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.