CARDIO: Angina and ACS Flashcards
Presentation of stable angina?
Chest discomfort/ pain provoked by effort, emotion and relieved by rest
How may severe angina present?
Accompanied by autonomic features- fear, sweating and nausea
ddx for chest pain/discomfort
angina, GORD, MSK discomfort, pulmonary disease
RF for angina?
cigarette smoking, hypertension, DM, hypercholesterolaemia, Fhx of premature coronary artery disease presence of other acquired vascular disease
What drugs do you prescribe to someone with angina?
Aspirin 75mg OD
Sublingual GTN
Statin
Beta blocker OR CCB- depending on contraindications, co-morbities and pt preference- first line. If using CCB monotherapy, use rate limiting one- verapamil or diltiazem.
If pt is still symptomatic on CCB or Beta blocker monotherapy, add the other. Ensure CCB is now a is long-acting dihydropyridine one e.g modified release nifedipine.
If patient on monotherapy cannot tolerate addition of a CCB or Beta blocker, consider long-acting nitrate, ivabradine ( when B blocker is not tolerated and not prescribed with verapamil or diltiazem), nicorandil or ranolazine
if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG
Hx for someone presenting with angina?
precipitants of anginal attacks relieving factors stability of symptoms risk factors (smoking history, high BP, lipids, diabetes, prior CV disease) • occupation assessment of the intensity, length and regularity of exercise basic dietary assessment alcohol intake drug history family history
Examination for someone presenting with angina?
- weight and height (to allow calculation of BMI) or waist / hip ratio
- blood pressure
- Cardio exam: look for presence of murmurs, especially that of aortic stenosis
evidence of hyperlipidaemia
evidence of peripheral vascular disease and carotid bruits (especially in diabetes).
Investigations for someone presenting with angina?
FBC and biochem screen incl glucose and HbA1c
Full lipid profile
Resting 12 lead ECG- provides info on rhythm, presence of heart block, previous MI, myocardial hypertrophy and iscahemia
What investigations for Cardiac tamponade?
ECG - low voltage QRS complexes or electrical alternans (alternating QRS amplitude)
Chest x-ray - show a large globular heart
ECHO - fluid around the heart and quantify the level of ventricular compromise.
Pericardiocentesis - sampling of the fluid to find the underlying cause and treat the immediate problem.
What is first line management for cardiac tamponade in a haemodynamically unstable pt?
pericardiocentesis
using a needle and small catheter to drain excess fluid
Causes of non-cardiac chest pain?
Costo-chondritis Gastro-oesophageal PE Pneumonia Pneumothorax Psychogenic/psychosomatic
When do you offer invasive coronary angiography to a pt for angina?
If estimated likelihood of CAD is between 61-90%
When do you offer functional imaging as the first- line diagnostic investigation (stress MRI, echo or myoview) of angina?
If the estimated likelihood of CAD is 30 - 60%
When do you offer CT calcium scoring as the first- line diagnostic investigation in angina?
If the estimated likelihood of CAD is 10 - 29%
How do you interpret CT calcium scoring?
0- minimal likelihood there is significant coronary disease
1-400: Consider CTCA or stress perfusion imaging
Above 400- coronary angiography should be seriously considered
When should you NOT use exercise ECG to diagnose stable angina?
If they do NOT have known CAD
For men older than 70 with atypical or typical symptoms what risk do you assume of having CAD
> 90%
For women older than 70, with typical or atypical symptoms, what risk do you assume of CAD?
61-90%
When do you assume women over 70 has a risk of CAD of >90%?
If she has high risk factors AND typical symptoms
What are the acute coronary syndromes?
STEMI
NSTEM
Unstable angina
What is a STEMI ?
Cardiac sounding chest pain
with: ST segment elevation >1mm in limb >2mm in chest
or
New LBBB on ECG
hs-Tnl (Troponin I ) - >100ng/L
CK usualluy > 400
What is an NSTEMI ?
Cardiac sounding chest pain
with: ST depression, T wave inversion (can be normal)
hs-Tnl (Troponin I ) - >100ng/L
+ previous ECG changes: old MI (pathological Q waves), LV hypertrophy / Afib may be present on ECG
What is unstable angina?
Cardiac sounding chest pain
with ST depression, T wave inversion (can be normal)
hs-Tnl (Troponin I ) - NORMAL RANGE
Apart from Troponin I (Tnl) levels what else should be measured in STEMI pts?
Creatinine Kinase
What levels of Tnl (troponin) in men and women suggest high likelihood of myocardial necrosis?
men: hs-Tnl levels >34 ng/L
women: hs-Tnl levels >16 ng/L
if suspect ACS when should you take a Tnl (troponin)?
1 on admission and then 1 hour later
only 1 needed if onset of symptoms was >3 hours ago
What other conditions can cause a rise in Tnl (Troponin) and therefore give a false positive result when investigating for suspected ACS?
Non cardiac: sepsis Advanced renal failure (rhabdmyolysis - CTF) Large PE Congestive cardiac failure malignancy stroke
Cardiac: Myocarditis - post tacchyarrythmias aortic dissection aortic stenosis hypertrophic cardiomyopathy
What ECG findings do you need for a STEMI diagnosis?
ST elevation on 2 or more leads from the same zones e.g. II, III , AVF (inferior)
or
presence of LBBB
What conditions can mimic STEMI on ECG?
Early repolarisation causes up-sloping ST elevation V1-V2 -Younger athletic / afro Caribbean pts.
Pericarditis - concave ST elevation. Widespread changes
If there are raised troponins, and / or ECG changes such as ST depression, T wave inversion, pathological Q waves) what is diagnosis?
NSTEMI
If troponin is normal and ECG shows no pathological changes, what is diagnosis?
Unstable angina
or
musculoskeletal chest pain
If a pt presents with a STEMI within 12 hours of onset of symptoms what are the two treatment options that are time dependant ?
PCI - Percutaneous coronary intervention w/in 2 hours of presentation
Thrombolysis
- if PCI not available w/in 2 hours
How is PCI for STEMI performed?
catheter is fed through pts femoral / brachial artery up to the coronary arteries.
A dye is injected so that the blockage can be visualised.
Balloons to widen or devices to aspirate and remove the blockage are performed.
Stent is then placed to keep the artery open
What does thrombolysis involve?
Fibrinolytic material is injected to rapidly break down clots
e.g. alteplase
streptokinase
tenectplase
What is the management for an STEMI -? This is workbook one
- IV access
- Pain relief (morphine + antiemetic)
- O2 (ONLY IF hypoxic aim >94%)
- Aspirin (300mg loading dose)
4 a. Prasugrel (Ticagrelor if contra)
4 b. Clopidogrel - PCI
- Biochem - lipid progile, glucose, HbA1c, FBC
- Meds (Bblocker, statin, ACEi)
- Diabetic control
- HTN control
- Smoking cessation
- Triple therapy - AF pts
- complication monitoring - HF diuretics etc.
What is the risk with pts who have AF and then get a STEMI in terms of their drug regimine?
AF taking anticoagulation (not
anti-platelets such as asprin).
They will be on 3 medications - increasing the risk of bleeding.
SO - limit time on all 3 drugs and give a PPI
What is NSTEMI treatment? Dr Tom mnemonic
BATMAN
B – Beta-blockers unless contraindicated
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk)
M – Morphine titrated to control pain
A – Anticoagulant: Fondaparinux (unless high bleeding risk)
N – Nitrates (e.g. GTN) to relieve coronary artery spasm
Give oxygen only if their oxygen saturations are dropping (i.e. <95%).
SANDILANDS PLUS:
repeat ECG
Grace score for elevated troponins
What are some complications of MI?
(Heart Failure DREAD)
D – Death
R – Rupture of the heart septum or papillary muscles
E – “Edema” (Heart Failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome
Secondary Prevention Medical Management for Acute Coronary Syndromes / STEMI DR TOM
Aspirin 75mg once daily
Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
Atorvastatin 80mg once daily
ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily)
Atenolol (or other beta blocker titrated as high as tolerated)
Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)
What is some secondary Prevetion lifestyle advice for ACS (acute coronary syndromes - STEMI/ NSTEM/UA)
Stop smoking
Reduce alcohol consumption
Mediterranean diet
Cardiac rehabilitation (a specific exercise regime for patients post MI)
Optimise treatment of other medical conditions (e.g. diabetes and hypertension)
What is Grace score ? who is used for ?
gives a 6-month risk of death or repeat MI after having an NSTEMI:
<5% Low Risk
5-10% Medium Risk
>10% High Risk
If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.
Coronary arteries anatomy :
The Left Coronary Artery becomes the _____1___and _____2_____
The Left Coronary Artery becomes the ___Circumflex___and __Left anterior descending (LAD)___
What part of the heart does the Right Coronary Artery (RCA) supply?
Curves around the right side and under the heart and supplies the:
Right atrium
Right ventricle
Inferior aspect of left ventricle
Posterior septal area
What part of the heart does the Circumflex Artery supply?
curves around the top, left and back of the heart and supplies the:
Left atrium
Posterior aspect of left ventricle
What part of the heart does the Left Anterior Descending (LAD) supply?
it travels down the middle of the heart and supplies the:
Anterior aspect of left ventricle
Anterior aspect of septum
What ECG leads correspond with Left Coronary Artery?
I, aVL, V3-6
Anterolateral
What ECG leads correspond with LAD Artery?
V1-4
Anterior
What ECG leads correspond with Circumflex Artery?
I, aVL, V5-6
Lateral
What ECG leads correspond with the Right Coronary Artery?
II, III, aVF
Inferior
What is dresslers syndrome?
central, pleuritic chest pain and fever 4 weeks following a myocardial infarction. The ESR is elevated - Dressler’s syndrome
How does GTN spray help alleviate symptoms of angina
CVS revision
1) Nitric oxide causes vascular smooth muscle relaxation. NO activates granulate cyclase which increases cGMP. this lowers intracellular calcium levels so causes relaxation of vascular smooth muscle.
2) It acts primarily on veins - ventilation will lower preload. So the heart will fill less so force of contraction is reduced. This lowers oxygen demand needed.
3) GTN also acts on coronary collateral arteries - so improves oxygen delivery to the ischaemic heart muscle.
Early Complications of MI? < 2 weeks?
- Cardiac Arrest
- Rupture of L ventricular wall
- Arrythmias
- Pericarditis (Dresslers syndrome)
- Heart Block
- Mitral regurg
How does GTN spray help alleviate symptoms of angina
CVS revision
1) Nitric oxide causes vascular smooth muscle relaxation. NO activates granulate cyclase which increases cGMP. this lowers intracellular calcium levels so causes relaxation of vascular smooth muscle.
2) It acts primarily on veins - ventilation will lower preload. So the heart will fill less so force of contraction is reduced. This lowers oxygen demand needed.
3) GTN also acts on coronary collateral arteries - so improves oxygen delivery to the ischaemic heart muscle.