Cardio Flashcards

Question

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

Answer 1

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.

Answer 2

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)

Answer 3

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)

Answer 4

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

Answer 5

Benign, often haemoorhagic Usually pedunculated and over variable size Usually in the LA attached to the interatrial septum in the fossa ovale region

Answer 6

![]() 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.

Answer 7

Metastatic pericardial disease

Answer 8

Mitral valve prolapse

Answer 9

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.

Answer 10

Cardiac mechanical prosthesis (St Jude)

Answer 11

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

Answer 12

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

Answer 13

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

Answer 14

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

Answer 15

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

Answer 16

≥ 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)

Answer 17

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

Answer 18

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.

Answer 19

Severe pulm HT - markedly prominent main pulm artery (MPA) - RPA enlarged - prominent right atrial contour (RA dilation due to RVH) ![]()

Answer 20

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)

Answer 21

Combination of: Dyspnoea - esp with exercise Right heart failure including peripheral oedema and abdominal distension ECG - RV strain and hypertrophy

Answer 22

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

Answer 23

Emphysema of any kind Asthma Bronchiectasis of any kind Lymphangiomyomatosis Langerhans cell histiocytosis Pulmonary fibrosis (any cause ie scleroderma, dermatomyositis, rheumatoid, SLE) Pneumoconiosis

Answer 24

Chronic pulmonary emboli Arteritis - PAN, SLE, Takayau, Wegeners Pulmonary artery stenosis

Answer 25

Eisenmenger phenomenon (inc ASD, VSD, PDA)

Answer 26

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

Answer 27

calcium channel antagonists nitric oxide prostanoids, e.g. epoprostenol, treprostinil, iloporst endothelin antagonists e.g. bosentan, sitaxsentan, ambrisentan phosphodiesterase inhibitors

Answer 28

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

Answer 29

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.)

Answer 30

Hyperdynamic (fever, exercise) Mitral stenosis Atrial myxoma (rare)

Answer 31

Soft First Sound Low cardiac output (rest, heart failure) Tachycardia Severe mitral reflux (caused by destruction of valve)

Answer 32

Variable Intensity of First Sound Atrial fibrillation Complete heart block

Answer 33

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

Answer 34

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

Answer 35

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

Answer 36

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

Answer 37

LVH in absence of other loading conditions Prevalence 0.2% or 1 in 500!

Answer 38

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

Answer 39

Jerky rapidly rising pulse Prominent LV impulse Apical systolic murmur that increases with valsalva (related to dynamic obstruction) Fourth heart sound

Answer 40

LVH TWI Q waves

Answer 41

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

Answer 42

Identifies at-risk earlier Avoids unecessary screening of non-carriers Can distinguish between other causes of LVH Pick up rate of 50-50%

Answer 43

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

Answer 44

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

Answer 45

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

Answer 46

Elective PCI - 2 days MI - 2 weeks CABG - 4 weeks Arrest - 6 months

Answer 47

DVT - 2 weeks Cardiogenic syncope - 4 weeks PE - 6 weeks

Answer 48

Sx on moderate exertion = no licence

Answer 49

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

Answer 50

4 weeks - 2 if TIA SAH - 3 months

Answer 51

Chronic hypertension - hypertension before 20 weeks gestation, often diastolic - no or stable proteinuria (if after 20 weeks gestation and no proteinuria --\> gestational hypertension)

Answer 52

'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

Answer 53

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

Answer 54

'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

Answer 55

S1 closure of mitral and tricuspid valves soft if long PR or mitral regurgitation loud in mitral stenosis

Answer 56

S2 closure of aortic and pulmonary valves soft in aortic stenosis splitting during inspiration is normal

Answer 57

- 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.

Answer 58

ejection systolic murmur fixed splitting of S2 embolism may pass from venous system to left side of heart causing a stroke

Answer 59

Stroke Volume = End Diastolic Volume– End Systolic Volume

Answer 60

Cardiac Output = Heart Rate x Stroke Volume

Answer 61

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

Answer 62

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)

Answer 63

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).

Answer 64

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

Answer 65

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

Answer 66

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

Answer 67

- 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

Answer 68

- 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

Answer 69

Amoxicillin 2g 1 hour before procedure If hypersensitive/already on long-term/or in last month Clindamycin 600mg 1 hour beforehand

Answer 70

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

Answer 71

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

Answer 72

A- wave (S1) - atrial contraction C-wave - tricuspid valve closure X-descent - atrial relaxation V-wave (S2) - atrial filling Y-descent - rapid ventricular filling

Answer 73

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

Answer 74

Internal jugular vein is preferred (although does correlate well with external This is lateral to the SCM

Answer 75

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

Answer 76

- 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

Answer 77

(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

Answer 78

Inferior = II, III, aVF Lateral = I, aVL, V5-6 Anterior = V2-6

Answer 79

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.

Answer 80

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.

Answer 81

AD Prevalence in offspring of 50% Mediterraneans

Answer 82

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

Answer 83

Protected prior to menopause Natural hx delayed by about one decade But still accelerated b y 2 decades in both women and men

Answer 84

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.

Answer 85

Arcus and xanthelasma Premature CHD/CVD Aortic stenosis

Answer 86

Increased LDL Increased remnants including precursor IDL

Answer 87

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

Answer 88

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.

Answer 89

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.

Answer 90

LDL receptor (most common) LDL receptor ligand (apolipoprotein B100) - second most common Proprotein Convertase Subtilsin Kexin 9 (PCSK-9) - third most common

Answer 91

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

Answer 92

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.

Answer 93

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

Answer 94

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

Answer 95

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%.

Answer 96

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.

Answer 97

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

Answer 98

Bile acid binding resin

Answer 99

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)

Answer 100

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.

Answer 101

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

Answer 102

Statins are first line

Answer 103

Statin plus fish oil Fibrate plus ezetimibe Statin plus fenofibrate or statin plus nicotinic acid can be done but only with caution.

Answer 104

Steatorrhea Myalgia and rhabdo have been repeated Raise ALT/AST NOT CYP450 so limited drug interactions Avoid in mod-severe liver impairment (no data)

Answer 105

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.

Answer 106

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

Answer 107

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.

Answer 108

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

Answer 109

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.

Answer 110

CK: statin \> fibrate \> nicotinic acid or ezetimibe ALT: nicotinic acid \> ezetimibe \> fibrate \> statin

Answer 111

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

Answer 112

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

Answer 113

Reduce liver cholesterol synthesis Increased LDLr and SREBP gene expression Receptors produced by normal gene (even in familial disease) will reduce LDL cholesterol levels.

Answer 114

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

Answer 115

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

Answer 116

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.

Answer 117

Broad QRS \>120ms RSR pattern in V1-V3 Wide slurred S wave in lateral leads (I, AVL, V5-V6) RBBB

Answer 118

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

Answer 119

Symptoms of known or probably ischaemic heart disease Stable chest pain Unstable chest pain stabilised by medical therapy Post MI Post revascularisation

Answer 120

Acute MI Unstable angina Symptomatic uncontrolled cardiac arrhythmia Severe AS Acute PE or pulm infarct Acute myocarditis or pericarditis Acute aortic dissection

Answer 121

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

Answer 122

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).

Answer 123

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.

Answer 124

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.

Answer 125

Evaluation of acute chest pain (emergency department): normal ECG and cardiac enzymes low-to-intermediate pretest probability of CAD.

Answer 126

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.

Answer 127

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

Answer 128

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

Answer 129

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.

Answer 130

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

Answer 131

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

Answer 132

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

Answer 133

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.

Answer 134

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.

Answer 135

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.

Answer 136

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.

Answer 137

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

Answer 138

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).

Answer 139

QRS is positive (dominant R wave) in leads I and aVL QRS is negative (dominant S wave) in leads II and aVF

Answer 140

LVH Inferior MI LBBB WPW

Answer 141

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

Answer 142

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.

Answer 143

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.

Answer 144

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_

Answer 145

Constant PR interval until P waved dropped with P-P interval twice normal This the Mobitz II (the bad one)

Answer 146

Lengthening PR interval until P waved dropped with P-P interval variable. Grouped beats. Need follow up but less likely to progress to CHB

Answer 147

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.

Answer 148

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

Answer 149

QRS is positive (dominant R wave) in leads III and aVF QRS is negative (dominant S wave) in leads I and aVL

Answer 150

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

Answer 151

![]() 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

Answer 152

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

Answer 153

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.

Answer 154

Severe pneumonia Exacerbation of COPD / asthma Pneumothorax Recent pneumonectomy Upper airway obstruction

Answer 155

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

Answer 156

Obesity COPD Pericardial effusion Severe hypothyroidism Massive damage Infiltrative/restrictive disease ie amyloid

Answer 157

- 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.

Answer 158

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

Answer 159

Increase 5 year survival

Answer 160

Decrease PAP Decrease PVR Increase survival Increase six minute walk Bosentan is the same but also increases cardiac output

Answer 161

Decreases PAP Decreases PVR Increases 6min walk test

Answer 162

Both increase 6 minute walk test and decrease symptoms

Answer 163

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

Answer 164

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

Answer 165

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

Answer 166

Secondary (ie disease associated) - much more common

Answer 167

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

Answer 168

_RV infarct_ (need high filling Pa to maximize filling of LV) Venodilatation and hypotension with _inferior MI._

Answer 169

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

Answer 170

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.

Answer 171

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.

Answer 172

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

Answer 173

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).

Answer 174

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.

Answer 175

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)

Answer 176

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.

Answer 177

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

Answer 178

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%)

Answer 179

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

Answer 180

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%.

Answer 181

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).

Answer 182

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.

Answer 183

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.

Answer 184

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.

Answer 185

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.

Answer 186

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

Answer 187

\>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.

Answer 188

preload reduction: diuretics, opioids, decrease intake, spironolactone

Answer 189

afterload reduction: ACE-I, GTN, IABP

Answer 190

increase contractility: milrinone, dobutamine, adrenaline, VAD

Answer 191

decreased myocardial work: beta-blockers, IABP, VAD

Answer 192

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

Answer 193

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

Answer 194

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.

Answer 195

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

Answer 196

dilutional hyponatraemia, exacerbated by high-dose diuretic therapy

Answer 197

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

Answer 198

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

Answer 199

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

Answer 200

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

Answer 201

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

Answer 202

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

Answer 203

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.

Answer 204

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.

Answer 205

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

Answer 206

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

Answer 207

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.

Answer 208

Systolic dysfunction (LVEF \< 40%) Diastolic dysfunction (LVEF \> 40%

Answer 209

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).

Answer 210

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.

Answer 211

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.

Answer 212

Male patients frequently suffer from erectile dysfunction. Sildenafil is contraindicated in patients receiving nitrate therapy, or those who have hypotension, arrhythmias or angina pectoris

Answer 213

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

Answer 214

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

Answer 215

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

Answer 216

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

Answer 217

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

Answer 218

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

Answer 219

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.

Answer 220

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.

Answer 221

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.

Answer 222

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.

Answer 223

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.

Answer 224

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

Answer 225

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

Answer 226

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.

Answer 227

Valuable for therapy of AF in CHF patients Increased mortality of women even in therapeutic range, survival advantage for men.

Answer 228

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

Answer 229

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

Answer 230

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.

Answer 231

Avoid unless beta-blockers or amiodarone

Answer 232

Avoid TCAs and Clozapine

Answer 233

Avoid thiazolidendiones Metformin is safe unless concomitant renal impairment

Answer 234

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

Answer 235

Avoid Moxonidine has been associated with increased mortality in patients with heart failure and is contraindicated in such patients.

Answer 236

Severely symptomatic despite appropraite doses of ACEI's and diuretics

Answer 237

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.

Answer 238

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)

Answer 239

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

Answer 240

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

Answer 241

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

Answer 242

\<65 Class IV heart failure and no major comorbidities, refractory or intolerant to beta-blocker therapy

Answer 243

Symptomatic on therapy and LVEF \>40 = spironolactone Symptomatic on therapy and LVEF \<40 = eplerenone

Answer 244

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.

Answer 245

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

Answer 246

NYHA symptoms Class III/IV despite optimal medical therapy dilated heart failure with an ejection fraction ≤ 35% QRS duration ≥ 120 ms sinus rhythm

Answer 247

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

Answer 248

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%.

Answer 249

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.

Answer 250

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

Answer 251

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

Answer 252

- 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

Answer 253

Infections (particularly pulmonary) due to haemodynamic changes Renal failure --\> fluid overload Anaemia or pulm emboli impairing oxygen delivery Thyroid imbalance

Answer 254

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.

Answer 255

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

Answer 256

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.

Answer 257

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.

Answer 258

Systolic LV dysfunction—CHD, dilated cardiomyopathy, mitral regurgitation Diastolic LV dysfunction—hypertensive heart disease, hypertrophic cardiomyopathy, aortic stenosis Normal LV function—mitral stenosis

Answer 259

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

Answer 260

- 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

Answer 261

Echo - restrictive or pseudonormal mitral inflow filling pattern - LA enlargement - reduced septal annular velocity Angio - elevated LVEDP - Prolonged Tau

Answer 262

- 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

Answer 263

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.

Answer 264

Poorly to medical therapy Arterial vasodilators including ACEIs are contraindicated due to the risk of coronary hypoperfusion Appropriate medical therapy = digoxin and diuretics

Answer 265

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)

Answer 266

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

Answer 267

Nonselective CCB Last line for angina CYP450 - watch out for liver toxicity

Answer 268

- 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

Answer 269

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

Answer 270

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

Answer 271

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.

Answer 272

Severe of decompensated - risk of lactic acidosis Glitazones should avoided in patients with Class III or IV sx

Answer 273

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.

Answer 274

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.

Answer 275

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

Answer 276

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.

Answer 277

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

Answer 278

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

Answer 279

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

Answer 280

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.

Answer 281

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

Answer 282

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

Answer 283

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%

Answer 284

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

Answer 285

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

Answer 286

Primary failure - evidence of continuing or worsening myocardial ischemia Threatened reocclusion - early recurrent ischemia after apparently successful fibrinolysis

Answer 287

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

Answer 288

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.

Answer 289

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

Answer 290

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).

Answer 291

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

Answer 292

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.

Answer 293

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.

Answer 294

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).

Answer 295

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.

Answer 296

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.

Answer 297

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

Answer 298

Stable coronary sx as opposed to acute and dynamic

Answer 299

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.

Answer 300

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

Answer 301

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

Answer 302

Sedation and coma Seizures Hypotension Tachycardia Broad complex dysrhythmias Anticholinergic syndrome

Answer 303

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

Answer 304

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

Answer 305

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

Answer 306

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

Answer 307

A – impaired LOC -\> intubate consider whole bowel irrigation for massive acute ingestion activated charchoal does not bind Liberal fluid resuscitation with normal saline

Answer 308

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

Answer 309

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.

Answer 310

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.

Answer 311

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

Answer 312

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.

Answer 313

38% Around 7%

Answer 314

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.

Answer 315

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

Answer 316

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)

Answer 317

Output from left ventricle to body surface area - in L/m Under 1.8 = cardiac shock Used in ICU

Answer 318

Cardiogenic shock

Answer 319

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

Answer 320

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

Answer 321

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

Answer 322

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.

Answer 323

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.

Answer 324

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.

Answer 325

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.

Answer 326

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