Cardiac Contraction, Starling's Law and MI Management Flashcards
Where does the left anterior descending artery extend and what does it supply?
Ventricular groove
Supplying anterolateral wall, apex and anterior 2/3 of ventricular septum
What does the left circumflex artery supply?
Wraps around back of heart and supplies lateral + posterolateral walls of left ventricle
What are the branches of the right coronary artery?
Right ventricular branch (Supplies RV free wall)
Sino atrial nodal artery (supplies SA node so with large inferior STEMI can cause complete heart block)
Posterior descending artery (terminal end branch of right coronary artery) supplies inferior wall of RV
Coronary territories
The LAD supplies the anterior wall of the LV
It gives off branches (septals and diagonals) which supply the anterior 2/3 of the interventricular septum, and the lateral wall of the LV respectively
The LCx supplies the posterolateral wall of the LV
The RCA supplies the RV, the posterior third of the interventricular septum and the sino-atrial nodal artery (supplies the SA node)
ECG shows inferior posterior STEMI (ST elevation in inferior leads 3, 2 and AVF, supplied by RCA or LCx)
What chest leads correspond to each artery?
RCA = 2, 3, AVF- inferior leads
LCx = 1, AVL, V5 and V6- lateral leads
LAD = V1 and V2 (septal leads) V3 and V4 (anterior leads)
Branch of LAD = AVL, lateral chest
Stable vs unstable plaques
Stable: thicker fibrin cap and smaller lipid core
Unstable: thinner fibrin cap and lipid rich core thicker, eccentric so subject to haemodynamic turbulence and shear stress
What are fatty streaks?
Collection of lipid laden foam cells residing beneath endothelial layer, may evolve into atherosclerotic plaque or remain stable.
When the endothelium gets injured how does this lead to fatty streaks?
Triggers myocytes sticking to endothelial layer causing loosening of cell junctions between them and monocytes migrate beneath endothelium becoming macrophages.
Permeable areas of endothelium allow in LDL to intima where macrophages eat it up and become lipid laden = foam cells seen in fatty streaks
What kind of plaque is more likely to cause acute coronary syndrome (ACS)?
Unstable plaques (vulnerable)
Thin cap fibroatheroma (TCFA)
Criteria for type 1 MI (ruptured plaque)
Rise/fall of troponin values with at least one value above the 99th percentile URL and with at least one of the following:
Symptoms of acute myocardial ischaemia;
New ischaemic ECG changes;
Development of pathological Q waves;
Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischaemic aetiology; (echo)
Identification of a coronary thrombus by angiography including intracoronary imaging or by post- mortem.
Criteria for type 2 MI (imbalance between myocardial oxygen supply and demand)
Rise and/or fall of cTn values with at least one value above the 99th percentile URL, and evidence of an imbalance between myocardial oxygen supply and demand unrelated to acute coronary thrombosis, requiring at least one of the following:
Symptoms of acute myocardial ischaemia;
New ischaemic ECG changes;
Development of pathological Q waves;
Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischaemic aetiology.
What are the different types of acute coronary syndrome?
Stable angina
Unstable angina
NSTEMI
STEMI
Common causes of type 2 MI
anaemia, rapid tachyarrythmias, sepsis or hypoxia
Assessing a patient with STEMI (via PPCI pathway)
Get handover from the paramedic crew
Interpret ECG – confirm STEMI diagnosis
Perform a clinical assessment of the patient:
Take the history and examine at the same time – is the patient in cardiogenic shock? What is the access route for PPCI?
Gain IV access if not already done by paramedics
Correct any haemodynamic instability (e.g. atropine if in complete heart block)
Give analgesia (IV morphine plus anti-emetic)
Perform a bedside echocardiogram (LV function/valves/Aortic dissection/pericardial effusion/mechanical complications (VSD/papillary muscle rupture))
Load with second antiplatelet (ASA usually given by crew)
Explain coronary angiogram and PCI and gain consent
Define STEMI
ST-Elevation Myocardial Infarction (STEMI) is a very serious type of heart attack during which one of the heart’s major arteries (one of the arteries that supplies oxygen and nutrient-rich blood to the heart muscle) is blocked. ST-segment elevation is an abnormality detected on the 12-lead ECG.
Define NSTEMI
Non-ST-elevation myocardial infarction (NSTEMI) is an acute ischaemic event causing myocyte necrosis. The initial ECG may show ischaemic changes such as ST depression, T-wave changes, or transient ST elevation; however, it may also be normal or show non-specific changes
What is PPCI and why do we use it?
Primary percutaneous coronary intervention (PCI)
Primary PCI is a form of reperfusion therapy which should be done as soon as possible. This is because heart muscle starts to be lost once a coronary artery is blocked and the sooner reperfusion therapy is delivered the better the outcome for the patient. If too much time elapses the benefits of primary PCI may be lost. Because of the difficulty in timely delivery, in some areas primary PCI is no longer the preferred coronary reperfusion strategy over fibrinolysis. However, when performed early, primary PCI is more effective.
STEMI with cardiogenic shock
Usually results following large anterior infarct
Patient will be sick: hypotensive, cool, clammy and in pulmonary oedema
Bleep anaesthetic SpR to intubate the patient for the procedure
May have to use the femoral route if shut down radials
Will require haemodynamic support with vasopressors (metaraminol boluses +/- infusion)
May require intra-aortic balloon pump (IABP)
STEMI with cardiogenic shock
Usually results following large anterior infarct
Patient will be sick: hypotensive, cool, clammy and in pulmonary oedema
Bleep anaesthetic SpR to intubate the patient for the procedure
May have to use the femoral route if shut down radials
Will require haemodynamic support with vasopressors (metaraminol boluses +/- infusion)
May require intra-aortic balloon pump (IABP)
IABP
Large balloon catheter inserted via the femoral artery and balloon placed in the proximal descending aorta
Goal is to increase aortic diastolic pressure which may increase coronary artery perfusion (bc perfusion here occurs during diastole)
Inflates immediately after Ao valve closure and deflates just before Ao valve opens
Initial management of NSTEMI
These patients are often pain-free when you see them
BUT – if ongoing pain, and ischaemic ECG, this is a ”High Risk ACS” and may be treated in a similar manner to STEMI, i.e. with immediate PCI.
Generally these patients are treated with an “ACS protocol” of medications (ASA aka aspirin, ticagrelor, fondaparinux, high dose statin)
They are admitted to a cardiology or medical bed and listed for an angiogram ?proceed.
Different types of chest pain:
a) Typical angina
b) Atypical angina
c) Non-specific chest pain
a) Typical (classic) angina chest pain consists of
(1) Substernal chest pain or discomfort that is
(2) Provoked by exertion or emotional stress and
(3) relieved by rest or nitroglycerine GTN (or both).
b) Atypical (probable) angina chest pain applies when 2 out of 3 criteria of classic angina are present.
c) Non-specific chest pain: If ≤ 1 of the criteria of classic angina is present, symptoms are classified as non-specific.
Early invasive strategy with 24 hours is recommended in patients with any of the following high risk criteria:
Diagnosis of NSTEMI
Dynamic/new contiguous ST/T-segment changes suggesting ongoing ischaemia
Transient ST segment elevation
GRACE risk score >140
GRACE risk score
Determines mortality risk from myocardial infarction within 6 months to 3 years, for patients with acute coronary syndrome
- patient age
- HR
- systolic BP
- creatinine
- Killip class
- cardiac arrest at admission
- ST segment deviation
- abnormal cardiac enzymes
Read the ECG
Anterolateral ST elevation
Read the ECG
ST elevation in inferior leads 2, 3 and AVF
Read the ECG
Patient with evolving inferior STEMI
Evolving ST elevation V1 to V4 and V5
Also ST elevation in lead 1 and AVL
Large anterolateral STEMI
Access routes for coronary angiography
Right radial or right femoral artery
How is a stent put in an artery?
Primary PCI
Primary angioplasty
- > catheter inserted with stent crimped around stent balloon
- > balloon inflated and stent deployed, compressing plaque against artery wall
Nodal action potential
SA node:
resting membrane potential -60mV slow influx of Na funny current channel -> rapid influx of calcium once membrane potential is -40mV (threshold) depolarisation occurs then outflux of K+ repolarises cell
Myocyte action potential
membrane potential -96mV, more negative than nodal AP
maintained by K+ channels
Na influx depolarisation
K+ efflux
Cl- influx (L type calcium channel maintains contractility phase)
AP gets negative again due to continued K+ efflux
What is the functional unit of the muscle cell?
Sarcomere
What is the critical delivery mechanism through which calcium and sodium rapidly move in and out myofibrils?
T tubules
Heart with preload reserve
Leads to small increase in preload but larger increase in stroke volume
ideal area to be in
Heart with maximum filling and optimal sarcomere length
See no increase in stroke volume, so giving fluid is not going to help
Higher right atrial pressure (RAP) the same as Pms means…
…lose venous return, so very low cardiac output
So you want a patient to have a lower RAP to assist venous return and enhance cardiac output.
Add starlings curve.
I want to increase Pms by adding fluids and increase my venous return curve.
By increasing my venous return curve I have increases my cardiac output to match.
If I was measuring CVP at the same time this would result in a very small increase in RAP and therefore the extra venous return is being coped with by the heart.
If however the heart was not functioning well or close to the plateau. By increasing the Pms , going up on the venous return will not increase CO and the CVP shoot up and therefore there is no benefit and possible harm with the pressure gradient driving flow decaresing.
Healthy heart vs failing heart muscle
Healthy: easily increase CO by increasing VR- bc more sympathetic tone with SMALL increase in RAP
Failing: as Pms increases, lots more filling and pressure but very little improvement in CO, heart unable to increase CO beyond this level
Starling’s curve:
1. Want to increase Pms by adding fluids and increase my venous return curve.
- By increasing my venous return curve I have increases my cardiac output to match.
- If however the heart was not functioning well or close to the plateau. By increasing the Pms , going up on the venous return will not increase CO and the CVP shoot up and therefore there is no benefit and possible harm with the pressure gradient driving flow decreasing.
What is their cardiac output? (high, low, normal, can’t say…)
How to improve cardiac output?
Low- due to low BP, cold peripheries (blood diverted to brain, kidneys, liver so less blood to peripheries) high HR so compensating and failing
Improve- give O2 because hypoxic (88 sats) and high RR, give fluid because hypovolaemic, give inotropes like NA, dopamine, butadiene, NORAD due to poor vascular tone (borderline hypotensive)
What is her cardiac output?
What interventions are needed to help her?
Anterior surface of heart comprises of..
Right ventricle
What are sulci?
External grooves created by internal divisions of heart
CORONARY SULCUS- separates atria and ventricles
ANTERIOR/POSTERIOR INTERVENTRICULAR SULCI- separate ventricles and are continuous inferiorly
