Cardiac & Respiratory Nursing

Left ventricle fails to pump blood forward → blood backs up into pulmonary circulation. Symptoms: dyspnea, orthopnea, paroxysmal nocturnal dyspnea (PND), crackles/rales on auscultation, pink frothy sputum (pulmonary edema), tachycardia, S3 gallop, fatigue, decreased urine output. Elevated BNP (>100 pg/mL). CXR: pulmonary congestion, cardiomegaly. Most common cause: CAD, hypertension. Think 'Left = Lung.'

Right ventricle fails → blood backs up into systemic venous circulation. Symptoms: jugular venous distension (JVD), peripheral/dependent edema, ascites, hepatomegaly (liver engorgement), weight gain, anorexia/nausea. Most common cause: LEFT-sided heart failure. Other causes: COPD (cor pulmonale), PE, pulmonic stenosis. Treatment: diuretics, fluid/sodium restriction, ACE inhibitors/ARBs, beta-blockers, daily weights. Think 'Right = Rest of body.'

Daily weights (same time, same scale — report gain >2 lbs/day or 5 lbs/week). Low sodium diet (<2 g/day). Fluid restriction (1.5-2 L/day if severe). I&O monitoring. Elevate HOB. O2 as needed. Medications: ACE inhibitors, beta-blockers (carvedilol, metoprolol succinate), diuretics, digoxin, aldosterone antagonists (spironolactone). Activity: regular low-intensity exercise as tolerated. Teach: monitor for edema, weigh daily, report dyspnea, medication compliance, avoid NSAIDs (fluid retention).

Assessment: crushing substernal chest pain (may radiate to jaw, left arm, back), diaphoresis, N/V, dyspnea, anxiety, denial. Women/diabetics/elderly: may present atypically (fatigue, indigestion, jaw pain). ECG: ST elevation (STEMI) or depression (NSTEMI), T-wave inversion. Troponin elevated (rises 3-6 hrs, peaks 12-24 hrs). Immediate interventions — MONA (modified): Morphine (if pain unrelieved), Oxygen (only if SpO2 <94%), Nitroglycerin (SL), Aspirin (162-325 mg chewed). Activate cath lab for STEMI (door-to-balloon <90 min).

Bed rest → progressive activity. Continuous cardiac monitoring (watch for arrhythmias — #1 cause of death in first 24 hrs). Serial troponins and ECGs. Medications: dual antiplatelet therapy (aspirin + P2Y12 inhibitor), statin, ACE inhibitor, beta-blocker. Monitor for complications: cardiogenic shock, heart failure, ventricular arrhythmias, papillary muscle rupture (new murmur), ventricular septal defect, Dressler syndrome (pericarditis weeks later), cardiac tamponade. Cardiac rehab referral. Teach: lifestyle modification, when to call 911.

Rate: 60-100 bpm. Regular rhythm. P wave before every QRS, QRS after every P. P-R interval: 0.12-0.20 sec (3-5 small boxes). QRS duration: <0.12 sec (<3 small boxes). Each small box = 0.04 sec, each large box = 0.20 sec. P waves upright and uniform in Lead II. Isoelectric baseline between beats. Calculating rate: 300 / # of large boxes between R-R intervals (regular rhythm) or count R waves in 6-second strip x 10 (irregular rhythm).

ECG: irregularly irregular rhythm, no identifiable P waves (fibrillatory baseline), variable R-R intervals, narrow QRS (unless aberrant conduction). Rate: can be rapid (>100 = afib with RVR) or controlled. Risk: blood stasis in atria → thrombus → stroke. Management: rate control (beta-blocker, diltiazem, digoxin), rhythm control (amiodarone, cardioversion), anticoagulation (CHA2DS2-VASc score determines need — DOACs or warfarin). If onset <48 hrs: may cardiovert. If >48 hrs: anticoagulate 3 weeks before cardioversion or rule out clot with TEE.

V-Tach: wide QRS (>0.12 sec), regular, rate 150-250 bpm, no identifiable P waves. If pulseless: treat as Vfib (defibrillation). If pulse present: stable → amiodarone or lidocaine; unstable → synchronized cardioversion. V-Fib: chaotic, no organized rhythm, no identifiable waves, no pulse. Immediately fatal if untreated. Treatment: CPR + defibrillation (unsynchronized shock) ASAP. ACLS: CPR → shock → epinephrine 1 mg q3-5 min → shock → amiodarone 300 mg → shock → amiodarone 150 mg. Continue CPR between interventions.

1st degree: prolonged PR interval >0.20 sec, all P waves conducted — benign, monitor only. 2nd degree Type I (Wenckebach): progressive PR prolongation until a QRS is dropped — usually benign. 2nd degree Type II (Mobitz II): constant PR interval with suddenly dropped QRS — dangerous, may progress to 3rd degree, may need pacemaker. 3rd degree (complete): no relationship between P waves and QRS complexes (AV dissociation) — atria and ventricles beat independently. Requires transcutaneous pacing → permanent pacemaker. Treat symptomatic bradycardia with atropine first.

Pre: assess allergies (contrast dye, shellfish/iodine — may need premedication), NPO 6-8 hrs, baseline peripheral pulses (mark with marker), labs (BUN/Cr — contrast is nephrotoxic, PT/INR), consent, IV access, remove jewelry. Post: bedrest with affected extremity straight (femoral: 4-6 hrs; radial: 1-2 hrs). Monitor: site for bleeding/hematoma (apply pressure if bleeding), circulation of affected limb (5 P's: pain, pallor, pulselessness, paresthesia, paralysis), VS q15 min x 4 → q30 min x 2 → q1h. Hydrate to flush contrast (monitor I&O). Report: chest pain, back pain (retroperitoneal bleed), loss of pulse.

Mitral stenosis: narrowed mitral valve → impaired filling of LV. Causes: rheumatic heart disease (#1). Symptoms: dyspnea, fatigue, afib, hemoptysis, rumbling diastolic murmur. Mitral regurgitation: mitral valve doesn't close fully → blood leaks back to LA during systole. Causes: MI (papillary muscle dysfunction), endocarditis, mitral valve prolapse. Symptoms: dyspnea, fatigue, high-pitched blowing systolic murmur radiating to axilla. Both lead to left atrial enlargement → pulmonary congestion → right heart failure eventually. Treatment: medical management, valve repair/replacement.

Narrowed aortic valve → LV outflow obstruction. Classic triad: syncope, angina, dyspnea on exertion. Harsh systolic crescendo-decrescendo murmur at right upper sternal border, radiating to carotids. Causes: calcific degeneration (elderly), bicuspid valve (younger). Leads to LV hypertrophy → heart failure. Avoid strenuous activity (risk of sudden death). Monitor for heart failure symptoms. Treatment: surgical aortic valve replacement (SAVR) or transcatheter (TAVR). Post-valve replacement: anticoagulation (mechanical valve: lifelong warfarin, INR 2.5-3.5; bioprosthetic: short-term).

Normal: <120/80. Elevated: 120-129/<80. Stage 1 HTN: 130-139 or 80-89. Stage 2 HTN: >=140 or >=90. Hypertensive crisis: >180/120. Management: lifestyle first (DASH diet, sodium <2.3 g/day, exercise 150 min/week, limit alcohol, weight loss, smoking cessation). Medications: Stage 1: thiazide diuretic, ACE/ARB, or CCB. Stage 2: two-drug combination. African American patients: CCB or thiazide preferred initially. Diabetic or CKD: ACE or ARB (renoprotective). Teach: BP monitoring, medication compliance (no symptoms doesn't mean stop meds), avoid NSAIDs.

Both: BP >180/120. Hypertensive urgency: severely elevated BP WITHOUT target organ damage (headache, anxiety). Lower BP gradually over 24-48 hrs with oral meds. Hypertensive emergency: severely elevated BP WITH target organ damage (encephalopathy, stroke, MI, aortic dissection, pulmonary edema, acute kidney injury). Requires ICU, IV meds (nitroprusside, labetalol, nicardipine, nitroglycerin). Lower MAP by no more than 25% in first hour (too rapid → stroke, MI). Arterial line for continuous BP monitoring. Neuro checks frequently.

Indications: pneumothorax, hemothorax, pleural effusion, post-thoracic surgery. System: collection chamber, water seal chamber (2 cm H2O — should see tidaling with respirations; continuous bubbling = air leak), suction control chamber. Nursing care: keep system below chest level, maintain airtight connections, never clamp except for brief assessment, encourage coughing and deep breathing. Monitor drainage: report >100 mL/hr (hemorrhage). Assess for subcutaneous emphysema (crepitus). If disconnected: place tube end in sterile water. If pulled out: cover site immediately with petroleum gauze occlusive dressing taped on ALL 4 sides. Document drainage amount, color, and character.

Notify provider: drainage >100 mL/hr (hemorrhage), continuous bubbling in water seal chamber (persistent air leak), sudden cessation of drainage (possible clot/kink), subcutaneous emphysema increasing, signs of tension pneumothorax (tracheal deviation, absent breath sounds, hypotension, JVD), patient develops respiratory distress, change in drainage color (bloody → serous is expected; sudden return to bloody is not). After removal: monitor for recurrent pneumothorax (dyspnea, decreased breath sounds, CXR). Chest tube removal: end of expiration or during Valsalva maneuver.

Low-flow systems: Nasal cannula: 1-6 L/min (FiO2 ~24-44%, adds ~4% per liter). Simple face mask: 5-8 L/min (FiO2 40-60%) — minimum 5 L/min to prevent CO2 rebreathing. Partial rebreather: 6-15 L/min (FiO2 60-75%). Non-rebreather: 10-15 L/min (FiO2 80-95%) — keep reservoir bag inflated. High-flow systems: Venturi mask: precise FiO2 (24-50%) — best for COPD. High-flow nasal cannula (HFNC): up to 60 L/min, FiO2 21-100%.

CPAP (Continuous Positive Airway Pressure): delivers constant pressure during inhalation AND exhalation. Keeps alveoli open. Indications: obstructive sleep apnea, acute pulmonary edema. One pressure setting. BiPAP (Bilevel Positive Airway Pressure): delivers higher pressure on inhalation (IPAP) and lower on exhalation (EPAP). Easier to exhale against. Indications: COPD exacerbation, neuromuscular disease, sleep apnea intolerant of CPAP. Both are non-invasive ventilation. Contraindications: unprotected airway, facial trauma, vomiting, hemodynamic instability. Monitor for gastric distension, skin breakdown from mask.

Normal values: pH 7.35-7.45, PaCO2 35-45 mmHg, HCO3 22-26 mEq/L, PaO2 80-100 mmHg, SaO2 >95%. Step 1: Look at pH (acidosis <7.35 or alkalosis >7.45). Step 2: Check PaCO2 — if abnormal and matches the pH direction, respiratory cause (CO2 is acid — high CO2 = acidosis). Step 3: Check HCO3 — if abnormal and matches pH direction, metabolic cause (HCO3 is base — low HCO3 = acidosis). Step 4: Check compensation — the other system will move to try to normalize pH. Partially compensated: pH still abnormal. Fully compensated: pH normal (look at which value moved first to determine primary cause).

ABG: pH <7.35, PaCO2 >45 mmHg (elevated CO2 retained). Cause: hypoventilation — CO2 not being blown off. Common causes: COPD, sedation/opioids, neuromuscular disease, pneumonia, airway obstruction, respiratory failure. Compensation: kidneys retain HCO3 (takes 24-48 hrs). Treatment: improve ventilation — bronchodilators, reverse sedation (naloxone), BiPAP/CPAP, intubation if severe. For COPD patients: low-flow O2 (1-2 L). Note: The traditional 'hypoxic drive' theory is largely outdated; the actual mechanism of O2-induced hypercapnia in COPD is worsening V/Q mismatch and the Haldane effect.

ABG: pH >7.45, PaCO2 <35 mmHg (too much CO2 blown off). Cause: hyperventilation — anxiety/panic attacks, pain, fever, early sepsis, PE, high altitude, mechanical ventilation (rate too high). Compensation: kidneys excrete HCO3 (takes 24-48 hrs). Treatment: treat underlying cause. Anxiety: coaching to slow breathing, rebreathing into paper bag (controversial), anxiolytics. Mechanical vent: decrease rate or tidal volume. Monitor for tetany, numbness/tingling (alkalosis decreases ionized calcium).

ABG: pH <7.35, HCO3 <22 mEq/L. Causes — MUDPILES: Methanol, Uremia, DKA, Propylene glycol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates. Also: severe diarrhea (loss of bicarb), renal failure. Compensation: Kussmaul respirations (deep, rapid breathing to blow off CO2). Treatment: treat underlying cause (insulin for DKA, dialysis for uremia), sodium bicarbonate if pH <7.1 (severe), fluid resuscitation. Monitor potassium (acidosis shifts K+ out of cells — may appear normal but drop rapidly with treatment).

ABG: pH >7.45, HCO3 >26 mEq/L. Causes: prolonged vomiting or NG suction (loss of HCl), excessive antacid use, excessive NaHCO3 administration, hypokalemia (kidneys retain H+ to excrete K+), loop/thiazide diuretics, Cushing syndrome. Compensation: slow, shallow respirations (retain CO2). Treatment: treat underlying cause, replace potassium and chloride (normal saline with KCl), antiemetics for vomiting, discontinue offending meds. Monitor for hypokalemia, hypocalcemia (increased neuromuscular excitability).

Assessment: productive cough (rust-colored sputum = pneumococcal), fever/chills, dyspnea, tachypnea, pleuritic chest pain, crackles on auscultation, dullness to percussion (consolidation). Types: community-acquired (CAP) — S. pneumoniae #1 cause; hospital-acquired (HAP) — onset >48 hrs after admission; ventilator-associated (VAP). Diagnostics: CXR (infiltrate), sputum C&S, CBC (elevated WBC), blood cultures. Nursing: O2 therapy, antibiotics (obtain cultures BEFORE first dose), encourage fluids, incentive spirometry, HOB elevated, isolation if needed (TB: airborne). Prevention: pneumococcal vaccine, flu vaccine, hand hygiene.

Chronic bronchitis + emphysema. Chronic bronchitis: 'blue bloater' — productive cough, hypoxemia, cyanosis, cor pulmonale. Emphysema: 'pink puffer' — barrel chest, pursed-lip breathing, dyspnea, thin, uses accessory muscles. Both: irreversible airflow limitation. Assessment: decreased breath sounds, wheezing, prolonged expiration, hyperinflation on CXR. Management: smoking cessation (#1 intervention), bronchodilators (SABA rescue + LAMA maintenance +/- LABA +/- ICS), pulmonary rehab, O2 therapy (low flow 1-2 L/min — titrate to SpO2 88-92%), flu + pneumococcal vaccines. O2 CAUTION: The hypoxic drive theory is largely outdated; the actual mechanism of O2-induced hypercapnia in COPD is V/Q mismatch worsening and the Haldane effect. Still use low-flow O2 and titrate carefully.

Assessment: wheezing (expiratory initially → may become silent if severe = ominous sign), dyspnea, chest tightness, cough (especially nocturnal), tachypnea, use of accessory muscles. Triggers: allergens, exercise, cold air, infection, stress. Acute management: SABA (albuterol) first-line + ipratropium for severe exacerbation + systemic corticosteroids (prednisone or methylprednisolone) + O2 to maintain SpO2 >90%. Maintenance: ICS (fluticasone) +/- LABA (salmeterol). Status asthmaticus: life-threatening, not responding to initial treatment — may need IV magnesium sulfate (bronchodilator), heliox, intubation. Monitor peak flow: <50% of personal best = severe.

Risk factors: Virchow's triad — venous stasis, hypercoagulability, endothelial injury. DVT, immobility, surgery, OCP use, malignancy, obesity. Assessment: sudden dyspnea (most common), pleuritic chest pain, tachycardia, tachypnea, anxiety, hypoxemia, possible hemoptysis, JVD. ABG: respiratory alkalosis (early). Diagnosis: CT pulmonary angiography (gold standard), D-dimer (sensitive but not specific — rules out if negative), V/Q scan if CT contraindicated. Management: anticoagulation (heparin → warfarin or DOAC), thrombolytics (alteplase) for massive PE with hemodynamic instability, IVC filter if anticoagulation contraindicated. Prevention: early ambulation, SCDs, DVT prophylaxis.

Settings: FiO2 (21-100% — wean to <60% ASAP to prevent O2 toxicity), Tidal Volume (6-8 mL/kg ideal body weight — lung-protective), RR (12-20), PEEP (Positive End-Expiratory Pressure — keeps alveoli open, improves oxygenation, typically 5 cm H2O). Modes: Assist-Control (AC): vent delivers set rate + assists patient-initiated breaths. SIMV: set rate + patient breathes independently between vent breaths (used for weaning). Pressure Support: augments spontaneous breaths only. Nursing: HOB 30-45 degrees (prevent VAP), oral care q2h with chlorhexidine, sedation vacation daily, spontaneous breathing trial (SBT) assessment, monitor ABGs, alarm settings ON, secure ETT (note cm mark at lip), suction PRN.

VAP bundle: HOB elevation 30-45 degrees, daily sedation vacation and assess readiness to extubate, DVT prophylaxis, PUD/stress ulcer prophylaxis (PPI or H2 blocker), oral care with chlorhexidine 0.12% q2-4 hrs, hand hygiene, subglottic suctioning (if available), avoid unnecessary circuit changes, maintain ETT cuff pressure 20-30 cm H2O. Diagnosis: new or progressive infiltrate on CXR + fever + purulent secretions + elevated WBC. Treatment: empiric broad-spectrum antibiotics → narrow based on sputum cultures.

Fluid accumulation in pericardial sac → compresses heart → decreased cardiac output. Beck's Triad: hypotension, muffled/distant heart sounds, JVD. Also: tachycardia, pulsus paradoxus (>10 mmHg drop in SBP during inspiration), narrowed pulse pressure, anxiety, dyspnea. Diagnosis: echocardiogram. Emergency treatment: pericardiocentesis (needle aspiration of pericardial fluid). Keep patient upright to pool fluid away from heart. Causes: trauma, post-cardiac surgery, MI (ventricular rupture), pericarditis, malignancy.

Inflammation of pericardium. Assessment: sharp, pleuritic chest pain that worsens with inspiration and lying flat, IMPROVES with sitting up and leaning forward (key distinguishing feature from MI). Pericardial friction rub on auscultation (scratchy, high-pitched sound). ECG: diffuse ST elevation (concave up — saddle-shaped), PR depression. Diagnosis: echo (may show effusion), elevated ESR/CRP. Treatment: NSAIDs (ibuprofen) + colchicine (reduces recurrence). Avoid anticoagulants (risk of hemopericardium). Monitor for cardiac tamponade (complication).

Infection of heart valves/endocardium. Risk factors: IV drug use (tricuspid valve), prosthetic valves, dental procedures, congenital heart defects, poor dentition. Common organisms: S. aureus (#1), Streptococcus viridans (dental). Assessment: persistent fever, new or changing murmur, Janeway lesions (painless red spots on palms/soles), Osler nodes (painful nodules on fingers/toes), Roth spots (retinal hemorrhages), splinter hemorrhages (nails), splenomegaly, petechiae. Diagnosis: Duke criteria — positive blood cultures (draw 3 sets before antibiotics) + echo findings (vegetations). Treatment: IV antibiotics 4-6 weeks. Teach: prophylactic antibiotics before dental procedures for high-risk patients.

Thoracic aortic aneurysm (TAA) or abdominal aortic aneurysm (AAA). AAA: pulsatile abdominal mass (DO NOT palpate vigorously), bruit, back/flank/abdominal pain (if rupturing). Screen: one-time ultrasound for men aged 65-75 who ever smoked. Dissecting aneurysm: tearing/ripping pain radiating to back, BP difference between arms >20 mmHg, diaphoresis, hypertension. Nursing: strict BP control (SBP <120, HR <60 — IV labetalol, nitroprusside), pain management, prepare for emergency surgery if rupturing (cross-match blood, large-bore IVs, consent). Monitor hemoglobin, renal function. Post-op: monitor graft site, peripheral pulses, neuro checks (spinal cord perfusion).

Keep trach ties secure (1-2 finger breadth looseness). Clean inner cannula q8h or PRN (or replace if disposable). Trach care: clean stoma site with normal saline only (H2O2 is no longer recommended), apply pre-cut gauze (never cut gauze — loose threads can be aspirated). Keep obturator at bedside (for reinsertion). Keep same-size and one-size-smaller trach at bedside. Suctioning: preoxygenate with 100% O2, sterile technique, insert without suction, apply suction on withdrawal (max 10-15 seconds), max 3 passes. Cuff: keep 20-30 cm H2O (check with manometer). Accidental decannulation: <7 days post-op = surgical emergency (stoma may close); >7 days = reinsert or ventilate via stoma.

Air enters pleural space but cannot escape → pressure builds → mediastinal shift → compresses opposite lung and heart. Assessment: severe dyspnea, tracheal deviation (away from affected side), absent breath sounds on affected side, JVD, hypotension, tachycardia, cyanosis, hyperresonance to percussion. EMERGENCY treatment: needle decompression — large-bore needle (14-16 gauge) at 2nd intercostal space, midclavicular line on affected side → followed by chest tube placement. Do NOT wait for CXR if clinical signs are present and patient is unstable. Causes: trauma, barotrauma from mechanical ventilation, central line insertion.

Non-cardiogenic pulmonary edema with diffuse alveolar damage. Berlin criteria: acute onset (within 1 week), bilateral opacities on CXR (white-out), PaO2/FiO2 ratio <=300 (mild <=300, moderate <=200, severe <=100), not fully explained by heart failure. Causes: sepsis (#1), pneumonia, aspiration, trauma, pancreatitis. Management: lung-protective ventilation (low tidal volume 6 mL/kg, PEEP optimization), prone positioning (16+ hrs/day — improves oxygenation), conservative fluid management, neuromuscular blockade if severe, treat underlying cause. Nursing: continuous SpO2/hemodynamic monitoring, oral care, DVT/stress ulcer prophylaxis, nutrition, skin assessment when prone.

Caused by Mycobacterium tuberculosis. Transmission: airborne droplet nuclei. Testing: Mantoux (TST/PPD) — read in 48-72 hrs, measure induration (not redness): >=5 mm positive (HIV, close contacts, CXR changes), >=10 mm (high-risk groups — immigrants, healthcare workers, IV drug users), >=15 mm (no risk factors). Positive PPD → CXR. QuantiFERON-TB Gold (blood test) — preferred in BCG-vaccinated. Isolation: airborne precautions (negative-pressure room, N95 respirator, patient wears surgical mask during transport). Treatment: RIPE therapy — Rifampin (orange body fluids, drug interactions), Isoniazid (INH — give with vitamin B6/pyridoxine to prevent peripheral neuropathy, hepatotoxic), Pyrazinamide, Ethambutol (monitor vision — optic neuritis). Duration: 6-9 months. Monitor LFTs.

FEV1 (Forced Expiratory Volume in 1 sec): amount exhaled in first second — decreased in obstructive disease (COPD, asthma). FVC (Forced Vital Capacity): total amount exhaled — decreased in restrictive disease (pulmonary fibrosis). FEV1/FVC ratio: <70% = obstructive disease; normal or increased in restrictive disease. Peak Expiratory Flow Rate (PEFR): effort-dependent, used for asthma monitoring (green >80%, yellow 50-80%, red <50% of personal best). TLC (Total Lung Capacity): increased in COPD (air trapping), decreased in restrictive disease.

Occurs when FiO2 >60% for prolonged periods (>24-48 hrs). Pathophysiology: high O2 concentrations generate free radicals → damage alveolar-capillary membrane → inflammation, atelectasis (absorption atelectasis — nitrogen washout), ARDS-like picture. Signs: substernal chest pain, cough, dyspnea, decreased lung compliance. Prevention: use lowest FiO2 to maintain adequate oxygenation (SpO2 >=92% or PaO2 >=60 mmHg), wean FiO2 as tolerated, use PEEP to allow lower FiO2. Special populations: neonates — retinopathy of prematurity (ROP) with excessive O2; COPD — target SpO2 88-92%.

Cardioversion: synchronized shock — machine senses R wave and delivers shock during QRS (avoids R-on-T phenomenon → Vfib). Used for unstable tachyarrhythmias WITH a pulse (afib, aflutter, SVT, Vtach with pulse). Sedation required (patient is conscious). Start at lower energy. Defibrillation: unsynchronized shock — delivers immediately regardless of cardiac cycle. Used for pulseless Vtach and Vfib ONLY. No sedation (patient is pulseless). Start at manufacturer-recommended energy (biphasic: 120-200J). If a synchronized shock is attempted on Vfib, the machine may not fire (no R wave to sync to).

Immediate post-op: ICU, intubated on ventilator, hemodynamic monitoring (arterial line, PA catheter, CVP). Chest tubes (mediastinal and/or pleural). Monitor for: bleeding (>100 mL/hr x 3 hrs), cardiac tamponade, arrhythmias (afib most common post-CABG), MI, infection. Assess neurological status (stroke risk from bypass). Sternal precautions: no pushing/pulling >10 lbs for 6-8 weeks, hug pillow when coughing, no driving for 4-6 weeks. Leg incision care (if saphenous vein graft) — monitor for swelling, elevate leg. Assess peripheral pulses. Incentive spirometry q1h while awake. Progressive ambulation. Cardiac rehab referral.

12-lead ECG views the heart from 12 angles. Limb leads: I, II, III, aVR, aVL, aVF. Precordial leads: V1-V6. Leads II, III, aVF = inferior wall (RCA). Leads V1-V4 = anterior wall (LAD). Leads I, aVL, V5, V6 = lateral wall (LCx). Leads V1-V2 = septal wall. V3-V4 = anterior. Reciprocal changes (ST depression) appear in leads opposite the infarct. Right-sided leads (V4R) for right ventricular MI (avoid nitroglycerin and morphine — preload dependent). Posterior MI: tall R waves and ST depression in V1-V3 (mirror image).

CVP (Central Venous Pressure/Right Atrial Pressure): 2-8 mmHg — reflects right heart preload. Elevated: right heart failure, fluid overload. Low: hypovolemia. PAP (Pulmonary Artery Pressure): systolic 15-30, diastolic 4-12, mean 9-18 mmHg. PCWP (Pulmonary Capillary Wedge Pressure): 6-12 mmHg — reflects left heart preload. Elevated >18: left heart failure, fluid overload. CO (Cardiac Output): 4-8 L/min. CI (Cardiac Index): 2.5-4.0 L/min/m2. SVR (Systemic Vascular Resistance): 800-1200 dynes/sec/cm-5. Cardiogenic shock: high PCWP, low CO, high SVR. Septic shock (warm phase): low SVR, high CO, low PCWP.