVR.

TCA overdose

Question 333

What are the important points about acute vs chronic lithium toxicity?

Answer 333

acute overdose is usually benign if adequate hydration is maintained and renal function is normal

chronic toxicity can be difficult to manage and result in devastating neurotoxicity

Question 334

What are the features of lithium toxicity (acute or chronic)?

Answer 334

acute ingestion or chronic accumulation

CNS: confusion -> coma, cerebella symptoms, seizure, basal ganglia symptoms (choreiform movements, Parkinson-like)

GIT: nausea, vomiting, bloating

CVS: syncope

RENAL: polyuria, polydipsia, renal insufficiency

NEUROMUSCULAR: peripheral neuropathy, myopathy

ENDOCRINE: hypothermia, hyperthermia

Question 335

What are the normal and toxic lithium levels?

Answer 335

Lithium level:

0.7-1.2mEq/L (therapeutic)

> 1.5mEq/L (toxic)

levels can be very high following acute ingestion, but do not correlate with outcome

as clinical features determine

Question 336

What is the acute resuscitation mx of Lithium overdose?

Answer 336

A – impaired LOC -> intubate

consider whole bowel irrigation for massive acute ingestion

activated charchoal does not bind

Liberal fluid resuscitation with normal saline

Question 337

What are the specific interventions for lithium toxicity?

Answer 337

A – impaired LOC -> intubate

consider whole bowel irrigation for massive acute ingestion

activated charchoal does not bind

Liberal fluid resuscitation with normal saline

Avoid hyponatraemia as this will decrease lithium clearance

Question 338

What is the clinical significance of and RV infarct?

Answer 338

Right ventricular infarction complicates up to 40% of inferior STEMIs. Isolated RV infarction is extremely uncommon.

Patients with RV infarction are very preload sensitive (due to poor RV contractility) and can develop severe hypotension in response to nitrates or other preload-reducing agents.

Hypotension in right ventricular infarction is treated with fluid loading, and nitrates are contraindicated.

Question 339

Which two ECG changes are most suggestive of an RV infarct?

Answer 339

ST elevation in V1 - the only standard ECG lead that looks directly at the right ventricle.

ST elevation in lead III > lead II – because lead III is more “rightward facing” than lead II and hence more sensitive to the injury current produced by the right ventricle.

Question 340

What does this ECG show?

Answer 340

There is an inferior STEMI with ST elevation in lead III > lead II.

There is subtle ST elevation in V1 with ST depression in V2.

There is ST elevation in V4R.

RV infarct

Question 341

How can leads V1 and V2 help you in spotting an RV infarct?

Answer 341

If the magnitude of ST elevation in V1 exceeds the magnitude of ST elevation in V2.

If the ST segment in V1 is isoelectric and the ST segment in V2 is markedly depressed.

NB. The combination of ST elevation in V1 and ST depression in V2 is highly specific for right ventricular MI.

Question 342

What is the percent survival to hospital discharge with use of an AED for a shockable rhythm?

What is the overal percent survival to hospital discharge for an out of hospital arrest?

Answer 342

38%

Around 7%

Question 343

Do AEDs work for hospitalised patients with cardiac arrest?

Answer 343

Compared to usual resuscitative measures (including external defibrillation when indicated), AED use in hospitalized patients with cardiac arrest did not improve survival in a large, multi-center observational study.

Question 344

What is Hypoalphalipoproteinemia?

Answer 344

Hypoalphalipoproteinemia is a high-density lipoprotein deficiency, inherited in an autosomal dominant manner.

Question 345

Three points about LCAT deficiency

Answer 345

LCAT esterifies cholesterol so you get accumulation of unesterified cholesterol

Renal failure is the major cause of morbidity and mortality

Patients get very low HDL and very high TGL, as well as corneal opacities with hepatosplenomegaly (fish eye disease)

Question 346

What is the cardiac index? How is it used?

Answer 346

Output from left ventricle to body surface area - in L/m

Under 1.8 = cardiac shock

Used in ICU

Question 347

PCWP 25 + v-waves to 40mmHg is…

Answer 347

MR

Question 348

PCWP of 25 with CI 1.5

Answer 348

Cardiogenic shock

Question 349

RA 20 mmHg PAP 40/20mmHg PCWP 20 mmHg consistent wit…

Answer 349

tamponade

Question 350

Saturation of 88% in the pulmonary artery consistent with…

Answer 350

VSD

Question 351

PAP 50/30 PCWP of 4 consistent with…

Answer 351

PE

Question 352

What is the evidence of the methacholine challenge in the dx of asthma?

Answer 352

Highly specific HOWEVER it’s sensitivity is reduced in Caucasians and non-atopic asthmatics when using the test for asthma.

Question 353

What is the evidence behind methacholine and mannitol testing in the dx of asthma?

Answer 353

Similar sens and spec - around 75% specific, poorly sensitive but increases when two exercise tests are positive

Question 354

How do you define asthma reversibility?

Answer 354

Reversibility is demonstrated by an increase of 12% and 200 mL after the administration of a short-acting bronchodilator.

Question 355

What is the most important limitation of PEF?

Answer 355

A limitation of PEF is that it is dependent on effort by the patient. FEV1 is also effort dependent but less so than PEF. FEV1 is not often used in the ED except in research settings.

Question 356

When is the bronchoconstriction of asthma at it’s greatest?

Answer 356

Bronchoconstriction is highest between the hours of 4:00 am and 6:00 am (the highest morbidity and mortality from asthma is observed during this time). These patients may have a more significant decrease in cortisol levels or increased vagal tone at night. Studies also show an increase in inflammation compared with controls and with patients with daytime asthma.

Question 357

What happens to pa02 and Sp02 in methaemoglobinaemia and CO2 poisoning?

Answer 357

In carbon monoxide poisoning SpO2 will read in the 90s despite high levels of COHb — but the PaO2 should still be high.

In methemoglobinemia, the SpO2 plateaus at about 86% with increasing levels of MetHb, but again the PaO2 will not be decreased.

Question 358

What is methemoglobinemia?

Answer 358

presence of a higher than normal level of methemoglobin (metHb, i.e., ferric [Fe3+] rather than ferrous [Fe2+] haemoglobin) in the blood. Methemoglobin is a form of hemoglobin that contains ferric [Fe3+] iron and has a decreased ability to bind oxygen. However, the ferric iron has an increased affinity for bound oxygen.[1] The binding of oxygen to methemoglobin results in an increased affinity of oxygen to the three other heme sites (that are still ferrous) within the same tetrameric hemoglobin unit. This leads to an overall reduced ability of the red blood cell to release oxygen to tissues, with the associated oxygen–hemoglobin dissociation curve therefore shifted to the left. When methemoglobin concentration is elevated in red blood cells, tissue hypoxia can occur.

Question 359

What effect does flying have on PAH?

Answer 359

Pulmonary hypertension — Patients with pulmonary hypertension may be at particular risk for in-flight hypoxemia, as a low inspired oxygen tension can trigger pulmonary artery vasoconstriction and exacerbate hypoxemia [22,39]. The combination of exertion and low in-flight oxygen tension may lead to further oxygen desaturation