CCRN Cardiovascular: ACS/Dysrrhythmias

What is ACS? What are the three (3) types?

Acute coronary syndrome- results from sudden reduction or blockage of blood flow to myocardium.

Three types: Unstable angina, Non-ST Elevated Myocardial Infarction (NSTEMI), and ST-Elevated Myocardial Infarction (STEMI)

Explain general ACS pathophysiology.

1. Starts with rupture of atherosclerotic plaque in a coronary artery- triggers platelet aggregation and adhesion, thrombin activation and fibrin formation, vasoconstriction and thrombus propagation

2. Results in in partial or total occlusion blocking coronary artery, reducing O2 and nutrients

Explain the 3 ACS type pathophysiology

1. UA- partial occlusion of coronary artery, but no myocardial necrosis- biomarkers (troponin/CK-MB) stay normal, ischemic symptoms present

2. NSTEMI- partial occlusion accompanied by elevated troponin, no ST elevation on ECG (infarctio n is subendocardial, or not full thickness)

3. STEMI- complete occlusion with ST elevation on ECG, needs immediate reperfusion therapy to save myocardium and prevent death

Key Differences (Chart): Type/ Biomarkers/ ECG findings/ Degree of Occlusion

UA- Normal Biomarkers/ ST depression, T-wave inversion/ partial, transient occlusion

NSTEMI- Elevated Biomarkers/ ST depression, T-wave inversion/ Partial, prolonged occlusion

STEMI- Elevated Biomarkers/ ST elevation, Q waves/ Complete

Signs/Symptoms

1. Mostly have some form of chest discomfort, can be atypical (older adults, diabetics, women)

2. Chest pain/pressure- retrosternal, may radiate to L arm, neck, jaw or back- crushing, squeezing, or heavy. Lasts ~20 mins, not relieved by rest or nitro

3. SOB (may also indicate HF/ pulmonary congestion)

4. Diaphoresis

5. Nausea/vomiting/anxiety or syncope- frequently reported in inferior wall MI

6. Fatigue/weakness

S/S: ECG Findings/ Diagnostics

1. ST elevation > 1mm = STEMI (transmural infarction)

2. ST depression = NSTEMI/ UA

3. T wave inversion = ischemia/ evolving infarct

4. Q waves (late sign) = Previous infarction or late STEMI

5. New LBBB = may be equivalent to STEMI

ST elevation on continuous leads + rise in troponin = STEMI > needs urgent PCI or thrombolytics

ST depression or T wave inversion + troponin rise = NSTEM > non-emergent PCI, medical therapy

Lab Markers/Tests

1. Troponin I/T (most specific) - rises 3-6 hours after symptom onset. Peaks at 12-24 hours, may stay elevated for 7-10 days. Elevated in NSTEMI/STEMI, normal in UA.

2. CK-MB (less specific)- rises earlier but returns normal faster. Can indentify reinfarction

3. BNP or NT-proBNP- may be elevated of LV dysfunction or HF is present

*If trop is negative, but symptoms persist and ECG suggestive of ischemia, repeat lab Q6 hours to capture delayed elevation

4. CXR- r/o other causes of chest pain (pneumothorax, aortic dissection)

5. Echocardiogram- may show wall motion abnormalities in affected area

6. Coronary angiography (LHC)- definitive test for dx and tx

Goal of Treatment/ Initial Tx

Goal: relieve ischemia, restore perfusion, and prevent further thrombus formation or myocardial damage.

Initial tx: MONA

1. Morphine- provides analgesia, reduces anxiety, and decreases sympathetic tone. Reduces preload via venodilation. Can cause hypotension or RV infarct

2. Oxygen- only administer if SpO2 <90%, respiratory distress is present or signs of hypoxemia present.

3. Nitrates- sublingual or IV can relieve CP and reduce preload. Contraindicated to those w/ hypotension, bradycardia, or recent use of phosphodieterase inhibitors (Sildenafil).

4. Aspirin- give immediately unless contraindicated (recent GIB/true allergy). Use 162-325 to inhibit platelet aggregation.

Reperfusion Strategies

1. PCI (Percutaneous Coronary Intervention)- Gold Standard in STEMI if available within 90 minutes (door-to-balloon time). Also considered in high risk NSTEMI

2. Thrombolytics (fibrinolytics)- Used only in STEMI if PCI unavailable within time frame. Most effective within 3 hourse of symptom of onset. Contraindicated in recent surgery, bleeding disorders, or stroke

3. NSTEMI/UA- medically managed first, the assess risk for need for PCI

Antithrombotic & Anti-Ischemic Therapy

Antiplatelets-

1. Asa- continue indefinitely

2. P2Y12 inhibitors (Clopidogrel/ticagrelor)- added to asa for dual anti-platelet therapy (DAPT), especially post-PCI

Anticoagulants

1. Heparin- reduced clot propagation

2. Bivalirudin/fondaparinux

Beta-Blockers

1. Reduce myocardial O2 demand by decreasing HR and BP

2. Contraindicated in acute decomp. HF, bradycardia, or severe hypotension

Statins

1. Started early regardless of cholesterol level. High intensity statin therapy improves outcomes

ACE Inhibitors/ARBS

1. Started within 24 hours if LV dysfunction, HF or anterior MI present

Nursing Priorities

1. Monitor for recurrent CP or ECG changes

2. Serial troponins to assess infarct progression

3. Continuous telemetry for arrhythmias

4. Watch for signs of bleeding if thrombolytics or anticoagulants are used

5. Educated pts on importance of medication adherence and risk factor modification

Complications (3 Major)

A. Arrhythmias- most common

1. Ventricular- VT/VF, common in first 48 hours most-MI d/t myocardial irritability. Defib if pulseless

2. Bradyarrhythmias- seen especially in inferior wall MI d/t AV node ischemia, may require atropine or pacing

3. Afib- may occur from atrial ischemia or increased left atrial pressure; can compromise cardiac output of rapid or persistent

4. PVCs- may precede more serious arrhythmias, monitor closely

B. Pericarditis- inflammation of pericardial sac following MI

1. Typically occurs 2-4 days post-MI (early) or weeks later (Dressler’s syndrome)

2. Pleuritic CP (worse when lying down), pericardial friction rub, and diffuse ST elevation on ECG (not localized like in STEMI)

3. Tx include NSAIDs for inflammation and pain, avoid AC unless strongly indicated, d/t bleeding risk. | *recognize pattern as it can mimic reinfarction, but different ECG pattern and tx approach

C. Pappilary Muscle Rupture- rare but catastrophic mechanical complication, typically occuring within 3-7 days post-MI, spec. an inferior MI > post papillary muscle

1. Leads to acute mitral regurgitation > sudden pulmonary edema, hypotension, cardiogenic shock

2. Physical exam may reveal new, loud systolic murmur at apex, often accompanied by signs of Left HF.

3. DX confirmed by echo

4. Requires urgent surgical intervention- mortality extremely high w/o repair

5. HF and cardiogenic shock- d/t to large size of infarct and poor contractibility

6. Ventricular septal rupture- causes new harsh systolic murmur and biventricular failure

7. Left ventricular aneurysm- may form weeks after MI, can lead to embolic events or HF

*If post-MI pt develops hypotension, dyspnea and new murmur > think papillary muscle rupture or vent. septal defect | If chest pain with diffuse ST elevation and friction rub > pericarditis

Explain dyshythmia pathology

• Result from disturbances from hearts electrical conduction system. They may involve the following:

  • Automaticity- cells firing when they shouldnt (ectopic pacemakers in VT)

  • Conductivity- failure or delay in signal transmission (i.e. AV blocks)

  • Reentry circuits; impulses looping repeatedly through cardiac tissue (i.e. SVT)

• Can also result from underlying myocardial ischemia, electrolyte imbalances (esp. in K/Mg/Ca levels), hypoxia, or medication effects (digoxin, antiarrythmics)

• Common precipitating factors include acute coronary syndrome, heart failure, and post cardiac surgery states.

What can arrhythmias affect and how?

It can affect cardiac output by increasing or decreasing heart rate, reducing stroke volume (loss of atrial kick in afib) or cause uncoordinated contractions (V-fib)

Explain pathophysiology of the following key rhythms: Tachyarrhythmias (SVT/VT)/, Bradyarrhythmias (Sinus Bradycardia/ High grade AV blocks), Pulseless rhythms (VF/Pulseless VT/ asystole/PEA), Atrial arrhythmias (A-fib/flutter), Heart Blocks

• Tachyarrhythmias- increase myocardial O2 demand, reduce ventricular filling time = decrease in CO, increase ischemic risk

• Bradyarrhythmias- slow HR = decrease in CO → HYPOperfusion

• Pulseless Rhythms- No effective circulation, requires ACLS protocols

• Atrial arrythmias- loss of atrial kick = decrease in preload, risk of thromboembolism

• Heart blocks- delay/block signal from atria to ventricles → bradycardia of AV dissociation, depending on type

Signs/Labs (General/Brady/Tachy)

• Hemodynamic instability

• Altered mental status

• Based on HR, rhythm origin, and impact on cardiac output

• Bradycardia (HR <60 BMP)

  • Fatigue, dizziness, lightheadedness

  • Syncope/presyncope

  • Hypotension, especially in high AV grade block/SN dysfunction

  • Possible altered mental status → drop in cerebral perfusion

• Tachycardia (HR >100 BPM)

  • Palpitations, anxiety, chest discomfort

  • SOB → decreased filling time

  • Hypotension/signs of hypoperfusion

  • Syncope if unstable/poorly tolerated rhythms

• Syncope/sudden colllapse

  • Seen in VT, complete HB, torsades, VF

  • Always investigate arrhythmic causes in unexplained syncope in ICU pts

• Pulses may be weak/irregular and perfusion markers (urine output, cap refill may deteriorate)

ECG Patterns: VT

• Wide QRS complex (>0.12 sec), regular rhythm

• May have pulse or pulseless

• Monomorphic or polymorphic (Torsades)

ECG Patterns: VF

• Chaotic, irregular no identifiable waves

• No cardiac output → immediate defibrillation required

ECG Patterns: SVT

• Narrow QRS

• HR >150

• P waves often hidden in T waves

• Sudden onset and termination

ECG Patterns: Afib/Aflutter

Afib

• Irregularly irregular rhythm

• No discernable P waves, variable ventricular response

• Risk of thromboembolism

Aflutter

• Sawtooth flutter waves (best seen in leads II, III, aVF)

• Ventricular rate often REGULAR and FAST (2:1 or 4:1 conduction)

ECG Patterns: AV Blocks

First Degree

• Prolonged PR interval (>0.20 sec)

Second Degree Mobitz I

• Wenkebach)- Progressive PR prolongation → dropped beat

• Longer, longer, longer, drop, now we have a Wenkebach

Second Degree Mobitz II

• Dropped beats WITHOUT PR change

Third Degree (Complete)

• Atria and ventricles beat independently (AV dissociation)

• If your P’s and Q’s dont agree, now you have a third degree

Rhythm Insight: What to look for

• Assess rate and regularity, QRS width, P wave presence, and PR interval

• Is this rhythm perfusing the patient? What is the immediate intervention?