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
Impact of cocaine on heart
Coronary vasospasm (in MI) Accelerates atherosclerotic process
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
After primary PCI
Patient is admitted to CCU for haemodynamic and rhythm monitoring
Reperfusion arrythmias are common, e.g. frequent premature ventricular complexes
Initiation of secondary prevention medications
Departmental TTE for assessment of LV function
Secondary prevention aims and lifestyle changes
Secondary prevention aims to prevent complications or reduce impact, and to prevent further cardiovascular events
Secondary prevention include cardiac rehabilitation, addressing relevant lifestyle risk-factors, and drug treatment
Lifestyle changes that can reduce the risk of having further MI or other cardiovascular events following an MI include:
Smoking cessation.
A healthy diet.
Aiming to be moderately physically active for at least 150 minutes per week.
Losing weight if overweight or obese.
Keeping alcohol consumption within recommended limits.
All patients w MI should be offered cardiac rehab w exercise
Secondary prevention medications
- Dual antiplatelet therapy (ASA 75 mg OD lifelong + ticagrelor 90 mg BD for 12 months)
- Statin (atorvastatin 80 mg nocte) stabilises plaque
- Beta blocker (bisoprolol 2.5 mg OD)
- ACE inhibitor (ramipril 2.5 mg OD)
- Mineralocorticoid antagonist (eplerenone 12.5 mg OD)
Secondary prevention: Control risk factors
Lipids check- cholesterol below 5
Check HbA1c (long term measure of blood sugar control, 48mm or above = diabetes)
What is the process of cardiac myocyte contraction?
- Automaticity- An Action Potential (AP) is generated by nodal tissue with the ability of automaticity
- This electrical current travels through myocytes via gap junctions
- To sarcomeres activating L Type calcium channels in T Tubules -> Ca2+ influx into cell cytoplasm
- Calcium binds to ryanodine receptors on the SR, causing more calcium to enter cytoplasm.
- Calcium binds to troponin C -> conformational change in troponin -> binding of troponin and exposure of ATP binding sites
- Actin and Myosin bind together
- The myosin head binds to ATP -> shortening of myosin, pulling actin filaments towards the centre
- Calcium is pumped back into SR and the extra-cellular space, and once low enough, it dissociates from Troponin C, resulting in the end of the contraction cycle.
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
How are T tubules clinically relevant to heart failure?
T tubules allow the line up of calcium and ryanodine receptors clusters and sodium channels, making heart contraction more efficient.
In heart failure this line up is more obtuse angle than direct so less efficient capture of calcium so contractility is less rapid.
What are the thin and thick filaments in a sarcomere?
Thin- actin
Thick- myosin (has little heads on it that bind to actin)
Starling’s law of the heart
The greater the heart muscle is stretched,
greater is the force generated and the
output from the ventricle.
In practice, within some limits the heart
needs to pump all the venous return.
(as heart is distended, recruits more cross bridges, more myosin heads -> more efficient contraction)
more filling = more stretch = more bonds between actin and myosin = more force of contraction (independent from external influences)
What is preload?
Preload- amount of fluid in circulating system (filling pressure) keeps stretch of heart muscle
Filling is the most important determinant of
cardiac output in a healthy heart
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
No preload reserve
Leads to heart failure, heart overstretched and cant form actin-myosin bonds to contract
Stroke volume is dependant on…
Preload- need filling to eject
Contractility- efficiency
Afterload- pressure heart has to work against to force ejection
Cardiac output depends on…
Pressure difference between arterial system
and venous system (or MAP/Pms and RAP)
SV X HR = CO
Venous return = Cardiac output
Venous return is dependant on…
Pms (mean systemic pressure)
RAP (right atrial pressure)
Resistance (to flow)
Unstressed volume- what is it and how do we make it stressed volume?
Unstressed volume: No pressure generated
No additional stretch on vessel walls and no pressure generated (need degree of stress to create pressure)
Do this via mean systemic pressure (Pms) = Stressed volume, has pressure generated
What lowers stressed volume in preload?
Sepsis
Decreased venous resistance
(give patient fluid to improve this)
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.
Clinical signs of failing heart
Decreased exercise tolerance (breathlessness)
or a loss of redundancy (cannot increase C.O
during exertion)
Chronic deterioration
– SOB (shortness of breath)
– Fluid retention and oedema
Acute deterioration
– Paroxysmal nocturnal dyspnoea (SOB at night)
– Orthopnea (SOB lying down)
Why do humans suck at coping with heart failure?
We evolved to deal with hypovolaemia…
Any drop in cardiac output is considered hypovolaemia
so
– Sympathetic system increases venous tone, heart rate and
contractility (increasing afterload as well)
– Fluid recruited from interstitial space and intracellular
spaces into vascular space
– Renin-angiotensin-aldosterone system activated due to
renal hypo-perfusion, resulting in water and salt retention
These result in fluid retention and increased resting
symapthetic tone
Compensatory mechanisms of the heart: normal vs failing
Normal heart – contracts well (EF 60%) and is compliant, so filling pressures are low and cavity is small (energy efficient)
Failing heart – contracts less well (EF 40%) and is stiff, so filling pressures are high and cavity DILATES to maintain stroke volume
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?
Atherosclerosis
Atherosclerosis may effect all arteries but most commonly is seen in the aorta, coronary, ilio-femoral, carotid and cerebral arteries.
Atherosclerosis can result in a number of pathological sequelae:
- Occlusion, resulting in ischaemia of the tissue supplied by the artery
- Thrombosis, may occlude the artery or break of to form emboli and possible occlude a distant vessel
- Aneurysm, damage to the wall weakens its elastic/muscular properties allowing localized area of dilation which may rupture.
Thrombus
Thrombus formation can result from three major factors, which act singularly or in combination:
- Damage to the vessel wall
- Disordered blood flow
- Abnormal properties of blood, such as increased platelet concentration.
Thrombus formation in the veins can result in vessel occlusion and embolisation
Anterior surface of heart comprises of..
Right ventricle
Where do atria sit in anatomical position?
Behind ventricles
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
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
