N123 - Week 3 ACS/CAD

What is the etiology and pathophysiology of CAD?

CAD is the narrowing of coronary arteries to the point where blood flow is obstructed.

Atherosclerosis is the main cause of CAD in most people. It is characterized by lipid deposits in the inner layer of coronary arteries. The pathogenesis is as follows:

1) Chronic endothelial damage due to a variety of factors including smoking, hypertension, hyperlipidemia, diabetes, and hyperhomocysteinemia (from red meat consumption)

2) Fatty streak forms under areas of endothelial damage

3) Collagen covers the fatty streak and the vessel is narrowed outward, and fissures in the endothelium form. This is known as an atherosclerotic plaque, and it obstructs blood flow.

4) The fissures on the plaque ruptures, and a thrombus is formed that further narrows or totally occludes the vessel.

Describe the nursing role in the promotion of therapeutic lifestyle changes in patients at risk for CAD, distinguishing between modifiable and non-modifiable risk factors.

Non-modifiable:

1) Age

2) Sex

3) Ethnicity/Race

4) FHx/Genetics

Modifiable:

1) High serum lipids - Nursing can encourage diet change

2) Sedentary lifestyle and obesity - Nursing can encourage exercise and weight loss

3) Hypertension - Nurses can encourage adherence to blood pressure medications and provide education on sticking to a regimen

4) Tobacco use - Nurses can encourage tobacco use cessation and provide products such as nicotine replacement therapies

5) Diabetes - Nurses can educate patients on managing risk factors or the disease itself

6) Metabolic syndrome (a combination of central obesity, HTN, high serum lipids, and high fasting BGL): Utilize the above strategies to prevent

Drug therapy for HTN and CAD

1) Adrenergic inhibiting agents: These can either directly inhibit the release of norepinephrine to decrease sympathetic tone (ex: clonidine) OR block adrenergic receptors to cause vasodilation and lowered heart rate (ex: beta blockers).

2) ACEIs (-Prils): These block the formation of angiotensin II and thus reduce vasoconstriction. They also block aldosterone release, thus leading to increased elimination of sodium and water.

3) ARBs: (-Sartans): These prevent angiotensin II from binding to receptors in blood vessel walls, thus reducing vasoconstriction.

4) Calcium channel blockers (-Pines, Diltiazem, and Verapamil): These prevent the movement of extracellular calcium into cells, thus causing ARTERIAL VASODILATION (dilates coronary arteries!!!).

-Diltiazem and Verapamil in particular also have this effect on cardiac cells, so they lower heart rate as well.

5) Direct vasodilators (nitrates, hydralazine): These relax vascular smooth muscles to promote vasodilation.

-Hydralazine is a ARTERIAL vasodilator so it REDUCES AFTERLOAD

-Nitrates are VENOUS vasodilator so it REDUCES PRELOAD, but this is a desired effect in hypertension/HF/angina since we want to reduce the cardiac workload and myocardial oxygen demand. THEY ALSO DIRECTLY DILATE COROANRY ARTERIES.

6) Diuretics (Lasix, HCTZ, Bumex) reduce plasma volume by increasing sodium/water excretion and reducing vascular response to DA/NE/Epi.

Drug therapy for Hyperlipidemia and CAD

1) HMG-CoA reductase inhibitors (-STATINS) inhibit cholesterol synthesis, decrease LDL, decrease C reactive protein, and increase HDL. Examples:

-Atorvastatin (most common)

-Rosuvastatin is the most potent but also most associated with serious adverse effects such as liver damage and myalgia (muscle pain)

-Simvastatin

2) Ezetimibe (Zetia) decreases absorption of dietary/biliary cholesterol. It is often used in conjunction with a -statin.

What is C reactive protein?

The liver produces C-reactive protein (CRP) during periods of acute inflammation.

It is a predictor of cardiac events and is emerging as an independent risk factor for CAD.

Antiplatelets used for CAD

Antiplatelets are used to prevent the formation of blood clots that can completely occlude the coronary arteries. However, they RELATIVELY contraindicated if the patient already has increased risk of bleeding, such as due to hemophilia. Examples:

1) Aspirin 81 mg

2) Clopidogrel (Plavix)

Why do patients with CAD have increased O2 demand? What are clinical consequences?

In normal conditions, our heart only uses 75% of the O2 in our arterial blood supply. However, in CAD/ACS, the heart is using at least 85% of this supply. Contributors to this are:

1) Coronary arteries will vasodilate to increase blood supply in CAD. However, this only works up to a certain point before the blood/oxygen supply is inadequate to support normal functioning.

2) When the heart has chronic oxygen deprivation due to CAD, ventricular hypertrophy occurs, thus increasing wall stress and O2 demand. This leads to a chronically increased O2 demand.

3) CAD is often associated with hypertension, which increases the afterload that the heart has to pump against, thus also increasing myocardial workload.

The resulting consequence of increased O2 demand is that it means cardiac cells can also infarct more easily. Thus, the primary goal of managing CAD/ACS is to decrease O2 demand and increase O2 supply. Principles of this:

1) Heart rate control is of particular importance since a faster heart uses more oxygen. The coronary arteries also supply the bulk of blood during DIASTOLE, and higher heart rates shorten diastole.

2) Afterload (arterial blood pressure) control is also of importance since it decreases the pressure that the heart has to pump against.

3) Nitrates in particular decrease preload. This may seem counterintuitive, but decreased preload leads to decreased wall-stress, which is linked to increased O2 demand. Nitrates also DIRECTLY dilate coronary arteries and collateral blood vessels.

What is the etiology and pathophysiology of Chronic Stable Angina?

Chronic stable angina is chest pain/pressure that occurs due to TRANSIENT myocardial ischemia, which occurs during periods of increased O2 demand such as exercise. It is a SYMPTOM of CAD.

The chief symptom is chest pain or pressure that may radiate to the arms, neck, or back.

Chronic stable angina is, by definition, able to be relieved by rest (usually 5 minutes is enough) or nitroglycerin, which both decrease myocardial O2 demand.

THERE IS ECG CHANGE ASSOCIATED WITH STABLE ANGINA. IT'S ST SEGMENT DEPRESSION AND T WAVE INVERSION.

What interventions can we implement to address increased O2 demand in CAD/chronic stable angina?

1) Administer O2

2) Administer beta blockers, calcium channel blockers, and/or ACEIs to lower heart rate and/or afterload

3) Administer nitrates to lower preload and increase supply to the heart by coronary arteries.

4) Administer antiplatelets, which prevent further narrowing of coronary arteries.

-324 mg of aspirin for any patient with chest pain (unless they already have bleeding issues or liver damage)

5) Promote relaxation and rest and address underlying causes of stress such as pain or infection

-Opioids also independently decrease sympathetic tone, thus making them helpful for stable angina

6) Deep breathing and/or vagal nerve stimulation

7) Position patients semi-fowler to decrease preload and WOB

Nitroglycerin 101

Procedure:

1) Give 1 tablet SL (0.4 mcg per dose) at a time

2) Expect relief in 5 minutes. If not, you can repeat every 5 minutes for a maximum of 3 tablets in 15 minutes.

3) ACTIVATE EMS IF NO RELIEF AFTER 1ST DOSE NITROGLYCERIN.

Contraindicated in patients with:

1) Right ventricular infarction or inferior wall MI since such patients already have a difficult time moving venous blood.

2) SBP < 90 mmHg

3) Use of sildenafil (Viagra) or similar drugs in the past 24 hours

Patient teaching:

1) Side effects include headache, dizziness, flushing, and orthostatic hypotension

2) Patients should store these away from sunlight and in a dark amber bottle.

What is percutaneous coronary intervention for CAD? What are nursing considerations? What are complications?

PCI is the gold standard diagnostic and curative intervention for CAD and associated problems. It involves CT angiography and/or IV ultrasound for diagnostic purposes and placing a balloon/catheter stent for interventional purposes. This is done in a cardiac catheter lab (which not all hospitals have).

Nursing assessments and considerations:

1) Assess for allergies to IV contrast

2) Assess VS, heart/breath sounds, neurovascular status of extremities, and 12-lead before/during/after procedure

3) Perform baseline lab studies including CBC, Chemistry Panel, and cardiac biomarkers prior to procedure

4) Administer drugs. Anticoagulants and antiplatelets including heparin, LMWH, direct thrombin inhibitors, and eptifibatide (Integrilin) are common during placement. Patients will need to stay on aspirin and clopidogrel after placement as well.

5) Provide pre and post procedure education, emphasizing:

-NPO status prior to procedure and diet progression to DASH diet after intervention

-Clot prevention techniques while in-hospital and the importance of staying on anticoagulants after discharge

-Necessary follow-up with cardiology and cardiac rehabilitation

-S/S to report to providers.

Common complications:

1) The coronary artery an re-occlude due to plaque migration distal from the insertion site and other reasons.

2) The stent can break or migrate, thus causing re-occlusion and possible emboli as well.

3) Clots form more easily around the stent. Anticoagulant therapy is paramount.

What other diagnostics are relevant for acute episodes of CAD/ACS?

What are specific nursing considerations for patients post-PCI?

What to do:

1) Monitor CSM, vascular access site, and cardiac status/symptoms q15 minutes until patient is stable

2) Monitor VS, telemetry, and fluid status/UO continuously

3) Positioning/mobility:

-KEEP THE AFFECTED EXTREMITY STRAIGHT FOR 2-6 HOURS AFTER THE PROCEDURE DEPENDING ON THE APPROACH/CLOSURE.

-HOB < 30 degrees initially

-Mobility as ordered

4) Administer antiplatelets (aspirin and clopidogrel) and other cardiac medications

What to look out for:

1) Acute vessel closure/thrombosis/psuedoaneurysm in accessed vessel

2) Bleeding or hematoma at access site

3) Contrast-induced nephropathy

4) Dysrhythmias

Why do ECG changes occur in ACS?

Increased O2 demand and subsequent ischemia leads to ATP depletion, which then leads to impaired active ion transporters. This then leads to uneven repolarization of the heart.

What is the etiology and pathophysiology of ACS. What differentiates it from stable angina?

ACS is the final stage of CAD, in which the plaque ruptures and leads to thrombus formation. This results in partial occlusion (UA or NSTEMI) or a full occlusion (STEMI). It is separated by severity into unstable angina, NSTEMI, and STEMI.

Differentiators of ACS:

1) Biomarkers may be present

2) Chest pain is more severe, frequent, and persistent regardless of rest or nitroglycerin use. However, silent MI without chest pain can occur.

3) ECG changes may occur

What is variant (Prinzmetal) angina?

This is angina that occurs due to coronary artery spasm rather than occlusion. It can be induced by sympathomimetic abuse. Interventions are different, but it can cause the same symptoms and outcomes as ACS.

What biomarkers are present in ACS/MI?

Cardiac specific troponins (T and I) are present during an MI (not present in unstable angina). They are released when cardiac cells infarct.

1) Usually not detected until 3-6 hours after MI onset. It's a good idea to get baseline labs BEFORE troponin is elevated.

2) Peak 10-24 hours after MI onset.

3) Do not return to baseline until 10-14 days later.

High-sensitivity cardiac troponin (HS-cTn) increases 3 hours after an MI onset and is the gold standard. Other biomarkers such as CK-MB (CK specific to myocardial cells) or myoglobin are less specific to MI.

What is unstable angina?

Unstable angina is characterized by chest pain that is not relieved by rest or nitroglycerin. It does NOT have positive biomarkers because cells are not dying (yet), but ECG changes such as ST depression and/or T wave inversion may be present.

Unstable angina is still worked up like an MI because it reflects significant vessel occlusion that MAY progress to an MI if untreated.

What is NSTEMI?

NSTEMI is a progression of CAD in which the coronary arteries are occluded enough by a thrombus to cause significant ischemia and cardiac infarction. However, the occlusion is still PARTIAL.

Characteristics of STEMI:

1) Biomarkers are always POSITIVE

2) ECG changes may show DEPRESSED ST segment and/or inverted T waves

3) Echocardiogram can reveal small areas of hypokinesis or akinesis in necrotic areas.

NSTEMI is differentiated from unstable angina because biomarkers are POSITIVE due to myocardial infarction. ECG changes will also show ST depression or T wave inversion.

What is STEMI?

STEMI is a total coronary artery occlusion due to a thrombus. This can cause severe and irreversible myocardial cell death, and it is the more severe form of MI.

Characteristics of STEMI:

1) Biomarkers are always POSITIVE

2) ECG changes show ELEVATED ST segment with possible T wave inversion

-An elevation of 1 mm (1 small box) or more in 2 or more contiguous leads is criteria for STEMI

-QRS complex may look inverted due to deep Q waves, which reflect lack of depolarization current in dead tissue, and ST elevation.

3) Lactic acid may be increased due to anaerobic metabolism in the heart

4) Echocardiogram can reveal WIDESPREAD hypokinesis (less contraction) or akinesis (NO contractions) of necrotic areas.

What is meant by "contiguous leads"?

Leads are grouped based on regions of electrical activity that they read.

What is the influence of collateral circulation on MI?

Heart cells can only survive for 20 minutes without oxygen, and the damage is irreversible if there is no collateral circulation to support the heart in place of the occluded coronary artery. More collateral circulation = Less severe MI.

What is the progression of an MI?

Necrosis always spreads from inside-out since coronary arteries supply the inner layers of the heart first.

1) For STEMI, the entire full thickness of the affected area is necrotic in up to 4-6 hours

2) For NSTEMI, the entire full thickness of the affected area is necrotic in up to 12 hours.

What are the clinical manifestations of an MI?

1) Severe chest pain not relieved by rest, position change, or nitrates

-Often occurs in the morning

-Women and people with DM are more likely to not present with chest pain

2) Signs associated with SNS activation, including diaphoresis, increased HR/BP, vasoconstriction of peripheral blood vessels (reflected by cool, clammy skin).

3) Nausea/vomiting

4) Fever, which develops over 24-48 hours can can last for 4-5 days due to inflammation caused by heart cell death

VOMIT MNEMONIC

Use this IN ORDER OF THE MNEMONIC for any suspected cardiac related complaints:

1) Assess responsiveness, pulse, and breathing. If pulseless, initiate defib/CPR. Then perform quick scan of ABCs.

2) V - Take vitals and establish telemetry

-May consider doing focused OPQRST and cardiopulmonary assessment, but do not delay interventions if patient is unstable.

2) O - Apply O2 if

How should chest pain be assessed? What diagnostics? Nursing interventions?

Nursing Assessment: See VOMIT term

Diagnostic studies:

1) 12-lead within 10 minutes for ALL chest pain followed by continuous telemetry

2) Obtain baseline CBC, BMP, coagulation panel, and CARDIAC BIOMARKERS such as cardiac troponin for ALL chest pain

3) Obtain CXR, which can R/O aortic aneurysm/dissection

-ECHO and CT angiography might be done as well

4) Fibrinolytic checklist

Nursing interventions:

1) Give aspirin, opioid analgesia, and nitroglycerin if no contraindications

2) Implement the same strategies used for chronic stable angina to decrease O2 demand.

3) If BP unstable, give fluids

What is medical management for all MIs?

1) Definitive treatment: PCI and balloon catheter within 90 minutes of presentation.

-Fibrinolytics within 30 minutes of presentation may be considered if the expected door-to-PCI time is >120 minutes.

2) Anticoagulation is established before PCI. It must be maintained after PCI due to increased clot risk.

3) Antiarrhythmics including amiodarone, beta blockers, and calcium channel blockers are used to maintain normal HR/BP/cardiac rhythm in the long-term.

-ARBs and ACEis may also be added for further prevention of ventricular remodeling

What is criteria and contraindications for fibrinolytic therapy in the context of MI?

Inclusion criteria:

1) Chest pain >15 minutes and < 12 hours

2) 12-lead shows STEMI

3) Estimated door-to-PCI time is >120 minutes.

4) No contraindications

Absolute contraindications (patient is disqualified without question):

1) Prior intracranial hemorrhage EVER or significant head trauma within 3 months

2) Known cerebral vascular lesion or brain tumor

3) Ischemic stroke within 3 months (except acute stroke

What should you assess during fibrinolytic therapy?

1) VS

2) ST segment changes

3) Reperfusion dysrhythmias:

-Benign: Accelerated idioventricular rhythms, minimal PVCs, short runs of VTach, and sinus bradycardia (if stable)

-BAD: Frequent PVCs, sustained VTach, high degree AV blocks, and VFib.

4) Heart/lung sounds

5) Neurologic status and CSMs

What are signs of failed reperfusion after fibrinolytic therapy? What to do after fibrinolytic administration?

Signs of failed reperfusion or re-occlusion:

1) Ongoing or returning ischemic symptoms despite drug administration

2) Persistent or returning ST-segment elevation

3) Hemodynamic or electrical instability

What to do after:

1) In the case of suspected failed reperfusion, you should immediately initiate CT angiography with rescue PCI.

2) In the case of successful reperfusion, you should still initiate early angiography with intent to perform PCI within 2-24 hours of drug administration.

What education to provide patients after fibrinolytic therapy?

Be cautious of injuries and bleeding d/t increased risk of bleeding

How is Inferior Wall MI and RV MI treated differently from LV MI?

40% of all MIs involve the inferior wall, with half of those also having associated right ventricular involvement as well. For these patients:

1) NO NITROGLYCERIN. WE NEED HIGH PRELOAD Reducing venous tone will definitely cause BP to crash since these patients already have a hard time moving blood from veins.

2) Instead, provide IV fluid bolus and possible vasopressors to encourage venous vasoconstriction and keep pre-load high.

Discharge education for a patient after an MI and appropriate referrals?

Educate on:

1) S/S that would indicate another MI and the importance of activating EMS quickly in such a case

2) Modifiable risk factors such as diet (glucose and fat control), obesity, smoking, exercise, and managing BP

3) New medications that are prescribed, including anticoagulants, antiplatelets, lipid reducers, stool softeners, and anti-hypertensives and importance of compliance.

-Important to teach about orthostatic hypotension and necessity of getting up slowly

4) Instill appropriate expectations about recovery and rehabilitation and the importance of gradual, progressive resumption of activity.

Appropriate referrals:

1) Outpatient or home-based cardiac rehab program

2) Dietitian to help with healthy diet

3) Community support groups or therapist

Factors affecting cardiac output: Preload

Decreases:

1) Venous vasodilators, such as nitrates and OPIOIDS

2) Diuretics, which increase urinary excretion

3) PEEP, which increases intrathoracic pressure and inhibits venous return

Increases:

1) Fluids

2) Colloids

3) Crystalloids

4) Blood

Factors affecting cardiac output: Afterload

Decreases:

1) Beta blockers and calcium channel blockers

2) ACEi/ARB

3) Arterial vasodilators like hydralazine

4) ANP/BNP in CHF → vasodilation

5) Aortic balloon for aortic stenosis (percutaneous transluminal balloon valvuloplasty)

Increases:

1) Hypertension

2) Smoking (vasoconstriction)

3) Atherosclerosis (narrows arteries)

4) Sympathomimetics/Inotropes (Epi/NE/DA/Midodrine)

Factors affecting cardiac output: Contractility

Decreases:

1) Beta blockers → decrease SNS stimulation

2) Calcium channel blockers → decrease cardiac cell depolarization

Increases:

1) Inotropes including Epi/NE, dobutamine, and milrinone

2) Circulatory assist devices including Impella, VAD, intra-aortic balloon pump