Cardiovascular Disorders Charts

Definition

Inflammation of the pericardium (the fibrous sac surrounding the heart). It can interfere with normal heart movement and may lead to pericardial effusion or cardiac tamponade.

Causes

• Viral infection (most common)
• Autoimmune disease
• Myocardial infarction (MI)
• Trauma

Pathophysiology

Inflammation of the pericardium → Pericardial layers become rough → Friction develops between layers → Sharp chest pain and friction rub → Fluid may accumulate (pericardial effusion) → Large effusion compresses the heart (cardiac tamponade) → ↓ Ventricular filling → ↓ Cardiac output

Clinical Manifestations

• Sharp, pleuritic chest pain ⭐
• Pain improves when sitting up and leaning forward ⭐
• Pericardial friction rub ⭐
• Dyspnea
• Signs of cardiac tamponade if severe

Diagnostics

• Echocardiogram ⭐
• ECG
• Laboratory markers of inflammation

Management

• Monitor for pericardial effusion
• Monitor for cardiac tamponade
• Treat underlying inflammation
• Monitor cardiac function

⭐ NCLEX Pearls / Nursing Priorities

⭐ Chest pain improves when leaning forward = classic finding.
⭐ Pericardial friction rub is the hallmark assessment finding.
🚨 Watch for cardiac tamponade, which is life-threatening because ventricular filling is impaired.

Definition

Inflammation of the myocardium (heart muscle). The inflammation weakens the heart muscle, reducing its ability to pump blood effectively.

Causes

• Viral infection (most common)

Pathophysiology

Viral infection → Inflammation damages myocardial cells → ↓ Contractility → ↓ Cardiac output → Heart failure and dysrhythmias may develop

Clinical Manifestations

• Flu-like symptoms
• Chest pain
• Tachycardia
• Dysrhythmias
• Fatigue
• Dyspnea
• Heart failure symptoms

Diagnostics

• ECG
• Echocardiogram
• Cardiac biomarkers

Management

• Monitor cardiac function
• Monitor for dysrhythmias
• Monitor for signs of heart failure
• Treat the underlying cause

⭐ NCLEX Pearls / Nursing Priorities

⭐ Viral illness followed by heart failure symptoms should make you think myocarditis.
⭐ Damaged myocardium can cause decreased contractility, heart failure, and dysrhythmias.

Definition

Infection of the endocardium and heart valves, usually caused by bacteria. The infection damages the valves and can lead to embolization.

Causes

• Bacterial infection
Major Risk Factors:
• Prosthetic heart valves
• Structural heart disease
• Intravenous drug use
• Recent invasive procedures

Pathophysiology

Bacteria enter the bloodstream → Attach to damaged endocardium or valves → Vegetations form on valves → Valve destruction → Pieces of vegetation may embolize → Stroke or organ damage

Clinical Manifestations

• Fever and chills
• New or changing heart murmur ⭐
• Petechiae
• Splinter hemorrhages
• Signs of embolization (stroke or organ damage)
• Vegetations visible on echocardiogram

Diagnostics

• Blood cultures ⭐
• Echocardiogram ⭐

Management

• Identify organism with blood cultures
• Monitor for valve damage
• Monitor for embolization
• Treat underlying infection

⭐ NCLEX Pearls / Nursing Priorities

⭐ Blood cultures BEFORE antibiotics is a classic nursing exam concept.
⭐ New murmur + fever = Think infective endocarditis.
⭐ Biggest complications are valve destruction and systemic emboli (stroke) because vegetations can break loose.

❤ Pericarditis

Pericardium

Friction rub + pain relieved by leaning forward

Cardiac tamponade

❤ Myocarditis

Myocardium

Heart failure symptoms, dysrhythmias

Dilated cardiomyopathy, heart failure

❤ Infective Endocarditis

Endocardium & valves

New murmur + vegetations

Septic emboli, valve destruction

Definition

Persistent elevation of blood pressure. Hypertension increases the workload of the heart and damages blood vessels over time. Often called the "Silent Killer" because most patients have no symptoms until organ damage occurs.

Causes

Primary (Essential): ~90–95% of cases; no single identifiable cause.

Secondary: Kidney disease, endocrine disorders, medications.

Risk Factors: Increasing age, family history, genetics, male sex, obesity, high sodium diet, smoking, excess alcohol, inactivity, chronic stress, diabetes, CKD, obstructive sleep apnea, certain medications.

Pathophysiology

↑ Cardiac output and/or ↑ peripheral vascular resistance → Persistent elevation of blood pressure → Endothelial damage → Arterial remodeling and stiffening → Progressive target organ damage (heart, brain, kidneys, eyes, blood vessels). SNS activation increases heart rate and vasoconstriction; RAAS causes vasoconstriction plus sodium and water retention, further increasing blood pressure.

Clinical Manifestations

Usually asymptomatic ⭐
Headache
Blurred vision
Dizziness
Fatigue
Chest pain
Shortness of breath
Epistaxis
Altered mental status (hypertensive emergency).

Complications: Stroke, heart failure, kidney injury, vision loss.

Diagnostics

Multiple BP measurements on separate visits ⭐
Home/ambulatory BP monitoring
History & physical
BMP, urinalysis, glucose/A1C, lipid profile
ECG
Echocardiogram if indicated.

Management

Lifestyle modifications: weight loss, DASH diet, reduced sodium, exercise, smoking cessation, limit alcohol, stress management.

Medications: Diuretics, ACE inhibitors, ARBs.

⭐ NCLEX Pearls / Nursing Priorities

⭐ "Silent Killer."
Most patients feel normal until organ damage develops.
Lifestyle modifications are recommended even when medications are prescribed.
Remember: SNS increases HR & vasoconstriction; RAAS retains fluid & causes vasoconstriction.

Definition

Abnormal levels of blood lipids, including increased LDL, decreased HDL, and/or elevated triglycerides. It promotes plaque formation and cardiovascular disease.

Causes

Genetics
Poor diet
Smoking
Obesity
Diabetes

Pathophysiology

↑ LDL enters artery wall → Inflammation develops → Plaque formation begins → Atherosclerosis develops → Blood flow decreases → Risk for CAD, PAD, and stroke increases.

Clinical Manifestations

Usually no symptoms until vascular disease develops.

Diagnostics

Lipid panel ⭐

Management

Lifestyle modifications to reduce cardiovascular risk.

⭐ NCLEX Pearls / Nursing Priorities

⭐ High LDL = plaque formation.
Low HDL = less cholesterol removal.
Dyslipidemia itself usually causes no symptoms—complications occur later.

Definition

A chronic inflammatory disease of the arteries caused by plaque buildup, resulting in arterial narrowing and reduced blood flow.

Causes

Endothelial injury
LDL cholesterol accumulation
Chronic inflammation

Pathophysiology

Endothelial injury → LDL enters vessel wall → Inflammation develops → Plaque forms → Arterial stenosis → Reduced blood flow → Tissue ischemia. Plaque rupture can lead to thrombus formation and infarction.

Clinical Manifestations

Usually asymptomatic early.

Coronary arteries → Angina
Carotid arteries → Stroke/TIA symptoms
Peripheral arteries → Claudication.

Diagnostics

Lipid panel
Ultrasound/vascular studies
Cardiac imaging when indicated.

Management

Reduce cardiovascular risk factors and monitor progression.

⭐ NCLEX Pearls / Nursing Priorities

⭐ Stenosis = narrowing.
Plaque location determines symptoms.
Plaque rupture is what commonly triggers myocardial infarction.

Definition

Narrowing of the coronary arteries due to atherosclerosis, reducing oxygen-rich blood flow to the myocardium.

Causes

Atherosclerosis.

Risk Factors: Smoking, hypertension, dyslipidemia, diabetes, obesity, family history.

Pathophysiology

Coronary plaque narrows arteries → Reduced coronary blood flow → Myocardial ischemia → Stable angina (reversible) → Plaque rupture may cause coronary occlusion → Myocardial infarction (irreversible).

Clinical Manifestations

Chest pressure, squeezing, or heaviness ⭐
Pain radiating to jaw, neck, shoulder, arm, or back
Dyspnea
Diaphoresis
Nausea/vomiting
Fatigue
Dizziness
Anxiety.

Types: Stable angina, unstable angina, Prinzmetal's angina.

Diagnostics

Evaluation of myocardial ischemia and coronary blood flow.

Management

Reduce myocardial ischemia and prevent progression to myocardial infarction.

⭐ NCLEX Pearls / Nursing Priorities

⭐ Angina = reversible ischemia.
Unstable angina is a medical emergency.
Prolonged ischemia = myocardial infarction.

Hypertension

Elevated blood pressure

Usually asymptomatic ("Silent Killer")

Stroke, HF, CKD

Dyslipidemia

Abnormal lipid levels

↑ LDL / ↓ HDL

Atherosclerosis

Atherosclerosis

Plaque buildup

Progressive arterial narrowing

CAD, PAD, Stroke

Coronary Artery Disease

Coronary artery narrowing

Angina

Myocardial infarction

Definition

Irreversible death of myocardial (heart muscle) cells caused by prolonged interruption of coronary blood flow. Commonly called a heart attack. Cell death begins within 20–40 minutes if blood flow is not restored. "Time is Muscle."

Causes

Most common: Coronary artery occlusion caused by plaque rupture and thrombus formation.

Nonmodifiable Risk Factors: Increasing age, family history, male sex (until menopause), genetics.

Modifiable Risk Factors: Smoking, hypertension, dyslipidemia, diabetes mellitus, obesity, physical inactivity, poor diet, chronic stress.

Pathophysiology

Atherosclerotic plaque ruptures → Platelets aggregate → Thrombus forms → Partial (NSTEMI) or complete (STEMI) coronary artery occlusion → Oxygen delivery to myocardium stops → Myocardial ischemia develops → Irreversible myocardial cell death begins after 20–40 minutes → Decreased cardiac output → Dysrhythmias, heart failure, or cardiogenic shock may occur.

Clinical Manifestations

Classic Symptoms:
• Crushing, pressure-like chest pain ⭐
• Pain radiating to left arm, jaw, neck, shoulder, or back ⭐
• Shortness of breath
• Diaphoresis (cold, clammy skin)

Other Symptoms:
• Nausea/vomiting
• Dizziness or syncope
• Anxiety or feeling of impending doom
• Fatigue or weakness

Diagnostics

⭐ ECG – First diagnostic test; distinguishes STEMI from NSTEMI.
⭐ Troponin – Most specific marker of myocardial injury; rises within hours after MI.
Echocardiogram – Evaluates heart function.
Cardiac catheterization – Identifies and opens blocked coronary arteries.

Management

Restore Blood Flow: PCI (preferred), fibrinolytics when PCI is unavailable and appropriate.

Reduce Myocardial Workload: Nitroglycerin, beta blockers (when appropriate).

Prevent Further Clot Formation: Aspirin, antiplatelet therapy, anticoagulants.

Support Oxygen Delivery: Oxygen only if hypoxemic, continuous cardiac monitoring.

⭐ NCLEX Pearls / Nursing Priorities

⭐ TIME IS MUSCLE.
⭐ ECG is the FIRST diagnostic test.
⭐ Troponin is the MOST SPECIFIC laboratory marker.
⭐ PCI is the preferred treatment.
⭐ Oxygen is not given routinely—only if the patient is hypoxemic.
🚨 Rapid recognition and reperfusion are the priorities to save myocardium.

Definition

Complete coronary artery occlusion causing full-thickness myocardial infarction

Partial coronary artery occlusion causing subendocardial infarction

Cause

Complete blockage of a coronary artery

Partial blockage of a coronary artery

Pathophysiology

Complete occlusion → Total loss of blood flow → Full-thickness myocardial necrosis

Partial occlusion → Reduced blood flow → Inner layer of myocardium becomes ischemic and infarcts

ECG Findings

⭐ ST-segment elevation

⭐ No ST-segment elevation

Troponin

Elevated

Elevated

Treatment

🚨 Immediate PCI (preferred); fibrinolytics if indicated

Medical management followed by PCI if needed

⭐ NCLEX Pearls

Complete blockage = ST elevation = Emergency PCI

Partial blockage = No ST elevation = Positive troponin

Risk Factors

Smoking, hypertension, diabetes, obesity, dyslipidemia, family history

↓

Dyslipidemia

Increased LDL promotes plaque formation

↓

Atherosclerosis

Plaque narrows coronary arteries

↓

Coronary Artery Disease

Reduced blood flow to myocardium

↓

Angina

Reversible myocardial ischemia

↓

Myocardial Infarction

Irreversible myocardial cell death due to prolonged ischemia

Heart Failure

Damaged myocardium cannot pump effectively

Dysrhythmias

Ischemic myocardial tissue disrupts electrical conduction

Cardiogenic Shock

Extensive myocardial damage causes severe pump failure

Death

Large infarction or fatal dysrhythmias prevent adequate circulation

Definition

A disease of the heart muscle in which the ventricles become enlarged (dilated) and weakened, reducing the heart's ability to pump blood effectively.

Causes

Idiopathic, viral infection, alcohol use, genetics

Pathophysiology

Ventricles enlarge and stretch → Myocardial contraction weakens → ↓ Ejection fraction → ↓ Cardiac output → Blood backs up into the lungs and systemic circulation → Heart failure develops

Clinical Manifestations

Dyspnea
Fatigue
Pulmonary congestion
Peripheral edema
Palpitations
Dysrhythmias

Diagnostics

Echocardiogram showing enlarged ventricles and reduced ejection fraction

Management

Treat heart failure, improve cardiac output, monitor dysrhythmias

⭐ NCLEX Pearls / Nursing Priorities

⭐ Can't Pump = Dilated Cardiomyopathy.
⭐ Reduced EF is the hallmark.
Often progresses to systolic heart failure (HFrEF).

Definition

A genetic disease in which the ventricular muscle becomes abnormally thick, reducing ventricular filling and sometimes obstructing blood flow leaving the heart.

Causes

Genetic (autosomal dominant)

Pathophysiology

Left ventricle and septum thicken → Ventricle cannot relax normally → ↓ Ventricular filling during diastole → May obstruct outflow → ↓ Cardiac output

Clinical Manifestations

Dyspnea
Chest pain (angina)
Palpitations
Syncope with exercise ⭐
Dysrhythmias

Diagnostics

Echocardiogram showing ventricular hypertrophy

Management

Improve ventricular filling and monitor for dysrhythmias

⭐ NCLEX Pearls / Nursing Priorities

⭐ Too Thick to Fill.
⭐ Syncope during exercise is a classic NCLEX clue.
⭐ Greatest complication is sudden cardiac death.

Definition

A disease in which the ventricles become stiff and cannot relax normally, limiting ventricular filling.

Causes

Infiltrative disease (amyloid)

Pathophysiology

Ventricles become stiff → Impaired ventricular relaxation → ↓ Diastolic filling → Congestion develops despite relatively normal pumping strength early in the disease

Clinical Manifestations

Dyspnea
Fatigue
Exercise intolerance
Peripheral edema
Pulmonary congestion

Diagnostics

Echocardiogram demonstrating impaired filling

Management

Improve ventricular filling and reduce congestion

⭐ NCLEX Pearls / Nursing Priorities

⭐ Can't Relax = Can't Fill.
⭐ Ejection fraction is often normal early because contraction is preserved.

Definition

A condition in which the heart cannot pump enough blood to meet the body's metabolic needs.

Causes

Myocardial infarction
Hypertension
Cardiomyopathy
Valvular heart disease

Pathophysiology

Cardiac damage → ↓ Cardiac output → ↓ Tissue perfusion → SNS and RAAS activation → Fluid retention + vasoconstriction → ↑ Workload on heart → Progressive heart failure

Clinical Manifestations

Dyspnea
Crackles
Pulmonary congestion
Peripheral edema
JVD
Fatigue
Weight gain

Diagnostics

BNP/NT-proBNP ⭐
Echocardiogram ⭐
Chest X-ray
ECG

Management

Diuretics
Sodium restriction
Daily weights
ACE inhibitors/ARBs
Beta blockers
SGLT2 inhibitors
Activity as tolerated
Heart-healthy diet
Smoking cessation
Medication adherence

⭐ NCLEX Pearls / Nursing Priorities

⭐ Daily weights are the best indicator of fluid status.
⭐ BNP is elevated.
⭐ Echocardiogram determines ejection fraction.
⭐ Heart failure is primarily a problem of decreased cardiac output plus fluid overload.

Definition

Failure of the left ventricle to pump blood effectively, causing blood to back up into the lungs.

Causes

Myocardial infarction
Hypertension
Cardiomyopathy

Pathophysiology

Left ventricular failure → Blood backs up into pulmonary circulation → Pulmonary edema develops → Gas exchange decreases → Tissue oxygenation decreases

Clinical Manifestations

Dyspnea ⭐
Orthopnea
Paroxysmal nocturnal dyspnea (PND)
Crackles
Pulmonary edema
Pink frothy sputum
Fatigue
Cool skin
Cyanosis

Diagnostics

BNP, Echocardiogram, Chest X-ray, ECG

Management

Standard heart failure treatment to reduce pulmonary congestion and improve cardiac output

⭐ NCLEX Pearls / Nursing Priorities

⭐ LEFT = LUNGS.
Crackles, orthopnea, and pink frothy sputum indicate pulmonary congestion.

Definition

Failure of the right ventricle to pump blood effectively, causing blood to back up into the systemic circulation.

Causes

Left-sided heart failure (most common)
Pulmonary disease (Cor Pulmonale)

Pathophysiology

Right ventricular failure → Blood backs up into systemic veins → Venous congestion develops → Peripheral edema, hepatomegaly, and ascites occur

Clinical Manifestations

Peripheral edema ⭐
JVD
Ascites
Hepatomegaly
Weight gain
GI congestion
Fatigue

Diagnostics

BNP, Echocardiogram, Chest X-ray, ECG

Management

Standard heart failure treatment to reduce systemic congestion and improve cardiac output

⭐ NCLEX Pearls / Nursing Priorities

⭐ RIGHT = REST OF THE BODY.
Think edema, JVD, ascites, hepatomegaly, and weight gain.

Definition

A disorder in which one or more heart valves fail to open or close properly, disrupting normal blood flow through the heart.

Causes

Valve stenosis (does not open completely) or regurgitation (does not close completely).

Pathophysiology

Stenosis: Valve opening narrows → Forward blood flow is obstructed → Pressure overload → Ventricular hypertrophy.

Regurgitation: Valve fails to close → Blood leaks backward → Volume overload → Ventricular dilation.

Clinical Manifestations

Heart murmur ⭐
Dyspnea
Fatigue
Palpitations
Peripheral edema (advanced)
Syncope (especially aortic stenosis)
Chest pain

Diagnostics

⭐ Echocardiogram (gold standard)
ECG
Chest X-ray
Cardiac catheterization (selected patients)

Management

Medications for symptom management
Valve repair
Valve replacement
TAVR for selected patients with aortic stenosis

⭐ NCLEX Pearls / Nursing Priorities

⭐ Murmur = Think valve disease.
⭐ Echocardiogram is the gold standard.
Stenosis = Pressure overload.
Regurgitation = Volume overload.

Dilated Cardiomyopathy

Weak, enlarged ventricle

Can't Pump

↓ Ejection Fraction

Hypertrophic Cardiomyopathy

Thick ventricle

Too Thick to Fill

Syncope with exercise

Restrictive Cardiomyopathy

Stiff ventricle

Can't Relax

Normal EF early

Left HF

Blood backs into lungs

LEFT = LUNGS

Crackles, pulmonary edema

Right HF

Blood backs into body

RIGHT = REST OF BODY

Edema, JVD, ascites

Valvular Disease

Valve doesn't open or close properly

Stenosis = Pressure; Regurgitation = Volume

Heart murmur

Pericarditis

Friction rub + pain relieved by leaning forward

Endocarditis

Blood cultures + new murmur + vegetations

Myocarditis

Viral infection → heart failure symptoms

Hypertension

Silent Killer

Dyslipidemia

↑ LDL, ↓ HDL

Atherosclerosis

Plaque buildup → stenosis

CAD

Reversible ischemia = angina

MI

Time is Muscle

Dilated Cardiomyopathy

Can't Pump

Hypertrophic Cardiomyopathy

Too Thick to Fill

Restrictive Cardiomyopathy

Can't Relax

Left HF

LEFT = LUNGS

Right HF

RIGHT = REST OF BODY

Valvular Disease

Murmur = Think Valve

Definition

A supraventricular dysrhythmia characterized by chaotic atrial electrical activity that causes the atria to quiver instead of contracting effectively. AFib significantly increases the risk of thrombus formation and ischemic stroke.

Causes

Multiple ectopic atrial foci override the SA node.

Pathophysiology

Multiple ectopic atrial foci → Chaotic atrial depolarization → Atria quiver instead of contracting → Blood pools in atria → Thrombus formation → Embolization → Ischemic stroke risk increases.

Clinical Manifestations

• Irregularly irregular pulse ⭐
• Palpitations
• Dyspnea
• Fatigue
• Dizziness/lightheadedness
• Increased risk for thrombus formation and ischemic stroke ⭐

Diagnostics

ECG showing an irregularly irregular rhythm.

Management

Monitor cardiac rhythm and assess for thrombus/stroke risk.

⭐ NCLEX Pearls / Nursing Priorities

⭐ Irregularly irregular = AFib.
⭐ Biggest complication = ischemic stroke.
⭐ Blood pools because the atria quiver instead of squeeze.

Definition

A supraventricular dysrhythmia caused by a single reentry circuit that produces rapid, organized atrial contractions.

Causes

Single reentry circuit within the atria.

Pathophysiology

Single reentry circuit → Rapid organized atrial depolarization (250–350 bpm) → Ineffective atrial contraction → Reduced ventricular filling → Stroke risk increases.

Clinical Manifestations

• Rapid, usually regular pulse ⭐
• Palpitations
• Dyspnea
• Fatigue
• Dizziness/presyncope
• May progress to atrial fibrillation

Diagnostics

ECG showing sawtooth waves. ⭐

Management

Monitor rhythm and assess stroke risk.

⭐ NCLEX Pearls / Nursing Priorities

⭐ Sawtooth ECG = Atrial Flutter.
⭐ Can progress to AFib.
⭐ Stroke risk remains elevated because atrial contraction is ineffective.

Definition

A life-threatening ventricular dysrhythmia characterized by an extremely rapid ventricular rhythm that produces minimal cardiac output.

Causes

Extremely rapid ventricular electrical activity (250–350 bpm).

Pathophysiology

Ventricles beat extremely rapidly → Minimal ventricular filling → Severely reduced cardiac output → Cerebral hypoperfusion → Syncope → Frequently progresses to ventricular fibrillation.

Clinical Manifestations

• Palpitations (brief episodes)
• Chest pain
• Dizziness
• Syncope
• Pulseless if sustained ⭐
• May rapidly progress to VFib

Diagnostics

ECG showing sine-wave pattern. ⭐

Management

Immediate CPR and defibrillation. ⭐

⭐ NCLEX Pearls / Nursing Priorities

⭐ Think "Almost VFib."
⭐ Can quickly deteriorate into ventricular fibrillation.
⭐ Immediate intervention is required.

Definition

A life-threatening ventricular dysrhythmia in which chaotic electrical activity causes the ventricles to quiver instead of contract, producing no effective cardiac output.

Causes

Chaotic ventricular electrical activity.

Pathophysiology

Chaotic ventricular impulses → Ventricles quiver → No ventricular contraction → No cardiac output → No cerebral or coronary perfusion → Cardiac arrest.

Clinical Manifestations

• Immediate collapse ⭐
• Unresponsive
• No pulse
• No blood pressure
• No effective breathing
• Cardiac arrest

Diagnostics

ECG showing chaotic rhythm. ⭐

Management

Immediate CPR and defibrillation. ⭐

⭐ NCLEX Pearls / Nursing Priorities

⭐ No pulse = Shock immediately.
⭐ VFib is a shockable rhythm.
⭐ This is a true cardiac arrest rhythm.

Definition

Complete absence of ventricular electrical activity and cardiac contraction ("flatline").

Causes

Complete absence of ventricular electrical activity.

Pathophysiology

No ventricular electrical activity → No ventricular contraction → No cardiac output → Complete loss of tissue perfusion.

Clinical Manifestations

• Unresponsive
• No pulse ⭐
• No breathing
• Flatline ECG

Diagnostics

Flatline ECG. ⭐

Management

CPR. Not a shockable rhythm. ⭐

⭐ NCLEX Pearls / Nursing Priorities

⭐ Flatline = Do NOT defibrillate.
⭐ Asystole is not shockable.
⭐ Begin CPR immediately.

Atrial Fibrillation

✅ Yes

❌ No

Irregularly irregular rhythm

Atrial Flutter

✅ Yes

❌ No

Sawtooth waves

Ventricular Flutter

⚠ Usually absent if sustained

✅ Yes

Sine-wave pattern

Ventricular Fibrillation

❌ No

✅ Yes

Chaotic rhythm

Asystole

❌ No

❌ No

Flatline

❤ Atrial Fibrillation

Irregularly irregular = Stroke risk

❤ Atrial Flutter

Sawtooth ECG

❤ Ventricular Flutter

Almost VFib

❤ Ventricular Fibrillation

No pulse = Shock immediately

❤ Asystole

Flatline = Do NOT shock

Definition

A disease in which narrowed peripheral arteries reduce blood flow to the extremities (most commonly the legs), resulting in tissue ischemia.

Causes

Atherosclerosis causing plaque buildup inside arteries.

Pathophysiology

Atherosclerosis → Plaque narrows arteries → ↓ Blood flow → ↓ Oxygen delivery → Tissue ischemia → Poor wound healing → Tissue necrosis → Gangrene if untreated.

Clinical Manifestations

6 P's: Pain (claudication), Pallor, Pulselessness, Paresthesia, Paralysis, Poikilothermia ⭐

Thin, shiny skin
Hair loss
Thick toenails
Painful punched-out ulcers (toes/feet)
Delayed wound healing
Dependent rubor
Gangrene (late)

Diagnostics

Vascular assessment and evaluation of arterial blood flow.

Management

Improve tissue perfusion and monitor for ischemia and gangrene.

⭐ NCLEX Pearls / Nursing Priorities

⭐ 6 P's = Acute arterial ischemia.
⭐ Intermittent claudication is the classic early symptom.
⭐ Painful, punched-out ulcers occur on the toes and feet.
⭐ Extremity is cool with decreased or absent pulses.

Definition

Weakening and ballooning of an arterial wall that may enlarge and rupture. The abdominal aorta is the most common location.

Causes

Weakening of an arterial wall.

Pathophysiology

Arterial wall weakens → Vessel dilates → Aneurysm enlarges → Wall tension increases → Risk of rupture rises as aneurysm grows.

Clinical Manifestations

Often asymptomatic until large or ruptured. Symptoms depend on location and size.

Diagnostics

Ultrasound ⭐
CT angiography
Echocardiogram (thoracic aneurysms)

Management

Blood pressure control
Monitor aneurysm size
Surgical repair if large or ruptured.

⭐ NCLEX Pearls / Nursing Priorities

⭐ AAA = Most common aneurysm.
⭐ Rupture is life-threatening.
⭐ Blood pressure control helps reduce rupture risk.

Definition

A disorder in which damaged venous valves impair blood return to the heart, causing venous pooling, edema, and skin changes.

Causes

Damaged venous valves.
Risk factors: prolonged standing, pregnancy, obesity, immobility, advanced age, family history.

Pathophysiology

Venous valve failure → Blood pools in legs → ↑ Venous pressure → Fluid leaks into tissues → Edema → Chronic skin changes → Venous ulcers.

Clinical Manifestations

Edema ⭐
Aching/heaviness
Brown discoloration (hemosiderin staining)
Thickened skin
Warm extremity
Normal pulses
Shallow irregular ulcers near medial ankle.

Diagnostics

Physical assessment.

Management

Improve venous return and reduce edema.

⭐ NCLEX Pearls / Nursing Priorities

⭐ Warm leg + edema + brown skin = Venous disease.
⭐ Venous ulcers = medial ankle, shallow, draining.
⭐ Pulses are usually normal.

Definition

Dilated, tortuous veins caused by incompetent venous valves and increased venous pressure.

Causes

Improper venous valve function causing venous pooling.

Pathophysiology

Valve incompetence → Blood pools → Venous pressure increases → Veins enlarge and become tortuous.

Clinical Manifestations

Bulging purplish veins
Pedal edema.

Diagnostics

Physical examination
Duplex ultrasound.

Management

Improve venous circulation and reduce venous pressure.

⭐ NCLEX Pearls / Nursing Priorities

⭐ Valve failure causes blood pooling.
⭐ Think bulging superficial veins.

Definition

Thrombus: Blood clot attached to the vessel wall.
Embolus: A clot or other material that breaks loose, travels through the bloodstream, and blocks another vessel.

Causes

Blood clot formation.

Pathophysiology

Thrombus forms → May obstruct blood flow → If clot dislodges → Embolus travels → Occludes another vessel → Tissue ischemia or infarction develops.

Clinical Manifestations

Depend on location and amount of blood flow lost.

Diagnostics

Ultrasound
CT imaging
Echocardiogram (if cardiac source suspected).

Management

Prompt diagnosis and restoration of blood flow.

⭐ NCLEX Pearls / Nursing Priorities

⭐ Thrombus stays. Embolus travels.
⭐ Symptoms depend on where the clot lodges.

Definition

Chronic accumulation of protein-rich fluid caused by impaired lymphatic drainage.

Causes

Primary (congenital) or secondary to surgery, radiation, cancer, infection, or trauma.

Pathophysiology

Lymphatic obstruction → Protein-rich fluid accumulates → Chronic inflammation → Fibrosis → Non-pitting edema.

Clinical Manifestations

Non-pitting swelling ⭐
Heaviness
Tightness
Thickened skin
Decreased ROM
Increased cellulitis risk.

Diagnostics

Physical assessment.

Management

Compression garments
Exercise
Manual lymph drainage
Skin care.

⭐ NCLEX Pearls / Nursing Priorities

⭐ Non-pitting edema is the hallmark.
⭐ Compression therapy and meticulous skin care help prevent infection.

Cardiogenic Shock

Pump failure causing inadequate tissue perfusion.

Usually MI.

Heart cannot pump effectively → ↓ Cardiac output → Organ hypoxia.

Chest pain, pulmonary edema, hypotension, tachycardia, cool clammy skin.

Clinical assessment.

Improve pump function, oxygen, medications.

⭐ Pump problem. Think MI + pulmonary edema.

Hypovolemic Shock

Shock caused by severe blood or fluid loss.

Hemorrhage, burns, dehydration.

↓ Blood volume → ↓ Preload → ↓ Cardiac output → Poor tissue perfusion.

Tachycardia, hypotension, cool clammy skin, decreased urine output.

Clinical assessment.

Stop fluid loss, IV fluids, blood if needed.

⭐ Volume problem. Replace fluids first.

Septic Shock

Distributive shock caused by severe infection.

Severe infection.

Inflammatory response → Widespread vasodilation → Hypotension → Poor tissue perfusion.

Warm flushed skin early ⭐, tachycardia, hypotension, altered mental status.

Clinical assessment.

IV fluids, antibiotics, vasopressors.

⭐ Warm early = Septic shock.

Neurogenic Shock

Distributive shock caused by loss of sympathetic tone.

Spinal cord injury.

Loss of SNS activity → Vasodilation → Hypotension + bradycardia.

Warm dry skin, hypotension, bradycardia ⭐.

Clinical assessment.

Fluids, vasopressors, stabilize spine.

⭐ Only shock with bradycardia.

Anaphylactic Shock

Distributive shock caused by a severe IgE-mediated allergic reaction.

Allergen exposure.

Histamine release → Vasodilation + increased capillary permeability + airway edema.

Hives, wheezing, airway swelling, hypotension, tachycardia.

Clinical assessment.

IM epinephrine first, airway, oxygen.

⭐ Epinephrine is the priority intervention.

Peripheral Arterial Disease

6 P's, painful punched-out ulcers

Cold leg = arterial

Chronic Venous Insufficiency

Edema, brown skin, medial ankle ulcer

Warm leg = venous

Varicose Veins

Bulging superficial veins

Valve failure

Aneurysm

Ballooning artery

AAA most common

Thrombus

Clot stays attached

Stays

Embolus

Clot travels

Travels

Lymphedema

Non-pitting edema

Protein-rich fluid

Cardiogenic Shock

Pump failure

MI

Hypovolemic Shock

Fluid loss

Replace volume

Septic Shock

Warm skin early

Infection

Neurogenic Shock

Bradycardia

Spinal cord injury

Anaphylactic Shock

Airway swelling

Epinephrine first

Causes

Severe IgE-mediated allergic reaction

Manifestations

Hives, wheezing, airway swelling, tachycardia, hypotension

Diagnostics

Clinical assessment

Management

IM epinephrine first ⭐, airway management, oxygen

Atrial Fibrillation

Irregularly irregular = Stroke risk

Atrial Flutter

Sawtooth ECG

Ventricular Flutter

Can quickly become V-Fib

Ventricular Fibrillation

No pulse = Shock immediately

Asystole

Flatline = NO shock

Peripheral Arterial Disease

6 P's of ischemia

Venous Disease

Edema + Brown skin + Medial ankle ulcer

Varicose Veins

Valve failure → Bulging veins

Aneurysm

Weak artery wall that balloons

Lymphedema

Non-pitting edema + Compression therapy

Cardiogenic Shock

Pump problem

Hypovolemic Shock

Volume problem

Septic Shock

Warm early + Infection

Neurogenic Shock

Bradycardia + Warm dry skin

Anaphylactic Shock

Epinephrine first