📚 Exam 3 KCRs

NUR198 Cardiovascular — Key Concept Reviews | Modules 7 & 8

Joyce University · Summer 2026 · the course faculty

Major Topics

ECG Rhythms

370+

Quiz Questions

Drug Classes

🎯 What's on Exam 3 (Modules 7 & 8)

📋 Learning Objectives

Normal vs abnormal cardiovascular assessment findings
Diagnostic tests & nursing implications
Pathophysiology, manifestations & treatment of coronary vascular disorders
Nursing process for HTN, angina, ACS, post-revascularization
ECG interpretation & dysrhythmia management

⚡ High-Yield Topics

HTN classifications, crisis treatment, med side effects
Stable vs unstable vs variant angina
STEMI vs NSTEMI — ECG changes + troponin
Dysrhythmias: recognize → intervene
Cardioversion vs defibrillation
Pacemaker vs ICD teaching
PCI/CABG post-op care
Dosage calculation WILL be on the exam

📦 Module Deliverables — Key Concepts

🩺 For ALL Disorders, Know:

Causes & risk factors Pathophysiology Diagnostic procedures Clinical manifestations Medical management Nursing management & priorities Client teaching/education

📘 Module 7 — Coronary, Conduction & HTN

Learning Objectives

Discuss normal & abnormal cardiovascular assessment findings (CO 1)
Identify diagnostic tests of the CV system & related nursing implications (CO 1)
Describe patho, manifestations & treatment of coronary vascular disorders (CO 1–4)
Use the nursing process for HTN, angina pectoris, ACS, or post-revascularization/cardiac surgery (CO 1–4)

Conditions & Concepts

Coronary artery disease · Angina · Acute coronary syndrome · Myocardial infarction
ECG interpretation · Electrical conduction system · PQRST · Depolarization/repolarization
Cardiac arrhythmias: bradycardia, tachycardia, atrial fibrillation, V-tach, V-fib, asystole
Synchronized cardioversion · Defibrillation · Pacemaker · AICD
Coronary revascularization procedures · Hypertension

📙 Module 8 — Valves, Infection, HF & Vascular

Learning Objectives

Define patho & etiology of cardiac valve disorders, infectious cardiac disorders & cardiomyopathy (CO 1)
Describe nursing care of the adult with a valvular disorder, cardiomyopathy, or infectious cardiac disorder (CO 1–4)
Use the nursing process for the adult client with heart failure (CO 1–4)

Conditions & Concepts

Cardiac valve disorders · Pulmonary HTN
Heart failure · Pulmonary edema
Cardiomyopathy · Myocarditis · Pericarditis · Endocarditis
Peripheral vascular disorders: PAD, peripheral venous disease, DVT
Raynaud syndrome · Aortic aneurysm

Dosage calculation and/or math problems WILL be included on this exam.

The key concepts list is a resource of topics drawn from module content and required readings.

🔍 Quick Navigation Guide

💉 Hypertension

Classifications · Risk Factors · BP meds · Hypertensive crisis · Nursing care

💔 CAD & Angina

Atherosclerosis · Angina types · Diagnostics · Stress tests · Revascularization

🚨 ACS & MI

STEMI/NSTEMI · Troponin · ECG changes · MONA · PCI/CABG

📈 ECG Interpretation

PQRST · Intervals · Rate calculation · 6-step approach

⚡ Rhythms

14 rhythms with ECG patterns · Treatments · Key differences

🔧 Procedures

Cardioversion · Defibrillation · Pacemaker · ICD · Pre/Post care

Know the DIFFERENCE: Cardioversion (synchronized, for living patient with pulse, needs anticoagulation first) vs Defibrillation (unsynchronized, pulseless VF/VT, NO anticoagulation needed first).

💉 Hypertension (HTN)

The "Silent Killer" — often no symptoms until end-organ damage

📊 Blood Pressure Classifications

Category	Systolic		Diastolic	Action
Normal	<120	AND	<80	Maintain healthy lifestyle
Elevated	120–129	AND	<80	Lifestyle changes
Stage 1 HTN	130–139	OR	80–89	Lifestyle + possibly meds
Stage 2 HTN	≥140	OR	≥90	Lifestyle + meds
Hypertensive Crisis	≥180	AND/OR	≥120	EMERGENCY — IV meds

Goal of HTN CRISIS treatment: Reduce BP by 20–25% in the FIRST HOUR, then gradually. NOT to normal immediately — rapid drop → stroke, MI, renal failure.

🔎 Primary vs Secondary HTN

Primary (Essential) HTN — 95%+ of cases

No identifiable cause. Treated with lifestyle + medications.

Secondary HTN — Rare

Caused by a specific condition:

Renal failure / CKD
Cushing's disease (high cortisol)
Pheochromocytoma (adrenal tumor)
Aldosterone-secreting tumor
Pre-eclampsia
Exogenous steroids
Sleep apnea

Only check for secondary if BP resistant to all treatments.

⚠️ Risk Factors

✅ Modifiable

Excessive Na+ intake
Physical inactivity
BMI >25 (obesity)
High alcohol intake
Tobacco / smoking
Hyperlipidemia
Diabetes mellitus
Stress

❌ Non-Modifiable

Family history
Age >60
Postmenopausal women
African American ethnicity (highest risk)
Male sex
Pre-existing CV disease

👁️ Clinical Manifestations

😶 Usually ASYMPTOMATIC — "Silent Killer"

Most people with HTN feel FINE. Damage occurs silently to target organs.

When symptoms occur: headaches, facial flushing, visual changes, nausea, dizziness

💥 End-Organ (Target Organ) Damage from Uncontrolled HTN:

👁️ Eyes → Blindness/retinopathy 🫀 Heart → Heart failure, MI, CAD 🧠 Brain → Stroke, TIA 🫘 Kidneys → CKD, renal failure 🩸 Vessels → Atherosclerosis, PAD, aneurysm

🔵 How to Accurately Assess BP:

Client seated, feet flat, back supported, legs uncrossed
No caffeine or exercise 30 min prior
Correct cuff size — too small = falsely HIGH reading; too large = falsely LOW
Arms bare (not over clothing)
Check BOTH arms on first visit — use higher reading
Manual BP is most accurate

💊 Antihypertensive Medications — ABCD + More

Class	Examples ("Last Name")	Mechanism	Key Nursing Points
A — ACE Inhibitors	Lisinopril, Ramipril, Enalapril (-PRIL)	Block conversion of angiotensin I → II → vasodilation, ↓aldosterone	Dry cough (hallmark SE), hyperkalemia, angioedema, hypotension. Hold if AKI. Monitor K+, creatinine.
A — ARBs	Valsartan, Losartan, Candesartan (-SARTAN)	Block angiotensin II receptors → vasodilation	NO cough (vs ACEi). Can cause hyperkalemia, angioedema. Monitor K+. Often used if ACEi cough intolerable.
B — Beta Blockers	Metoprolol, Atenolol, Carvedilol (-OLOL)	Block β1 (heart) → ↓HR, ↓CO; β2 (lungs) in non-selective	Monitor HR — hold if <60. Can mask hypoglycemia signs. NEVER stop abruptly — rebound HTN. Contraindicated in severe asthma/COPD (non-selective).
C — CCBs (Dihydropyridines)	Amlodipine, Nifedipine, Nicardipine (-PINE)	Block Ca2+ channels in vascular smooth muscle → vasodilation	Peripheral edema, flushing, headache. No grapefruit juice.
C — CCBs (Non-DHP)	Diltiazem, Verapamil	Block Ca2+ in heart AND vessels → ↓HR, vasodilation	Bradycardia, constipation (verapamil). Used for rate control in AFib.
D — Diuretics (Thiazide)	Hydrochlorothiazide (HCTZ), Chlorthalidone	↓ Na+ reabsorption in distal tubule → ↓ fluid volume	Hypokalemia, hyponatremia. Take in AM. Monitor electrolytes.
D — Diuretics (Loop)	Furosemide (Lasix), Bumetanide (-MIDE)	Block Na/K/Cl reabsorption in loop of Henle → massive diuresis	Hypokalemia (wasting!), ototoxicity. Monitor K+ closely. Take AM.
D — Diuretics (K+ sparing)	Spironolactone, Triamterene	Aldosterone antagonist → ↓ Na+ retention, HOLD K+	Hyperkalemia. Avoid in renal failure. Often combined with loop/thiazide.
α2 Agonist	Clonidine (Catapres)	Central α2 stimulation → ↓ sympathetic outflow → ↓ HR, ↓ BP	NEVER stop abruptly — severe rebound HTN. Sedation, dry mouth. Rebound crisis if missed doses.
α1 Antagonist	Prazosin, Doxazosin (-ZOSIN)	Block α1 receptors in vessels → vasodilation	First-dose hypotension/syncope — give at HS, have patient stay supine.

🧠 Memory Tricks for Drug Classes:

-PRIL = ACE inhibitor -SARTAN = ARB -OLOL = Beta blocker -PINE = CCB (DHP) -MIDE or -THIAZIDE = Diuretic

🚨 Hypertensive Crisis

⚡ Hypertensive URGENCY

Diastolic BP >120 mmHg WITHOUT acute target organ damage

Can be managed with oral medications over 24–48 hours

🔴 Hypertensive EMERGENCY

Elevated BP WITH acute target organ damage

Symptoms: severe headache, blurred vision, confusion, chest pain, epistaxis, decreased urine output

Requires IV medications

🏥 Treatment of Hypertensive Emergency:

Goal: Reduce BP by 20–25% in the FIRST HOUR
Then: Very gradual reduction over next 24 hours — NOT to normal immediately
IV vasodilators used: Nitroprusside, Hydralazine, Nicardipine IV, Labetalol IV
Nursing: BP q5–15 min, continuous cardiac monitor, ICU setting, titrate per protocol
After stabilization: Patient education on medication compliance

Never drop BP too fast in hypertensive crisis — can cause ischemic stroke, MI, or renal failure. The goal is controlled, gradual reduction.

📝 HTN Case Study — Dosage Calculation:

Nitroprusside 0.5 mcg/kg/min for 236 lb patient:

1. Convert weight: 236 lb ÷ 2.2 = 107.3 kg

2. Dose: 0.5 mcg/kg/min × 107.3 kg = 53.6 mcg/min

Clonidine 0.2 mg PO BID / available 0.1 mg tabs: 2 tabs per dose × 2 doses = 4 tabs/24 hr

👩‍⚕️ HTN Nursing Management

✅ DO

Monitor BP both arms on first visit
Assess for target organ damage
Teach DASH diet (low Na, low fat, fruits/veg)
Emphasize medication adherence
Weight loss if BMI >25
Regular aerobic exercise (30 min most days)
Smoking cessation
Limit alcohol
Stress management

❌ NEVER

Abruptly stop beta blockers or clonidine
Drop BP too fast in crisis
Ignore "silent" elevated BP readings
Give K+-sparing diuretic + ACEi without monitoring K+
Use non-selective beta blocker in asthmatic patient

💔 Coronary Artery Disease (CAD)

Progressive plaque buildup → narrowing → ischemia → infarction

🔬 Pathophysiology

Normal Coronary Artery

→

Fatty streak deposits (childhood)

→

Atherosclerotic plaque builds up

→

Lumen narrows → Ischemia

→

Plaque ruptures → Thrombus

→

Occlusion → MI

Atherosclerosis

Progressive buildup of lipid-rich plaques (atheromas) in the intima of arterial walls. Begins in childhood. LDL is the primary culprit.

Arteriosclerosis

Hardening and loss of elasticity of arterial walls — calcification. Reduces ability of arteries to dilate and respond to increased demand.

⚠️ CAD Risk Factors

✅ Modifiable

Hypertension Tobacco use Hyperlipidemia Diabetes Obesity (BMI >30) Sedentary lifestyle Excessive alcohol Stress Poor sleep Cocaine/meth use

❌ Non-Modifiable

Age (risk ↑ with age) Male sex Postmenopausal women Family history / genetics Race/ethnicity

📊 Key Lipid Panel Values to Know:

Lab	Desired Level	Notes
Total Cholesterol	<200 mg/dL	Main screening value
LDL ("Bad")	<130 mg/dL (or <70 for high-risk)	Primary driver of plaque
HDL ("Good")	>60 mg/dL	Protective — carries cholesterol away
Triglycerides	<150 mg/dL	Elevated → atherosclerosis risk
Homocysteine	<10 μmol/L	Elevated damages arterial lining

Client must be NPO for lipid panel!

😣 Angina Pectoris — 3 Types

Type	Trigger	Relief	Troponin	Key Feature
Stable (Exertional)	Exercise, emotional stress, cold	Rest + nitroglycerin (within 15 min)	Normal	Predictable, reproducible pattern. Does NOT indicate MI.
Unstable (Pre-Infarction)	At rest OR with minimal exertion	NOT relieved by rest or nitro	May be elevated	NEW, WORSENING, or at REST = medical emergency! Part of ACS.
Variant (Prinzmetal)	Coronary artery SPASM (not plaque)	Calcium channel blockers, nitrates	Normal	Occurs at REST, often at night. Not always plaque-related. Treated with CCBs.

Unstable angina = ACS even if troponin is normal. The key is that it's NEW, occurs at REST, or is WORSENING from prior pattern.

🔬 Cardiac Diagnostics

💉 Serum Tests

Troponin I & T — Gold standard for MI. Rises 3–6 hr post-MI, peaks 12–24 hr, stays elevated 7–14 DAYS. >0.4 = positive (99% specific to cardiac injury)
CK-MB — rises 4–6 hr, peaks 18–24 hr. More specific than CK alone
Myoglobin — earliest marker (1–2 hr) but NOT cardiac-specific
BNP/NT-proBNP — elevated in heart failure (normal <100). Correlates with severity.
Lipid panel — NPO required
CRP & ESR — inflammation markers

🔌 Non-Invasive Tests

12-lead ECG — "sixth vital sign," get in 10 min of chest pain. ST elevation = STEMI; ST depression/T-wave inversion = NSTEMI/ischemia
Telemetry — continuous 1–2 lead cardiac monitoring
Chest X-ray — cardiomegaly, pulmonary congestion
Echocardiogram (Echo) — visualize heart structure, valves, EF
Exercise stress test — walk treadmill, reach 85% max HR, monitor for ST changes
Nuclear stress test — radiotracer injected, images at rest & stress

🏃 Stress Test — Nursing Care:

Before:

NPO except water (no caffeine 24 hr prior)
No smoking before test
Start IV (for nuclear tracer injection)
Informed consent
Hold certain cardiac meds per order

Stop test if:

Chest pain develops
Extreme dyspnea
ST changes on ECG
Severe dysrhythmias
Dizziness, syncope
BP drops significantly

For patients who CANNOT walk: Pharmacologic stress with Dobutamine or Adenosine/Dipyridamole

🩺 Cardiac Catheterization (Coronary Angiography)

Invasive procedure — catheter threaded through femoral or radial artery to heart
Contrast dye injected — visualizes blockages
Pre: NPO 8–12 hr, assess for dye/shellfish/iodine allergy, check BUN/Cr (contrast → nephrotoxicity), hold metformin, IV access, informed consent, baseline VS & neurovascular check
Post: Assess access site for bleeding/hematoma, maintain bedrest 2–6 hr, monitor neurovascular status of extremity q15min → q1hr, push fluids (flushes contrast), monitor for chest pain, monitor I&O
Femoral site: Keep leg STRAIGHT; Radial site: TR band compression device applied

🔧 Revascularization Procedures

🎈 PCI (Percutaneous Coronary Intervention)

Balloon angioplasty + stent placement
Done through cardiac cath lab
GOAL: PCI within 90 minutes of STEMI ("door-to-balloon")
Drug-eluting stents release medication to prevent re-stenosis
Post: Same as post-cath + antiplatelet therapy (clopidogrel/aspirin LONG-TERM — do NOT stop without cardiology approval)

✂️ CABG (Coronary Artery Bypass Graft)

Surgical — open chest (sternotomy) or minimally invasive
Harvests saphenous vein (leg) or internal mammary artery to bypass blocked coronary artery
Post-op ICU: continuous telemetry, VS q1hr, monitor chest tube drainage (>150 mL/hr = notify provider), watch for cardiac tamponade, rhythm changes
Activity restriction 6 weeks, no lifting, sternal precautions

After stent placement, patients take antiplatelet agents (clopidogrel + aspirin) for at least 1 year for drug-eluting stents. NEVER tell patient to stop on their own — risk of sudden in-stent thrombosis.

🚨 Acute Coronary Syndrome & MI

ACS = Spectrum: Unstable Angina → NSTEMI → STEMI

📊 ACS Spectrum

Condition	Troponin	ECG	Definition
Unstable Angina	NORMAL	May have ST depression or T-wave changes	Chest pain at rest or worsening — no myocardial death yet
NSTEMI	ELEVATED	ST depression / T-wave inversion (2 contiguous leads)	Partial-thickness myocardial infarction — subendocardial
STEMI	ELEVATED	ST ELEVATION in 2 contiguous leads	Full-thickness MI — complete occlusion. TRUE emergency.

😰 MI Clinical Manifestations

👨 Classic Symptoms (Male typical)

Crushing, substernal chest pressure — "elephant on chest"
Radiates to LEFT arm, neck, jaw, shoulder
Diaphoresis (cold, clammy skin)
Dyspnea, anxiety, sense of impending doom
Nausea, vomiting
Tachycardia, tachypnea
Pallor, cool extremities
NOT relieved by rest or nitroglycerin

👩 Atypical Symptoms (Females, Elderly, Diabetics)

Pain between shoulder blades
Jaw or neck ache
Extreme fatigue, weakness
Nausea/vomiting MORE prominent
Shortness of breath
Indigestion-like sensation
May NOT have classic chest pain

NEVER dismiss atypical symptoms in women or diabetics!

🏥 MI: Initial Nursing Management

🔑 "MONA" — Initial Orders to Anticipate:

M — Morphine (pain, ↓anxiety, ↓preload) O — Oxygen (if SpO2 <90%) N — Nitroglycerin (vasodilation, ↓preload) A — Aspirin 325mg (chewed, antiplatelet)

Note: Morphine use is now more selective — fentanyl sometimes preferred. Oxygen only if SpO2 <90%

📋 Nursing Priorities:

Continuous cardiac monitoring + 12-lead ECG within 10 min
2 large-bore IVs
Pain assessment (0–10 scale), location, radiation
VS q5 min until stable, then q1hr
SpO2 monitoring; O2 if <90%
Serial cardiac enzymes (troponin q6–8hr × 3)
Urine output ≥30 mL/hr (renal perfusion)
NPO (anticipate PCI)
Bed rest / energy conservation
Cluster care to reduce cardiac workload

💊 Pharmacotherapy:

Aspirin — immediate antiplatelet (chewed)
Clopidogrel (Plavix) — antiplatelet
Heparin/LMWH — anticoagulation
Nitroglycerin — vasodilation (3 doses q5 min SL, then IV drip)
Beta blockers — ↓workload, ↓HR (metoprolol)
Thrombolytics (Alteplase/tPA) — if PCI not available within 90 min (best within 6 hr of onset)
Statins — Atorvastatin 80mg ASAP
ACE inhibitors — within 24 hr post-MI

Nitroglycerin is CONTRAINDICATED if: BP <90, HR <50 or >100, right ventricular MI (inferior MI), or patient took PDE-5 inhibitor (sildenafil/Viagra) within 24–48 hr.

📈 ECG Changes in MI — What to Look For

🔴 STEMI Pattern

ST segment is ELEVATED above the isoelectric (baseline) line in 2+ contiguous leads. Looks like a "tombstone" pattern. Indicates FULL-thickness MI (complete occlusion).

Troponin: ELEVATED Type: Full thickness MI Action: CATH LAB in 90 min

🟡 NSTEMI / Ischemia Pattern

ST segment is DEPRESSED below baseline, or T-wave is inverted. Indicates partial-thickness MI or ischemia (NSTEMI / unstable angina).

Troponin: ELEVATED Type: Partial thickness MI Action: Urgent (not emergent)

⚠️ MI Complications

⚡ Dysrhythmias

#1 cause of death post-MI. Continuous telemetry monitoring essential. VFib most lethal.

💔 Heart Failure

Pump failure after significant myocardial death. Watch for crackles, S3, JVD, edema.

🫀 Cardiogenic Shock

Signs: hypotension, tachycardia, tachypnea, weak pulses, altered LOC, ↓urine output. Medical emergency.

🩺 Cardiac Tamponade

Beck's Triad: JVD + hypotension + muffled heart sounds. Pericardiocentesis needed.

🔴 Pericarditis (Dressler's)

Post-MI inflammation. Pleuritic chest pain worse when supine, better leaning forward. Pericardial friction rub.

📉 Reinfarction

New onset ST elevation + troponin rise after initial event. Repeat PCI may be needed.

📈 ECG Interpretation

The 6-Step Approach — Master this framework!

⚡ Electrical Conduction System

🗺️ Conduction Pathway (MEMORIZE THIS ORDER)

SA Node
Pacemaker
60–100 bpm

→

Atrial Myocardium
P wave formed

→

AV Node
Delays 0.12–0.20s
40–60 bpm if SA fails

→

Bundle of His
Only atria→ventricle route

→

Bundle Branches
L and R branches

→

Purkinje Fibers
Ventricular walls
20–40 bpm (last resort)

🧠 Key Concepts:

SA Node = "The Boss" — highest intrinsic rate (60–100 bpm), controls everything under normal conditions
AV Node — introduces a delay (PR interval = 0.12–0.20 sec) to let atria CONTRACT before ventricles
Backup pacemakers: AV node takes over if SA fails (40–60 bpm); Purkinje/ventricular cells last resort (20–40 bpm)
Depolarization = electrical activation → muscle contraction
Repolarization = electrical reset → muscle relaxation

Structure	Location	Intrinsic Rate	Function
SA Node	Right atrium near superior vena cava	60–100 bpm	Primary pacemaker; initiates each heartbeat
AV Node	Lower right atrium, near tricuspid valve	40–60 bpm	Delays conduction (0.12–0.20s); secondary pacemaker
Bundle of His	Upper interventricular septum	—	Only pathway from atria to ventricles
Bundle Branches	Left & right along septum	—	Carry impulse to respective ventricles
Purkinje Fibers	Ventricular myocardium	20–40 bpm	Final distribution to ventricular muscle; tertiary pacemaker

📊 PQRST Waveform — Every Component Explained

🔌 Normal PQRST Complex with Annotations

Wave/Interval	What It Represents	Normal Value
P wave	Atrial depolarization (SA→AV)	Smooth, rounded, <0.12 sec
PR interval	Atrial depolarization + AV node delay	0.12–0.20 sec (3–5 small boxes)
QRS complex	Ventricular depolarization	<0.12 sec (3 small boxes)
ST segment	Early ventricular repolarization	0.08–0.12 sec; at isoelectric line
T wave	Ventricular repolarization	Positive deflection, upright
QT interval	Total ventricular depolarization + repolarization	Varies with HR; <0.44 sec

📏 ECG Paper Measurements:

1 small box = 0.04 seconds (horizontal)
1 large box = 0.20 seconds (5 small boxes)
30 large boxes = 6 seconds (a "6-second strip")
To calculate rate: Count QRS complexes in 6-second strip × 10
Or: Count R-R interval boxes: 300 ÷ number of large boxes between Rs

🔢 Rate Calculation Example:

On a 6-second strip: count 7 QRS complexes

7 × 10 = 70 BPM

R to R interval = 4 large boxes

300 ÷ 4 = 75 BPM

🔢 6-Step Rhythm Interpretation Approach

STEP 1: What is the RATE?

Count QRS complexes in 6-second strip × 10
Normal: 60–100 bpm
Bradycardia: <60 bpm
Tachycardia: >100 bpm

STEP 2: Is the rhythm REGULAR or IRREGULAR?

Measure R-to-R intervals — are they equal?
Irregular = NOT sinus origin (think AFib, PVCs)
"Irregularly irregular" = hallmark of AFib

STEP 3: Are there P WAVES?

Yes, one before every QRS = sinus rhythm
No P waves = AFib or ventricular origin
P waves present but not before every QRS = AV block

STEP 4: What is the PR INTERVAL?

Normal: 0.12–0.20 sec (3–5 small boxes)
>0.20 = 1st degree AV block
Progressively lengthening = 2nd degree Type I (Wenckebach)
Constant but some P waves not followed by QRS = 2nd degree Type II
No relationship P to QRS = 3rd degree (complete) heart block

STEP 5: What is the QRS DURATION?

Normal: <0.12 sec (narrow = supraventricular origin)
Wide (>0.12): ventricular origin OR bundle branch block
Wide + bizarre = VTach or VFib

STEP 6: What are the T WAVES doing?

Normal: upright, positive
ST elevation: STEMI until proven otherwise
ST depression: ischemia/NSTEMI
T-wave inversion: ischemia

⚡ Quick-Fire ECG Analysis Steps (IN ORDER):

1. Calculate heart rateCount QRS × 10 (on 6-sec strip)

2. Determine rhythm regularityR-to-R equal = regular; unequal = irregular

3. Assess for P waveOne before every QRS? Visible? Upright?

4. Measure PR intervalNormal = 0.12–0.20 sec

5. Measure QRS durationNormal = ≤0.12 sec

6. Observe T wave and ST segmentElevated? Depressed? Inverted?

⚡ Cardiac Dysrhythmias

14 Rhythms — Recognize → Identify Symptoms → Treat

🏃 Approach to Dysrhythmias

⚠️ TREAT THE PATIENT, NOT THE MONITOR!

First ask: Is the patient stable or unstable? Any symptoms (hypotension, decreased LOC, chest pain, dyspnea)? Treatment urgency depends on hemodynamic stability, not just the rhythm.

Common Causes of Dysrhythmias:

Myocardial ischemia or infarction
Hypoxemia / hypoxia
Electrolyte imbalances (especially K+, Mg2+)
Acid-base imbalances (acidosis)
Sympathomimetic drugs (epinephrine, dopamine)
Drug toxicity (digoxin, antiarrhythmics)
Caffeine, alcohol, cocaine, meth

Clinical Manifestations of Dysrhythmias:

Subjective: Anxiety, palpitations, dizziness, syncope, chest pain, dyspnea, weakness

Objective: BP changes, altered LOC, hypotension, cold/pale extremities, ↓ pulses, ↓ urine output

Severity depends on cardiac status AND rhythm type

💚 Sinus Rhythms (Originate from SA Node)

1️⃣ Normal Sinus Rhythm (NSR)

Rate: 60–100 bpm Rhythm: Regular P wave: One before every QRS PR: 0.12–0.20 sec QRS: <0.12 sec

✅ Treatment: None — continue to monitor

2️⃣ Sinus Bradycardia

Rate: <60 bpm Rhythm: Regular P wave: Present, one before each QRS PR: 0.12–0.20 (WNL) QRS: <0.12 (WNL)

If SYMPTOMATIC: IV Atropine 0.5–1mg (max 3mg) → Transcutaneous Pacing → Permanent Pacemaker
If asymptomatic: Monitor only (athletes may have baseline HR in 50s)

3️⃣ Sinus Tachycardia

Rate: >100 bpm Rhythm: Regular P wave: Present, one before each QRS PR/QRS: WNL

✅ Treat the CAUSE (fever, pain, anxiety, dehydration, hyperthyroidism). Not the rhythm itself.

🔷 Atrial Rhythms

4️⃣ Atrial Fibrillation (AFib) — "Irregularly Irregular"

Rate: Atrial 300–600, Ventricular variable Rhythm: IRREGULARLY IRREGULAR P waves: ABSENT — fibrillatory baseline QRS: WNL when conducted Hallmark: "Irregularly irregular" + no P waves

⚠️ The atria quiver (300–600 times/min) rather than contracting effectively. Blood pools → clots → STROKE risk. A "pulse deficit" may be present (apical > radial rate).

3 Goals: 1) Rate control (metoprolol, diltiazem, digoxin) 2) Rhythm control (amiodarone, synchronized cardioversion) 3) Prevent stroke (anticoagulation: warfarin, apixaban/Eliquis, rivaroxaban/Xarelto)
⚠️ Must be anticoagulated BEFORE cardioversion (unless emergency) — risk of clot embolism

5️⃣ Atrial Flutter — "Sawtooth Pattern"

Atrial rate: 240–360 bpm Ventricular: Usually <150 (2:1, 3:1, 4:1 conduction) Hallmark: Sawtooth F waves, no PR interval

Synchronized cardioversion, beta blockers or CCBs for rate control, amiodarone for rhythm control, anticoagulation for stroke prevention

6️⃣ Paroxysmal Supraventricular Tachycardia (PSVT / SVT)

Rate: 100–280 bpm (typically 150–200) Rhythm: Regular P waves: Not identifiable (hidden in QRS or T) QRS: Narrow (0.06–0.10 WNL)

Vagal maneuvers first (Valsalva, bearing down, coughing) → Adenosine IV (6 mg rapid push, then 12 mg) → Beta blockers → Synchronized cardioversion if unstable

🔴 Ventricular Rhythms (Life-Threatening)

7️⃣ Premature Ventricular Contraction (PVC)

Rhythm: Irregular (when PVC occurs) P wave: Absent before PVC QRS (PVC): WIDE and BIZARRE (>0.12) Cause: Ectopic ventricular focus fires early

If symptomatic or frequent: beta blockers or antiarrhythmics. Reduce stimulants (caffeine, smoking). If asymptomatic: may just monitor. Concerning if: >6/min, "R on T", runs of 3+ in a row (V-tach warning)

8️⃣ Ventricular Tachycardia (VTach / VT) — ⚠️ LIFE-THREATENING

Rate: 100–250 bpm Rhythm: Regular P waves: Absent/not identifiable QRS: WIDE (>0.12), bizarre "tombstone" shape ⚠️ MEDICAL EMERGENCY

Pulseless VTach: CPR + Defibrillation (NOT synchronized) + Epinephrine
With pulse + unstable: Synchronized cardioversion
With pulse + stable: IV Amiodarone, Lidocaine, Procainamide → Synchronized cardioversion if no response
Prevent recurrence: ICD placement

9️⃣ Ventricular Fibrillation (VFib / VF) — 🔴 CARDIAC ARREST

Rate: Too chaotic to count Rhythm: CHAOTIC, irregular P/QRS/T: NONE identifiable 🔴 NO PULSE — CARDIAC ARREST

IMMEDIATE CPR + DEFIBRILLATION (unsynchronized, NO anticoag needed, NO sync mode)
Epinephrine 1mg IV q3–5 min + Amiodarone 300mg IV push after 3rd shock

🔟 Asystole — "Flatline"

Rate: NONE Rhythm: None All waves: ABSENT ⚫ FATAL without immediate intervention

CPR + Epinephrine 1mg IV q3–5 min + Treat reversible causes (H's and T's)
❌ NO Defibrillation (nothing to shock) | ❌ NO Synchronized cardioversion
H's: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo/Hyperkalemia, Hypothermia
T's: Tension pneumothorax, Tamponade, Toxins, Thrombosis

🔶 AV Blocks

Block	PR Interval	P:QRS Ratio	QRS	Treatment
1st Degree	>0.20 sec (prolonged)	1:1 (every P has QRS)	Normal	None — monitor
2nd Degree Type I (Wenckebach)	Progressively lengthens until QRS dropped	1:1 until a dropped QRS	Normal	Usually none; monitor
2nd Degree Type II (Mobitz II)	Consistent, then suddenly no QRS	2:1, 3:1, etc. (some P waves not conducted)	WNL	Atropine, pacemaker (can deteriorate to 3rd degree)
3rd Degree (Complete Heart Block)	No relationship	NO relationship — atria and ventricles beat independently	Wide if ventricular escape; narrow if junctional	IMMEDIATE pacemaker

2nd Degree Type II and 3rd Degree are the dangerous AV blocks — can progress rapidly to cardiac arrest. Both require PACEMAKER.

📊 Quick-Reference Rhythm Summary

Rhythm	Rate	Rhythm	P Wave	QRS	Treatment
NSR	60–100	Regular	Yes, 1:1	Normal	None
Sinus Brady	<60	Regular	Yes	Normal	Atropine if symptomatic
Sinus Tachy	>100	Regular	Yes	Normal	Treat cause
AFib	Ventricular: varies	Irreg. irregular	Absent	Narrow	Rate/rhythm/anticoag
Atrial Flutter	Atrial: 240–360	Regular saw-tooth	F-waves (sawtooth)	Narrow	Cardioversion, meds
SVT/PSVT	150–250	Regular	Hidden	Narrow	Vagal, adenosine
PVC	Variable	Irregular when present	Absent (PVC)	Wide, bizarre	Monitor, beta blocker
VTach	100–250	Regular	Absent	Wide, bizarre	Defib if pulseless / Cardiovert if pulse
VFib	None	Chaotic	None	None	CPR + Defibrillation STAT
Asystole	None	None	None	None	CPR + Epinephrine, NO defib

🔧 Cardiac Procedures

Cardioversion · Defibrillation · Pacemaker · ICD

⚡ Cardioversion vs Defibrillation

🔄 Synchronized Cardioversion

SYNCHRONIZED with ECG — fires during QRS complex (R wave)
Used for tachyarrhythmias WITH pulse (AFib, VTach with pulse, SVT)
Elective: Must anticoagulate FIRST (prevent clot embolism)
Requires informed consent + sedation
Lower energy than defibrillation
Nursing: Monitor VS, administer sedation, monitor rhythm before/during/after

⚡ Defibrillation (Unsynchronized)

UNSYNCHRONIZED — delivers shock immediately, no timing with ECG
Used for PULSELESS VFib and Pulseless VTach ONLY
NO anticoagulation needed
NO consent needed (emergency)
Higher energy level
"Clear!" — ensure no one touching patient before shock
Earlier = better survival rate

KEY DISTINCTION: Cardioversion = SYNCHRONIZED, for rhythms WITH PULSE, needs anticoag if AFib >48hr. Defibrillation = UNSYNCHRONIZED, for PULSELESS arrest rhythms (VFib/pulseless VTach).

🩺 Pacemaker

📌 Types:

Temporary (Transcutaneous): External pads on chest → emergency use (while awaiting permanent)
Temporary (Transvenous): Catheter through jugular/subclavian to right ventricle → ICU
Permanent: Surgically implanted under skin — small pectoral incision

📋 Indications:

Symptomatic bradycardia not responsive to atropine
2nd degree Type II AV block
3rd degree (complete) heart block
Sick sinus syndrome

🏥 Post-Op Nursing Care (Permanent):

Document insertion: time, date, model, settings
Continuous cardiac monitoring — compare ECG to pacemaker settings
Chest X-ray — lead placement, rule out pneumothorax
Pain management PRN
Sling for affected arm (~2 weeks) — minimize shoulder movement
Monitor incision for bleeding, hematoma, infection
ASSESS FOR HICCUPS — may mean generator is pacing the DIAPHRAGM (lead displacement)

👩‍⚕️ Pacemaker Client Teaching:

✅ TEACH PATIENT TO:

Always carry pacemaker ID card
Take daily pulse — report rate below set rate
Report: dizziness, syncope, hiccups, palpitations, shortness of breath
Tell ALL healthcare providers (including dentist)
Tell airport security — do NOT let them wand directly over device
Household items with small magnets are FINE
Attend follow-up appointments for device checks
Battery lasts ~10 years — will need generator replacement

❌ AVOID:

Large magnets (MRI may be issue — check with cardiologist)
Direct blows to pacemaker site
Heavy lifting for 6 weeks post-op
Arm exercises that stress the shoulder (4–6 weeks)
Airport security wands directly over device

📈 ECG Evidence of Pacing

A pacing SPIKE precedes each paced event. If ventricular pacing: wide QRS follows spike. Presence of QRS after spike = "capture" — confirms pacemaker is working.

💉 ICD (Implantable Cardioverter-Defibrillator)

📌 Indications:

Survivors of VFib or VTach cardiac arrest
Ejection fraction ≤35% with heart failure
High-risk patients with structural heart disease
After large MI with low EF

🔌 What it does:

Continuously monitors cardiac rhythm
Can PACE if bradycardia occurs
Can perform CARDIOVERSION for VTach
Can DEFIBRILLATE for VFib/Pulseless VTach

👩‍⚕️ ICD Client Teaching:

Always carry ICD ID card
If ICD fires, you may feel a "blow to the chest" — report to provider
If someone touches you when ICD fires, they feel a small tingle — NOT harmful
You may lose consciousness briefly BEFORE device fires
Avoid direct blows to generator site
Avoid large magnets (same as pacemaker)
Remote monitoring — scheduled follow-ups
Battery lasts ~10 years; will need generator replacement
Feeling a shock ≠ device malfunctioning (it detected dangerous rhythm)

Pacemaker vs ICD: A pacemaker prevents the rate from going TOO SLOW. An ICD prevents sudden cardiac death from lethal FAST rhythms (VFib/VTach). An ICD can ALSO pace if bradycardia occurs.

🦺 Zoll Vest (External Defibrillator Vest):

Worn externally while awaiting ICD implantation. Continuously monitors rhythm. Can detect VF/VT and automatically defibrillate. Temporary bridge to permanent ICD. Client must wear it at all times (except showering) and must NEVER sleep without it if prescribed.

🗺️ Visual Mind Maps

Big-picture visual organization — great for ADHD brains

💉 Hypertension — Mind Map

💔 CAD/ACS — Treatment Algorithm

🔄 ACS Decision Tree

📖 Key Terms & ATI Flashcards

All ATI terms from your Quizlet sets — review before quiz!

🫀 Heart Anatomy — Illustrated Diagram

📸 What the ATI/Quizlet heart diagrams show — explained with an interactive SVG

🗺️ Cross-Section: Heart Chambers, Valves & Blood Flow

📸 What the Quizlet Anatomy Images Show:
Each heart diagram in the ATI flashcards highlights a specific structure with an arrow. The images show a cross-sectional view similar to this diagram, with blue coloring for deoxygenated blood (right side) and red for oxygenated (left side).

🩸 Blood Flow Pathway (MEMORIZE IN ORDER)

Body → Superior/Inferior Vena Cava

↓

RIGHT ATRIUM

↓ (through Tricuspid valve)

RIGHT VENTRICLE

↓ (through Pulmonic valve)

Pulmonary Artery → LUNGS (gets O₂!)

↓ (Pulmonary Veins)

LEFT ATRIUM

↓ (through Mitral/Bicuspid valve)

LEFT VENTRICLE

↓ (through Aortic valve)

AORTA → BODY (delivers O₂)

🧠 Memory: "Try Pulling My Aorta"

Valve order (right to left): Tricuspid → Pulmonic → Mitral → Aortic

📸 Quizlet Image Descriptions:

Arteries image: Red/pink vessels carrying blood AWAY from heart — thick muscular walls
Veins image: Blue/purple vessels returning blood TO heart — thinner walls, valves
Closed circulatory system: Double-loop diagram showing pulmonary (right) and systemic (left) circuits
Open lymphatic system: Diagram of lymph vessels throughout body draining into circulatory system
Plasma tube image: Test tube showing 55% plasma (top), 1% WBCs/platelets, 45% RBCs (bottom)
Valve images: Cross-section showing each valve location with arrows indicating blood flow direction
Blood flow diagrams: Labeled pathway with numbered arrows showing circulation sequence
SA node image: Heart with electrical conduction system highlighted in yellow/gold
Coronary arteries image: Heart with red arteries branching from aorta to myocardium surface

📸 ECG Rhythm Strip Images — What They Show

Each Quizlet ATI Cardiac Dysrhythmias flashcard shows a pink-gridded rhythm strip image. Here is what each one looks like and what to look for:

Rhythm	What the Image Shows	Key Identification Feature
Normal Sinus Rhythm	Regular upright P waves, consistent PR intervals, narrow QRS complexes, upright T waves — all evenly spaced at ~70 BPM	Everything is regular, P before every QRS, normal intervals
Sinus Tachycardia	Same morphology as NSR but complexes are COMPRESSED together — more waves per second, rate ~140 BPM	Fast version of NSR — identical P waves and QRS, just faster
Sinus Bradycardia	Same morphology as NSR but complexes are SPREAD FAR APART — rate <60 BPM. Looks like NSR with huge gaps	Slow version of NSR — tall single beat with a long pause before next
Premature Atrial Beat (PAC)	Mostly regular NSR-like rhythm but ONE beat comes EARLY — slightly different P wave morphology before early QRS	Early beat with slightly different (abnormal-looking) P wave, then normal QRS follows
PSVT/SVT	Very RAPID, regular, narrow QRS complexes packed tightly together — P waves buried in preceding T waves or absent	Extremely fast regular narrow complexes — looks like a fence of rapid spikes
Atrial Flutter	Classic SAWTOOTH baseline — F waves zigzag up and down at 240-360/min, with QRS complexes appearing at regular intervals within the sawtooth (2:1, 3:1, 4:1)	Sawtooth! Looks like mountains between QRS complexes
Atrial Fibrillation	Chaotic, irregular wavy baseline (fibrillatory line) instead of P waves — QRS complexes appear at IRREGULAR intervals, varying R-R distances	Irregularly irregular — no two R-R intervals are equal, messy baseline
PVC	Normal beats interrupted by ONE very WIDE, TALL, BIZARRE-looking complex that looks completely different — followed by a flat "compensatory pause" before normal beats resume	One huge ugly complex stands out from all the normal ones
VTach	Series of WIDE, BIZARRE, regular complexes that all look the same — like repeating tombstones. Rapid (100-250 BPM), no visible P waves	"Tombstone" pattern — rapid regular WIDE complexes
VFib	Completely CHAOTIC, irregular wavy line — no recognizable P, QRS, or T waves at all. Looks like a seismograph during an earthquake	Total chaos — no organized pattern at all
1st Degree AV Block	Looks like normal NSR but the space between P wave and QRS (PR interval) is LONGER than usual — visible as a bigger gap between P and QRS	NSR with a noticeably long flat PR segment (>0.20 sec)
2nd Degree Type I (Wenckebach)	P waves visible; QRS complexes appear at first, then PR interval GRADUALLY gets longer with each beat until a QRS is dropped (missing) — then the cycle resets	Longer, longer, longer... DROP! Then cycle restarts
2nd Degree Type II (Mobitz II)	P waves appear regularly; most are followed by QRS but occasionally a QRS is missing (P wave with no QRS after it) — PR intervals are CONSTANT before the dropped beat	Consistent PR interval until QRS suddenly drops — no warning
3rd Degree (Complete Heart Block)	Two independent rhythms visible — P waves march through at one regular rate, QRS complexes occur at a slower SEPARATE rate — they march through each other with NO relationship	Two rhythms happening independently — they march through each other
Asystole	Flat or nearly flat line with minimal artifact — no cardiac electrical activity visible	FLATLINE — confirmed in 2+ leads

🫀 Anatomy & Physiology Terms

Term	Definition
Arteries	Carry blood AWAY from heart. Typically oxygen-rich (except pulmonary artery)
Veins	Carry blood TOWARD heart. Typically oxygen-poor (except pulmonary veins)
Systole	Heart muscle CONTRACTION → blood ejected
Diastole	Heart muscle RELAXATION → chambers fill
Pulmonary loop	Right ventricle → lungs (deoxygenated) → oxygenated blood to left atrium
Systemic loop	Left ventricle → body → deoxygenated blood to right atrium
Mitral/bicuspid valve	Between LEFT atrium and LEFT ventricle
Tricuspid valve	Between RIGHT atrium and RIGHT ventricle
Pulmonic valve	Between right ventricle and pulmonary artery
Aortic valve	Between left ventricle and aorta (prevents backflow)

Term	Definition
SA node	Primary pacemaker — 60–100 bpm, initiates electrical impulse
AV node	Secondary pacemaker — 40–60 bpm if SA fails; delays impulse 0.12–0.20 sec
Bundle of His	ONLY route between atria and ventricles
Purkinje fibers	Last-resort pacemaker — 20–40 bpm; initiates ventricular depolarization
Coronary arteries	Originate from aorta; deliver O2 and nutrients to myocardium
Inferior vena cava	Returns deoxygenated blood from body below diaphragm to right atrium
Superior vena cava	Returns deoxygenated blood from upper body to right atrium
Cyanosis	Bluish discoloration of skin/mucous membranes from hypoxia; assess nailbeds, lips
Cardiac output	HR × Stroke Volume = amount of blood pumped per minute (normal 4–8 L/min)
Ejection fraction	% of blood pumped out of LV with each beat; normal 55–70%

⚡ Dysrhythmia Key Terms

Term	Definition
Electrocardiogram (ECG/EKG)	Graphic record of the electrical activity and contractions of the heart. EKG = German spelling (K = Kardia).
Cardiac monitoring	Continuous viewing of electrical activity via ECG machine or cardiac monitor
Valsalva maneuver	Forceful exhalation against a closed glottis → ↑ intrathoracic pressure → ↓venous return → slows HR. Used for SVT treatment.
Synchronized cardioversion	Electrical shock TIMED with R wave on ECG; for tachyarrhythmias WITH a pulse
Defibrillation	Unsynchronized electrical shock; terminates VFib/pulseless VTach; no timing needed
Pacemaker	Implanted/external electronic device that takes over function of natural cardiac pacemaker
Pacemaker capture	Ability of pacing stimulus to successfully generate a cardiac depolarization (spike followed by complex)
ICD	Implantable cardioverter-defibrillator — small device implanted in chest to sense arrhythmia and terminate with shock
Asynchronous pacing	Pacemaker fires at set rate REGARDLESS of patient's intrinsic cardiac activity
ABI (Ankle-Brachial Index)	Ratio of ankle to brachial BP. Normal ≥1.0; <0.9 = PAD; <0.4 = severe PAD
Sudden Cardiac Death (SCD)	Death within 1 hour of cardiac symptoms; most common cause in healthy people = hypertrophic cardiomyopathy causing VFib
BNP/NT-proBNP	B-type natriuretic peptide — released when heart chambers are stretched. Normal <100 pg/mL. Elevated in heart failure. Used to diagnose/monitor HF severity.

💊 CAD Terms from ATI Flashcards

Term	Definition/Notes
Atherogenesis	Process of forming plaques in the intima of arteries; begins in CHILDHOOD
Atherosclerosis	Progressive plaque buildup in arteries causing narrowing or occlusion (lipid-rich)
LDL	"Bad" cholesterol — primary source of plaque. Target: <130 mg/dL (<70 for high-risk)
HDL	"Good" cholesterol — carries cholesterol AWAY from arteries. Target: >60 mg/dL
Triglycerides	Type of blood fat — elevated levels cause atherosclerosis. Target: <150 mg/dL
Homocysteine	Amino acid — elevated levels damage arterial lining → increased MI/stroke risk
Stable angina	Chest pain with exertion, relieved by rest or nitroglycerin within 15 min. Troponin normal.
NSTEMI	Non-ST elevation MI — partial thickness, elevated troponin, ST depression or T-wave inversion
STEMI	ST elevation MI — full thickness, complete occlusion, ST elevation in 2+ contiguous leads. CATH LAB in 90 min!
Angioplasty (PCI)	Balloon catheter inflated in narrowed coronary artery to push plaque against wall + stent placement
CABG	Coronary artery bypass graft — surgical bypass using saphenous vein (leg) or internal mammary artery
DASH diet	Dietary Approaches to Stop Hypertension: fruits, vegetables, low-fat dairy, whole grains, low sodium, lean proteins

📙 Module 8 — Heart Failure, Valves, Infection & Vascular

Cardiovascular II: HF · cardiomyopathy · pericarditis/myocarditis/endocarditis · valves · aneurysm · PAD · venous & DVT

💔 Heart Failure — The Big Picture

Definition: the heart muscle can't pump effectively → inadequate cardiac output, myocardial hypertrophy/remodeling, and pulmonary & systemic congestion (fluid overload). Chronic disease with acute exacerbations (like COPD) — managed, not cured.

🏷️ Classifications

Left vs Right (always refers to the ventricle)
Systolic (poor contraction, EF < 40%) vs Diastolic (stiff ventricle won't relax/fill; EF may look normal)
Acute vs Chronic

⚠️ Top Causes / Risk Factors

#1 cause = prior MI (lost muscle). Also: HTN, CAD, valve disease, cardiomyopathy, myocarditis, COPD/pulmonary HTN, aging, alcohol/tobacco, sepsis, family hx. One side eventually drags the other down → most patients have both.

↔️ Left vs Right HF — HIGH YIELD

Memory hook: LEFT = LUNGS · RIGHT = REST of the body. Backed-up blood shows where the failing ventricle receives blood from.

LEFT-sided HF (backs up into lungs)	RIGHT-sided HF (backs up into body)
Dyspnea, orthopnea (props on pillows), PND Crackles, cough, pink frothy sputum S3 gallop ↓ SpO₂, altered mental status (low O₂ to brain)	JVD (jugular venous distention) Dependent/pitting edema, weight gain Ascites / abdominal distention Hepatomegaly + liver tenderness, nausea/anorexia

🔬 HF Diagnostics & Key Numbers

🩸 BNP

> 100 pg/mL supports HF. Trend it to judge response (lower = improving). Specific to HF; drawn with the CBC/BMP.

❤️ Ejection Fraction

Normal 50–70%. < 40% = systolic HF. Obtained by echo or cath.

🖥️ Echo

TTE (noninvasive). TEE = clearer images of LA/LV but needs sedation, NPO, aspiration precautions.

DAILY WEIGHT = #1 monitoring tool. Same time each morning, after voiding, before dressing, same scale. Call provider for a gain of 2 lb in a day or 5 lb in a week. Restrict fluids (~2 L) and sodium (~2 g/2000 mg).

💊 HF Pharmacotherapy — Preload vs Afterload

⬇️ Preload reducers (volume coming IN)

Loop diuretics (furosemide) — pull third-space fluid → vasculature → out via kidneys
Fluid & sodium restriction

Biggest risk = HYPOkalemia (+ hyponatremia) → telemetry. IV furosemide ≤ ~10 mg/min (ototoxicity/tinnitus).

⬇️ Afterload reducers (pressure LV pumps AGAINST)

ACE inhibitors / ARBs, vasodilators (isosorbide), CCBs
Beta blockers — ↓ workload & remodeling
Entresto = sacubitril/valsartan; digoxin = inotrope

Lowering afterload effectively improves ejection fraction.

🚨 Cardiogenic Pulmonary Edema (LEFT-sided emergency)

Fluid floods the alveoli. Hallmark = pink frothy sputum + crackles rising from the bases, dyspnea at rest, anxiety, tachycardia. Priority: High-Fowler's → O₂ / positive pressure (maybe intubation) → IV loop diuretic → vasodilators/ACEI; morphine may ↓ preload & anxiety in severe cases.

🫀 Cardiomyopathy — 3 Types

Type	What happens	Pearls
Dilated (most common)	LV stretches & thins → low EF	Causes: alcohol, viral (HIV/hep), genetic, cardiotoxic chemo. Treat as HF → CRT/biventricular pacing, VAD, transplant.
Hypertrophic	Thick septum → ventricle can't fill	Leading cause of sudden death in young athletes. Syncope, chest pain. Septal ablation; avoid exertion.
Restrictive	Stiff/scarred walls won't relax (diastolic)	Amyloidosis, sarcoidosis, connective tissue dz. Treat as HF + steroids.

🔧 VAD / LVAD

Pumps blood from the ventricle; bridge to transplant or permanent. Patients are highly anticoagulated (bruise easily), depend on battery power, and may have NO palpable pulse (continuous-flow pump).

🫁 Pulmonary Hypertension & Cor Pulmonale

Elevated pulmonary arterial pressure — cannot be measured indirectly (needs a Swan-Ganz/right-heart cath); often silent until late. Manifestations: dyspnea, weakness/fatigue, syncope.

Cor pulmonale = RIGHT-sided HF caused by pulmonary HTN (most often from COPD). Management: treat the cause, O₂, diuretics, vasodilators, digoxin, daily weight, low-Na diet, fluid restriction; definitive = lung transplant.

🦠 Inflammatory & Infective Cardiac Disorders

Pericarditis

Inflamed pericardium (recent viral illness, lupus, post-MI). Chest pain like a "hot iron", worse lying flat / deep breath, better sitting & leaning forward. Pericardial friction rub at left lower sternal border. Tx: rest + NSAIDs, colchicine, corticosteroids. Usually self-limiting.

Myocarditis

Inflamed myocardium, usually viral (COVID-19 ↑ risk). Tachycardia, murmur, cardiomegaly, chest pain, dysrhythmias. Tx: rest, avoid strenuous exercise & alcohol (anything that ↑ HR). Usually resolves on its own.

🚨 Cardiac Tamponade (complication of pericarditis/effusion): fluid in the pericardial sac compresses the heart so it can't fill. Beck's Triad = hypotension + JVD + muffled heart sounds. Emergency tx = pericardiocentesis.

Rheumatic Heart Disease

Endocardial damage from Group A strep ("strep throat") / rheumatic fever → inflammation & scarring of valves. ↑ in children; now uncommon with early strep treatment.

Endocarditis

Life-threatening infection of chamber/valve lining (strep/staph). Hits the tricuspid valve first/most (first valve returning venous blood reaches). Risk: IV drug use, prosthetic valves/pacemakers, central lines, prior endocarditis. Tx: IV antibiotics 4–8 weeks; valve repair/replace only after infection clears.

🚪 Valvular Heart Disease

Stenosis

Stiff/narrow valve obstructs forward flow (often scar tissue).

Regurgitation (insufficiency)

Leaky valve allows backward flow ("incompetent" valve).

Mostly LEFT-sided (highest pressures); top risk factor = HTN (also aging, rheumatic fever, endocarditis, Marfan). Hallmark sign = a MURMUR (turbulent flow). Acts like HF → daily weights, diuretics, inotropes (digoxin), afterload reducers, Na/fluid limits.

Therapeutic Procedures

Percutaneous balloon valvuloplasty — catheter + balloon opens a stenotic valve
Valve replacement — mechanical, xenograft (animal), or allograft (cadaver)

Mechanical vs Tissue valve

Mechanical: lasts for life, but lifelong anticoagulation — INR ~2.5–3.5 (higher than the 2–3 for DVT)
Tissue: no long-term anticoagulation, but wears out in 7–10 years

Client teaching: prophylactic antibiotics before any dental/invasive procedure (prevents endocarditis); weigh daily; report HF signs, fever, or petechiae; avoid OTC meds with alcohol, ephedrine, or epinephrine (dysrhythmias).

🎈 Aneurysm & AAA

Weak, dilated section of artery (abdomen/thorax). #1 cause = atherosclerosis + uncontrolled HTN. AAA is usually silent until rupture: constant gnawing abdominal/low-back ache, pulsating mass, bruit. Dx by CT.

NEVER palpate a pulsating abdominal mass — can cause rupture. Nursing priority = control BP (titratable IV agents). Monitor < 5.5 cm with serial CT; repair if larger/symptomatic. Rupture = sudden severe pain, hypotension, syncope → high mortality.

Post-op (open repair)

Watch graft bleeding (hypotension, tachycardia) and occlusion (cold/pulseless legs). Report flank bruising, abd swelling, urine < 30 mL/hr. Keep HOB < 45° (avoid flexing graft), warm room, IS, avoid lifting > 15 lb, VTE prophylaxis.

🦵 Peripheral Arterial Disease (PAD)

Findings & Dx

ABI < 0.9 = diagnostic (ankle-brachial index)
Dependent rubor, pallor on elevation, cool, hairless, thin shiny skin, weak pulses
Ulcers on TOES / top of foot
Intermittent claudication — leg pain with exertion ("stable angina of the leg")

🚨 6 P's of Acute Arterial Occlusion

Pain · Pallor · Polar (cold) · Paresthesia · Paralysis · Pulselessness — limb emergency. Use a Doppler before declaring "no pulse", then call the provider.

Arterial teaching: keep legs DEPENDENT (do NOT elevate above heart), keep warm, no direct heat (burn risk—can't feel it), avoid cold/nicotine/caffeine/constriction; antiplatelets (aspirin/Plavix); walk regularly; good foot hygiene.

🆚 Arterial vs Venous Ulcers — HIGH YIELD

	ARTERIAL (PAD)	VENOUS (CVI)
Location	Toes, top of foot, bony points	Medial malleolus (inner ankle)
Pain	Painful; worse with elevation/activity	Aching/heavy; better with elevation
Skin	Pale, cool, shiny, hairless; dependent rubor	Brown stasis dermatitis, edema, warm
Position	Keep DEPENDENT, do NOT elevate	ELEVATE above heart + compression
Pulses	Weak/absent	Usually present

🤍 Raynaud Syndrome

Arteriole/capillary spasm in fingers (± toes) → color changes (white → blue → red), numbness, stinging on warming. More common in females; triggered by cold, smoking, beta-blockers. Tx: keep hands warm / run under warm (not hot) water; CCBs (nifedipine, amlodipine) or alpha blockers for severe cases.

🩸 Venous Disorders & VTE

Varicose veins

Dilated veins w/ incompetent valves → backflow/pooling. Risk: female, prolonged standing, pregnancy, obesity. Tx: compression stockings, sclerotherapy, vein stripping.

Chronic venous insufficiency

Leaky deep-vein valves → edema, stasis dermatitis, venous ulcers (medial malleolus), cellulitis risk. Tx: compression, elevate legs, wound care, protein/zinc/vit A&C diet.

Venous ulcers

Chronic, recurrent. Occlusive/hydrocolloid dressing left 3–7 days; wound vac/hyperbaric; debridement + antibiotics PRN. Toenails trimmed only by a provider.

🚨 DVT / VTE

Virchow Triad: venous stasis + endothelial injury + hypercoagulability. Unilateral calf pain/warmth/swelling + ↑ calf circumference (may be silent). Dx: ultrasound with Doppler (D-dimer is nonspecific). Tx: anticoagulation (heparin/LMWH/warfarin/Factor Xa inhibitors), then ambulate; dorsi/plantar-flexion in bed; compression/anti-embolism stockings.

NEVER massage the affected limb — can dislodge the clot → pulmonary embolism.

🧠 Case Study Quick-Review (Clinical Judgment)

Case 1 — Mr. Smith, 78 (HF)

SOB, fatigue, leg/abdominal edema, orthopnea; hx HTN, T2DM, CKD; BP 160/90, HR 102, RR 24, SpO₂ 92%; JVD, S3, pitting edema, crackles, abdominal distention.

Recognize/analyze cues: acute decompensated biventricular HF — LEFT (crackles, orthopnea, S3, low SpO₂) + RIGHT (JVD, edema, ascites).
Prioritize: the umbrella problem is fluid overload, but the priority is airway/breathing (ABC) — impaired gas exchange first.
Generate/Take action: High-Fowler's → O₂ for SpO₂ ≥94% → IV loop diuretic (furosemide) → strict I&O + daily weight → telemetry (K⁺) → labs (BNP, BMP, ABG) → ACEI/ARB/vasodilators (± morphine if severe) → 2 g Na/fluid restriction → energy conservation. Protect kidneys (CKD).
Evaluate outcomes: SpO₂ ≥94%, clearing crackles, urine >30 mL/hr, weight down to baseline, ↓ edema/JVD, normal K⁺, stable BUN/Cr, falling BNP; verbalizes 2 lb/day–5 lb/week rule + Na/fluid limits.

Case 2 — Mrs. Johnson, 82 (Venous ulcer / CVI)

Venous ulcer left lower leg with increased swelling, pain, redness; hx HTN, OA, chronic venous insufficiency.

Prioritize hypotheses: CVI with a venous stasis ulcer at the medial malleolus, now likely infected/cellulitis; impaired skin integrity, infection/sepsis risk, pain. (Venous pattern, not arterial.)
Generate solutions: improve venous return (compression + elevate legs), occlusive dressing (3–7 days)/wound vac/debridement, cultures + systemic antibiotics, pain control, protein/zinc/vit A&C diet.
Take action: elevate left leg, apply compression (after confirming arterial flow/ABI), sterile dressing, give antibiotics/analgesics, monitor circulation & DVT signs — do NOT massage; teach skin/foot care (toenails by provider only).
Evaluate outcomes: ulcer granulating/smaller with less drainage, redness/swelling/pain resolving, afebrile, ↓ edema, adherence to compression/elevation, intact distal pulses.

🎯 Module 8 — High-Yield Traps

Left = lungs, Right = body. Crackles/orthopnea = left; JVD/edema/ascites = right.
Daily weight beats I&O for fluid status — report 2 lb/day or 5 lb/week.
Beck's Triad (hypotension + JVD + muffled tones) → tamponade → pericardiocentesis.
Endocarditis → tricuspid valve first; IV antibiotics 4–8 weeks.
Mechanical valve INR 2.5–3.5 (vs 2–3 for DVT); tissue valves last 7–10 yr.
Arterial = dependent + warm, no heat; ulcers on toes. Venous = elevate + compression; ulcers at medial malleolus.
Do NOT palpate a pulsating abdominal mass; do NOT massage a DVT.
Diuretics → watch potassium → telemetry.

📇 Flashcards — Adult Med Surg Exam 3

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📂 Materials — Decks, ATI & Diagrams

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🧠 Interactive Quiz — Modules 7 & 8

370+ questions — 120 written MCQs plus 252 auto-generated from the 286 flashcards. Pick how many and how hard, then start.

🎯 Exam Prep Quiz

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🫀 Heart Rhythms

From your HEART-RHYTHMS document — EKG basics, rate calculation & arrhythmia reference

📏 EKG Paper Basics

The EKG paper moves at 25 mm/second.

Small Box

Width = 0.04 sec
Height = 0.1 mV

Large Box

5 small boxes
Width = 0.20 sec
Height = 0.5 mV

Entire Strip

5 large boxes = 1 sec
30 large boxes = 6 sec

🧮 Method 1: The 300 Rule (most common for NCLEX)

Count the number of large boxes between two R waves.

Formula

Heart Rate = 300 ÷ Number of Large Boxes

Memorize: 300 – 150 – 100 – 75 – 60 – 50

Example: 4 large boxes between R waves → 300 ÷ 4 = 75 bpm

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300 Rule reference

⏱️ Method 3: The 6-Second Method

Used for irregular rhythms such as atrial fibrillation.

Find a 6-second strip (30 large boxes)
Count the number of QRS complexes
Multiply by 10

Example: 8 QRS complexes in 6 seconds → 8 × 10 = 80 bpm

On NCLEX

6 large boxes between R waves → ~50 bpm → Bradycardia
2 large boxes between R waves → ~150 bpm → Tachycardia
1.5 large boxes → ~200 bpm → Severe tachycardia (often SVT)

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Rate calculation reference

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ECG strip detail

📈 ECG Pattern Quick Breakdown

Understanding ECG patterns can be life-saving. A quick breakdown:

✅ Normal Sinus Rhythm – Regular P wave before every QRS, HR 60–100 bpm.
⚡ Tachycardia – HR >100 bpm. Physiological or pathological.
🐢 Bradycardia – HR <60 bpm. Normal in athletes, may indicate conduction issues.
🔁 Atrial Flutter – Saw-tooth flutter waves, atrial rate ~300 bpm.
🎯 Atrial Fibrillation – Irregularly irregular, no distinct P waves. Stroke risk!
🚨 Ventricular Tachycardia – Wide complex, fast. Potentially life-threatening.
💥 Ventricular Fibrillation – Chaotic, no cardiac output. Immediate defibrillation.

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ECG pattern comparison

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ECG pattern comparison (cont.)

🗂️ Electrocardiogram Arrhythmias Chart

Rhythm	Description
Sinus Arrhythmia	A normal variation where heart rate slightly increases during inhalation and decreases during exhalation.
Sinus Tachycardia	Heart rate exceeds 100 bpm while maintaining a normal sinus rhythm.
Sinus Bradycardia	Slower-than-normal heart rate, typically below 60 bpm, with a normal sinus rhythm.
Atrial Fibrillation	Irregular, often rapid rhythm from chaotic atrial activity. P waves absent; irregularly irregular. Stroke risk.
Atrial Flutter	Rapid, regular atrial contractions producing a sawtooth pattern; ventricular conduction at fixed or variable ratio.
Atrioventricular (AV) Block	Atrial-to-ventricular signals delayed or partially blocked at the AV node, causing missed beats or slower conduction.
Ventricular Fibrillation	Life-threatening: ventricles quiver, no output. Chaotic waves, no identifiable P/QRS/T. Immediate defibrillation.
Ventricular Tachycardia	Rapid rhythm from the ventricles; wide QRS complexes; can reduce cardiac output if sustained.
Second-Degree Partial Block	Some atrial impulses fail to reach the ventricles, causing occasional dropped QRS while P waves continue.
Third-Degree Partial Block	Complete heart block: no atrial impulses reach the ventricles. Atria and ventricles beat independently (AV dissociation).

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Arrhythmias chart