Radiating Chest Pain And Dyspnea, Ischemic Heart Disease And ACS (Quiz 2) Flashcards
Myocardial oxygen supply
What are the 2 factors that affect coronary blood flow?
Perfusion pressure
—occurs during diastole
— = aortic diastolic pressure ➡️ LVEDP
Coronary vascular resistance
—modulated by:
—forces that compress the coronaries, such as contracting myocardium
—forces that alter intrinsic tone, i.e vasodilators to meet O2 demands by metabolic, endothelial and neural auto reg.
What are the 3 factors that affect auto regulation of coronary vascular resistance? (Metabolic, endothelial, neural)
How do these affect vasodilation/constriction?
-
Metabolic
—during hypoxia:
—aerobic metabolism is impaired
➡️ can’t produce ATP,
∴ more ADP/AMP
➡️ degraded to adenosine
= vasodilator -
Endothelial
—regulated by NO & prostacyclin which are vasodilators
—DM, tobacco and HTN cause endothelial dysfunction
∴ less NO and prostacyclin -
Neural
—alpha adrenergic ➡️ vasoconstriction (bind to α-receptors on vascular smooth muscle and induce smooth contraction and vasoconstriction)
—beta 2 receptors ➡️ vasodilation
What are the three sources of myocardial oxygen demand from the heart?
- Stress
- Heart rate
- Contractility
Myocardial O2 demand:
What are the three major determinants?
What is the Layplace law?
- Ventricular wall stress
- Heart rate
- Contractility
Ventricular wall stress:
=forces acting on myocardial fibres trying to pull them apart
Layplace Law
Directly proportional to:
1. Diameter of ventricle
2. Ventricular pressure
bigger diameter or greater ventricular pressure = more wall stress
Inversely proportional to:
1. Thickness of ventricle
thicker ventricle = less wall stress (stronger muscle
man on tightrope between two buidlings
—aortic stenosis, HTN cause ⬆️ wall stress & O2 consumption
—anti HTN meds ⬇️ ventricular pressure ∴ O2 consumption decreases
—MR and AR increase LV filling and thus wall stress and consumption
—diuretics & nitrates decrease LV size and filling thus decreasing wall stress & O2 consumption
—thick ventricular wall spreads stress over greater mass
— ∴ hypertrophied heart as less stress and O2 consumption per gram of tissue than a thin walled heart (this logic doesn’t make sense to me! Doesn’t a thick walled heart have higher O2 demand?)
Heart rate
—ATP consumed increases w/ higher rates
Contractility
—force of contraction
—more forceful = more O2 consumption
Ischemia — Pathophysiology
What is it?
Which two processes could cause ischemia?
What is coronary reserve?
What is the difference between 70% and 90% stenosis?
Ichemia from a reduction of blood depends on
-
Atherosclerosis
—in proximal coronary arteries ➡️ stenotic plaque ➡️ limited flow -
Endothelial Dysfunction (Vasomotor tone)
—distal coronaries don’t have stenotic plaque but have abnormal vasomotor tone such as endothelial dysfunction and don’t dilate like they should
Coronary reserve
= small vessels act as reserve if plaque stenosis is present. They will dilate when O2 demand goes up
70% stenosis
—at this point, vasomotor dilation can’t maximise blood flow with exertion ∴ O2 demand mismatch ∴ ➡️ ischemia
90% stenosis
—ischemia occurs at rest
4 consequences of ischemia
- Conversion from aerobic to anaerobic metabolism ➡️ lack of ATP = decrease contractile proteins ➡️ BOTH systolic and diastolic dysfunction (SOB)
- increase of LV diastolic pressure (SOB)
- Transmits to LA and pulmonary circulation ➡️ congestion (SOB)
- Lactate accumulates ➡️ activating pain receptors (chest pain) and ➡️ arrhythmias
What are the four Ischemic syndromes? (that involve obstructed coronary arteries)
3 are ACS, 1 is not
Describe the patho for each
- STABLE ANGINA
—chest pain with exertion
—fixed plaque obstruction in one or more coronary arteries
—small component of endothelial dysfunction (inability to vasodilate and increase coronary reserve)
Acute Coronary Syndrome:
2. UNSTABLE ANGINA
—stable angina with INCREASED frequency, intensity, or duration of chest pain during same activity as well as longer recovery time with rest.
- NSTEMI
—Type I MI: incomplete occlusion of the artery from plaque rupture and thrombus formation
—Type II MI: supply-demand mismatch (vasospasm/endothelial dysfunction): NO plaque rupture. GI bleed/cocaine use leads to increase demand > heart works harder and doesn’t get as much perfusion. Type II does not involve the coronaries
—only difference between NSTEMI and unstable angina is release of cardiac markers d/t myocyte damage.
—must go to cath lab - STEMI
—Type I MI: complete occlusion of the artery from plaque rupture and thrombus formation
—no distal perfusion. 100% blockage. Need to get to cath lab ASAP.
Ischemic syndrome: MINOCA
Myocardial infarction with non-obstructive coronary arteries
What are the two types?
Myocardial Infarction With Nonobstructive Coronary Arteries (MINOCA):
VARIANT (Prinzmetal’s Angina)
—coronary artery vasospasm w/o atherosclerotic disease
—reduces oxygen supply related to increased sympathetic activity (recreational stimulant use) or endothelial dysfunction
—can occur at rest
MICROVASCULAR ANGINA
—angina w/o atherosclerotic coronary stenosis
—inadequate vasodilatory reserve during periods of increased myocardial oxygen demand
Chest pain
What is the pain like?
Where?
What makes it worse/better?
How long does it last?
Radiation?
A/w ?
What is the pain NOT?
Pain is:
—pressure-like or burning or heaviness
—feeling of “impending doom”
—diffuse across the precordium
—exertional (more concerning if occurs at rest)
—relieved with rest or nitroglycerin
—lasts 5-15 minutes
—radiates to neck or down left arm
—a/w nausea/emesis, diaphoresis (cool/clammy), shortness of breath, palpitations (if arrhythmias), and fatigue
—women > GI symptoms
—elderly > can just be fatigue
STEMI/NSTEMI
—might not relieve with rest or NTG
Pain is NOT
—stabbing
—increased with inspiration or palpation
—a few seconds / several continuous hours/days, to a pinpoint location, or relieved with exertion
What is the universal sign for distress in angina pectoris (chest pain) & MI
Levine’s sign
—chest/hand clutching
—lasts for >20 mins
Chest pain — what might you find on exam?
What are 3 atypical symptoms, who are they associated with?
—risk factors
—HTN and tachycardia from increased sympathetic activity
—S4 (gallop) from from a MI causing a stiff LV
—S3 (gallop), crackles, elevated JVD, edema
—MR murmur from papillary muscle dysfunction (supplied by LAD)
—+/- carotid bruit = atherosclerosis elsewhere
atypical symptoms
—25% of patients > silent ischemia; diabetics
—elderly may present with fatigue or weakness
—women may have more GI symptoms
How do you diagnose ischemia? 6
—cardiac markers (serial labs to see elevation in troponin)
—EKG
—echo: structural heart disease (specifically regional wall motion abnormality, valves, and LV function)
—stress imaging: determine exercise preferred over chemical. Determine exercise capacity and potentially reproduce angina. Use nuclear (SPECT MIBI). we don’t stress test pts w/ active ACS
—CTA coronary scan (noninvasive image of coronaries)
—coronary angiography (gold standard) (invasive)
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What are the 4 stages on EKG that determine ischemia?
- Injury: ST elevation
- Ischemia: fully inverted T waves in 24h
- Acute infarction: pathologic Q waves
- Old infarction: ST segment normal. Perm Q waves
With ST depression: concerned about how “deep” the depression is
T wave inversion: not v. Helpful unless the pt has symptoms and cardiac markers OR if the T wave suddenly inverts between EKGs
What are the 3 cardiac markers?
Troponin I — 100% sensitive
CK-MB — 88.2% sensitive
Total CK — 73.5% sensitive
Troponin
—concerned about the patten, rise and fall
—always need serial values
—b/c there are other reasons for slightly elevated troponin levels: athletes, impaired renal clearance, inflammation
Acute stable angina — what is the medical management?
rest
nitro
relieves ischemia by venodilation to reduce preload, wall stress, and myocardial oxygen consumption as well as dilate the coronaries to increase flow
—limitation is tolerance but can be overcome w/ nitrate free periods daily
—this is only for symptom relief
Ischemia — stable angina
How do BBs, CCBs and Ranolazine help?
beta blockers
—suppress angina by reducing myocardial O2 demand
—decreasing HR and contractility
—FIRST LINE for CAD b/c reduce recurrent rates of infarction —DECREASE MORTALITY after an acute MI
non-DHP CCB
—decrease myocardial O2 demand by decreasing HR and contractility
DHP CCB
—decrease O2 demand via decreasing preload/wall stress and increase oxygen supply by increasing coronary perfusion
CCBs 3rd line, but all CCBs decrease occurrence of vasospasm (1st line for these pts). No proven survival benefit in chronic/stable angina or to slow/reverse atherosclerotic process
ranolazine — last line
—inhibits late phase AP inward Na+ current in ventricular myocytes thereby reducing intracellular calcium to restore contractility and diastolic function
—like CCBs, no proven survival benefit in chronic stable angina or to slow/reverse atherosclerotic process
Ischemia, medical management to PREVENT ACS?
4 drug categories
ANTIPLATELETS
—prevent platelet aggregation and thrombosis
—aspirin (81 mg daily)
—P2Y12 antagonists if ASA allergy (clopidogrel/Plavix)
—combination of ASA + P2Y12 inhibitors is superior to ASA monotherapy
LIPID LOWERING THERAPY
—statins lower MI and death rates in CAD patients
—high intensity (>50%) is superior
—ezetimibe and PCSK9 inhibitors added to statin therapy
—icosapent Ethyl reduces resistant triglyceride levels and reduces CAD events when added to a statin
GLUCOSE LOWERING THERAPY
—SGLT2 inhibitors and GLP-1 receptor agonists
ACE INHIBITORS
—some studies have shown reduced rates of death, MI and CVA in pts w/ stable CAD
Ischemia —non pharm management
What are the two procedures?
When are they used?
Coronary Revascularization used when:
—non responsive to meds / persistent pain / side effects / high risk CAD (> 50% or significant three vessel disease)
Percutaneous Coronary Intervention (PCI)
—balloon angioplasty (recurrent symptoms within 6 months)
—coronary stents: reduce rate of restenosis
Coronary Artery Bypass Grafting (CABG)
—bypass obstructions
—venous grafts > SVG (vulnerable to atherosclerosis and decline in patency 10% per year)
—arterial grafts > LIMA (patency rate of 90% at 10 years)
—CABG has improved survival over PCI in patients with significant LM disease, three vessel disease w/ reduced EF and diabetics w/ multi vessel disease «_space;only these three patient types !
ACS — Pathophysiology
What is it related to?
What are the 4 steps?
—related to PLAQUE RUPTURE (chemical factors that destabilize it or physical stressors)
- Fibrous cap rupture exposes plaque to circulating blood and platelets
- Platelets activate and aggregate
- Tissue factor is released ➡️ the coagulation cascade ➡️ formation of thrombus
-
Vasoconstriction
—thrombus can completely occlude the artery (STEMI)
—or partially occlude (UA/NSTEMI).
—A MI results from eventual myocyte necrosis
UA (unstable angina) does not result in necrosis; NSTEMI and STEMI do
ACS — what are the non-atherosclerotic causes ?5
- Coronary embolism (emboli from mechanical or infected valves)
- Coronary trauma
- Coronary dissection
- Coronary spasm (cocaine)
- Vasculitic syndromes causing coronary occlusion from inflammation
What is unstable angina
What can it progress to?
—increase in frequency, duration, and intensity of symptoms
—occurs at rest; without provocation
—new chest pain in a pt w/o previous symptoms
—can progress & develop evidence of necrosis (NSTEMI or STEMI) unless recognised & treated
ACS — which risk score can you use?
—GRACE or TIMI to predict probability of an adverse cardiac event in pts w/ chest pain
Thrombolysis in Myocardial Infarction (TIMI)
—7 factors:
—age > 65
—three or more risk factors for CAD
—prior catheterization demonstrating CAD
—ST segment deviation
—2 or more anginal events over 24 hours
—ASA use within 7 days
—elevated cardiac markers to predict an adverse cardiac outcome
Global Registry of Acute Coronary Events (GRACE)
—evaluates age, HR, SBP, creatinine, CHF class, cardiac arrest on admission, ST segment deviation, and elevated markers to predict in hospital death
ACS diagnosis
UA
NSTEMI
STEMI
—physical exam same as ischemia
UA:
(+) chest pain, EKG normal or with ST depression or T wave inversions
(-) biomarkers
NSTEMI:
(+) chest pain, EKG with ST depression or T wave inversion (+) biomarkers
STEMI:
(+) chest pain, ST elevations on EKG,
(+) biomarkers
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Describe the EKG progression of a STEMI
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What are the ST elevation morphologies?3
—concave
—convex
—obliquely straight
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STEMI EKG
What are reciprocal changes?
There is usually RECIPROCAL ST DEPRESSION in the electrically opposite leads.
Ex: If have ST elevation in lead III, can have ST depression to lead aVL
Inferior leads — lateral leads (and vice versa)
II — AVR
III — AVL
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Memorise the coronary anatomy and ECG leads
Which leads relate to which coronary arteries?
V1 V2 = more septum
V3 V4 = anterior wall
Lateral = LCx (for this class)
AVR could be left main disease, although it’s a “forgotten” lead
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What is the DX of this EKG?
Upper
V1-V4 : ST elevation
Heightened T wave
Not too much reciprocal change
Anterior/septal = LAD
Lower
I and AVL ST elevation
Lateral STEMI
LCx
Reciprocal changes in III (reciprocal from AVL)
see annotations in notability
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What is the DX of this EKG
ST elevation in II, III and AVF
Inferior MI
RCA
RCA = more common because the left main MI patients usually die. The RCA supplies a lot of the right ventricle, still have a lot of LV available to squeeze and preserve cardiac output
Right side supplies a lot of conduction (SA and AV node)
A lot of these patients will present w/ heart block and bradycardia
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Right-sided ECG lead placement:
When would you do this?
Which lead are you looking at?
Which med don’t you give?
Confirm inferior MI w/ right ventricular wall involvement
(Confirm this)
II, III, AVF = inferior MI
If someone comes in with this, don’t give nitro, becuase it’s a preload reducer, and you need to INCREASE preload.
Always get a right sided EKG before giving nitro!
Aortic stenosis is the other reason you SHOULDN’T give nitro (could cause syncope)
If you have ST elevation in V4. You have a RV infarct
Acute marginal artery
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Right sided EKG lead placement
To confirm RV infarct
DO this before giving nitro because RV is preload dependent
Needs preload to SQUEEZE
V4 is the lead to follow
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Right sided EKG lead placement
Confirm what this is showing
Not super clear
But right sided EKG would be ordered to confirm an inferior MI of the RV wall / RCA
Posterior MI EKG lead placement
Normal placement of V1-V6 plus V7-9
V1 and V2 should have ST depression on standard EKG
Take EKG, flip it and look in light, should flip to ST elevation and voila, it’s a posterior MI
Another way is a posterior EKG
Put 3 leads on the back
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What is this?
Posterior MI
From posterior EKG
The original EKG is attached to this side.
There is no ST elevation on this EKG
But it is: R wave in V1 and V2. Should not have a prominent R wave in V1 or V2 (bigger than S wave) — indicates RV hypertrophy. Another reason is posterior MI!
And you have ST depression
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What is this
LBBB
W in V1
M in V6
QRS duration >120ms
—normal conduction : septum activated from left to right
—In LBBB = conduction delay : R to L
—The overall depolarisation vector from the right to left ventricle produces tall R waves in lateral leads (I, V5-6)
—and deep S waves in the right precordial leads (V1-3). — = “M-shaped” R wave seen in lateral leads
—Delayed overall conduction time to the LV extends the QRS duration to > 120 ms
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What is this
LBBB
M in V6
ST elevation in the setting on LBBB
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AVR ST elevation
What can it indicate? 2
What are the 2 mechanisms in EKG?
—Left Main insufficiency
—OR diffuse multi vessel disease
Two mechanisms:
—DIFFUSE subendocardial ischemia with ST depression producing RECIPROCAL ST elevation in aVR — 3 vessel disease
—Or infarction of the basal septum producing aVR STEMI
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What is this?
Look at AVR
AVR ST elevation
—Left Main insufficiency
—OR diffuse multi vessel disease
Two mechanisms:
—DIFFUSE subendocardial ischemia with ST depression producing RECIPROCAL ST elevation in aVR
—Or infarction of the basal septum producing aVR STEMI
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What is considered a STEMI equivalent?
LBBB
—EKG pattern has a ST elevation at baseline making it impossible to use the standard STEMI criteria
—Any new LBBB must be considered as a STEMI equivalent ⭐️
—Sgarbossa’s criteria: (don’t memorise)
1. Discordant ST elevation w/5mm
2. Concordant 1mm
3. Concordant V1-3
LBBB
Where is the impulse travelling
What happens to septal activation ?
Which direction does the depolarisation vector go?
Which 4 findings on EKG would you see because of this?
—normal = left to right
—in LBBB septal activation is REVERSED
—impulses travel via the right bundle branch to the RV then to the LV via the septum
Depolarization vector from right to left produces:
—Tall R waves in the lateral leads
—prolonged QRS
—“M” shaped R wave in the lateral leads due to delay in activation between the RV and LV
—Deep S waves in the precordial leads
—Delayed conduction > 120 msec
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What is this?
[CONFIRM]
LBBB
—impulses must travel via the right bundle branch to the RV then to the LV via the septum
—Septal activation is REVERSED
Depolarization vector from right to left produces:
—Tall R waves in the lateral leads
—“M” shaped R wave in the lateral leads due to delay in activation between the RV and LV
—Deep S waves in the precordial leads
—Delayed conduction > 120 msec
Pink EKG is ST elevation in the setting of LBBB (V6)
What is Wellens Syndrome / Waves?
—EKG is showing what in the vasculature of the heart?
—what are the symptoms?
—when do you see the EKG changes?
—which treatment is indicated in 75% of patients?
—EKG seen in critical, proximal LAD stenosis (either plaque or spasm)
—Pattern seen during chest pain free episodes (not active pain). Otherwise normal EKG during pain.
—history of chest pain
—no pathological precordial Q waves or loss of R wave progression
—pain free ST elevation in V2 and V3 (minimally elevated)
—pain free symmetrical deep T wave inversion or biphasic T waves in V2-V5
—PRE-INFARCT state rather than a complete occlusion.
—URGENT PCI is indicated however as 75% of patients will have an anterior wall MI within 8.5 days
This pattern is associated with proximal LAD disease (bad territory to have an MI!)
Deep inverted symmetrical T waves also in:
—Takautso
—Intracranial haemorrhage
—HOCUM
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What is this?
What do you notice in the pattern on the left?
On right right?
Wellen’s syndrome
wellen will get an MI
Pattern A: BIPHASIC T waves (up then down) in V2-3
Pattern B: DEEP INVERTED T waves, symmetrical
Critical LAD stenosis > urgent PCI > MI in 8.5d
What is benign early repolarisation or
“J point elevation”
What do you see on EKG ? 2
Seen in which pts?
What do you NOT see on EKG?
What does it mimic
—Causes MILD ST elevation
—with TALL T waves in the precordial leads
NORMAL VARIANT
—commonly seen in young, healthy patients
—less common in people > 50
—rare in those > 70 years old.
EKG
—Notching at the J point (fish-hook pattern)
The J point is the junction between the termination of the QRS complex and the beginning of the ST segment (end of depolarization and beginning of repolarization)
—NO RECIPROCAL ST depression
—MIMICS pericarditis or STEMI.
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What is this?
Benign early repolarisation or J point elevation
—Causes MILD ST elevation
—with TALL T waves in the precordial leads
NORMAL VARIANT
—commonly seen in young, healthy patients
—less common in people > 50
—rare in those > 70 years old.
EKG
—Notching at the J point (fish-hook pattern)
The J point is the junction between the termination of the QRS complex and the beginning of the ST segment (end of depolarization and beginning of repolarization)
—NO RECIPROCAL ST depression
—MIMICS pericarditis or STEMI.
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What is this?
J point elevation in the smiley face
benign early repolarisation
Technically:
“Upward concavity or ST coving”
This image is taken from litfl
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What are the three main cardiac markers?
What are their clinical significances?
Troponin:
—regulatory protein in muscle cells that control interactions between myosin and actin.
—there are three subunits: TnC, TnI, and TnT.
—TnT and TnI are structurally unique and sensitive to myocyte damage. However, other conditions such as myocarditis, hypertensive emergency, and heart failure can also cause cardiac strain and release of markers.
—troponin should be normal, so any troponin level is concerning
CK-MB
—isoenzyme of CK localized to the heart and improves specificity of its origin
Creatine Kinase
—found in heart, skeletal muscle, brain, and many other organs therefore elevation can come with damage to any of these organs
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Cardiac markers
How do you approach ordering them and interpreting them? 4
—not released into the serum until a few hours after the onset of myocardial necrosis
—single normal value drawn early does not rule out a MI.
Approach:
1. Draw serial sets of biomarkers:
—a 2nd set 1-2 hours after the first
—then every few hours after
- With coronary occlusion
—the rate of rise is rapid with serial sets of enzymes - If a patient has a STEMI
—total troponin and CK/CK-MB levels useful to gauge size of the infarct
—draw until levels peak - If pt presents w/
—hx of a 1w of chest pain
—+ elevated troponin level
—w/ normal CK/CK-MB
—Q waves on the EKG
= he likely already had evolution of his MI
ACS — revascularisation pathways
What is the ward to balloon time?
STEMI
Vs
UA NSTEMI
ST elevation (STEMI)
—emergent PCI available w/i 90 minutes
—120 mins if transferring to a PCI capable hospital
—if yes ➡️ primary PCI
—if no ➡️ fibrinolytic therapy if no c/i
UA and NSTEMI
—risk assessment (troponin, ECG, TIMI score)
—low ➡️ conservative strategy
—high ➡️ invasive strategy: early cardiac cath w/ PCI or CABG
ACS management — medications
What are the anti-Ischemic therapies
Antithrombotic therapies
Adjunctive therapies
Anti-Ischemic therapies
—BBs
—Nitrates
— +/- CCB
Antithrombotic therapies
1. Antiplatelets
—ASA
—P2Y12 inhibitor (Clopidogrel/Plavix)
+/- GP IIb/IIIa
2. Anticoagulants
—UFH
—LMWH
—Bivalirudin
Adjunctive therapies
—statin
—ACE inhibs
When is thrombolytic therapy contraindication?
Absolute = anything to do w/ the brain
ACS STEMI management
If artery is completely occluded, to minimise myocardial damage and improve survival, what is the first revascularisation option?
How does it compare to fibrinolytics?
When is it ideally performed?
What is it called when it’s for pts who didn’t respond to fibrinolytics?
What about for pts who attained vessel patency?
Percutaneous Coronary Intervention:
—higher survival than fibrinolytics and is termed primary PCI as it is the preferred reperfusion strategy
—Goal is within 90 minutes for angioplasty and eventual stenting
—Even if you give a fibrinolytic, STILL go to cath lab. Sometimes only 50% effective
—“Rescue PCI” is for those patients that did not respond to fibrinolytics
—“Facilitated PCI” are patients who attained vessel patency with medical therapy and later will undergo PCI
ACS management — ICD
For which two patient populations?
What are the criteria 2
What about a wearable cardioveter-defibrillator, who is this for?
—pts w/ an EF < 35% AND NYHA class II-III symptoms secondary to a MI that occurred at least 40 days prior
—pts w/ VT/VF 48 hours after the MI and reperfusion completed
Wearable cardioverter-defibrillators:
—pts who at risk of ventricular arrhythmias but do not meet the above criteria for an ICD can wear an external defibrillator as a bridge to therapy
—basically during the 40 days while they’re waiting
What is the arterial supply for these conduction pathways?
SA node
AV node
Bundle of His
RBB
LBB:
Left anterior fascicle
Left posterior fascicle
SA node — RCA
AV node — RCA
Bundle of His — LAD
RBB: proximal = / distal = RCA
LBB:
Left anterior fascicle = LAD
Left posterior fascicle = LAD & PDA
