NURS 471 Week 3: Acuter Coronary Syndrome and Code Blue

Immediate Actions

Obtain 12‑lead EKG within 10 minutes and get provider to sign/date/time interpretation.

Draw labs: troponin (expect normal 0–0.04), plus CBC, BMP, BNP for HF, coags.

Do full set of vital signs before everything else.

Assess pain with PQRST; ask radiation, provoking/relieving factors, severity, timing, and risk factors (smoking, HTN, hypothyroidism, female atypical symptoms).

Emergency Department Meds for Suspected Acute Coronary Syndrome

aspirin

nitroglycerin

morphine

heparin

plus a P2Y12 inhibitor (e.g., clopidogrel, prasugrel, ticagrelor).

Oxygen only if SpO₂ < 90%; do not give routine oxygen at 96–98% since it does not help and may be harmful.

Acute MI

defined as the presence of acute myocardial injury detected by abnormal cardiac biomarkers in the setting of evidence of acute myocardial ischemia.

Clinical MI classification

Types 1–5

Type 1: Atherothrombotic CAD with plaque disruption.

Type 2: O₂ supply–demand mismatch (vasospasm, dissection, severe anemia).

Type 3: Sudden death or classic ischemic changes/vfib without biomarker confirmation.

Type 4a/4b: MI related to PCI / stent thrombosis within 48 hours of procedure.

Type 5: CABG‑related MI within 48 hours post‑CABG.

MI Type 1

ACS leading to rupture of a plaque or erosion of a plaque

MI Type 2

Vasospasm or endothelial dysfunction

fixed atherosclerosis and supply-demand imbalance

supply-demand imbalance alone

Severe Anemia

MI Type 3

Sudden death or classic ischemic changes/vfib without biomarker confirmation.

Death happens without measuring biomarkers

MI Type 4a

MI associated with percutaneous coronary intervention (PCI)

MI Type 4b

MI related to stent thrombosis within 48 hours of PCI procedure

MI Type 5

CABG‑related MI within 48 hours post‑CABG.

Percutaneous Coronary Intervention (PCI)

(balloon angioplasty ± stent) done within 48 hours can define procedure‑related MI (Types 4a/b).

Hospital Care in an Acute Myocardial Infarction

•Pain relief

•Tests

•Anti-ischemic therapy

•Anti-thrombolytic Therapy

•Intervention

•Post intervention management

•Potential complications

Pre‑cath ED/hospital care

-Door‑to‑ECG < 10 minutes and door‑to‑balloon < 60 minutes for STEMI if cath lab available.

-If no cath lab, consider TPA/fibrinolytic if eligible to open the vessel.

Door‑to‑ECG

< 10 minutes

Door‑to‑balloon

< 60 minutes for STEMI if cath lab available.

Pre‑Procedure Nursing Care

Confirm patient understands the procedure and verify signed informed consent.

Obtain medication history and allergies, especially to contrast media, aspirin, clopidogrel.

Review routine pre‑procedure labs (e.g., creatinine, CBC, coags) and report abnormal values.

Ensure adequate hydration to reduce contrast‑induced nephrotoxicity risk.

Establish IV access with fluids at KVO rate.

Document baseline peripheral pulses (radial, brachial, femoral) using 0–4 scale.

What happens in the Cath lab

Transluminal coronary angioplasty: guidewire → sheath → catheter under fluoroscopy to coronary arteries; dye injected to visualize blockages (angiograms).

Balloon‑tipped catheter inflated at the lesion: pushes plaque against wall; plaque remains but lumen widens.

Patients may feel flushing or nausea when dye injected, and chest discomfort during balloon inflation (same symptoms that brought them in).

DES LAD: drug‑eluting stent deployed in LAD for anterior MI; stent props artery open permanently after balloon removal.

Post‑stent: repeat 12‑lead EKG to confirm ST‑segment elevation has improved.

Patient remains awake but receives analgesics and sedatives to keep comfortable.

Peri-Procedure Monitoring and Vasovagal Reactions

Continuous monitoring of vital signs and pulse oximetry during procedure.

Assess for chest pain, shortness of breath, signs of bleeding, rhythm changes, and ST/T‑wave abnormalities.

Monitor neurologic status and peripheral vascular status (especially access limb).

Watch for vasovagal reactions during sheath insertion/removal: BP and HR drop, dizziness, nausea, vomiting.

Treat vasovagal episode with IV fluids and atropine per ACLS until HR/BP normalize.

Post-Procedure Monitoring: ischemia, thrombosis, bleeding

Monitor for myocardial ischemia and thrombosis: chest pain, ST‑segment changes (especially new elevation), and dyspnea.

Vital sign changes: ↓ SpO₂, ↓ BP, HR up or down.

Assess for dysrhythmias and hemodynamic compromise; common rhythms post‑PCI: ventricular tachycardia, atrial bradycardia, heart blocks.

Watch for bleeding: hematuria, insertion‑site oozing, or bleeding from other orifices.

Hematoma at insertion site suggests local/internal bleeding, especially femoral approach.

Retroperitoneal bleeding is the most common serious internal bleed with femoral access; track vitals and Hgb/Hct.

Monitor platelets, particularly with GP IIb/IIIa inhibitors or tPA, which can cause thrombocytopenia.

If bleeding occurs, apply manual pressure or use a closure clamp/device over site.

PCI Access Preferences and Closure Devices

Two main approaches: femoral and radial.

Radial approach is preferred over femoral in ACS PCI.

Femoral: risk of brisk arterial bleeding; manual pressure is physically demanding; FemStop device helps maintain pressure and requires frequent leg circulation checks.

After femoral access: keep leg straight and maintain bedrest 4–6 hours until hemostasis.

Early sheath removal reduces vascular complications.

Radial: patients return with TR band on wrist; they can sit up and move arm but must avoid flexing wrist; band is gradually deflated over ~60 minutes while monitoring for bleeding.

Monitor for peripheral thrombosis/ischemia in accessed limb; any change in pulses from pre‑procedure baseline must be reported promptly.

Complications of Acute Coronary Syndrome

Heart Failure

Cardiogenic Shock

Dysrhythmias

Pericarditis

HF after MI

Types: Systolic and Diastolic

Common etiologies post‑MI:

-LV dysfunction from poor blood supply and decreased wall motion.

-Intraventricular septal rupture.

-Papillary muscle rupture causing acute valvular regurgitation.

-Right ventricular infarction.

Heart failure after ACS may present as reduced contractility, pulmonary congestion, and poor forward flow.

All decrease effective cardiac output.

HFrEF

heart failure with reduced ejection fraction

EF less than about 35-40%.

HFpEF

heart failure with preserved ejection fraction

EF above about 40-50%.

Cardiogenic Shock

Leading cause of death among ACS complications; mortality 50–60% even with maximal therapy.

Often occurs when ≥ 40% of LV is damaged.

Assessment findings: tachycardia, hypotension, urine output < 0.5 mL/kg/hr, cold clammy skin, agitation.

Dysrhythmias

Occur in up to 95% of MI patients and are frequent cause of post‑MI mortality.

Anterior MI: associated with serious dysrhythmias; catecholamine surge → sinus tachycardia, SVTs (AFib, atrial flutter, PAT, accelerated junctional rhythms) and ventricular irritability.

Hypokalemia is a common cause of ventricular irritability; replace K⁺ if < 3.5 mEq/L.

Inferior/posterior MI: associated with bradycardia and heart block because of RCA/SA node involvement in some patients; parasympathetic response → nausea, vomiting, hypotension, bradycardias, junctional escape rhythms.

AV Blocks

First‑degree and second‑degree type I: often with inferior MI, usually transient; often need no treatment.

Second‑degree type II: more common with anterior/anteroseptal MI.

Third‑degree (complete) block: occurs with inferior and anterior MI; less common but indicates large LV damage and is life‑threatening.

Second‑ and third‑degree blocks often require a temporary pacemaker until they resolve or permanent pacing is placed.

Pericarditis and Post‑Pericardiotomy

Pericarditis: inflamed pericardium with chest pain and ECG changes; pain is anterior, can radiate to abdomen/arms/back, worsens with inspiration and improves leaning forward.

Post‑pericardiotomy syndrome after cardiac surgery: pericarditis plus low‑grade fever, pericardial effusion, pleuritis, leukocytosis; thought autoimmune.

Often associated with pericardial friction rub; appears days–weeks after MI or surgery; often self‑limited but treated with ASA, NSAIDs, corticosteroids for pain/inflammation.

CABG Indications

Bypasses diseased coronary arteries using saphenous vein, internal mammary artery, or radial artery.

Indicated when:

PCI/PTCI fails.

>70% stenosis of three major coronaries.

>50% left main stenosis.

Mild–moderate LV dysfunction (LVEF 35–50%) with proximal LAD disease.

Multivessel CAD with diabetes mellitus.

CABG patients go directly from OR to ICU (not PACU) with ventilator, multiple lines, chest tubes; need pre‑op teaching about tubes/ventilator and inability to speak.

Teach sternal precautions: hugging pillow to splint, no pushing off bed/chair, avoid lifting > 10 lb, 6‑week healing similar to a broken bone.

Postop chest tubes drain blood and air; drainage amount and air leaks must be monitored closely.

Post‑ACS Pharmacology and Guidelines

•Dual antiplatelet therapy (Ticagrelor or prasugrel) and Aspirin 12 months or longer

•High-intensity statin therapy is recommended for all patients with ACS, and with the option to initiate concurrent ezetimibe. A nonstatin lipid-lowering agent (eg, ezetimibe, evolocumab, alirocumab) is recommended for patients already on maximally tolerated statin who have a low-density lipoprotein cholesterol level of ≥70 mg/dL (1.8 mmol/L).

•Two procedural strategies are recommended in patients with ACS who are undergoing PCI: (a) radial approach is preferred over femoral approach in patients with ACS.

At discharge Referral to cardiac rehabilitation

Aspirin

81-325 mg/day indefinitely, unless contraindicated; reduces MI, stroke, vascular death. Monitor platelets and bleeding.

Beta blockers

continued long‑term reduces mortality by ~23%; choose cardioselective vs mixed based on comorbidities; monitor HR, BP, HF signs, hypoglycemia masking.

ACE inhibitors

reduce afterload, prevent remodeling, lower BP and stroke risk; monitor BP, creatinine, Na⁺, K⁺, and cough.

Statins

increase HDL, reduce LDL/total cholesterol; monitor LFTs, muscle pain, INR if on warfarin; avoid grapefruit juice.

Nitroglycerin

dosing regimens for SL, patch, and ointment; counsel on sitting/lying before dose and storage; monitor for hypotension and headaches; absolutely avoid with erectile‑dysfunction meds due to hypotension risk.

Takotsubo Cardiomyopathy (Broken Heart Syndrome)

Japanese origin of the name: resemblance to a Japanese octopus pot.

Typical presentation: chest pain, ECG changes, elevated troponin, dyspnea, nausea, weakness, and possible heart failure/shock symptoms despite no obstructive coronary stenosis on angiography.

Key pathophysiology point: transient left ventricular apical ballooning with reduced contractility and reduced EF without coronary stenosis.

Coronary Arteries Are Clear.

90% of diagnosed patients described as postmenopausal women.

About 1–2% of women presenting with suspected MI may actually have broken heart syndrome.

Takotsubo Cardiomyopathy: Common Trigger

acute emotional or physical stress.

Takotsubo Cardiomyopathy: Nursing/clinical management

Treat according to severity, like heart failure/cardiogenic shock supportive care.

Most cases resolve within about 4 weeks.

Supportive care, monitor for heart failure and cardiogenic shock due to decreased LV contractility, reduce stress, and follow-up echocardiogram in 4-6 weeks because many cases resolve

Management Post Cardiac Arrest

First steps: call for help, assess responsiveness, confirm pulselessness, and begin high-quality CPR.

Once the defibrillator is available, attach pads, identify the rhythm, and treat shockable rhythms such as VF/pulseless VT with defibrillation.

Biphasic shock commonly 120-200 J depending on device; monophasic 360 J.

After each shock, resume CPR immediately for 2 minutes/5 cycles before rhythm reassessment. Defibrillate again if still shockable.

Epinephrine 1 mg IV is given during pulseless arrest management and repeated every 3-5 minutes. Do not stop CPR.

For persistent shockable rhythms, antiarrhythmics discussed were amiodarone or lidocaine. Amiodarone dose in code mentioned as 300 mg. (Torsades treatment mentioned: magnesium; Torsades treatment mentioned: magnesium).

If VF recurs after bradycardia scenario, defibrillate again at same or higher effective dose.

High-quality CPR was emphasized, including correct rate and consistent compressions.

Targeted Temperature Management (TTM)

Was previously called therapeutic hypothermia.

It is active treatment to achieve and maintain a target temperature, commonly 32°C to 36°C.

The goal is preservation of neurologic function after cardiac arrest.

Mechanism: slows cerebral metabolism, decreases oxygen consumption, and lessens cerebral edema.

Targeted Temperature Management: Post Cardiac Arrest

Initiated once a patient in cardiac arrest returns to a sinus rhythm or Return of Spontaneous Circulation (ROSC).

It is the controlled regulation of a patient's core temperature (typically 32-36 °C) for a period of time after return of spontaneous circulation following cardiac arrest to improve neurologic outcomes and prevent fever.

It was found that cooling improved neurologic outcomes and increased favorable discharge outcomes in post-arrest patients.

Every hour delay in cooling increased the risk of death by 20%.

If the post-arrest patient is not following commands, or if neurologic status is uncertain, targeted temperature management should be considered.

Ongoing post-arrest critical care also includes optimization of oxygenation, hemodynamics, and evaluation for coronary angiography when indicated.

Outcomes vary: full recovery, severe anoxic brain injury, or failure to awaken.

Post Cardiac Arrest Care

Cardiac arrest → initial brain injury → reperfusion → additional brain injury → compromised neurological function.

Cardiac arrest causes decreased systemic perfusion and decreased cerebral oxygen delivery, leading to anoxic brain injury and cerebral edema.

Reperfusion after ROSC can worsen cerebral edema, alter inflammatory response, and contribute to further neurologic injury.

Temperature Management Overview

Induction phase: first 0-8 hours, with emphasis on cooling as early as possible.

Maintenance phase: maintain the target temperature for about 24 hours.

Rewarming phase: rewarm slowly, around 0.25°C/hour, until target temp is achieved. Target time is 48hrs.

ICU Management TTM

This patient is managed 1:1 during TTM.

Core temperature monitoring may be via urinary catheter probe or rectal probe.

Mild sedation may be required, and shivering must be prevented because it increases metabolic demand.

Expected systemic effects discussed in lecture include bradycardia, hypotension, decreased GI motility, and renal/metabolic/hematologic changes.

Hyperthermia/fever should be treated aggressively because it worsens neurologic injury risk.

Highlights of the 2025 American Heart Association Guidelines

•2025 (New): In-hospital code teams should comprise members with ALS training. Designated or dedicated code teams with clearly defined roles, diverse expertise, and adequate training that incorporates simulation can be beneficial in improving patient outcomes following IHCA.

•2025 (New): EMS systems should be prepared to perform termination of resuscitation on scene; this involves EMS professionals receiving training on death notification.

2025 (New): Institutions should develop systems of care focused on facilitating and evaluating organ donation after cardiac arrest consistent with local legal and regulatory requirements.

•2025 (New): In adult patients with persistent hemodynamically unstable bradycardia refractory to medical therapy, temporary transvenous pacing is reasonable to increase heart rate and improve symptoms.

•2025 (New): In highly selected adult patients with refractory cardiogenic shock after cardiac arrest and ROSC, temporary mechanical circulatory support may be considered.

•2025 (New):Special populations : pregnant, opioid OD, LVAD

•2025 (New):Team, training, technology