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
D. all of the above
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.
A. Patients with recurrent AF after ablation had significantly less MR than those in sinus rhythm.
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
B. catheter ablation in patients with symptomatic paroxysmal AF who have not responded to antiarrhythmic medications
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.
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.
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.
C. Twenty years after smoking cessation, PAD risk in former smokers approached that of nonsmokers.
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.
B. aspirin was equivalent to aspirin plus warfarin.
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
B. male sex
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
C. major bleeding
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.
B. The international normalized ratio of warfarin recipients was in the therapeutic range about 50% of the time.
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.
A. The rate of the primary outcome was more than twice as high in the aspirin group as in the apixaban group.
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
B. hemorrhagic stroke
Name the types of atrial septal defects
Ostium secundum (70% of ASDs)associated with Holt-Oram syndrome (tri-phalangeal thumbs)ECG: RBBB with RAD
Ostium primumpresent earlier than ostium secundum defectsassociated with abnormal AV valvesECG: RBBB with LAD, prolonged PR interval
Describe the heart sound S4
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
Which drug will cause complete heart block if combined with a beta-blocker?
What are the features of Ivrabadine?
Ivabradinea new class of anti-anginal drug which works by reducing the heart rateacts on the If ('funny') ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activityadverse effects: visual effects, particular luminous phenomena, are common. Bradycardia, due to the mechanism of action, may also be seenthere is no evidence currently of superiority over existing treatments of stable angina
What is the acute mx of SVT?
Acute managementvagal manoeuvres: e.g. Valsalva manoeuvreintravenous adenosine 6mg → 12mg → 12mg: contraindicated in asthmatics - verapamil is a preferable optionelectrical cardioversion
Describe the modified Duke criteria
pathological criteria positive, or2 major criteria, or1 major and 3 minor criteria, or5 minor criteria
Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)
Positive blood culturestwo positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, orpersistent 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, orpositive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci, orpositive molecular assays for specific gene targets
Evidence of endocardial involvementpositive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves), ornew valvular regurgitation
Minor criteriapredisposing heart condition or intravenous drug usemicrobiological evidence does not meet major criteriafever > 38ºCvascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpuraimmunological phenomena: glomerulonephritis, Osler's nodes, Roth spots
Criteria for AVR
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)
What is the classification of critical and severe AS?
Always done with TTE
Mean gradient (mmHg) >70 is critical, >40 is severe
Valve area <0.6 is critical, <1.0cm is severe
What are the lines of drug therapy in long term maintenance of AF in terms of ventricular control?
B- blocker first lineThen diltiazemthen verapamil
When would you consider Digoxin in the control of rapid AF?
Useful in the elderlyUseful 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
Rate or rhythm control for AF?
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.
What is atrial 'stunning'? Why is it important?
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.
What is post -cardioversion maintenance therapy?
Not required if AF was associated with a transient condition.Anticoagulate for 6-12 monthsLong-term antiarrhythmics - flecainide, sotalol, amiodaroneConsider ablation if poorly controlled on antiarrhythmic therapy
If using sotalol, watch out for prolonged QTc (>500ms or >20% from baseline, avoid in renal impairment)
What consideration do you need to make in Warfarinising an elderly person?
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.
Epidemiology of atrial myxoma
Most common primary cardiac tumor in adultsMean presentation around 50 (but can be any age)WomenAssociated with MEN (can have myxomas elsewhere too)
What are the clinical features of atrial myxoma?
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)
What is the characteristic heart sound of someone with an atrial myxoma?
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
What is the histopath of atrial myxoma?
Benign, often haemoorhagicUsually pedunculated and over variable sizeUsually in the LA attached to the interatrial septum in the fossa ovale region
What does an atrial myxoma look like on CT?
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.
What is this?
Metastatic pericardial disease
What complication does papillary muscle rupture or dysfunction lead to?
Mitral valve prolapse
What is cor triatriatum?
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.
What is this a picture of?
Cardiac mechanical prosthesis (St Jude)
What is the natural history of a VSD?
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
What is the clinical finding of a VSD
Holosystolic (pan systolic) murmur over lower left sternal edge +/- palpable thrill or heave
Smaller = louder + more palpable thrill
Displaced apex if big enough
Three points about VSD
- most common heart defect in children- most commonly membranous- most common cause of Eisenmengers syndrome (due to severe overload)
What is the purpose of stress ECG testing?
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
What are the factors predicting an adverse outcome in CHD?
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
What are the stress ECG findings that predict an increased risk of adverse outcome?
≥ 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)
What is the significance of early and late onset ST depression in stress testing?
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
What is the significance of PVCs in stress testing?
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.
What does this CXR show?
Severe pulm HT
- markedly prominent main pulm artery (MPA)
- RPA enlarged
- prominent right atrial contour (RA dilation due to RVH)
What is pulmonary hypertension?
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)
What is the clinical presentation of pulmonary hypertension
Dyspnoea - esp with exerciseRight heart failure including peripheral oedema and abdominal distensionECG - RV strain and hypertrophy
Name the causes of pulmonary hypertension caused by pulmonary vein and left heart pathology
- chronic left heart failure
- mitral valve stenosis
- hypoplastic left heart syndrome
Name the cause of pulmonary hypertension caused by pulmonary capillary and parenchymal pathology
Emphysema of any kindAsthmaBronchiectasis of any kindLymphangiomyomatosisLangerhans cell histiocytosisPulmonary fibrosis (any cause ie scleroderma, dermatomyositis, rheumatoid, SLE)Pneumoconiosis
Name the cause of pulmonary hypertension caused by pulmonary artery pathology
Chronic pulmonary emboliArteritis - PAN, SLE, Takayau, WegenersPulmonary artery stenosis
Name the causes of pulmonary hypertension caused by right heart pathology
Eisenmenger phenomenon (inc ASD, VSD, PDA)
What are the extra-cardiad findings on CT in pulmonary hypertension?
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 arteriesmural calcification in central pulmonary arteries most frequently seen in patients with Eisenmenger phenomenon
evidence of previous pulmonary embolia 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
What are the medical options in pulmonary hypertension?
calcium channel antagonists nitric oxide prostanoids, e.g. epoprostenol, treprostinil, iloporst endothelin antagonists e.g. bosentan, sitaxsentan, ambrisentan phosphodiesterase inhibitors
What are the causes of a split S2?
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
3 points about the second heart sound
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.)
What are the causes of a loud first heart sound?
Hyperdynamic (fever, exercise) Mitral stenosis Atrial myxoma (rare)
What are the causes of a soft first heart sound?
Soft First Sound
Low cardiac output (rest, heart failure) Tachycardia Severe mitral reflux (caused by destruction of valve)
What are the causes of variable intensity first heart sound?
Variable Intensity of First Sound
Atrial fibrillation Complete heart block
How do you define a split heart sound?
Audible expiratory splitting means > 30 msec difference in the timing of the aortic (A2) and pulmonic (P2) components of the second heart sound.
What is the significance of a 3rd heart sound?
Low frequency sound in early diastoleIncreased atrial pressure --> increased flow rateCHF is the most common cause but may be normal in people under 40
What is the significance of a 4th heart sound?
Presystolic portion of diastoleStiff left ventricle - i.e. hypertension, AS, ischemic or HOCMIf the patient has MR, may be due to acute regurgitation following chorda tendinae rupture
What's the best way to hear the 3rd and fourth heart sounds?
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
What is definition of HOCM and it's prevalence?
LVH in absence of other loading conditionsPrevalence 0.2% or 1 in 500!
Epidemiology of HOCM?
AD with variable penetranceOffspring of affected = 50%Can be benignCommonest cause of sudden cardiac death <35 yearsCan have angina, signs of pulm congestion (PND, orthopnoea), syncope, and palpitations
What are the clinical examination features of HOCM?
Jerky rapidly rising pulseProminent LV impulseApical systolic murmur that increases with valsalva (related to dynamic obstruction)Fourth heart sound
What are the ECG findings in HOCM?
What are the causative genes of HOCM?
Primarily encode sarcomere or sarcomere related proteins
Cardiac β-myosin heavy chain (β MHC) (45%)
Myosin binding protein C (MyBPC) (35%)
Cardiac troponin T, tropomyosin, cardiac
troponin I, essential and regulatory myosin light c
hain, and more recently, titin and actinin-2 genes
What is the role of genetic testing in HOCM?
Identifies at-risk earlierAvoids unecessary screening of non-carriersCan distinguish between other causes of LVHPick up rate of 50-50%
When does sudden death in HOCM most frequently occur?
Sudden death occurs most commonly in HCM either during or immediately after exercise, although death can also occur at rest
Who should be screened for HOCM and how often?
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
When should the physician report someone to the RTA?
The health professional should considerreporting 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
What are the driving rules for:
Elective PCI - 2 daysMI - 2 weeksCABG - 4 weeksArrest - 6 months
What are the driving rules for:
DVT - 2 weeksCardiogenic syncope - 4 weeksPE - 6 weeks
What is the driving license rule with regard to heart failure?
Sx on moderate exertion = no licence
What are the driving rules for seizures?
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
How long after a stroke can you drive?
4 weeks - 2 if TIASAH - 3 months
How do you differentiate between chronic hypertension and pre-eclampsia?
Chronic hypertension - hypertension before 20 weeks gestation, often diastolic - no or stable proteinuria
(if after 20 weeks gestation and no proteinuria --> gestational hypertension)
What does the a-wave of JVP mean?
'a' wave = atrial contractionlarge if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertensionabsent if in atrial fibrillation
coincides with first heart sound
What is a cannon a-wave?
Cannon 'a' wavescaused by atrial contractions against a closed tricuspid valveare seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular pacing
What is the v wave of the JVP?
due to passive filling of blood into the atrium against a closed tricuspid valve
giant v waves in tricuspid regurgitation - very reliable sign
What does the S1 of the heart sound refer to? Pathology?
closure of mitral and tricuspid valves
soft if long PR or mitral regurgitation
loud in mitral stenosis
What does the S2 of the heart sound refer to? Pathology?
closure of aortic and pulmonary valves
soft in aortic stenosis
splitting during inspiration is normal
What is the significance of an ASD?
- 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.
What are the features of an ASD?
ejection systolic murmur
fixed splitting of S2
embolism may pass from venous system to left side of heart causing a stroke
How do you calculate stroke volume?
Stroke Volume = End Diastolic Volume– End Systolic Volume
How do you calculate cardiac output?
Cardiac Output = Heart Rate x Stroke Volume
What is VO2 max?
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
Why is it useful to measure the mixed venous oxygen concentration?
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)
increased O2 delivery (increased FiO2, hyperoxia, hyperbaric oxygen)
decreased O2 demand (hypothermia, anaesthesia, neuromuscular blockade)
high flow states: sepsis, hyperthyroidism, severe liver disease
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)
How do you calculate venous oxygen content?
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).
What is Fick's principle?
CO = VO2 (oxygen consumption) / arteriovenous oxygen difference (Ca-Cv)
How do you measure VO2?
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
What happens to the heart in old people?
Heart rate decreases (really affects max CO)Stroke volume declines (major factor for the decline lower cardiac output in submax exercise)LV contractility declinesDecreased vascular capacity and local blood flow autoregulationPoor O2 deliveryPoor muscle oxidative capacityIncreased TPR
In which cardiac patients is antibiotic prophylaxis recommended if undergoing dental surgery?
- 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
For which dental procedures is antibiotic phrophylaxis always required in at-risk cardiac patients?
- 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
What is the standard antibiotic prophylaxis for IE in at-risk patients undergoing dental procedures?
Amoxicillin 2g 1 hour before procedure
If hypersensitive/already on long-term/or in last month
Clindamycin 600mg 1 hour beforehand
Which respiratory tract procedures require endocarditis prophylaxis in those at-risk?
Anything involving incision or bx of resp mucosa- tonsillectomy/adenoidectomy- bronch PLUS incision or bxAny surgery inc bronchial sinus, nasal or middle ear mucosa including tympanosomty tube insertion
For which GI and GUT procedures is antibiotic prophylaxis required in at-risk cardiac patients?
LithotripsyAny 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
Name the points on the JVP
A- wave (S1) - atrial contraction
C-wave - tricuspid valve closure
X-descent - atrial relaxation
V-wave (S2) - atrial filling
Y-descent - rapid ventricular filling
What is the definition of a raised JVP?
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
Define the anatomy of the JVP
Internal jugular vein is preferred (although does correlate well with external
This is lateral to the SCM
Why is the right sided internal jugular vein preferred for measuring the JVP?
The left sided veins cross from the left side of the chest before entering the right atrium so are less accurate
What does the pulmonary artery wedge pressure measure?
- 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
In what situations is the PAWP not equivalent to LVEDP?
(Wedge pressure greater) than LVEDP
Mitral stenosis or MRAtrial myxomaPulmonary venous obstruction (i.e. fibrosis, vasculitis)L-R shuntCOPDIPPV
Wedge pressure less than LVEDP- severe LV failure- high PEEP- noncompliant LV (i.e. hocm)- AR
What is the normal distribution of the ECG leads?
Inferior = II, III, aVF Lateral = I, aVL, V5-6 Anterior = V2-6
What does LBBB and RBBB do to the t-wave?
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.
How do you interpret a troponin?
A test should be interpreted as positive if levelis≥99th centile for reference population ORthere is a change of≥50% above an initial base-line level. A positive finding identifies patientsat increased risk, but does not provide defini-tive evidence of MI. A positive troponin resultshould be followed up by a search for analternative plausible diagnosis and/or cardiacconsultation if ACS is suspected in the contextof the clinical presentation.
What is the epidemiology of familial hypercholesterolaemia?
ADPrevalence in offspring of 50%Mediterraneans
What is the clinical presentation of familial hypercholesterolaemia?
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
How do women differ from men with regard to familial hypercholesterolaemia?
Protected prior to menopauseNatural hx delayed by about one decadeBut still accelerated b y 2 decades in both women and men
What are the specific signs of familial hypercholesterolaemia
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.
What are the nonspecific clinical presentations of familial hypercholesterolaemia?
Arcus and xanthelasmaPremature CHD/CVDAortic stenosis
What are the metabolic features of hypercholesterolaemia?
Increased LDLIncreased remnants including precursor IDL
What are the top 3 specific features of familial hypercholesterolaemia?
8 points DNA Mutation, or LDL-C > 8.56 points Tendon xanthomas5 points LDL-C 6.5 – 8.4----4 points Arcus senilis < 45 yrs3 points LDL 5.0 – 6.42 points Xanthomas or premature arcus in 1 st degree relative, childhood LDL > 95th percentile, or premature CHD1 point 1st deg relative with premature CVD or LDL > 95 th percentile, personal history of LDL 4.0 – 4.9 or premature CVD
When should you suspect familial hypercholesterolaemia?
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 andpremature 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.
What is the main value of molecular diagnosis of familial hypercholesterolaemia?
The major value in making a molecular diagnosis is its use in predictive testingof 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.
What genes are associated with familial hypercholesterolaemia?
LDL receptor (most common)
LDL receptor ligand (apolipoprotein B100) - second most common
Proprotein Convertase Subtilsin Kexin 9 (PCSK-9) - third most common
When would you be most likely to find a causative mutation for familial hypercholesterolaemia?
Definite clinical familial hypercholesterolaemia --> causative mutation found 80% of the time.
What is the management of predominantly elevated LDL-C?
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.
When is use of a bile acid binding resin inappropriate?
Addition of a bile acid binding resin can enhance LDL-C reduction, but is inappropriate when triglycerides are elevated because hypertriglyceridaemia can be exacerbated.
What does doubling the dose of a statin do to the LDL-C?
Each doubling of statin dose is likely to reduce LDL-C by an additional 5% to 10%.
What is the next step after maximal statin therapy fails to bring down the LDL-C enough?
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%.
Under what circumstances are bile acid binding resins used in dyslipidemia?
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.
What are the adverse effects of bile acid binding resins?
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
ConstipatingCan interfere with drdug absorption esp anticoagulants, thyroxine, cyclosporin, and digoxin
What is third line after a statin plus ezetimibe for dyslipidemia of LDL-C variant?
Bile acid binding resin
What is fourth line therapy for dyslipidemia of the LDL-C kind?
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)
Can you use fibrates with a statin to reduce LDL-C? What do you need to consider?
May lead to 5-10% reduction in LDL-CDoes 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.
How do you treat hypertriglyceridaemia?
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
High CVD riskElevated LDL-CMild to moderate elevation of TGLs
What is the treatment?
Statins are first line
High absolute CVD riskLDL-C elevatedTGLs >4
What is first line therapy?
How safely do you treat mixed hyperlipidaemia that is severe? (Mixed = high cholesterol and TGL)
Statin plus fish oilFibrate plus ezetimibe
Statin plus fenofibrate or statin plus nicotinic acid can be done but only with caution.
What are the side effects of Ezetimibe?
SteatorrheaMyalgia and rhabdo have been repeatedRaise ALT/AST
NOT CYP450 so limited drug interactionsAvoid in mod-severe liver impairment (no data)
What are the risk factors for developing liver and muscle problems from lipid-modifying therapy?
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.
How do you monitor lipid modifying therapy?
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
When should you stop lipid-modifying therapy?
Mild muscle sx - still benefit from max dose, try second daily or twice weekly
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.
What do you do if someones muscles or liver enzymes normalise after you stop lipid-modifying therapy?
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
Which lipid-modifying agents impair glucose metabolism?
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.
Which lipid modifying drugs affect the CK and ALT respectively?
CK: statin > fibrate > nicotinic acid or ezetimibe
ALT: nicotinic acid > ezetimibe > fibrate > statin
What lipid tests are required to calculate absolute CVD risk?
What are the drawbacks of this?
TC (total cholesterol) and HDL-C
TC may overestimate risk of HDL-C is raisedTC may underestimate risk of TGLs are raised
Predictive value is improved by considering LDL-C and HDL-C independently
What impact does significantly elevated triglycerides have on the measurement of cholesterol and LDL-C?
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
How do statins reduce LDL?
Reduce liver cholesterol synthesisIncreased LDLr and SREBP gene expressionReceptors produced by normal gene (even in familial disease) will reduce LDL cholesterol levels.
What are the target lipid levels for patients on lipid-modifying therapy?
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
What are the target LDL-C levels in those with familial hypercholesterolaemia?
Target plasma levels for LDL-cholesterol for low, intermediate an d high risk FH are < 4, < 3 and < 2 mmol/L, respectively
Which subset of familial hypercholesterolaemia patients benefits the most from statins?
Statin treatment of FH males is one of the most cost-effective medical interventions 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.
What does this ECG show?
Broad QRS >120msRSR pattern in V1-V3Wide slurred S wave in lateral leads (I, AVL, V5-V6)
What syndrome do you need to be mindful of when diagnosing a RBBB on ECG?
An RSR’ pattern in V1-3 may also be caused by Brugada syndrome – an ECG pattern associated with malignant ventricular arrhythmias.
When is treatment stress testing indicated?
Symptoms of known or probably ischaemic heart diseaseStable chest painUnstable chest pain stabilised by medical therapyPost MIPost revascularisation
What are the absolute contraindications to EST?
Acute MIUnstable anginaSymptomatic uncontrolled cardiac arrhythmiaSevere ASAcute PE or pulm infarctAcute myocarditis or pericarditisAcute aortic dissection
What are the most important pre-test predictive parameters of CAD?
Diagnostic power of EST is maximal when the pretest probability is intermediate (30-70%)
What are the indications for PCI?
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).
What is the evidence behind CTCA?
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.
What are the indications for CTCA in the evaluation of non-acute chest pain?
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.
What are the indications for CTCA with acute chest pain?
Evaluation of acute chest pain (emergency department):
normal ECG and cardiac enzymes
low-to-intermediate pretest probability of CAD.
What are the indications for CTCA outside of chest pain?
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.
What is the most appropriate application of CTCA?
It is used most appropriately in symptomatic patients with low to intermediate pretest probability of CAD.
When should CTCA not be used?
It should not be used in asymptomatic subjects, patients with known significant CAD or patients with a high pretest probability of CAD.
How does the radiation dose of CTCA compare with invasive coronary angio?
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.
What are the absolute contraindications to thrombolysis?
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
What are the indications for digoxin?
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
What does the ECG show?
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
What are the limitations of coronary artery calcium scoring?
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.
What are the indications for coronary calcium scoring?
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.
What are the scoring categories of the Framingham Risk Score?
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.
Give a scenario where a coronary calcium score would be useful
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.
What is CHD risk equivalent?
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)
Chronic Kidney Disease
What are the ECG changes in LVH?
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).
How do you recognise left axis deviation on ECG?
QRS is positive (dominant R wave) in leads I and aVL QRS is negative (dominant S wave) in leads II and aVF
What are the causes of left axis deviation?
What ECG finding is suggestive of left main coronary artery occlusion?
A pattern of widespread ST depression plus ST elevation in aVR > 1 mm is suggestive of left main coronary artery occlusion.
What do you make of ST depression localised to a specific territory on ECG?
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.
When is T-wave inversion considered to be evidence of myocardial ischemia?
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.
What is Mobitz II heart block?
A-V blockPR of constant interval
Constant PR interval until P waved dropped with P-P interval twice normal
Likely to progress to CHB
What does the ECG show?
Constant PR interval until P waved dropped with P-P interval twice normal
This the Mobitz II (the bad one)
What is Wenkebach block?
Lengthening PR interval until P waved dropped with P-P interval variable. Grouped beats.
Need follow up but less likely to progress to CHB
What does this ECG show?
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.
What ECG findings are best used to differentiate PE from ACS?
Negative T waves in both leads III and V1 (Part of an RV strain pattern - can be in other right sided things too)
How do you recognise right axis deviation?
QRS is positive (dominant R wave) in leads III and aVF QRS is negative (dominant S wave) in leads I and aVL
What does the ECG show?
QRS is positive (dominant R wave) in leads III and aVFQRS is negative (dominant S wave) in leads I and aVL
Right axis deviation
How is the cardiac axis defined?
RA is negativeLA 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
Name the different infarct patterns on ECG
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
ECG findings in PE
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.
What are the causes of acute cor pulmonale (i.e. any disease that causes right ventricular strain / hypertrophy due to hypoxic pulmonary vasoconstriction)?
Severe pneumonia Exacerbation of COPD / asthma Pneumothorax Recent pneumonectomy Upper airway obstruction
How do you define a low-voltage ECG?
Peak-to-peak QRS <5mm in the limb leads or <10mm in the precordial leads
What causes a low voltage ECG?
ObesityCOPDPericardial effusionSevere hypothyroidismMassive damageInfiltrative/restrictive disease ie amyloid
When using a right heart catheter to measure drug response in pulmonary hypertension, which two values are you looking at?
- 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.
What are the biomarkers used in pulm hypertension?
Pro-BNP – correlated with degree of RV dysfunctionUric acid: sign of tissue hypoperfusionTroponin
Also (not a biomarker but)
Key prognostic measure is pulmonary vascular resistance – higher is a worse prognosis
What is the evidence for CCB's in PHT?
Increase 5 year survival
What is the evidence for prostacyclin (Epoprostenol) in PHT?
What about an endothelin receptor antagonist (Bosentan)?
Decrease PAPDecrease PVRIncrease survivalIncrease six minute walk
Bosentan is the same but also increases cardiac output
What's the evidence for a PDE5 inhibitor (Sildenafil) in PHT?
Decreases PAPDecreases PVRIncreases 6min walk test
What's the evidence for epoprostenol and prostacyclin analogues in PHT?
Both increase 6 minute walk test and decrease symptoms
What is the role of atrial septostomy in PHT?
Atrial septostomy: creates R -> L shunt to decrease RHF. Last resortHeart-Lung Transplant for patients with class III-IV symptoms not responsive to medical treatment
What are the mitigating factors of CCBs in PHT?
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
What is the clinical definition of PHT?
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
Which is more common - primary or secondary PHT?
Secondary (ie disease associated) - much more common
What is the epidemiology of idiopathic PHT?
5 year survival 35%Women of childbearing years6-10% familial - AD w/ incomplete penetrance - PPH1 gene --> morphogenetic protein receptor II (BMPR2) --> normal protein inhibits muscle proliferation, abnormal protein --> vascular remodelling
In which infarct settings is more volume support required?
RV infarct (need high filling Pa to maximize filling of LV)
Venodilatation and hypotension with inferior MI.
What is the culprit lesion in an inferior STEMI?
The vast majority (~80%) of inferior STEMIs are due to occlusion of the dominant right coronary artery (RCA).
Why will up to 20% of patients with inferior stemi develop heart block?
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.
What do you do about heart block caused by an inferior MI?
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.
What does the ECG show?
Inferior STEMI with third degree heart block and slow junctional escape rhythm.
What are the general features of pericarditis?
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).
How do you recognise pericarditis on ECG?
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.
What are the ECG stages of pericarditis?
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)
What does the ECG show?
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.
How do you differentiate pericarditis from a STEMI?
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
What is the clinical presentation of aortic dissection in order of frequency of symptom?
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%)
What are the complications of aortic dissection?
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
What are the CXR findings in aortic dissection?
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%.
What is the role of d-dimer in acute aortic dissection?
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).
What is the role of echo in aortic dissection?
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.
What is the role of CT in aortic dissection?
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.
What is the role of MRI/MRA or aortography in acute aortic dissection?
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.
What is the management of type A ascending aortic dissection?
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.
What is the management of type A descending aortic dissection?
Medical control of BP with beta blockers, with surgery or endovascular stent grafting for selected patients with an unfavourable outlook.
What are the stats like for out of hospital VF arrest and AEDs?
>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.
Which drugs decrease preload?
preload reduction: diuretics, opioids, decrease intake, spironolactone
Which drugs decrease afterload?
afterload reduction: ACE-I, GTN, IABP
Which drugs increase contracitility?
increase contractility: milrinone, dobutamine, adrenaline, VAD
Which drugs degrease myocardial work?
decreased myocardial work: beta-blockers, IABP, VAD
What increases coronary perfusion and oxygenation?
increased coronary perfusion and oxygenation: O2, Hb, Stents, CABG, IABP
What is the role of assisted ventilation in heart failure
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
What is the role of TTE in heart failure?
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.
What is the significance of anaemia in CHF?
Mild anaemia may occur in patients with CHF and is associated with an adverse prognosis
What happens to serum sodium in heart failure?
dilutional hyponatraemia, exacerbated by high-dose diuretic therapy
What happens to serum potassium in heart failure?
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 totherapy, with thiazide or loop diuretics
What happens to serum magnesium in heart failure?
plasma magnesium levels may be reduced due to theeffects of diuretic therapy; magnesium replacement tonormal levels reduces ectopic beats and helps normalisepotassium levels
What happens to the LFTs in heart failure?
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
What is an "angina equivalent"?
Dyspnoea on exertion is a frequent manifestation of inducible myocardial ischaemia, sometimes referred to as an ‘angina equivalent’.
What is a frequent manifestation of inducible myocardial ischaemia that isn't pain? How is it assessed?
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
What is the role of a right heart cath in heart failure?
heart failure appears refractory to therapy
the diagnosis of CHF is in doubtdiastolic heart failure is recurrent and difficult to confirm by other means
What are BNP levels useful for?
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.
When are BNP levels less useful?
Better for systolic, not diastolic dysfunction.
In particular, BNP levels do not appear to discriminate well between elderlyfemale 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 othercauses, including corpulmonale and pulmonary embolism.
What is the CSANZ recommendation for use of plasma BNP in patitens with recent-onset dyspnoea?
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
What is the role of plasma BNP in therapy for CHF titration?
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
When would you do an endomyocardial biopsy?
Endomyocardial biopsy may be indicated in patients with cardiomyopathy with recent onsetof symptoms, where CHD has been excluded by angiography, or where an inflammatory orinfiltrative process is suspected.
How do you delineate between systolic and diastolic heart failure?
Systolic dysfunction (LVEF < 40%)Diastolic dysfunction (LVEF > 40%
Who are the high risk CHF patients?
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
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).
What type of exercise should be avoided in CHF?
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.
Can patients with heart failure have sex? Why?
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.
Male patients with CHF frequently experience erectile dysfunction. Would you give them viagra? Why?
Male patients frequently suffer from erectile dysfunction.
Sildenafil is contraindicated in patients receiving nitrate therapy, or those who have hypotension, arrhythmias or angina pectoris
How do you manage fluid status in CHF?
Weight diary with daily morning weights>2kg/ days --> see doctor ASAP, ditto with lossNo more than 2L fluid a day1.5L / day if fluid retainingCan self regulate diuretic dose based on weight monitoring and symptoms - can only ever double - drop back when dry weight/symptoms resolveMay need to have a bit more fluid in warmer weather esp if losing weight
What do you do about alcohol in CHF?
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
What is the role of psychosocial support in heart failure?
LVEF <20% --> depression --> increased mortalityDepression --> 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
What impact does CHF have on pregnancy?
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
Can people with CHF travel?
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
How do youprevent clinical deterioration post-discharge in a CHF visit?
Patient support by a doctor and pre-discharge review and/or home visit by a nurse is recommended to prevent clinical deterioration.
Why shouldn't you initiate beta-blockers in acute decompensated heart failure?
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.
What is the role of nebivolol in heart failure?
More recently, nebivolol (a selective beta-1 receptorantagonist) 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.
In someone with stable heart failure, which should you start first, a beta-blocker or an ACEI?
A randomised study has suggested that major clinicaloutcomes 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.
Why do beta-blockers work in heart failure?
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.
Which three beta blockers have the best evidence fo CHF and why?
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.
Carvedilol or metoprolol in CHF?
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
What effect does aldosterone have on the heart?
Aldosterone receptors within the heart can mediate fibrosis, hypertrophy and arrhythmogenesis.
What is eplenerone indicated for?
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.
What is the role of Digoxin in CHF?
Valuable for therapy of AF in CHF patients
Increased mortality of women even in therapeutic range, survival advantage for men.
What is the role of ARBs in CHF?
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
What is the role of direct sinus node inhibitors in CHF?
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
What is the role of CCBs in heart failure?
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.
Anti-arrhythmics in heart failure?
Avoid unless beta-blockers or amiodarone
Psych drugs in heart failure?
Avoid TCAs and Clozapine
Diabetic drugs in heart failure?
Metformin is safe unless concomitant renal impairment
TNF-abs and steroids in heart failure?
Trastuzumab and heart failure?
Trastuzumab has been associated with the development of reduced LVEF and heart failure.
It is contraindicated in patients with symptomatic heartfailure or reduced LVEF (< 45%). Baseline and periodic evaluation of cardiac status including assessment of LVEF should occur
Moxonidine in heart failure?
Moxonidine has been associated with increased
mortality in patients with heart failure and is
contraindicated in such patients.
When are aldosterone receptor antagonists (spironolactone and eplenerone) indicated in heart failure?
Severely symptomatic despite appropraite doses of ACEI's and diuretics
Indication for Ivrabidine in heart failure?
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.
First line heart failure drugs in order of prescription are...
ACEIsDiureticsBeta-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)
What are the second line agents in CHF?
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
Fish oil - symptomatic despite standard therapy
What is the general mx of asymptomatic LV dysfunction (NYHA class I)?
- Exercise and RF modification- ACEI- B-Blocker- Disease specific rx (i.e. CHD - aspirin, statin etc)
Which class of NYHA heart failure should you give b-blockers
These should be given irrespective of class, just need to not be fluid overloaded.
When would you consider cardiac transplant in heart failure?
<65Class IV heart failure and no major comorbidities, refractory or intolerant to beta-blocker therapy
How do you decide between spironolactone and eplerenone?
Symptomatic on therapy and LVEF >40 = spironolactone
Symptomatic on therapy and LVEF <40 = eplerenone
What are the contraindications to eplerenone?
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.
When is Levosimendan used in CHF?
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
What is the indication for biventricular pacing?
NYHA symptoms Class III/IV despite optimal medical therapy
dilated heart failure with an ejection fraction ≤ 35%
QRS duration ≥ 120 ms
What is the evidence behind biventricular pacing?
Significant mortality reduction
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
What are the indications for ICD?
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%.
What is the evidence behind ICD therapy?
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.
When would you consider ICD plus CRT?
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
What are the definite indicators for cardiac transplant?
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
What drug changes can precipitate decompensated CHF?
- 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
What comorbid conditions can precipitate decompensated heart failure?
Infections (particularly pulmonary) due to haemodynamic changes
Renal failure --> fluid overload
Anaemia or pulm emboli impairing oxygen delivery
What is the role of thiazide diuretics in decompensated CHF?
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.
What is the difference between APO and decompensated CHF?
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
Which drug should you avoid in bilateral renal artery stenosis?
What is the role of nitrates in decompensated CHF?
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.
In a patient with APO, what constitutes cardiogenic shock and what should you do?
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.
What are some causes of systolic, diastolic, and normal LV function CHF?
Systolic LV dysfunction—CHD, dilated cardiomyopathy, mitral regurgitation
Diastolic LV dysfunction—hypertensive heart disease, hypertrophic cardiomyopathy, aortic stenosis
Normal LV function—mitral stenosis
What is the hierarchy of emergency therapy of acute heart failure?
3 points about HFPSF (diastolic heart failure)
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
What is the epidemiology of HFPSF?
- 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
What investigations are done for diastolic heart failure and what are their findings?
Echo - restrictive or pseudonormal mitral inflow filling pattern- LA enlargement- reduced septal annular velocity
Angio- elevated LVEDP- Prolonged Tau
What are the diagnostic criteria for diastolic heart failure (HFPSF?)
- 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
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?
For patients with CHF due to LV systolicdysfunction 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.
In CHF patients, what is the strongest single predictor of suddent cardiac death?
How is the CHF of severe aortic stenosis managed?
Poorly to medical therapyArterial vasodilators including ACEIs are contraindicated due to the risk of coronary hypoperfusionAppropriate medical therapy = digoxin and diuretics
What is the management of angina in CHF?
Avoid nondihydropyridine CCBs in LVEFs <40%
Use betablockers wherever tolerated for angina
Severe angina + systolic heart failure + inoperable disease - consider perhexiline (last line, highly toxic)
How should you treat decubitus angina? (nocturnal angina associated with orthopnoea)
Treat as CHFLoop diuretic in the arvo to minimise filling pressures overnight and prophylactic night tiem nitrates
What is perhexiline?
Nonselective CCBLast line for anginaCYP450 - watch out for liver toxicity
What is the role of ACEIs in protecting against CHF?
- 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
What is the role of spironolactone in CHF and renal failure?
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
What is the link between chemotherapy and CHF?
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
What impact does diabetes have on CHF?
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.
In CHF, when should Metformin be avoided?
Severe of decompensated - risk of lactic acidosis
Glitazones should avoided in patients with Class III or IV sx
Which group of CHF is most at risk of hyperkalemia from dual ACE/ARB therapy?
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.
What is the thromboembolism risk of CHF patients?
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.
How is gout managed in CHF?
Plasma urate goes up in CHF and levels have adverse prognostic significance
Can't have NSAIDs or Cox-2sCan't have steroids
Xanthine oxidase inhibition does not demonstrate benefits on clinical outcomes
In what arrhythmias is EPS not indicated?
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.
What are the diagnostic indications of EPS?
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
Patients with high risk occupations
Sudden cardiac death with no established cause (presumed idiopathic VF)
Wide complex tachyarrythmias of unclear etiology on noninvasive measures
What are the risk stratification indications for EPS?
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
What are the absolute contraindications to EPS?
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
Where is the value of EP studies the greatest?
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.
In Mobitz II block, when is pacing indicated?
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
What is the risk with young people and pre-excitation syndromes?
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
What are the annual risk factors of untreated stroke?
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%
In patients who receive thrombolysis and are later found to have a total occlusion of a vessel on angio - should they get stented?
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
How long after thrombolysis should angio be performed?
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
What is the difference between primary failure of fibrinolysis and threatened reocclusion?
Primary failure - evidence of continuing or worsening myocardial ischemia
Threatened reocclusion - early recurrent ischemia after apparently successful fibrinolysis
In a patient who undergoes fibrinolysis for MI, when would you consider re-thrombolysing?
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
Which group of patients should get a bare metal stent?
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.
How long after PCI should you continue dual antiplatelet therapy for?
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
A patient has a DES and completes 12 months of dual antiplatelet therapy with no complications - how long should you continue it for?
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).
How long should you continue dual antiplatelet for in a high risk patient with a BMS?
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
When should you use clopidogrel over ticagrelor or prasugrel?
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.
When is Prasugrel used?
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.
What are the considerations with Ticagrelor and Prasugrel?
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).
What are the Glycoprotein IIB/IIA inhibitors?
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.
How do GPIIb/IIIa inhibitors work?
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.
What is the most important risk factor for stent thrombosis?
The premature cessation of dual antiplatelet therapy is the most important risk factor for ST.
How does stent restenosis present?
Stable coronary sx as opposed to acute and dynamic
What is the difference between stent thrombosis and stent restenosis?
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.
In what acute MI setting would you use beta-blockers immediately?
Failed thrombolysis with preserved blood pressure and tachycardia - aim is to get HR <70 while maintaining systolic BP >90
Why is amitriptyline so cardiotoxic?
As well as being an SNR it is also a sodium channel blocker and an L-type calcium channel blockerr
What are the clinical features of TCA overdose?
Sedation and comaSeizuresHypotensionTachycardiaBroad complex dysrhythmiasAnticholinergic syndrome
What does this ECG show and what is it consistent with?
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.
What are the important points about acute vs chronic lithium toxicity?
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
What are the features of lithium toxicity (acute or chronic)?
acute ingestion or chronic accumulationCNS: confusion -> coma, cerebella symptoms, seizure, basal ganglia symptoms (choreiform movements, Parkinson-like)GIT: nausea, vomiting, bloatingCVS: syncopeRENAL: polyuria, polydipsia, renal insufficiencyNEUROMUSCULAR: peripheral neuropathy, myopathyENDOCRINE: hypothermia, hyperthermia
What are the normal and toxic lithium levels?
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 outcomeas clinical features determine
What is the acute resuscitation mx of Lithium overdose?
A – impaired LOC -> intubateconsider whole bowel irrigation for massive acute ingestionactivated charchoal does not bindLiberal fluid resuscitation with normal saline
What are the specific interventions for lithium toxicity?
A – impaired LOC -> intubateconsider whole bowel irrigation for massive acute ingestionactivated charchoal does not bindLiberal fluid resuscitation with normal saline
Avoid hyponatraemia as this will decrease lithium clearance
What is the clinical significance of and RV infarct?
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.
Which two ECG changes are most suggestive of an RV infarct?
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.
What does this ECG show?
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.
How can leads V1 and V2 help you in spotting an RV infarct?
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.
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?
Do AEDs work for hospitalised patients with cardiac arrest?
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.
What is Hypoalphalipoproteinemia?
Hypoalphalipoproteinemia is a high-density lipoprotein deficiency, inherited in an autosomal dominant manner.
Three points about LCAT deficiency
LCAT esterifies cholesterol so you get accumulation of unesterified cholesterolRenal failure is the major cause of morbidity and mortalityPatients get very low HDL and very high TGL, as well as corneal opacities with hepatosplenomegaly (fish eye disease)
What is the cardiac index? How is it used?
Output from left ventricle to body surface area - in L/m
Under 1.8 = cardiac shock
Used in ICU
PCWP 25 + v-waves to 40mmHg is...
PCWP of 25 with CI 1.5
RA 20 mmHg PAP 40/20mmHg PCWP 20 mmHg consistent wit...
Saturation of 88% in the pulmonary artery consistent with...
PAP 50/30 PCWP of 4 consistent with...
What is the evidence of the methacholine challenge in the dx of asthma?
Highly specific HOWEVER it's sensitivity is reduced in Caucasians and non-atopic asthmatics when using the test for asthma.
What is the evidence behind methacholine and mannitol testing in the dx of asthma?
Similar sens and spec - around 75% specific, poorly sensitive but increases when two exercise tests are positive
How do you define asthma reversibility?
Reversibility is demonstrated by an increase of 12% and 200 mL after the administration of a short-acting bronchodilator.
What is the most important limitation of PEF?
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.
When is the bronchoconstriction of asthma at it's greatest?
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.
What happens to pa02 and Sp02 in methaemoglobinaemia and CO2 poisoning?
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.
What is methemoglobinemia?
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. 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.
What effect does flying have on PAH?
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