Patho 3PA2: Cardiovascular (part 2)

what does the QRS complex represent

ventricular depolarization

what does the T wave represent

Ventricular Depolarization

what is the ST segment?

the relationship between the S and T waves, measured from the end of the QRS complex to the onset of the T wave --> end of ventricular depolarization, start of vent. repol

what does a normal ST segment look like?

pretty flat

any depression or elevation > or = this is considered worthy of attention

1 mm

What does the P wave represent?

Atrial Depolarization

Unstable Angina is serious because:

the plaque is disrupted, exposing the injured endothelium to platelets and coagulant factors (kinda like ripping off a scab)

Unstable angina leads to this at the site of plaque disruption:

transient episodes of vessel occlusion

Perfusion in Unstable Angina:

typically restored before necrosis occurs, but the pain is due to the schema

Characteristic of unstable angina:

atherosclerotic plaque disruption, platelet aggregation, clot formation, pain is persistent and severe, can occur at rest, difficult to relieve

What does unstable angina look like on an ECG?

ST depression and T wave inversion during the painful periods

Cardiac enzymes in Unstable Angina:

creatinine kinase, lactic dehydrogenase, troponin are usually negative

If a pt with unstable angina were to have an echocardiogram, what would it look like?

Their contractility may be somewhat abnormal

tissue necrosis in NSTEMI

- necrosis occurs but not full thickness of the ventricular wall

- limited to the inner layer of the myocardium, the subendocardium

- inner 1/3 to 1/2 of the ventricle wall

ECG changes in NSTEMI

- ST depression

- T wave inversion

pain in NSTEMI

severe and abrupt, often difficulty getting relief

how do we know if an infarct has taken place?

serum levels of cardiac biomarkers

which biomarkers do we look at?

serum CK and Troponin

Creatinine Kinase (CK)

- enzyme found in the heart, brain, and SK muscle tissue

when is CK released?

when cells get damaged

drawback to CK measurement

it's present in all tissues, not just the heart

SK isoenzymes

- SK-MM (SK muscle)

- SK-BB (brain)

- CK-MB (myocardium)

which isoenzyme do we need to look for to determine if there has been heart damage?

CK-MB

CK-MB is usually this much of the total CK in the body

0-4%

CK-MB levels rise, peak, and return to normal at this time post-MI

rise: 3-6 hours

peak: 12-24 hours

return to normal: 12-48 hours

do we use measurement of CK-MB really anymore?

it's mostly been replaced by more sensitive and specific assays involving cardiac troponins and are not the preferred MI biomarkers anymore

Troponina

proteins found in cardiac and SK muscle fibers

Troponins in MI

T and I

they rise very quickly

Rise, Peak, Return of Troponins in MI

rise: 6-10 hours post-MI

peak: 18-24 hours post-MI

return: 5-6 days!!

diagnostic window with CK versus Trops

trops are better bc they stay high for the 5-6 days so we have more time to diagnose the MI and distinguish between infarct and unstable angina

which biomarker is the preferred one for MI diagnosis?

Troponins!

high sensitivity cardiac troponin T threshold

< or = 0.1 mcg/L

high sensitivity cardiac troponin I threshold

< or = 45 ng/L (VERY cardiac specific)

ST segment in NSTEMI

- ST depression

- T wave inversion

is there always ECG change in NSTEMI?

no!

how do we differentiate NSTEMI from unstable angina?

the presence of a detectable troponin level

STEMI

- complete arterial occlusion

- necrosis of full thickness of ventricular wall

pain in STEMI

- severe

- abrupt

- no relief

how is STEMI diagnosed?

- ST elevation on ECG

- Hx

- pain

- biomarkers

greater elevation in the ST segment indicates this:

damage to cells has occurred

clinical definition of MI

denotes the presence of acute myocardial injury detected by abnormal biomarkers in the context of acute myocardial ischemia (chest pain, ecg changes r/t ischemia)

pathophysiological definition of MI

cell death due to prolonged myocardial ischemia

is there a distinction between cardiac injury and MI?

yes, injury is considered acute with a rise/fall in troponin

is troponin change always associated with MI

no, it can rise in the absence of MI so it alone is not diagnostic of MI

non-MI factors that can cause a rise in troponin

- preload-induced myocardial stress

- physiological stress in otherwise normal hearts

how many types of MI are there?

5

how are the types of MI determined?

- pathological, clinical, prognostic differences

- differences in Tx strategies

Type 1 MI:

MI precipitated by atherosclerotic plaque disruption

how is type 1 MI detected?

rise or fall in troponin and at least one of the following:

- symptoms of ischemia

- ischemic ECG changes

- new pathological Q waves

- imaging evidence of loss of myocardium/wall kinetic changes

- visualization of thrombus by angio or autopsy

Type 2 MI:

ischemic myocardial injury in the context of a mismatch between O2 supply and demand (excludes plaque rupture)

how is Type 2 MI detected?

- rise/fall in troponin and at least one of:

- s/s of ischemia

- new ischemic ECG changes

- new pathological Q waves

- imaging evidence of loss of myocardium or change in wall kinetics

Type 3 MI:

pts that suffer cardiac death with symptoms suggestive of myocardial ischemia, but before biomarkers can be obtained

symptoms suggestive of myocardial ischemia with respect to T3 MI

- ischemic ECG changes

- V fib

T3 classification allows for:

differentiation from other disorders resulting in sudden death that may be cardiac (non-ischemic) or non-cardiac in origin

Type 4 MI:

- coronary procedure related MI

4a, 4b, 4c

Type 4a

PCI-related

Type 4b

PCI/stent/scaffold related

Type 4c

re-stenosis following PCI

how is T4 MI defined?

troponin > 5x the 99th percentile URL plus one of:

- new ischemic ECG change

- new pathological Q waves

- imaging evidence of loss of viable myocardium

- angiographic evidence of limited blood flow

Type 5 MI

CABG related MI

how is T5 MI defined?

troponin > 10x 99th percentile URL plus one of:

- new pahtological Q waves

- angiographic evidence of blood graft occlusion or new occlusion

- imaging evidence of loss of viable myocardium or altered wall kinetics

most immediate non-pharm interventions for a person having an MI include:

- 911/immediate transfer to an acute care facility

- supplemental O2 (NP 3-4L/min)

- SpO2 monitoring

- 12 lead to ID the likely area of the ventricle affected

- continuous cardiac monitoring after ECG is done

- vitals

- CXR

- echo

- bed rest

- Hx/Phys

- blood draw for biomarkers and CBC/lytes

why do we do an ECG?

to identify the likely area of infarct

why do we take VS?

to determine the effect of the infarct on cardiac output (low BP tells us that CO is likely compromised by a ventricle that is not contracting well)

why do we do a CXR?

not so much to look at the heart itself but examine potential effects the infarct may be having on the lungs, like fluid shifts

why is an echo done?

- for info on the state of the ventricle --> get a report on the 'kinetics' of the heart

- some ppl develop a papillary muscle rupture that leads to a failure of a valve because of an infarct

why do we put ppl on bedrest?

to decrease demand on the heart and preserve their energy

purpose of thorough Hx and Physical

determine potential effects caused by the infarct, ID past risk factors/conditions that precipitated the event

why do we draw blood?

- detect biomarkers

- CBC/Lytes, lipid profile, INR/PTT

- look for elevated WBCs bc of inflammation

- look at hgb for O2 carrying capacity

- lipids for atherosclerosis risk

- coag studies to determine the risk for clots as a baseline for anticoagulation going forward

Pharmacologic/more invasive methods of managing MI include:

- morphine

- O2

- nitro

- ASA

- beta blockers

- adenosine diphosphate receptor antagonist (clopidogrel)

- anticoagulant

- reperfusion therapy

- glycoprotein iib/iiia inhibitors

- ACE-is or ARBs

- statins

morphine in MI mgmt:

- narcotic analgesic

- decreases afterload through vasodilation

use with cause in pts with right ventricular infarct

why do we need to use caution with morphine in pts with R vent infarct?

bc fluid needs to return to the R ventricle to encourage it to stretch and fill, increasing the force of contraction --> it can't do this if it's too vasodilated

current recommendations are that supplemental O2 should not really be given unless pt's sats are:

< 90%

Nitroglycerin

- vasodilates vascular sm. muscle

- decreases afterload and myocardial O2 demand

- improves coronary artery blood flow

- sublingual spray, quickly absorbed

ASA

- prevents plt aggregation

- should be chewed

- given ASAP, preferably in the ambulance

Beta Blockers

block beta receptors, decreases cardiac workload and O2 demand by reducing contractility and HR

ADRA (Clopidogrel)

- prevent action of glycoprotein iib/iiia complex required for plt aggregation

what does giving an antiplt drug do?

helps prevent a thrombus - one of the reasons we do CBC on admission --> figure out the baseline plt count

Anticoagulant (Heparin)

accelerates antithrombin action, which inactivates thrombin to prevent clot formation

does heparin break down existing clots?

no, just prevents new ones from forming

Reperfusion therapy

Fibrinolysis is achieved with tenecteplase (TNK) to re-establish artery patency. Also known as clot busters, these medications DO lyse existing clots.

PCI

balloon tipped catheter is used to open occluded arteries in the cath lab

when is PCI done?

preferably immediately upon arrival to the hospital --> time is tissue!

what is a stent?

little metal mesh tube placed in a vessel to hold it open

CABG:

surgical technique where the pt's own vessels are harvested from a distant site and used to bypass an occluded artery

Glycoprotein iib/iiia inhibitors

decrease clot formation by making plts less 'sticky' so the risk of clotting decreases

ACE-inhibitors

- prevents conversion of angiotensin 1 to 2: results in relaxed vessels and decreased cardiac workload

- lessens afterload, ventricle can then contract against low pressure circulatory system

ARBs

- prevent angiotensin and receptor interaction, inhibit vasoconstriction, dec. LV workload

- same result as ACE-i they just do it in a different way

Statins

- inhibit HMG-CoA Reductase

- reduces cholesterol synthesis, dec. LDL lvls

- good to reduce and eliminate bad cholesterol

consequences of MI depend on:

- location

- size

of the infarct

an infarct causing 40% damage to the myocardium can result in:

significant decrease in LV function, leading to cardiogenic shock

cardiac enzymes are released and can be detected in serum when:

myocardial cells have been damaged due to inadequate perfusion

b/d of necrotic tissue post-infarct:

within a couple of days, WBCs and scavenger neutrophils invade the area, releasing enzymes that break down the necrotic tissue

consequence of breakdown of necrotic tissue post-infarct

thinning of the ventricle wall and potential for rupture

scar formation post-MI

occurs around 3 weeks post-MI and ventricular remodelling begins

ventricular remodeling post-MI

fibrous CT replaces necrotic tissue, but is not vascularized and can't do contraction

what happens to the remaining myocardial tissue in response to the non-function scar tissue formation?

it hypertrophies to compensate for the lack of contraction in the scar tissue

what happens to a ventricle full of scar tissue?

- non-compliance, an inability to stretch and/or relax

- ventricle wall no longer dilates/contracts efficiently

- damaged parts lag behind in contraction

wall motion post-MI

either diminished or absent (hypo or akinesis)

heart failure post-MI

for some ppl the heart is so damaged that the ventricle fails to pump adequately --> this is heart failure