Coronary artery disease and Hypertension Flashcards
Discuss differences between indications for beta-blockers in the surgical vs non surgical setting
indications for beta-blockers in non surg setting:
- hypertension
- svt
- vt
- angina
- ami
surgical indication
- conflicting evidence (small trials with differing methodology)
- POISE trial - large trial looking into topic (>45 undergoing noncardiac surg with CAD, PVD, stroke, prior CCF admission)
- Theory: stress response increase catecholamines lead to increase HR/BP/fatty acids - betablockers can attenuate this
- outcome from trial, treatment group had less non fatal MI and primary outcome of (CV death) but metoprolol had higher mortality and increased stroke and more hypotension/bradycardia
- downgraded periop betablockers post poise AHA
- all decreased non fatal MI in followup and increased stroke/hypo/brady
class 1 indication - continue in those who have been on them chronically - if recognised preop don't start or should start well before e.g. delay surgery.
What are some of the effects of beta blockers?
- b1 selective and nonselective
(atenolol, metoprolol, bisoprolol are all beta 1 selective)
Classic effects
- reduce myocardial O2 suppler/demand mismatch
- rapid onset
Non Classic effects
- complex interaction between heart, sympathetic nervous system and inflammatory system ?plaque stabilisation (specifically bisoprolol)
- slower onset
What is the outcomes of studies looking at perioperative outcomes of clonidine and aspirin?
Clonidine
- theory: decreased noradrenergic CNS transmission (anxiolysis, analgesia) suppress normal post op increase in fibrinogen and antagonise adrenaline induced platelet aggregation. May reduce stress response
- did not reduce atherosclerotic disease but did cause hypotension and increase in nonfatal cardiac arrest
Aspirin
- POISE 2 stratified based on continuation or initiation
- aspirin did not reduce nonfatal MI but did increase major bleeding
- result confounded by other forms of anticoagulation
What are the two types of stents? What are some considerations for each?
Bare metal stent
- cobalt and chrome or platinum chrome (thinner struts)
- restenosis due to smooth muscle cell proliferation and neointimal hyperplasia
- peaks between 3-6mths
- required repeat PCI in 12-20% (balloon angioplasty, re-stent, brachytherapy)
Drug eluting stent
- stent coated with thin polymer (drug carrier) with antiproliferative agent
- now 80% are DES now (>60% off label)
- lipo-philic molecule that are distributed into arterial wall
- reduce need for PCI from 20 to 5%
- stent remains uncovered therefore late thrombosis and need DAPT - length increases over years
- changing landscape 1st gen (sirolimus/paclitaxel) whereas new use everolimus and cobalt.
What are some complications from stenting?
bare metal stent thrombosis
- 2 weeks after stenting
- risk diminishes after endothelialization (4-6weeks)
bare metal stent restenosis
- peaks at 3-6mths
5-7 days clopidogrel post
6-12weeks post BMS can wait for surgery
What are some guidelines for surgery post PCI?
DES - delay for 1 year (clopidogrel therapy)
BMS - delay for 3-45days (6weeks)
Balloon angioplasty <14 days
wait for completion of clopidogrel therapy in elective
if semi-urgent take case by case basis
- risk of thrombosis and low risk bleeding intraop continue aspirin and clopidogrel and vice versa (e.g. intracranial surg/TURP stop aspirin)
if grey zone stop clopidogrel and continue aspirin
restart clopidogrel asap post surgery with loading dose if possible (>300mg 6hrs, >600mg 2hrs)
no evidence for bridging techniques currently but many case reports.
- monitor until anti-platelets re-established
- should be performed in centre with urgent PCI facilities
How do you determine risk of bleeding vs thrombosis?
- consider myocardium at risk (Left main, proximal LAD stent?)
- ?previous stent thrombosis
- ?multi-vessel or long/overlapping stents
Associated risk factors
- DM, CKD, low ejection fraction, advanced age
discussion with surgeon/cardio/home team
What is the common mechanism of myocardial injury perioperatively? What is the outcomes in these people?
- majority are ST depression in 24-48hrs (NSTEMI) post surgery (rare within a procedure)
- implies myocardial o2 supply/demand mismatch
- often silent (pain distractors, analgesia, nausea, baseline ECG changes (LBBB, paced), missed without trop level
Outcomes
- 10-15% mortality from cardiac complications, >50% are due to STEMI
- plaque fissure/rupture and thrombus
- Non cardiac surgery troponin rise predict prognosis for long term morbidity/mortality
What is the definition of an AMI? Prior MI?
- detection of a rise/fall of cardiac biomarkers (troponin) gold standard
- evidence of myocardial ischaemia (ECG changes, sxs, imaging evidence of loss of viable myocardium/regional wall abnormality)
- exclude alternative for trop increase
Prior MI:
- new pathological Q waves with or without prior symptoms
- imaging evidence of region of loss of viable myocardium
What are some downfalls of raised cardiac troponin?
- all patients with AMI is not the same
categorise associated prognostic factors/other causes:
- ablation, pacing, DCR, biopsy
- CCF (acute/chronic)
- aortic dissection
- tachy/bradyarrhythmias
- PE
- severe pul HTN
- Renal failure
- infiltrative disease (amyloid, sarcoid, scleroderma)
- inflammatory conditions (myocarditis)
- drug toxicity (snake, chemo)
- critically ill patients
- burns
What is the difficulty of measuring troponin in renal failure?
normally both trop T and I comparable for diagnostic accuracy
- in renal failure higher troponin T compared to troponin I
- chronic elevation secondary to presumed myocardial injury resulting from some aspect of renal failure
- troponin T carries prognostic significance
- an increase from baseline distinguishes acute IHD
What is highly sensitive troponin? What are some difficulties with its interpretation?
- 5th gen, in theory should have higher diagnostic rates and a higher negative predictive value
- in practice have lower specificity and lower positive predictive value
Guidelines for interpreting (MJA 2012)
- needs to be a dynamic change
- report conditions e.g. haemolysed sample/circulating antibodies
- should have pre-test probability (rule out rather than rule in AMI) - not elevated in 6hrs of symptom onset very low likelihood.
What is the management of MI? Can you stratify this management?
NSTEMI
- medical stabilisation/risk stratification
- O2,morph, GTN
- antiplatelet therapy (aspirin) ideally clopidogrel (CURE trial 20% reduction in death)
- anticoagulation (heparin/clexane)
- beta-blockade (if HR >50, nil CCF decompensation, no severe COPD and no major CI with improved mortality/cardiac arrest/re-infarction)
- ace-inhibitors - continue in long term with low EF, significant MR
- statin
STEMI
- acute re-perfusion (fibrinolytics/PCI)
- peri-operatively PCI recommended due to reduced bleeding risk (still require anticoag tirofiban and DAPT)
- consider risks and benefits in each patient.
What is a hypertensive crisis/emergency? What do you do in this sceanario?
SBP >180 or DBP >110
HTN emergency
- progressive organ dysfunction (encephalopathy, ICH, stroke, acute renal failure, infarct, dissection)
- reduce BP quickly to prevent end organ damage (10-15% over first hour and aim towards 160/1000 over next 2-4hrs)
HTN urgencies
- no end organ dysfunction
- control over days-weeks
What is the SBP targets for patients?
Based on 2014 JNC-8 guidelines
- CKD/DM aim <130/80 increased to <140/90
- contradict other guidelines
relaxed goals - producing a minority report
impact of change is large
- 8.5% increase in MI over 10 years
Currently following JNC 7 guideline
