Cardio
Chest Pain
Chest pain is a major cardiovascular symptom; clinicians in primary/urgent care must consider cardiovascular etiologies first, even though causes span pulmonary, GI, musculoskeletal, neurological, psychogenic, or idiopathic.
Mortality context and public health framing:
Coronary heart disease deaths declined over 40 years, with 2017 CHD deaths at 365,914; improvements largely from medical/surgical advances, not lifestyle changes yet.
Lifestyle changes reduce mortality risk: smoking cessation (~12% reduction), increased physical activity (~5% reduction).
Healthy People 2030 objectives target cholesterol reduction, hypertension control, and aspirin use for secondary prevention; educational efforts emphasize sex differences in heart attack presentations in women (Evidence-Based Nursing Practice 34.1).
Evidence-Based Nursing Practice 34.1 highlights NP roles in teaching women at risk for ACS to recognize symptoms and seek prompt care; case-vignette study showed NP accuracy higher for abrupt-onset classic ACS symptoms but gaps in recognizing need to call 911 for all ACS presentations; emphasizes educating on less typical ACS symptoms in women; action: call 911 within ~5 minutes of symptom onset if ACS suspected.
Diagnostic approach: Initial Chest Pain Differential uses focused history and physicals (Fig. 34.1). Critical history elements include:
Major symptoms: chest pain, dyspnea, syncope, heart failure symptoms; exercise tolerance and whether activity provokes symptoms.
Personal risk factors for cardiovascular disease.
Diagnostic reasoning algorithm (Chest Pain): key patterns
Cardiac pain: often diffuse retrosternal pressure or burning, may radiate, usually >1 minute but <10 minutes when typical; exertional pattern common with fixed atherosclerosis.
Angina vs MI: unstable angina/premarket ischemia patterns (crescendo/REST angina) signal higher ACS risk; rest pain with vasospasm also possible.
Costochondritis (CWS): focal, reproducible with palpation; diagnosis of exclusion.
GERD/hiatal hernia, peptic ulcer disease, pancreatitis, pneumothorax, pulmonary embolism, pneumonia, pericarditis, aortic dissection, PE, pleuritis among differentials.
Acute coronary syndrome (ACS) concepts:
Unstable angina vs NSTEMI vs STEMI: ACS spectrum; STEMI requires acute transmural myocardial ischemia with ST elevations; NSTEMI involves nontransmural infarction; unstable angina indicates ischemia without biomarker evidence of MI.
Some patients, especially women, older adults, or diabetics, present with minimal or atypical ACS symptoms; high index of suspicion is crucial.
Pain descriptors and actions:
Pain for angina: diffuse, retrosternal, sometimes radiating, often lasting >1 minute but typically <10 minutes; exertional symptoms common.
MI pain: anginal-like but lasts >20 minutes, may wax and wane; dyspnea, diaphoresis, nausea, dizziness common; radiation to neck/jaw/shoulder/left arm; variability in pain intensity; women/older adults/diabetics may have atypical presentations.
Additional presentation features:
Diaphoresis with chest pain is worrisome for significant hemodynamic compromise.
Dyspnea accompanying angina occurs in about one-third of patients due to transient pulmonary venous pressure rise during ischemia.
Accurate history phrasing: the word “pain” can be misleading; describe tightness, pressure, heaviness, etc.
Practical clinical pearls:
Changes in angina pattern may indicate accelerated atherosclerosis or vasospasm; urgent assessment advised.
Localized chest wall pain with reproducible chest wall tenderness suggests non-cardiac causes.
In ACS, rapid, accurate disposition and treatment are vital; time-sensitive interventions improve outcomes.
Palpitations
Definition: awareness of heartbeats; may be benign or pathologic.
Symptom description matters: strong regular rhythm after stress/exertion may be normal; skipped/missed beats may indicate ectopy (atrial or ventricular).
Medications, caffeine, alcohol, nicotine, and physical activity can cause palpitations.
Differential diagnosis:
Atrial ectopic beats most common benign cause; can be associated with COPD, rheumatic disease, valvular dysfunction when linked to pathology.
Ventricular ectopy more likely to indicate pathology than atrial ectopy; increased risk of sudden cardiac death with high-risk individuals.
Recurrent rapid rhythms with paroxysmal onset (e.g., PSVT, VT) may occur with abrupt cessation; may be regular or irregular (atrial fibrillation possible).
Evaluation and testing:
History and exam guide testing; thyroid studies (TSH, free T4), CBC, chemistries, hemoglobin/hematocrit to rule out thyroid disease, electrolyte imbalance, anemia.
Ambulatory Holter monitoring useful when at least one event is recorded; helpful for lethal rhythm disturbances.
Echocardiography may assess outflow tract patency and rule out valvular stenosis or hypertrophic cardiomyopathy.
Diagnostic algorithm (Fig. 34.2): integrates symptoms with ECG, labs, and imaging.
Intervention targets:
Treat underlying rhythm disturbance if identified (e.g., SVT, VT).
Refer to cardiology for rhythm disturbances; ensure patient safety and optimal outcomes.
Syncope
Definition: abrupt loss of consciousness lasting minutes, due to decreased cerebral blood flow from reduced cardiac output.
Epidemiology: bimodal distribution—peaks in late adolescence/early adulthood and after 70 years; older adults often have multiple comorbidities complicating diagnosis.
Cardiac-related syncope carries high mortality risk; common causes include arrhythmias (tachycardia-bradycardia syndromes, sick sinus syndrome), AV block, SVT/VT, and congenital conditions like long QT and Brugada syndromes.
Differential diagnosis:
Cardiac outflow tract obstruction (e.g., hypertrophic cardiomyopathy, aortic stenosis) often provoked by activity or stress.
Presyncope differs from syncope (lightheadedness, weakness) and vertigo involves spinning sensation.
Diagnostic work-up:
History/physical tailored to arrhythmia risk; tilt-table testing for orthostatic syncope.
Work-up mirrors palpitations (ECG, labs, imaging) to identify cause.
Intervention:
Treat underlying rhythm disorder (ablation, ICD, permanent pacemaker as indicated).
Refer to cardiology for specialized management.
DYSPNEA (Shortness of Breath)
Dyspnea is highly subjective and common; determine precipitating factors, quality, duration, alleviating factors, and duration after removal of trigger.
Dyspnea can be an anginal equivalent, especially in older adults and people with diabetes.
Diagnostic reasoning
Left-sided outflow tract obstruction (e.g., severe aortic stenosis, obstructive cardiomyopathy) reduces cardiac output and causes dyspnea.
Dyspnea with recurrent ischemia suggests pulmonary congestion from left heart failure or high LV filling pressures.
Right-sided valvular disease elevates pulmonary pressures and resistance to emptying of the right ventricle.
Pulmonary diseases (COPD, asthma, pleural effusion, pneumothorax, PE) and noncardiac causes (anemia, metabolic acidosis, obesity, deconditioning, anxiety).
Orthopnea: dyspnea when supine; may use multiple pillows (three-pillow orthopnea) and improve when upright.
Paroxysmal nocturnal dyspnea (PND): occurs 1-2 hours after sleep; redistribution of fluids increases left atrial pressure; relieved by upright posture within 10-30 minutes.
Assessment and red flags:
Severity correlation with objective findings varies; dyspnea is a poor specific marker for cardiovascular disease.
Evaluate daily activity impairment and co-symptoms (wheezing, weight gain) to distinguish HF.
LEG Aches (Peripheral Vascular Symptoms)
Peripheral vascular disease (PVD) can affect arteries (atherosclerosis) or veins (venous insufficiency).
Arterial disease: atherosclerosis with fatty streaks and plaques affecting lower extremities.
Venous disease: chronic venous insufficiency and varicose veins; leg pains due to venous obstruction.
Differential diagnosis for leg aches:
Thrombosis, phlebitis, polycythemia, anemia, Raynaud’s, Buerger’s disease, smoking, HTN, diabetes.
Peripheral arterial disease and DVT discussed in Chapter 37.
Diagnostic approach: history and exam; Doppler studies for DVT; imaging for edema etiologies; labs as indicated.
Diagnostic algorithm: peripheral edema (Fig. 34.3) guides distinguishing chronic vs acute edema and underlying etiologies.
Peripheral Edema (Diagnostic Reasoning Algorithm: Peripheral Edema)
Peripheral edema = accumulation of interstitial fluid in extremities; etiologies include cardiac (HF, chronic venous insufficiency, thrombophlebitis), renal/hepatic disease, trauma, tumors, inflammation, iatrogenic causes (high salt intake, sodium-retaining meds, vasodilators).
Diagnostic approach:
History and physical to identify underlying cause; labs to guide etiology: CBC, urinalysis, serum chemistries, thyroid profile; chest x-ray for cardiac/pulmonary involvement; CT for edema distribution and venous/lymphatic obstruction; ECG to assess rhythm; Doppler ultrasound for DVT.
Important to identify and treat the underlying cause; edema without treatment may progress to tissue ischemia.
HYPERTENSION (HTN)
Epidemiology and public health:
HTN affects ~85.7 million in the US; HP2030 aims to reduce HTN prevalence and improve control; ~50% of HTN patients lack BP control.
Pathophysiology: Essential (primary) HTN is multifactorial; endothelial dysfunction central; imbalance between nitric oxide (vasodilator) and endothelin-1/angiotensin II (vasoconstrictors); kidney sodium handling and renin-angiotensin-aldosterone system (RAAS) dysregulation; sleep apnea and metabolic syndrome contribute; genetic and ethnic factors; obesity increases risk.
Box 35.1 Metabolic Syndrome (3 of 5 factors; definitions below):
Central obesity: Waist circumference >40 inches (men) or >35 inches (women)
Fasting triglycerides ≥130-150 mg/dL (depending on criteria)
HDL-C: <40 mg/dL (men) or <50 mg/dL (women) considered adverse; ≥60 mg/dL protective
Blood pressure ≥130/85 mm Hg
Fasting glucose ≥100 mg/dL
Note: any three of these constitute metabolic syndrome; etiology linked to insulin resistance; central obesity is a key driver; obesity increases inflammation and thrombosis risk.
Secondary HTN: identifiable reversible causes (5-10% of cases in primary care); obesity, sleep apnea, renovascular disease, corticosteroids, Cushing’s syndrome, primary hyperaldosteronism, pheochromocytoma, coarctation, endocrine disorders; drugs (NSAIDs, COX-2 inhibitors, decongestants, stimulants, OCPs, erythropoietin, cocaine, amphetamines, corticosteroids, tacrolimus, cyclosporine, ephedra).
White coat hypertension: ~13% prevalence; transient BP rise in clinic; 30-40% of clinic HTN diagnoses show normal out-of-office BP; use ambulatory BP monitoring (ABPM) to confirm.
Masked hypertension: HTN present in daily life but absent in clinic; up to ~1 in 7 individuals; ABPM or home monitoring recommended for high-risk individuals.
Malignant hypertension (hypertensive emergency/crisis): BP ≥ mm Hg with acute TOD (e.g., stroke, myocardial ischemia, renal failure); hypertensive urgencies treated with oral meds over 24-48 hours; emergencies require inpatient IV therapy; TOD examples include cerebrovascular events, acute myocardial ischemia, HF, pulmonary edema, aortic dissection, acute renal failure, catecholamine excess states, eclampsia.
Clinical presentation and objective evaluation:
History: assess CV risk factors, medications (NSAIDs, sympathomimetics), sleep apnea, smoking, pregnancy status; ethnicity (African Americans higher risk and different drug responses).
Diagnosis requires multiple office readings; BP measurement technique matters:
Seated position, arm at heart level, 5-minute rest, appropriate cuff size (bladder length ~80% of arm circumference; width ~40%), take two readings 2 minutes apart; use bilateral measurements if feasible; stand for 2 minutes and re-measure; report higher reading.
Abnormal measurements warrant staged approach and TOD assessment including funduscopy, PMI, heart/lung exam, abdominal aorta/bruits, carotid bruits, peripheral pulses, neuro exam, ECG, urinalysis, creatinine, chemistries, and chest X-ray; head CT if mental status changes.
Assess for TOD signs: hypertensive retinopathy (arteriolar narrowing, AV nicking, hemorrhages, exudates, papilledema), abdominal bruit (renal artery stenosis or aneurysm), displaced PMI/S4 (LVH), S3/S4 heart sounds, crackles, edema, LV dysfunction indicators.
Diagnostic reasoning and tests:
ECG, echocardiography (LVH, wall thickness), urinalysis, BUN/creatinine, electrolytes, lipid panel, and glucose tests.
2017 ACC/AHA HTN classification (Executive summary):
Normal < 120/80
Elevated SBP 120-129 and DBP < 80
Stage 1: SBP 130-139 or DBP 80-89
Stage 2: SBP ≥140 or DBP ≥90
Management:
Lifestyle modifications (Box 35.2) are foundational for all HTN patients.
Pharmacologic therapy: typically start with one first-line agent (thiazide diuretic, ACEI, ARB, or CCB). Consider African American patients for thiazide or CCB first-line; CKD patients benefit from ACEI/ARB to achieve SBP < 130 and DBP < 80.
Be mindful of comorbidities: HF, CAD, diabetes; adjust therapy accordingly (ACEI/ARB, beta-blockers, CCBs, diuretics, aldosterone antagonists, etc.). Avoid ACEI-ARB combinations due to no added benefit and potential risk; monitor for hyperkalemia with RAAS inhibitors; monitor renal function.
Dosing strategy: start low, go slow; reassess in 1 month; if goal not achieved, up-titrate or add a second agent; if two agents fail, consider a third; referral to HTN specialist if refractory.
Combination therapies: ACEI-CCB, ACEI-diuretic, ARB-diuretic, central agent + diuretic, diuretic combos; fixed-dose combos can improve adherence and efficacy (e.g., low-dose chlorthalidone at 12.5 mg boosting other agents).
Special notes:
Obesity/metabolic syndrome increases HTN risk and may affect drug response.
Beers criteria for older adults; avoid potentially inappropriate antihypertensives.
Elderly: monitor for postural hypotension; counsel on gradual position changes; hydration is important.
Targets and risk estimation:
For diabetics and CKD patients, specific BP goals may differ (e.g., <130/80 for many with diabetes or CKD with proteinuria).
ASCVD 10-year risk calculation guides statin therapy decisions (see Dyslipidemia section).
Dyslipidemia
Definition and epidemiology:
Dyslipidemia = elevated lipids/lipoproteins; major CV risk factor; 2017 CDC data: many adults have TC > 200 mg/dL or TG > typical thresholds; dyslipidemia often coexists with HTN and diabetes.
ACC/AHA guidelines emphasize statin therapy for higher-risk groups to reduce ASCVD events; high-intensity statins for ASCVD patients or LDL ≥ 190 mg/dL; moderate-intensity for other indicated groups.
Lipid biology (pathophysiology):
Lipoproteins carry cholesterol; LDL, VLDL, IDL, Lp(a) contribute to atherogenesis; HDL mediates reverse cholesterol transport and protection from oxidation.
LDL cholesterol (LDL-C) deposits cholesterol in arterial plaques; oxidized LDL promotes foam cell formation and atherosclerosis.
Triglycerides (TG) contribute to atherogenesis; HDL-C protects by reversing cholesterol transport and inhibiting LDL oxidation.
LDL-C, TG, HDL-C values form the basis of lipid risk stratification; TC combines LDL-C, TG/5, and HDL-C per the equation below.
Important relation: Atherogenic non-HDL cholesterol includes LDL, IDL, Lp(a), and VLDL components; non-HDL is often a better risk predictor in certain populations.
Diagnostic reasoning and targets:
Four groups for primary prevention/statin therapy per ACC/AHA: ASCVD; LDL ≥ 190 mg/dL; diabetes age 40-75 with LDL 70-189 mg/dL; no ASCVD/diabetes but LDL 70-189 mg/dL with 10-year ASCVD risk ≥ 7.5%
Testing strategy targets high-risk groups with high-intensity statins and lower-risk groups with moderate-intensity statins to meet lipid goals.
Secondary causes of dyslipidemia should be ruled out (obesity, diabetes, hypothyroidism, nephrotic syndrome, liver disease, medications, estrogen, Cushing’s, alcohol, pregnancy, etc.).
Lipids and cutoffs (Table 35.3, NHLBI/NCEP framework):
TOTAL CHOLESTEROL (mg/dL): Desirable 125 ext{ to } <200; Borderline high ; High
TRIGLYCERIDES (mg/dL): Normal < ; Borderline high ; High ; Very high
HDL (mg/dL): Low < ; High > (cardioprotective if ≥60)
LDL (mg/dL): for high-risk patients (e.g., diabetes/ASCVD) targets often < ; for general patients, targets range from < to < depending on risk
Pathophysiology of dyslipidemia:
Abnormalities in LDL, VLDL, IDL, Lp(a) promote atherogenesis; HDL removes cholesterol from vessels; apolipoprotein and genetic factors (e.g., familial hypercholesterolemia) drive severe elevations.
Genetic and secondary factors interplay; metabolic syndrome often features dyslipidemia as part of a cluster with HTN and insulin resistance.
Clinical presentation and differential:
Most dyslipidemia patients are asymptomatic; physical findings include carotid bruit or corneal arcus; xanthomas/xanthelasma may appear in certain dyslipidemias.
Secondary causes listed in Table 35.4 (e.g., obesity, diabetes, hypothyroidism, nephrotic syndrome, hepatic disease, medications).
Diagnostic reasoning and risk stratification:
Four ASCVD-risk-based groups guide statin intensity: high-intensity statins for ASCVD or LDL ≥ 190 mg/dL or diabetes age 40-75 with LDL 70-189 mg/dL; moderate-intensity for others with 10-year ASCVD risk ≥ 7.5% or LDL 70-189 with risk but no ASCVD/diabetes.
Management:
Primary goals: lower LDL, lower TG, raise HDL to reduce CV events.
Diet: cholesterol-lowering diet for all; avoid very low-fat diets that reduce protective HDL-C; Mediterranean pattern recommended; restrict saturated fat and total fat.
Pharmacologic therapy: statins are first-line; LDL reduction ~50% on average with high-intensity statins; monitor liver enzymes and CK if myopathy symptoms; avoid gemfibrozil with statins due to interaction risk.
Statin dosing examples (Drugs Commonly Prescribed 35.2):
High-Intensity: Atorvastatin 40-80 mg; Rosuvastatin 20-40 mg
Moderate-Intensity: Atorvastatin 10-20 mg; Lovastatin 40-80 mg; Pravastatin 40-80 mg; Rosuvastatin 5-10 mg; Simvastatin 20-40 mg; Pitavastatin 2-4 mg
Combination therapies (statin-based) include statin+ezetimibe, statin+niacin, statin+PCSK9 inhibitors (not detailed in text), and fixed-dose combinations with diuretics or CCBs; adverse effects include myopathy, liver enzyme elevations, GI effects, and interactions with fibrates, niacin, grapefruit juice, anticoagulants; caution with pregnancy, liver disease, and renal impairment.
Patient education and follow-up:
Ongoing education about lifestyle and pharmacotherapy; use of risk calculators to discuss ASCVD risk and statin benefits; shared decision making encouraged (Circle of Caring model).
FH may require endocrinology referral; nutritionist involvement for diet adherence; regular follow-up to monitor lipids and adherence.
Coronary Heart Disease (CHD) and Acute Coronary Syndrome (ACS)
CHD is a leading cause of death in the U.S.; incidence increases with age; more than 18 million Americans affected; CHD costs ~ $219 billion/year.
Risk factors for CHD categorized as nonmodifiable, modifiable, and contributing.
Nonmodifiable: male gender, increasing age, family history of CAD, ethnicity (African, Indigenous, Hispanic descent).
Modifiable: HTN, smoking, excessive alcohol, sedentary lifestyle, unhealthy diet, hyperlipidemia, diabetes, obesity, stress (also racial/ethnic disparities).
Pathophysiology of CHD:
Coronary arteries supply myocardium; atherosclerosis leads to plaque formation, endothelial injury, inflammation, and plaque rupture leading to thrombus formation and myocardial ischemia.
Inflammation (ILs, TNF-α, CRP) and endothelial dysfunction reduce nitric oxide; foam cells form; plaques become calcified and brittle; rupture triggers thrombosis and possible embolization, causing ischemia.
Ischemia can progress to myocardial infarction if sustained; risk of arrhythmias and HF after ischemic injury.
Clinical presentation and diagnostic approach:
CHD often develops silently; exertional angina is common presenting symptom; angina may radiate to left arm/jaw; associated symptoms include nausea, dyspnea, lightheadedness.
In women and older patients, angina may present as anginal equivalents (dyspnea, fatigue, GI symptoms).
Objective exam: check peripheral pulses, carotid bruits, JVP, skin perfusion, BP in multiple positions, signs of vascular disease.
Diagnostic testing for CHD/ACS:
Exercise ECG (treadmill stress test) or nuclear stress imaging assesses inducible ischemia; dipyridamole thallium imaging for those unable to exercise; contraindicated in acute CVD.
CT coronary calcium scoring quantifies plaque burden;