ECCO: Treating Patients with ACS: STEMI, Non-STEMI, and Unstable Angina, ECCO: Pre- and Post-Procedure Care for Noninvasive and Invasive Cardiac Procedures, ECCO: Diagnosing Acute Coronary Syndrome, ECCO: Assessing the CV System In Critically Ill Pat…

When should you admin O2

SpO2 less than 90%

Respiratory distress

High risk for hypoxemia

If three sublingual NTG don't relieve pain

Consider IV NTG

Contraindications to NTG

1. Systolic <90

2. Drop in systolic of 30 or more from baseline

3. Marked bradycardia or tachycardia

4. Sildenafil within 24 hours or tadalafil within 48 hours

5. Suspected of having a right ventricular infarct

6. Hypotension secondary to nitrates that prohibits the administration of beta-blocking agents

What else does morphine decrease

Preload

Possible anticoagulants for ACS

1. Low-molecular weight heparin or unfractionated heparin IV

2. ASA

3. P2Y12 Receptor inhibitors

4. Bivalirudin

5. Glycoprotein (GP) IIb/IIIa antagonists

ASA admin

Non-enteric coated tablets for initial dose which should be chewed. Subsequent doses are PO

What other medications part of ACS protocol

1. Beta blockers

2. ACEi

3. ARBs

4. CCBs

Three reperfusion treatment options

1. Emergent PCI

2. Fibrinolytics

3. Urgent CABG

When are fibrinolytics used

Only in presence of STEMI because non-STEMI thrombus is composed of platelets and does not contain fibrin

Symptom onset within 12 hours and when PCI can't be used

How soon after presentation should anticoagulants + fibrinolytics be given

Fibrinolytic + ASA + Heparin + P2Y12 receptor inhibitor within 30 minutes

Absolute contraindications to fibrinolytic therapy

1. Any history of intracranial hemorrhage

2. Ischemic stroke, significant closed head injury, or facial trauma within the previous three months

3. Severe uncontrolled HTN

4. Suspected aortic dissection

5. Active known bleeding or bleeding diathesis (excluding menstruation)

6. Known structural cerebral vascular lesion or malignant intracranial neoplasm

Diathesis

a vulnerability or predisposition to developing a disorder

How soon after presentation should balloon angioplasty happen

Within 90 minutes

Is fibrinolytic therapy indicated in non-stemi

No, fibrin is not present. Thrombus is platelet-based

Types of unstable angina

1. Rest angina

2. New-onset severe angina

3. Increasing angina

Rest angina

Occurs at rest and lasts longer than 20 minutes

New-onset severe angina

Has been present for less than two months and causes marked limitation of ordinary activities

Increasing angina

Has been previously diagnosed but occurs more frequently, lasts longer, or produces symptoms with less and less exertion

Treatment flow chart for UA and Non-STEMI

ASA

ADD P2Y12 Receptor Inhibitor if high-risk

then

Invasive or ischemia guided treatment strategy

Invasive:

-Heparin

-P2Y12 receptor inhibitor and/or GP IIb/IIIa antagonist

-Non-urgent diagnostic angiography: based on findings, manage with either PCI, CABG, or medical management

Ischemia-Guided:

-Heparin

-P2Y12 receptor inhibitor and/or GP IIb/IIIa antagonist

then

Recurrent ischemic symptoms or EF<40?

Yes: coronary angiography

No: stress test

Hyperkinesis

Increased contractility

Hypokinesis

Decreased contractility

Dyskinesis

Motion opposite to what is expected

Position for trans-thoracic echo

Supine or left side-lying

Pre-procedure TEE prep

NPO 4-6 hrs prior

Procedural sedation and numbing medication applied to pharynx and is often usedto provide patient comfort during procedure

Post-procedure TEE assessment

For return of gag reflex and provide clear liquids

Monitoring after procedural sedation

TTE and TEE are better for viewing what

TTE: Ventricular walls and wall motion

TEE: Atria and valves

Left ventriculogram is for what

Measures EF and looks for wall motion abnormalities

How is right sided-angiography accessed

Venous system to get to IVC

Balloon angioplasty

Baloon across atherosclerotic lesion

What medication are patients on who receive stents

P2Y12 receptor inhibitor to avoid clot on stent

4 kinds of PCI

1. Balloon angioplasty

2. Stent placement

3. Atherectomy

4. Laser angioplasty

Pre-procedure PCI assessment

,Wt and labs

pulses distal to proposed catheter insertion site

Prep-procedure labs for PCI

CBC

Plt

Cr

BUN

Electrolytes

BG

INR

PTT

Diabetic pre-procedure prep

Hold metformin 24 hours pre-cath and 48 hours post-cath

NPO 8-12 hours

Post-procedure assessment includes

1. VS and pain

2. Distal circulation

3. UO

4. Post-sedation monitoring

5. Cardiac rhythm monitoring

6. Insertion site for bleeding, oozing, or evidence of hematoma formation

If access site is bleeding, oozing or hematoma

Manual compression for a minimum of 10 minutes at arterial puncture site. Slightly proximal to the skin puncture site

Avoiding AKI post-PCI

Lots of fluids, contrast is an osmotic diuretic

After post-PCI complication such as hematoma formation, what diagnostics are expected

US of insertion size to assess size and extent of hematoma

CT to assess for retroperitoneal bleeding

What is used following radial access for compression

Inflatable compression device occluding radial artery

What does precordial mean

Anterior portion of the heart. Normal V leads are referred to as precordial

How long would pressure, tightness, squeezing, heaviness, aching, or indigestion pain have to be to likely be an MI

20 minutes

What kind of heart sounds can be heard with STEMI

Possibly S3, S4 Gallop secondary to a stunned, noncompliant ventricle or

Mitral regurgitation murmur from papillary muscle dysfunction

Why do STEMIs lead to N/V

Blood is shunted away from GI tract and skin to vital organs

What are the steps in the progression of atherosclerosis

Atheroma, atherosclerosis, thrombogenesis, vessel blockage, occlusion

What is atheroma

Extracellular lipid accumulation in the intima of artery

Atherosclerosis

Lipid accumulation evolves to become a fatty-fibrous lesion and may contain a lipid interior and necrotic material covered by a fibrous cap

Thrombogenesis

Rupture of the fibrous cap exposes lipids and procoagulants stimulating platelet adhesion

How soon after occlusion does MI occur

Irreversible damage within 20 minutes

What is sudden cardiac death

Occurs when heart stops beating or is not beating adequately to sustain life within 1 hour of onset of symptoms

Possible causes of MI

1. Coronary artery thombosis

2. Vasospasm

3. Coronary artery embolism

4. Severe, prolonged hypotension

5. Severe aortic stenosis or insufficiency

6. Trauma

7. Cocaine abuse

What layer of the heart is first affected by ischemia and why

Subendocardium because it has the highest oxygen demand and most tenuous blood supply

What is the first zone

Zone of necrosis: where tissue is actually dead

Second zone

Zone of injury: surrounds zone of necrosis which may have severe cellular damage but may still be viable if perfusion is restored quickly

Third zone

Zone of ischemia, which has reduced blood flow but is viable

Is variant angina part of ACS

No

Stable angina cause, triggers, duration

Cause: atherosclerosis

Predictable onset, severity, and duration at a consistent level of exertion or stress

Triggers: physical or emotional stressors, factors decreasing oxygen delivery

Predictably relieved with rest and/or NTG

Unstable angina cause

Atherosclerosis with thrombus that partially occludes the lumen

No predictable pattern

MI-Associated angina

Atherosclerosis and thrombus completely or nearly completely occlude the lumen, not relieved with NTG and rest

Variant angina cause, timing of onset, treatment

Coronary artery spasm which narrows the arterial walls and slows or blocks blood flow

Usually occurs at rest, often in the early hours of the morning

Can occur both in people who have CAD and in those who don't

Tx chronically with nitrates and CCB to vasodilate the arteries and inhibit spasm

What is silent ischemia, who do you find it in, and how

Ischemia without symptoms.

Common in elderly and diabetics

Only detectable through continuous EKG monitoring

What sound would you hear with mitral insufficiency

holosystolic murmur

How soon after ACS protocol activation should you get a 12-lead

Within 10 minutes needs to be obtained and reviewed

What pathological EKG findings indicate ACS

1. T wave inversion

2. ST depression

3. Hyperacute t waves

4. ST elevation

5. New or developing Q waves

What does t wave inversion look like

T wave looks almost like U

What does ST depression look like

Sharp depression in S and T wave

How much t wave inversion suggest acute ischemia

1-2 mm (1-2 boxes)

How much ST depression seen with symptoms and resolves when patient is asymptomatic is highly indicative of severe CAD

0.5 mm or 1/2 small box

What is significant ST elevation defined as

1 mm or 1 box or greater in two contiguous leads (looking at the same area of the heart)

When do hyperacute t waves appear and what do they look like

Early sign of STEMI and should be treated as such

Look like spiked T wave

What other potential early sign of STEMI is there

Lost ST segment as they fuse together

What are pathologic Q waves defined as

At least one small box wide on 12-lead

Any widening or deepening is bad

How long do pathological Q waves last

Permanent and will indicate prior infarction o nsubsequent EKGs

Interpreting EKG steps

1. Look at T wave changes (inversion and hyperacute

2. Look for ST segment changes (elevation or depression)

3. Look for pathologic Q waves

What leads monitor anterior portion of ventricle and what artery supplies anterior wall

V3 and V4 (may also be V1-V4)

LAD

What leads monitor intraventricular septum and what artery

V1 and V2

Branch of LAD

Which leads monitor lateral surface of left ventricle

1, aVL, V5, V6

Left circumflex artery

1 and aVL monitor high lateral surface of left ventricle

V5 and V6 monitor the low lateral surface

What leads monitor inferior surface of heart and artery

2, 3, and aVF

RCA

What does LMCA supply

Left Main Coronary Artery supplies LAD and left circumflex artery

What does occlusion of LMCA result in

Infarction of anterior, septal, and lateral walls of the heart

When does posterior MI often occur

In presence of inferior or lateral MI

ST elevation posterior MI can occur in isolation

Do we directly monitor posterior MI

No, EKG can't, we indirectly monitor for it

What does posterior MI look like

V1-V3 and/or V4 show tall R waves with ST depression and an upright T wave

Timeline of troponin without reperfusion

Peaks around 36 hours and stedily decline to one week

Timelines of troponin with reperfusion

Peaks at 24 hours and steadily declines by 72 hours

CK-MB without reperfusion timeline

Peaks at 24 hours and declines by 48 hours

CK-MB with reperfusion timeline

Peaks in 12 hours and declines by 36 hours

How often are biomarkers obtained

Presentation

3-4 hours

6-9 hours

Normal male and female CK

Total 55-170 units/L

Female 30-135 units/L

Normal CK-MB

<10 ng/mL or less than 3% of total CK

tROPONIN I normal

<0.03 ng/mL

Troponin T normal

<0.2 ng/mL

What is abnormal in trend of cardiac biomarkers

Rise after 24 hours

How does decreased preload affect oxygen demand

Leads to increased HR leading to increased demand for oxygen

How does icnreased preload affect oxygen demand

Increased tension on ventricle leading to compression of smaller endocardial blood vessels, decreasing myocardial oxygen delivery

What does NTG also reduce

Preload and afterload

Dose/admin of NTG for ACS

Start at 5 mcg/min and increase 5 mcg/min every 3-5 minutes

Low dose effects of NTG

<100-150 mcg/min

Primarily venous dilation thus preload reduction

Higher dose effects of NTG

>150 mcg/min

Arterial vasodilation hthus decreased afterload

Phenylepherine MOA

Selective alpha 1 agonist causing arterial vasoconstriction increasing afterload without affecting HR

Low dose effects of dopamine

2-10 mcg/kg/min

Beta agonist increasing contractility and HR leading to increased CO and variable SVR