Week 3 · Cardiovascular Disorders II — Interactive Reading Report

Orientation

How to read this week

Week 3 is one disease with many faces. Coronary artery disease is the substrate; everything else is what it becomes. Half the week is the ischemic clock — angina, infarction, and the race to reopen the artery. The other half is structure and electricity — valves, inflammation, pulmonary and peripheral flow, and the rhythms that sustain or stop the pump.

Half one

The ischemic clock

Angina — stable, Prinzmetal, unstable, microvascular
Acute coronary syndromes — UA, NSTEMI, STEMI
Serum cardiac enzymes & the ECG
Reperfusion — fibrinolytics, PTCA/PCI, CABG
Cardiac tamponade

Diagnostic currency: the ECG, serial enzymes, and a clock.

Half two

Structure, flow & electricity

Pericarditis & endocarditis
Valvular disease — stenosis & regurgitation
Pulmonary hypertension & embolism
Peripheral arterial & venous disease
Cardiomyopathy
Arrhythmias & antiarrhythmics

Diagnostic currency: echo, cultures, right-heart catheter, and the rhythm strip.

Your reading map

The seven chapters behind this week
Ch.	Title	What it actually contains
14	Angina & Acute Myocardial Infarction	Angina types · ACS (UA/NSTEMI/STEMI) · cardiac enzymes · fibrinolytics · PTCA/PCI · CABG · tamponade Tables 14.1–14.4
17	Inflammatory Cardiac Diseases	Pericarditis · Endocarditis (organism-directed regimens) · prophylaxis Tables 17.1–17.7
19	Valvular Disease	Mitral stenosis · Mitral regurgitation · MVP · Aortic stenosis · Aortic regurgitation · interventions & anticoagulation
28	Pulmonary Hypertension & Vascular Disorders	PH/PAH WHO groups · PAH pharmacotherapy (Table 28.1) · Pulmonary embolism · Vasculitis
20	Cardiomyopathy	Dilated · Hypertrophic · Restrictive
16	Peripheral Vascular Disease	PAD · Buerger's · CVI · Superficial thrombophlebitis · DVT
21	Arrhythmias	Sinus → blocks · Afib/flutter · SVT · VT/VF · antiarrhythmics (Table 21.1) · anticoagulation (Table 21.5)

The organizing principle

Ischemia is treated with a clock; the rest is treated with a diagnosis. A STEMI gets a drug or a balloon measured in minutes. A valve, an organism, a rhythm, or a clot each gets a specific, named answer — then a drug, a device, or a procedure that follows.

The numbers worth carrying in

~10 M

Americans with angina

The population the ischemic half of this week is built around.

1 in 4

deaths from CHD

One of every four deaths in the United States is caused by coronary heart disease.

>525 K

new MIs each year

Plus 210,000 recurrent attacks and ~150,000 "silent" MIs annually.

90 min

door-to-balloon

The national STEMI target for angioplasty — versus 30 min door-to-fibrinolytic.

Chapter 13 · referenced throughout

Coronary Artery Disease & Hyperlipidemia

CAD is the substrate every other chapter sits on. This week's excerpt does not print Chapter 13 in full — it cites it as the shared risk-factor and lipid source for angina, MI, and peripheral disease. What follows is everything the reading gives you about the risk factors that build the plaque and the statin therapy that follows the event.

A note on the source

"Coronary Artery Disease and Hyperlipidemia" (Chapter 13) is referenced repeatedly ("same as for CAD — see Chapter 13"), but its full text is not in this week's excerpt. The reading covers CAD through its risk factors and its clinical expression (angina, MI, PAD), plus the statin prescribing that appears in those chapters. No LDL/HDL targets or lipid-panel thresholds are stated in the excerpt, so none are reproduced here.

Predisposing

What builds the plaque

Coronary artery disease
Hypertension
Metabolic syndrome
Obesity — BMI > 30 kg/m²
Cigarette smoking
Diabetes mellitus — type 1 and 2

Predisposing

What you cannot change

Male gender — more prevalent until age 65, then equal
Family history
Sedentary lifestyle
Diet
Psychological stress

Downstream

What CAD becomes

Angina — rupture of atherosclerotic plaques or coronary spasm
Acute myocardial infarction
Peripheral arterial disease — arteriosclerosis obliterans shares the same risk factors
Ischemic heart disease is the most common cause of VT/VF

The lipid therapy the reading actually gives you

Lifestyle: cholesterol control, blood pressure control, weight loss, and smoking cessation are first-line in stable angina.
Acute ACS: a high-intensity statin is part of the emergency/post-event regimen.
Post-MI: atorvastatin (Lipitor) 80 mg once daily or rosuvastatin (Crestor) 20–40 mg once daily.
PAD: a moderate-intensity statin is indicated in patients older than 75 with peripheral arterial disease.

The clinical expression of this substrate is the subject of the next two sections — the angina/MI story and the reperfusion machinery that treats it.

Chapter 14

Angina & Acute Myocardial Infarction

Angina is "squeezing and choking of the chest" from ischemia; MI is necrosis of myocardial tissue. Both share one pathology: a supply/demand mismatch — myocardial oxygen demand exceeds what the coronary arteries can supply.

80%

of MI deaths > age 65

Four of every five deaths related to MI occur in individuals older than 65.

~30%

no immediate ECG changes

About 30% of MI patients show no immediate 12-lead ECG changes.

15%

of MIs are painless

Lack of pain is especially common in diabetic patients and the elderly (neuropathy).

50%

mortality reduction

Fibrinolytic therapy within 1–3 hr of pain onset may cut STEMI mortality by up to half.

Unstable angina

New onset of symptoms, or a change in pattern or frequency of symptoms.

ECG may show ST depression with transient T-wave inversion; no enzyme elevation.

NSTEMI

Non-ST-elevation MI

Angina — or a "silent MI" — with elevated enzymes but no ST elevation on the 12-lead ECG.

May show ST depression or T-wave inversion.

STEMI

ST-elevation MI

Acute injury requiring the blocked artery be opened: chest pain not relieved by NTG, elevated enzymes, and ST elevation.

The four anginas

Stable

Chronic / classic

Predictable — same onset, intensity, duration
Induced by exertion or emotional upset
Lasts 1–5 min (max 10–20)
ST depression during pain
Relieved by NTG or rest

Prinzmetal

Variant / vasospastic

Coronary artery spasm
At rest, up to 30 min
May occur without atherosclerosis
ST elevation during the event
Managed with CCBs
Triggered by sumatriptan, amphetamines, alcohol, cocaine

Unstable

Preinfarction / crescendo

Pain > 20–30 min
New onset, or more severe; at rest or low activity
Progresses in frequency, duration, intensity
ST depression ± transient T inversion
Follow ACS protocol
Higher MI risk within 6 months

Microvascular

Syndrome X

Pain mimics angina
Stress test positive for ischemia
Normal angio / CT / no spasm
Coronary microvascular dysfunction

Pain — angina vs. infarction

Angina

More diffuse & vague

Discomfort, pressure, or squeezing
May radiate to upper chest, epigastrium, arm, jaw, neck, back
Relieved by NTG/rest

"Vise-like," crushing, substernal

Crushing substernal pressure; may radiate to jaw and/or left arm
Also aching, cramping, grinding, burning, stinging, tearing, gnawing
~15% have no pain — especially diabetic patients and the elderly (neuropathy)
Women report more GI-like symptoms, back radiation, fatigue, dyspnea
Not relieved by NTG

P-Q-R-S-T — the pain assessment

Provocative — what brings it on?
Quality — what does it feel like? Other symptoms?
Region/radiation — where, and does it radiate?
Severity — rate 0–10 (some institutions 0–5)
Timing/treatment — when did it start, how long, what relieved it?

If the pain is from an acute GI cause (esophagitis, gastritis, ulcer), a "GI cocktail" (Maalox/Mylanta, viscous lidocaine, Donnatal) should relieve it immediately.

Reading the ECG & the enzymes

ECG

Ischemia → injury → infarction

Ischemia: T-wave inversion, peaked T waves, ST depression (with angina, resolves once pain is relieved)
Injury: ST elevation > 1 mm above baseline
Infarction: pathologic Q waves — > 25% of QRS height or > 1 mm wide (0.04 s)
~30% of MIs show no immediate 12-lead ECG changes

Site by leads

Where is the infarct?

Inferior II, III, aVF — RCA (80–90%) or left circumflex (10–20%)
Anterior V3, V4 — LAD
Anteroseptal V1, V2, V3 — LAD
Lateral I, aVL, V5, V6 — LAD or left circumflex
Posterior reciprocal V1–V3 (tall R, ST depression) — RCA or left circumflex
Right ventricular V4R–V6R

Serum cardiac enzymes — how soon each one rises

Time to first detectable increase. Hover a bar for peak and duration; the full table follows.

Troponin — preferred, myocardial-specific Other markers

Table 14.2 — Serum cardiac enzymes
Marker	Earliest increase	Peak	Duration	Other causes of elevation
Troponin T	4–6 hr	10–24 hr	14–21 days	Regenerative muscular disorders, unstable angina
Troponin I	4–6 hr	10–24 hr	5–7 days	100% specific for myocardial necrosis
Myoglobin	2–3 hr	6–9 hr	3–15 hr	Regenerative muscular disorders, unstable angina
CK-MB	4–8 hr	15–24 hr	48–72 hr	Post-cardioversion, myocarditis, contusion, cardiac surgery, pericarditis
Total CK	3–6 hr	24–36 hr	18–30 hr	Smooth muscle injury, nonspecific
LD1	8–12 hr	72–144 hr	7–12 days	Hemolytic/megaloblastic anemias, renal infarction, hemolysis, testicular cancer
Total LD	10–12 hr	48–72 hr	10–14 days	Smooth muscle injury, nonspecific

Troponin is the preferred biomarker for ACS; troponin I rises slightly faster than troponin T (3 hr vs. 6 hr). Because enzymes rise at different times, serial testing every 6–8 hr is needed.

hs-CRP — the three risk strata

High-sensitivity C-reactive protein predicts future coronary events after UA/MI. Hover a bar for its value.

Low Average High

Emergency management of ACS

Step	Dose / route	Notes
Aspirin	162–325 mg PO, chew and swallow	If allergic, consider clopidogrel as a substitute.
Nitroglycerin	0.4 mg SL (1 every 5 min × 3); IV after opioid if needed	Use extreme caution in inferior MI — preload drop → hypotension.
Oxygen	2–4 L/min nasal cannula	Only if SaO₂ < 92% and cyanotic or in respiratory distress.
Morphine	0.1 mg/kg IV, 2–4 mg; repeat 2–8 mg q5–15 min	Class IIB recommendation — for pain not relieved by anti-ischemic therapy.
β-blocker	Metoprolol 25–50 mg PO, titrate; maintenance 50–100 mg BID	Start oral within 24 hr. No routine IV β-blockers. Taper over 1–2 weeks if stopping.
Heparin	60 mcg/kg IV bolus then 12 mcg/kg/hr infusion	PTT 1.5–2. Antagonist = protamine sulfate.
Enoxaparin	1 mg/kg SC q12h for 2–8 days	Alternative to UFH, especially NSTEMI/UA. Monitor platelets.
Tirofiban (GP IIb/IIIa)	0.4 mcg/kg/min × 30 min, then 0.1 mcg/kg/min	With heparin for NSTEMI; continue through angio and 12–24 hr after. Monitor bleeding.
NTG IV drip	Start 5–10 mcg/min, titrate +5–10 mcg/min q5min	Until pain relieved or systolic BP < 90 mmHg.
Statin	High-intensity	Part of the post-event regimen.

Admit to CCU or a 23-hr observation unit to rule out NSTEMI/STEMI pending enzymes. Bedside monitoring, IV access (draw enzymes), pulse oximetry, continuous pain assessment, and a 12-lead ECG within 10 min of presentation.

Abciximab (ReoPro) — for PCI only, not ACS: 0.25 mg/kg IV bolus, then 0.125 mcg/kg/min (max 10 mcg/min) for 12 hr.
Eptifibatide (Integrilin) — 180 mcg/kg IV (max 22.6 mg) over 1–2 min, then 2 mcg/kg/min (max 15 mg/hr) for up to 72 hr. If PCI planned, reduce infusion to 0.5 mcg/kg/min and continue 20–24 hr after the procedure (up to 96 hr total).

Outpatient & post-MI management

Nitrates: SL/buccal spray 0.4 mg ~5 min before exertion. Long-acting: isosorbide dinitrate (Isordil) 5–40 mg TID (most common); isosorbide mononitrate (Ismo) 20 mg BID (7 hr apart); NTG sustained-release 2.5–6.5 mg q8–12h; NTG patches 5–40 mg/24h with a nitrate-free interval (12–14 hr on, 10–12 hr off).
β-blockers: metoprolol 50 mg (in two doses) then 100 mg; carvedilol 6.25 mg BID → 25 mg BID; nadolol 20 → 40–80 mg (max 240); atenolol 25 → 100 mg; propranolol 40 → 180–240 mg divided; nebivolol 5 mg → max 40 mg.
CCBs (Class IB for ACS when β-blockers are contraindicated, with normal LV function): diltiazem, verapamil; amlodipine/felodipine as adjuncts with β-blockers.
Ranolazine 500–1000 mg BID — adjunct for refractory angina.
Antiplatelet: aspirin 81 mg daily; clopidogrel 75 mg daily if aspirin-intolerant. For UA/NSTEMI: aspirin plus clopidogrel for 12 months.

β-blocker — e.g., metoprolol succinate (Toprol XL) 50 mg once daily.
Aspirin 81 mg daily indefinitely.
ACE inhibitor — captopril 12.5–50 mg TID, especially for EF < 40%, beginning 3–16 days after infarction. ARB if ACEI-allergic.
Statin — atorvastatin 80 mg once daily or rosuvastatin 20–40 mg once daily.
Stress testing 3–4 weeks after MI; repeat ECG at 3 months, then every 1–2 years.
Cardiac rehabilitation; address DM, HTN, and post-MI depression.

Complications of MI

Arrhythmias · heart failure · pulmonary edema · cardiogenic shock (the most common fatal complication) · ventricular septal rupture · papillary muscle rupture · pericarditis · infection (leg wound, sternotomy, or systemic).

Chapter 14

Reperfusion — Fibrinolytics, PTCA/PCI, CABG

A STEMI is a clock, and reperfusion is the answer. 90% of all STEMI involve a thrombus, so the strategy is to lyse it, balloon it, or bypass it — with the fastest safe option winning.

The reperfusion clock

Door-to-needle vs. door-to-balloon, and where the "no preference" window sits. Hover each zone.

Fibrinolytic window Angioplasty window Greatest benefit

Fibrinolysis preferred if

Lysis first

Early presentation — ≤ 3 hr from symptom onset
Invasive strategy not an option (no skilled PCI access) or would be delayed
Door-to-balloon > 90 min; (door-to-balloon) − (door-to-needle) > 1 hr
No contraindications to fibrinolysis

Invasive preferred if

Balloon first

Late presentation — symptom onset > 3 hr ago
Skilled PCI facility with surgical backup; door-to-balloon < 90 min
Contraindications to fibrinolysis (bleeding/ICH risk)
High-risk STEMI (CHF, Killip class ≥ 3) · diagnosis in doubt

Fibrinolytic / thrombolytic therapy

Preferred treatment for STEMI if PCI is not available within 90 min. Indicated for unrelieved chest pain of recent onset (> 30 min but < 6 hr; variations used up to, but not beyond, 24 hr) and ST elevation (1 mm in limb leads, 2 mm in precordial leads, two contiguous leads), Q waves, or bundle branch block. Greatest benefit 1–3 hr — mortality may be reduced by 50%.

Agent	Dosage / infusion	Peak · Duration · Fibrin-specific
Alteplase (t-PA)	15 mg bolus, then 50 mg over 30 min, then 35 mg over 1 hr (max 100 mg)	Peak 45 min · duration 6 hr–2 days · fibrin-specific · reocclusion 10–30%
Streptokinase	750,000 units over 20 min, then 750,000 units over 40 min	Peak 20 min–2 hr · duration 6–24 hr · not fibrin-specific · allergic reactions possible · reocclusion 5–20% · single lifetime use
r-PA (reteplase)	10-unit bolus over 20 min, repeated in 30 min	Fibrin-specific · longer half-life than t-PA · reocclusion unknown
TNKase (tenecteplase)	IV bolus over 5 s, weight-based (max 50 mg): < 60 kg → 30 mg; 60–70 kg → 35 mg; 70–80 kg → 40 mg; 80–90 kg → 45 mg; > 90 kg → 50 mg	Half-life 20 min · fibrin-specific · reocclusion 5–20%

Anticoagulation after lysis: alteplase/r-PA → aspirin 325 mg daily + heparin 5,000-unit bolus then 1,000-unit/hr (maintain PTT 1.5–2 × control). Streptokinase → aspirin 325 mg daily (no heparin evidence). TNKase → baby aspirin 160 mg + heparin 5,000 units IV then 750–1,000 mg/hr continuous. Monitor for signs of reperfusion: abrupt pain relief, ECG normalization/Q waves, reperfusion arrhythmias (accelerated idioventricular rhythm, sinus bradycardia, VT, VF), improved capillary refill and oxygen saturation.

Absolute / major

Active bleeding
Major trauma or surgery < 3 months ago
History of hemorrhagic stroke, intracranial aneurysm, or tumor
Ischemic stroke within the past 3 months
Severe HTN — SBP > 180 mmHg or DBP > 110 mmHg uncontrolled
Pregnancy
Aortic dissection
Acute pericarditis

Relative

Recent GI bleeding
HTN > 165/95 mmHg
Prolonged/traumatic CPR > 10 min
Cardiogenic shock — consider PTCA instead
Ischemic stroke or cerebrovascular disease > 3 months ago
History of intraocular bleeding

Major complication: hemorrhage, including intracranial hemorrhage. ICH risk is doubled over age 75, and increased with weight < 70 kg or severe HTN.

Ischemic stroke or cerebrovascular disease > 3 months ago; history of intraocular bleeding.

PTCA / PCI

A balloon-tipped catheter is inserted percutaneously (radial or femoral artery) into the coronary arteries under fluoroscopy; the balloon compresses plaque against the arterial wall. Stents (bare-metal and drug-eluting) are used with PTCA to restore flow to TIMI 3.

Bare-metal stents

When you worry about bleeding

For patients at high bleeding risk, those who may need surgery within 12 months, or those unlikely to comply with 12 months of dual antiplatelet therapy.

Drug-eluting stents

Require 12 months of DAPT

Currently require 12 months of dual antiplatelet therapy (aspirin and clopidogrel).

PTCA is preferred when

Immediately available — < 90 min of arrival — or fibrinolytics are contraindicated
ST depression or elevation; evolving MI; angina (recent, or stable but unresponsive to medical treatment)
Adequate ventricular function and collateral circulation; relatively proximal, noncalcified lesions < 10 mm not involving a major bifurcation

Watch for: restenosis in 30–40% (angina, ST elevation, arrhythmias → emergency repeat PTCA or CABG); contrast dye allergy; hematoma/false aneurysm; retroperitoneal bleed if femoral access; coronary perforation/rupture, embolism, spasm, or MI.

CABG surgery

Grafts

What is used

Internal mammary artery — better long-term patency
Saphenous vein
Gastroepiploic artery
Radial artery

Indications

When to operate

Refractory unstable angina
MI
Failure of PTCA
> 50% left main occlusion
Triple-vessel coronary artery disease
LV failure from CHF or cardiogenic shock

PCI / PTCA

Catheter and balloon

Preferred if available < 90 min, or fibrinolytics contraindicated
Best for proximal, noncalcified, short (< 10 mm) lesions
Drug-eluting stents need 12 months DAPT
Restenosis 30–40%

CABG

Surgical grafting

For refractory UA, MI, PTCA failure, > 50% left main, triple-vessel disease, LV failure
Post-op AF in 20–30%; CVA in 5–10%
Extubate within 2–6 hr; K⁺ 4.5–5.0, Mg ~2.0 mEq/L
Re-explore if chest tube output > 400 mL/2 hr or 300–500 mL/1 hr

Warfarin INR targets (Table 14.4)

The same anticoagulant, different goals by indication. Hover each range. Normal INR is 0.8–1.2.

Normal Atrial fibrillation DVT / PE MI / mechanical valve

Implications for the elderly

The majority of elderly patients with an acute MI have nondiagnostic ECG changes or present with NSTEMI.
Age > 75 → more likely a silent MI; age > 85 → more likely LBBB or signs of heart failure.
Clopidogrel loading dose is 75 mg (not 300 mg) for patients > 75 receiving fibrinolysis.
Patients > 75 have better outcomes with PCI than with thrombolytic therapy; hemorrhagic stroke risk after thrombolysis is greater over age 85.

Chapter 16

Peripheral Vascular & Venous Disease

Disorders of the peripheral arteries and veins, affecting about 1 in 5 adults, with prevalence rising 15–20% over age 70. The risk factors are the same as for CAD — over 95% of patients have at least one, over 75% have two.

PAD / PAOD

Peripheral arterial disease

Occlusive arterial disease of the limbs — most common in the lower extremities. Strongest associations: diabetes mellitus and smoking.

The six Ps: Pain (intermittent claudication to calf, thigh, or buttock) · Pallor · Pulselessness (diminished distal to the obstruction) · Paresthesias · Paralysis · Poikilothermia.

CVI

Chronic venous insufficiency

Venous outflow disturbance of the limbs, with or without valvular insufficiency. Risk factors: female, obesity, prolonged standing, multiparity, age.

Legs ache with standing, improve with elevation; edema, hyperpigmentation, and "wet" shaggy ulcers near the medial malleolus (gaiter region).

Peripheral arterial disease — reading it

Rutherford categories of PAD
Category	Description	Ankle pressure findings
0	Asymptomatic	Normal treadmill
1	Mild claudication	Completes treadmill; post-exercise ankle pressure > 50 mmHg but ≥ 20 mmHg below resting
2	Moderate claudication	Between categories 1 and 3
3	Severe claudication	Cannot complete treadmill; post-exercise ankle pressure < 50 mmHg
4	Ischemic rest pain	Resting ankle pressure < 60 mmHg; toe pressure < 40 mmHg
5	Minor tissue loss	Nonhealing ulcer, focal gangrene; ankle < 40, toe < 30 mmHg
6	Major tissue loss	Extends above transmetatarsal level; same as category 5

The ABI

Ankle–brachial index > 1.0 = normal; < 1.0 = PAD. Diabetes, chronic renal failure, and the very elderly have dense, poorly compressible vessels that can produce a falsely elevated ABI — use the toe–brachial index (TBI) instead; a TBI < 0.7 is consistent with PAD.

Cilostazol (Pletal) 100 mg PO BID for claudication (inhibits platelet aggregation, induces vasodilation). Contraindicated in the elderly with heart failure. Side effects: headache, diarrhea, dizziness, palpitations.
Pentoxifylline (Trental) — not effective, no longer recommended.
Aspirin 81–325 mg daily or clopidogrel 75 mg daily to reduce MI/stroke/thrombotic risk.
Moderate-intensity statin in patients > 75 with PAD.
Anticoagulation should NOT be used to reduce cardiovascular events in PAD.
Foot care, well-fitting shoes, structured exercise, and smoking cessation. Avoid compression with ABI < 0.7 (unless coexistent arterial + venous disease under a vascular provider).
BP goal < 130/88 mmHg; ACEI/ARB to reduce ischemic CV events.

Specific disorders — filter by side of the circulation

Filter

Arterial

Arteriosclerosis obliterans (OAD)

Atherosclerotic stenosis/occlusion of the arterial lumen. Men 3:1, most common age 50–70; higher incidence in diabetic patients; lower extremities most affected.

Acute limb ischemia is a medical emergency — sudden severe pain, paresthesia, numbness, coldness, loss of distal pulse, cyanosis/pallor/mottling. Start heparin IV immediately; do not delay for imaging; emergent revascularization.

Arterial

Buerger's disease

Thromboangiitis obliterans — nonatherosclerotic inflammatory vasculopathy of small/medium arteries and veins in distal limbs. Men aged 20–40; strongly associated with smoking.

Smoking cessation is the only definitive treatment. Amputation occurs in 50% of those who continue to smoke.

Venous

Chronic venous insufficiency

Compression stocking tension by CEAP class: 20–30 mmHg (classes 2–3), 30–40 mmHg (classes 4–6), 40–50 mmHg (recurrent ulcers). Knee-length is most common. CEAP 4–6 often needs reconstructive treatment.

Venous

Superficial thrombophlebitis

IV cannulation is the most common cause; Staphylococcus is the most common infection. Palpable, cordlike, red, tender, warm vein; fever in 70%; 1 in 5 cases associated with DVT.

Management: elevation, warm compresses, NSAIDs.

Venous

Deep vein thrombosis

Virchow triad (stasis, endothelial injury, hypercoagulability) plus age > 40, surgery, female hormones, obesity, CHF, thrombophilia, autoimmune disease, varicose veins.

Aching throbbing pain, tenderness, Homan's sign (~40%, unreliable), edema distal to occlusion. D-dimer may be elevated; duplex ultrasonography confirms. See the treatment accordion below.

DVT treatment

Agent	Dose	Notes
Unfractionated heparin	80 units/kg bolus, then 18 units/kg/hr continuous IV	aPTT 1.5–2.5 × baseline, or anti-Xa 0.3–0.7 units/mL. Higher HIT risk.
Enoxaparin (Lovenox)	1 mg/kg SC q12h or 1.5 mg/kg SC once daily	Lower HIT risk. Contraindicated with HIT within 100 days or severe renal dysfunction.
Dalteparin (Fragmin)	200 units/kg SC q24h	LMWH alternative.
Tinzaparin (Innohep)	175 units/kg SC daily	May be contraindicated in morbid obesity or severe renal impairment.
Fondaparinux (Arixtra)	< 50 kg: 5 mg; 50–100 kg: 7.5 mg; > 100 kg: 10 mg SC daily	100% bioavailability; does not cause HIT.
Apixaban (Eliquis)	10 mg PO BID × 7 days, then 5 mg PO BID	Factor Xa inhibitor.
Rivaroxaban (Xarelto)	15 mg PO BID × 21 days, then 20 mg once daily	Factor Xa inhibitor.
Dabigatran (Pradaxa)	150 mg PO BID	Direct thrombin inhibitor; requires initial parenteral therapy first.
Warfarin (Coumadin)	First dose 5–10 mg PO daily	Continue heparin/LMWH until therapeutic. Goal INR 2–3 (> 2 on two consecutive checks, after ≥ 5 days).

Duration: usually 3–6 months for a first episode; indefinite for recurrent DVT or cancer, anticardiolipin antibodies, lupus anticoagulant, homozygous factor V, prothrombin gene mutation, antithrombin deficiency, protein C or S deficiency, or two or more thrombophilias.

Catheter-directed thrombolysis for thrombosis < 1 week extending above the inguinal ligament (or proximal in an upper limb) with severe symptoms and significant edema — contraindicated with bleeding risk. IVC filter when anticoagulation is contraindicated (e.g., the elderly with frequent falls) or for recurrent DVT despite anticoagulation.

Gerontologic considerations

60% of first-time DVTs occur in nursing home residents.
Presenting symptoms are often atypical; pain and swelling are common.
D-dimer has little predictive value for DVT in the elderly.
Pulmonary thromboembolism is a common complication of DVT in the elderly.
Coexisting osteoarthritis and spinal-stenosis neurogenic claudication are the two most common differentials for leg symptoms.

Chapter 17

Inflammatory Cardiac Diseases

Pericarditis, endocarditis, and the tamponade that can follow. Two of them are diagnosed by listening and one by culturing — and all three can hide behind a fever and a murmur.

Pericarditis

Inflammation of the pericardium

Acute, painful; may be mild or life-threatening
Viruses are the most common cause (coxsackie, echo, EBV, influenza, hepatitis, HIV, varicella, mumps)
Follows MI in 10–15% within the first week; higher incidence in males
Precordial/retrosternal pleuritic pain, worse with coughing, swallowing, inspiration, or recumbent — relieved by sitting forward
Pericardial friction rub — best with the patient sitting up, leaning forward

Endocarditis

Infection of the endothelium

Inflammation/infection of the endothelial layer, usually the valves
Most commonly bacterial — S. aureus, S. pyogenes, pneumococcus, Neisseria
Rule it out in any fever of unknown origin with a new murmur, or after valve surgery
Fever for weeks, night sweats, fatigue, exertional dyspnea
Blood cultures × 3 from three sites are the most important test

Pericarditis — ECG & treatment

Diagnostics

What to look for

Concave ST elevation in multiple leads — the "smiling face"
Depressed PR interval — highly diagnostic
Elevated ESR; leukocytosis
Echocardiogram to confirm pericardial fluid
BNP helps separate cardiac from pulmonary etiology

Management

Drugs & doses

Colchicine — weight-based: < 70 kg → 0.6 mg daily; > 70 kg → 0.6 mg BID
Ibuprofen 600 mg PO TID with meals — preferred NSAID
Aspirin 650 mg q8h × 2 weeks — preferred in post-MI pericarditis
Naproxen 500 mg BID; indomethacin 25–50 mg q8h
Corticosteroids (prednisone 60 mg daily, then taper) — only after NSAID failure/contraindication
Monitor closely for cardiac tamponade

Ketorolac (Toradol) — 60 mg IV/IM × 1, then 15–30 mg IV/IM q6h PRN (max 120 mg/day, ≤ 5 days). For adults ≥ 65 or < 50 kg: 15 mg IV single dose or 15 mg q6h (max 60 mg/day).
PPI may be needed for GI protection — e.g., pantoprazole 40 mg PO daily.
Hydrocodone 5 mg / acetaminophen 325 mg (Norco) PO q4h PRN for pain.
Corticosteroids may enhance viral replication — reserve for NSAID contraindication or failure of high-dose NSAIDs over several weeks; taper to avoid recurrent pericarditis.
Antibiotics as indicated for bacterial infection.

Endocarditis — the exam & the criteria

Peripheral stigmata

Skin, eyes, spleen

Osler's nodes — painful red nodules on distal phalanges
Splinter hemorrhages — linear subungual streaks
Janeway lesions — macules on palms/soles, smaller, not painful
Roth's spots — retinal infarcts with surrounding hemorrhage
Pallor, purpura, petechiae, splenomegaly

Duke criteria

How the diagnosis is built

Direct histologic evidence, or
Positive Gram stain/culture from surgery/autopsy, or
Two major criteria — positive blood culture of typical organisms; vegetations/abscess on echo; endocardial damage; Coxiella burnetii
One major + three minor criteria, or five minor criteria
Minor: fever, predisposing valve/IV drug use, vascular phenomenon, immunologic phenomenon, other positive cultures

Empiric therapy while cultures are pending

Cover Gram-positive organisms — S. aureus, viridans group streptococci, and enterococci — with vancomycin dosed to a trough of 15–20 mcg/mL (consult pharmacy for pharmacokinetic modeling). Length of treatment varies 2–6 weeks by organism. If risk factors for HACEK or other Gram-negative bacilli, add ceftriaxone 1–2 g IV q12h.

Regimen by organism

VGS / S. bovisNative valve

Highly penicillin-susceptible

Penicillin G 12–18 M units/24h IV × 4 wk, or ceftriaxone 2 g q24h IV/IM × 4 wk
Or 2-week course of penicillin/ceftriaxone + gentamicin (peak 3–4, trough < 1 mcg/mL)
Severe β-lactam allergy: vancomycin trough 10–15 mcg/mL × 4 wk

VGS / S. bovisProsthetic valve

Prosthetic valve / material

Penicillin G 24 M units/24h IV × 6 wk, or ceftriaxone ± gentamicin × 6 wk
Relatively/fully resistant: penicillin 24 M or ceftriaxone 2 g q24h + gentamicin (peak 3–4, trough < 1) × 2 wk
β-lactam allergy: vancomycin 30 mg/kg/24h (trough 10–20) × 6 wk

StaphylococciNative valve

MSSA vs. MRSA

Oxacillin-susceptible: nafcillin or oxacillin 12 g/24h IV × 6 wk; penicillin-allergic → cefazolin 6 g/24h × 6 wk
Oxacillin-resistant: vancomycin 30 mg/kg/24h (trough 10–20) × 6 wk, or daptomycin ≥ 8 mg/kg/dose × 6 wk

StaphylococciProsthetic valve

Prosthetic valve / material

Oxacillin-susceptible: nafcillin/oxacillin 12 g/24h IV
Oxacillin-resistant: vancomycin 30 mg/kg/24h + rifampin 900 mg/24h + gentamicin × 2 wk — all > 6 weeks

Enterococcus

Native or prosthetic valve

Ampicillin 2 g IV q4h or penicillin G 18–30 M units/24h + gentamicin × 4–6 wk
Or ampicillin + ceftriaxone 2 g IV q12h × 6 wk
Penicillin-resistant: vancomycin + gentamicin × 6 wk
VRE: linezolid 600 mg q12h or daptomycin 10–12 mg/kg × > 6 wk

HACEK

Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella

Ceftriaxone 2 g q24h IV/IM — 4 wk (native valve), 6 wk (prosthetic)
Or ampicillin 2 g IV q4h, or ciprofloxacin 1000 mg/24h PO / 800 mg/24h IV in 2 divided doses

Native valve — VGS & S. gallolyticus (bovis), highly penicillin-susceptible

Penicillin G 12–18 M units/24h IV × 4 wk, or ceftriaxone 2 g q24h IV/IM × 4 wk
Or (2-wk course): penicillin G or ceftriaxone + gentamicin (peak 3–4, trough < 1 mcg/mL) × 2 wk
Severe β-lactam allergy: vancomycin trough 10–15 mcg/mL × 4 wk

Native valve — staphylococci

MSSA: nafcillin/oxacillin 12 g/24h IV (4–6 divided doses) × 6 wk; nonanaphylactoid penicillin allergy → cefazolin 6 g/24h × 6 wk
MRSA: vancomycin 30 mg/kg/24h (trough 10–20) × 6 wk, or daptomycin ≥ 8 mg/kg/dose × 6 wk

Prosthetic valve — VGS & S. gallolyticus (bovis)

Penicillin-susceptible: penicillin G 24 M units/24h × 6 wk, or ceftriaxone ± gentamicin × 6 wk
Relatively/fully resistant: penicillin G 24 M or ceftriaxone 2 g q24h + gentamicin (peak 3–4, trough < 1) × 2 wk
Unable to tolerate β-lactams: vancomycin 30 mg/kg/24h (trough 10–20) × 6 wk

Prosthetic valve — staphylococci

MSSA: nafcillin/oxacillin 12 g/24h IV × > 6 wk
MRSA: vancomycin 30 mg/kg/24h (trough 10–20) × > 6 wk + rifampin 900 mg/24h IV/PO × > 6 wk + gentamicin (peak 3–4, trough < 1) × 2 wk

Enterococcus (native or prosthetic)

Ampicillin 2 g IV q4h (4–6 wk) or penicillin G 18–30 M units/24h (4–6 wk) + gentamicin (peak 3–4, trough < 1) × 2 wk
Or ampicillin 2 g IV q4h + ceftriaxone 2 g IV q12h × 6 wk
Penicillin-resistant / β-lactam intolerant: vancomycin 30 mg/kg/24h (trough 10–20) + gentamicin × 6 wk
VRE: linezolid 600 mg IV/PO q12h × > 6 wk, or daptomycin 10–12 mg/kg/dose × > 6 wk

HACEK (native or prosthetic)

Ceftriaxone 2 g q24h IV/IM — 4 wk (native), 6 wk (prosthetic)
Or ampicillin 2 g IV q4h; or ciprofloxacin 1000 mg/24h PO or 800 mg/24h IV in 2 divided doses

Setting	Agent	Regimen
Oral	Amoxicillin	2 g
Unable to take oral	Ampicillin	2 g IM or IV
Penicillin-allergic (oral)	Cephalexin · or clindamycin · or azithromycin/clarithromycin	2 g · 600 mg · 500 mg
Penicillin-allergic, unable oral	Cefazolin or ceftriaxone · or clindamycin	1 g IM/IV · 600 mg IM/IV

Prophylaxis is now reserved for the highest-risk cardiac conditions: prosthetic valve/material, previous IE, unrepaired cyanotic CHD (or repaired with prosthetic material within 6 months, or with residual defects), and cardiac transplant recipients who develop valvulopathy. Mitral valve prolapse alone is not an indication. Only dental/oral-mucosa, infected-skin, and select respiratory procedures qualify — not routine GI/GU procedures.

Cardiac tamponade

Beck's triad

The three signs

Jugular venous distention — rarely present with traumatic injury (hypovolemia)
Narrowing pulse pressure
Distant heart tones

Plus tachycardia, pulsus paradoxus, anxiety/confusion, oliguria, and other signs of shock.

Diagnosis & management

Drain it

Accumulation of blood/fluid in the pericardial space → life-threatening drop in cardiac output
Causes: chest trauma, post-cardiac-surgery/catheterization, pericarditis, acute MI, infection
Echocardiogram is the gold standard; CXR may show a widening mediastinum
Treat with pericardiocentesis + symptomatic shock management (oxygen, fluids, inotropes)

Chapter 19

Valvular Disease

Impaired unidirectional flow from damaged valves — stenosis ("narrowing: obstructed forward flow") or regurgitation ("insufficiency: backward flow"). Aortic stenosis and mitral regurgitation are the most common valvular diseases in the elderly.

Filter lesion

Mitral stenosis

Narrowed mitral valve

Rheumatic heart disease is the most common cause; ~⅔ of patients are female
Hallmark: shortening/fusion of chordae; leaflets immobilize
Fatigue, dyspnea, orthopnea, hemoptysis, palpitations (AF)
Loud S1, low-pitched mid-diastolic murmur at the apex, apical crescendo rumble

Mitral regurgitation

Backflow into the left atrium

Etiology: rheumatic, "floppy" valve, papillary muscle dysfunction (ischemia), IE, ruptured chordae, cardiomyopathy, SLE
Primary = valve disease; secondary = LV disease (worse prognosis)
S3 with holosystolic murmur at the apex (5th ICS, MCL), radiating to base or left axilla

MVP

Mitral valve prolapse

Protrusion of the MV into the left atrium during systole; usually benign
2–6% of the population (1 in 40); women aged 15–30
Midsystolic click followed by a late systolic murmur, best at the apex
MR is the most common complication; IE risk 2–3× general population

Aortic stenosis

Narrowed aortic valve

Most common valvular disorder in the US and the elderly; rheumatic overall, degenerative/senile in the elderly
Angina in ~70%; syncope in ~20%; dyspnea
Harsh systolic murmur at the 2nd right ICS, radiating to neck/apex; pulsus parvus et tardus; S4; softer S2 = more severe

Aortic regurgitation

Backflow into the left ventricle

Infective endocarditis is the most common acute cause
Corrigan's (water-hammer) pulse, Quincke's pulse, widened pulse pressure
High-pitched, blowing, decrescendo diastolic murmur at the 3rd left ICS — sitting up, leaning forward

Anticoagulation

Mitral stenosis: warfarin or heparin for MS with AF (paroxysmal, persistent, or permanent), a prior embolic event, or a left atrial thrombus.
All MV prostheses require postoperative anticoagulation. Mechanical valves require lifelong anticoagulation with a target INR > 2.5–3.5; "bridging" with IV UFH or LMWH until therapeutic INR is reached.
Aspirin 81 mg PO may be added in CAD + mechanical prosthesis after thromboembolism despite adequate INR.
MVP: aspirin 81–325 mg daily for documented focal neurologic events in sinus rhythm with no atrial thrombi.

Interventions

MS: percutaneous mitral balloon commissurotomy (PMBC) for symptomatic severe MS — no role when the valve is calcified. Otherwise MV repair, MitraClip, transcatheter MV replacement, or MV replacement/repair.
MR (acute): nitroprusside or nicardipine, intra-aortic balloon pump, then MV repair/replacement. MR (chronic): HF regimen (β-blockers, ACEI/ARB, diuretics) + MitraClip or surgery for severe disease.
AS: TAVR for severe AS with prohibitive surgical risk and predicted survival > 1 year; percutaneous balloon valvuloplasty for young adults with congenital noncalcific AS. Aspirin 81 mg ± clopidogrel 75 mg for 3–6 months after TAVR. Nitrates with caution; avoid diuretics if the LV is small.
AR (acute): surgery is not delayed; IABP is contraindicated; nitroprusside. AR (chronic): treat HTN (SBP > 140) with dihydropyridine CCB or ACEI/ARB.

10-year survival after AS surgery is 60%; 30% of bioprosthetic valves fail within 10 years. Antibiotic prophylaxis applies only to those with a prior history of endocarditis.

Chapter 20

Cardiomyopathy

An idiopathic disorder causing cardiac muscle dysfunction — systolic or diastolic — that is not due to atherosclerosis, hypertension, or valvular disease. Three types, and the type decides everything: the symptoms, the murmur, the echo findings, and the drugs.

of the general population

Affected by dilated cardiomyopathy — the most common type.

10%

of those patients are over 80

Dilated cardiomyopathy skews elderly.

autosomal dominant

The inheritance pattern of hypertrophic cardiomyopathy.

types, two failure modes

Dilated is systolic; hypertrophic and restrictive are diastolic.

Which failure does each type cause?

The single fastest way to orient: match the type to its failure mode. Hover a row.

Systolic dysfunction Diastolic dysfunction

The three types

Filter type

DilatedSystolic

Abnormal systolic pump function

Also known as heart failure with reduced ejection fraction (HFrEF). Dilated ventricles without proportionate compensatory hypertrophy — systolic heart failure.

Most common type of cardiomyopathy. Approximately 1% of the general population is affected, and 10% of those patients are older than 80.

HypertrophicDiastolic

Stiff left ventricle in diastole

An autosomal dominant disorder. The left ventricle is stiff during diastole, which restricts ventricular filling. Hypertrophy occurs without dilatation or a thickening septum.

Diastolic heart failure — heart failure with preserved ejection fraction (HFpEF).

RestrictiveDiastolic

Rigid ventricular walls

Inadequate diastolic filling from rigid ventricular walls — diastolic heart failure. Relatively uncommon.

Related to a variety of conditions: sarcoidosis, endomyocardial fibrosis (after open heart surgery), exposure, and idiopathic causes.

Etiology at a glance

Dilated

What causes it

Ischemic heart disease
Alcoholism
Persistent tachycardia — inappropriate sinus tachycardia, or AFib with rapid ventricular response
Systemic lupus erythematosus
Toxins; cocaine; stimulants such as amphetamine and dextroamphetamine (Adderall)
Idiopathic causes such as takotsubo

Hypertrophic

What causes it

Idiopathic causes
Chronic hypertension has been associated with increased incidence

Restrictive

What causes it

Sarcoidosis
Endomyocardial fibrosis — after open heart surgery
Exposure
Idiopathic causes

What you find on exam

Dilated

Left or biventricular CHF

Increased jugular venous distention
Low pulse pressure
S3 and/or S4 heart sounds
Peripheral edema; rales
Dyspnea, orthopnea, paroxysmal nocturnal dyspnea
Mitral or tricuspid regurgitation
Cardiomegaly

Hypertrophic

The murmur is the tell

Dyspnea, chest pain, syncope
Harsh "diamond-shaped" (crescendo–decrescendo) systolic murmur at the left sternal border — it decreases with squatting and increases with the Valsalva maneuver
S4 heart sound
Maximized apical pulse — double or triple

Restrictive

Right-sided heart failure

Dyspnea, fatigue, weakness
Edema; jugular venous distention
Ascites
Murmurs (regurgitant)
Kussmaul breathing (possibly)

The murmur maneuver worth memorizing

The hypertrophic murmur is a harsh, "diamond-shaped" (crescendo–decrescendo) systolic murmur at the left sternal border — it decreases with squatting and increases with the Valsalva maneuver.

Diagnostics by type

Chest x-ray: marked cardiac enlargement; pulmonary edema (interstitial)
ECG: ST segment/T-wave changes with left ventricular hypertrophy; right or left bundle branch block; arrhythmias are common — AFib, premature atrial contractions, premature ventricular contractions, ventricular tachycardia
Echocardiogram: left ventricular dilatation and dysfunction with a low ejection fraction
Routine blood including BNP or pro-BNP and urine chemistries

Chest x-ray: mild cardiomegaly or normal heart size
ECG: abnormal Q waves in anterolateral and inferior leads; left ventricular hypertrophy
Echocardiogram — diagnosis confirmed by the two-dimensional approach: left ventricular hypertrophy with an increased or at times normal ejection fraction
Exercise stress testing and 24-hour Holter monitor screening
Routine blood and urine chemistries

Chest x-ray: evidence of CHF, possibly including pleural effusion; cardiomegaly is usually mild to moderate
ECG: ST segment/T-wave changes; atrial fibrillation, left axis deviation, and other arrhythmias are possible
Echocardiogram: thickened cardiac valves, increased wall thickness, normal or small left ventricle size with mild to normal left ventricle function
Routine blood and urine chemistries
Cardiac catheterization / MRI to distinguish from constrictive pericarditis
- With restrictive cardiomyopathy, left ventricular impairment is more evident than right — pulmonary capillary wedge pressure is greater than central venous pressure
- MRI reveals greater thickening of the pericardium with restrictive cardiomyopathy
- With constrictive pericarditis, both ventricles are usually involved
Myocardial biopsy for definitive diagnosis

Management by type

Treat the underlying condition — discontinuing alcohol, treating endocrine causes and rapid heart rate arrhythmias
For heart failure (see Chapter 18): rest; daily weights; restricted sodium; diuretics; ACE inhibitors / angiotensin receptor blockers; digoxin if needed to reduce heart rate and thus workload in associated tachyarrhythmias; beta-blockers
Vasodilators, especially combined with ACE inhibitors and nitrates
Oral anticoagulation for emboli prophylaxis only in the setting of other anticoagulation indications — e.g. VTE, AFib, left ventricular thrombus

Beta-blocking drugs are recommended for symptoms (angina or dyspnea) in adults with obstructive or nonobstructive hypertrophic cardiomyopathy — but used with caution in sinus bradycardia or severe conduction disease.

If low doses are ineffective, titrate to a resting heart rate of less than 60–65 bpm, up to generally accepted maximum doses:

Agent	Starting dose	Maximum
Metoprolol	25 mg PO BID	400 mg/day
Atenolol	25 mg PO daily	200 mg/day
Verapamil (Calan)	120–480 mg daily to twice daily	For obstructive and nonobstructive disease in those for whom beta-blockers are contraindicated or intolerable

Antibiotic prophylaxis for invasive procedures may be indicated depending on individual valvular diagnoses
Avoidance of alcohol
Consider dual-chamber pacing to prevent progression of the disease, as indicated
Consider implantation of an implantable cardioverter defibrillator for the prevention of sudden death
Septal alcohol ablation

Avoid these in hypertrophic obstructive disease

Avoid afterload reducers and digoxin with hypertrophic obstructive disease. In dilated cardiomyopathy, by contrast, digoxin may be used if needed to reduce heart rate and thus workload in associated tachyarrhythmias.

Control the major cause(s) of death due to heart failure
- Restrict sodium intake
- Use diuretics as needed
- Administer antiarrhythmics as appropriate
Repeated phlebotomies to decrease iron deposition in the heart for patients with cardiomyopathy caused by hemochromatosis
Corticosteroids for sarcoidosis
Symptomatic treatment

The one-line summary

Dilated is the common one and fails on systole — treat it like heart failure. Hypertrophic is inherited and obstructs on diastole — beta-block it, and avoid afterload reducers and digoxin. Restrictive is rare and stiff — find the cause, because sarcoidosis and hemochromatosis are treatable.

Chapter 28

Pulmonary Hypertension & Vascular Disorders

Pulmonary hypertension (PH) is not the same as pulmonary arterial hypertension (PAH). PAH is a specific subgroup of PH — and the WHO's five groups keep the difference straight.

Filter group

Group I

PAH (or primary)

Idiopathic — seen most often in young women
Familial/heritable; associated PAH (scleroderma, congenital shunts, portal HTN, HIV, drugs, toxins)
Chronic thromboembolic PH (CTEPH)

Group II

Left heart disease

LV systolic or diastolic dysfunction
Valvular disease (e.g., mitral stenosis)
Left heart inflow/outflow obstruction; congenital cardiomyopathies

Group III

Lung disease / hypoxemia

COPD, interstitial lung disease
Sleep-disordered breathing, alveolar hypoventilation
Chronic high altitude; developmental lung abnormalities

Group IV

CTEPH

PE in proximal or distal pulmonary arteries
Embolization of tumor cells or parasites

Group V

Miscellaneous / hematologic / systemic

Myeloproliferative disorders
Sarcoidosis
Sickle cell disease

Right-heart catheterization — the numbers that define PH

The gold-standard thresholds. Hover each zone. PAP > 25 mmHg = PH; LAP < 18 mmHg points to WHO group 1.

Presentation

What you see

Dyspnea on exertion · fatigue · substernal discomfort
Dizziness, near/true syncope, palpitations
Increased P₂, split S2, RV heave, holosystolic murmur, elevated JVP, peripheral edema, ascites
More common in females

Diagnostics

Gold standard & the rest

Right-heart catheterization — PAP > 25 mmHg; LAP < 18 mmHg = group 1
Echo with bubble study; ECG shows RV hypertrophy, right axis deviation ± RBBB
BNP/proBNP to monitor; D-dimer if PE suspected
CXR — enlarged proximal pulmonary arteries, narrowing in the medial third

Treatment

Oxygen reduces peripheral vascular resistance (long-term benefit not shown); recommended with COPD, low PaO₂, symptomatic benefit, or correctable exertional desaturation.
Exercise / cardiopulmonary rehabilitation for all patients.
Loop diuretics for decompensated right-heart failure with fluid retention, ascites, edema.
Anticoagulation recommended for PAH.
Digoxin may improve cardiac output in idiopathic PAH and slow rate in tachyarrhythmias (chronic-use evidence lacking).
Treat underlying disorders (COPD, CHF, OSA); supplemental oxygen at night; if hematocrit > 60%, phlebotomy to ~55%; immunize against influenza and pneumococcus.

Class / agent	Dose	WHO-FC · Notes
CCB — amlodipine	PO 20–30 mg/day	II, III · only after a positive vasoreactivity test; effect can fade over time
CCB — nifedipine ER	PO 120–240 mg/day
CCB — diltiazem ER	PO 240–960 mg/day
ERA — ambrisentan	PO 5–10 mg/day	II, III · teratogenic (REMS, specialty pharmacy); not for moderate–severe liver disease; monitor LFTs
ERA — bosentan	< 40 kg max 125 mg/day; > 40 kg max 250 mg/day
ERA — macitentan	PO 10 mg/day
Prostacyclin — epoprostenol	IV start 1–2 ng/kg/min, titrate q15 min to 25–40 ng/kg/min	III, IV · bleeding risk (platelet inhibition); specialty pharmacy
Prostacyclin — iloprost	INH 2.5–5 mcg, 6–9×/day (≥ 2 hr apart), max 45 mcg/day
Prostacyclin — treprostinil	IV/SC start 1.25 ng/kg/min, titrate weekly to 40 ng/kg/min
Agonist — selexipag	PO max 3,200 mcg/day	II, III · bleeding risk; many drug–drug interactions
PDE-5 — sildenafil / tadalafil	PO max 60 / 40 mg/day	II, III · avoid with nitrates
sGC — riociguat	PO max 2.5 mg TID	II, III · avoid with nitrates

Oral drugs (monotherapy or combination) for less severe disease; parenteral prostacyclins for more severe disease. Two or more classes are usually needed. None of the targeted therapies slows pathological progression. Riociguat is contraindicated with nitrates or PDE-5 inhibitors.

Pulmonary embolism

A clot (or other undissolved material) lodges in the pulmonary arterial circulation, interrupting flow. Massive if > 50% of flow is obstructed; death occurs from right ventricular failure. Lower-extremity/pelvic DVT causes 70% of pulmonary emboli. Dyspnea (insidious or sudden) is the most common symptom; watch for the "impending doom," pleuritic pain, and hemoptysis with infarction.

Fat embolism — the pattern to recognize

Sudden marked dyspnea in a susceptible patient
Altered consciousness; temperature > 102 °F
Petechiae over the thorax, shoulders, and axillae

Agent	Dose	Notes
Heparin (weight-based)	80 units/kg bolus, then 18 units/kg/hr	Anti-factor Xa 0.3–0.7 units/mL; PTT institution-specific.
Enoxaparin	1 mg/kg SC q12h	Lower bleeding/HIT risk; anti-Xa monitoring in pregnancy, obesity, renal failure, bleeding risk.
Argatroban	Non-ICU 2 mcg/kg/min; ICU 0.2–0.5 mcg/kg/min	PTT 1.5–3 × baseline.
Fondaparinux	< 50 kg 5 mg · 50–100 kg 7.5 mg · > 100 kg 10 mg SC daily	Weight-banded.
Rivaroxaban	15 mg BID × 21 days, then 20 mg daily (with food)	Avoid if CrCl < 30 mL/min.
Apixaban	10 mg BID × 7 days, then 5 mg BID	Andexanet alfa reverses.
Warfarin	First dose 5 mg PO daily	Continue heparin until therapeutic (INR 2–2.5 × 2–3 days).

Duration: 3–6 months for a first episode; 6–12 months or longer for recurrent/unprovoked PE.

Fibrinolysis for massive proximal PE with persistent hypotension and right-heart strain: alteplase 100 mg IV over 2 hr (check contraindications first); start heparin/enoxaparin when PTT < 2 × control. Surgical embolectomy for massive central PE causing shock; IVC filter when anticoagulation risk is high; oxygen to keep SaO₂ > 90%. Pulmonary angiography remains the gold standard for diagnosis.

Geriatric caution

Heart failure with preserved ejection fraction is a commonly under-recognized cause of PH in the elderly. Older patients are very unlikely to have PAH — far more likely pulmonary venous hypertension from LV systolic/diastolic failure, aortic or mitral valve disease, or left atrial noncompliance.

Chapter 21

Arrhythmias & Their Treatment

The electricity that keeps the pump going — from the quiet rhythms of the sinus node to the lethal ones that stop it. Know the rate, know the P wave and QRS, and know the first move.

2.2–6.1 M

Americans with Afib

The most common sustained arrhythmia — associated with preventable stroke.

<20%

survive out-of-hospital VF

Versus 36% in-hospital survival. Every minute of defibrillation delay drops survival ~10%.

Afib at age ≥ 80

Prevalence climbs from 0.4–1% generally to as high as 8% in patients 80 or older.

95%

ablation success

For atrial flutter, AVNRT, and AVRT accessory pathways — though heart block is the complication risk.

The rate ladder — where each rhythm lives

Representative rate ranges in beats per minute. Hover a bar. (Afib's atrial rate is 400–700; its ventricular response 100–160.)

Sinus / normal Brady Tachy SVT Flutter

The rhythms in brief

Common rhythms — rate, hallmark, first move
Rhythm	Rate	Hallmark / first move
Normal sinus	60–100 bpm	Regular; PR ≤ 0.20 s, QRS ≤ 0.12 s.
Sinus bradycardia	≤ 60 bpm	Often asymptomatic; acute symptomatic → transcutaneous pacing; atropine/dopamine/epinephrine temporize.
Sinus tachycardia	≥ 100, usually < 150–160	Treat the underlying cause (fever, shock, pain, hypovolemia).
Junctional	40–60 (accelerated 60–100)	No P waves before QRS; stop AV nodal blockers; atropine 0.5 mg (max 3 mg) if unstable.
Atrial fibrillation	Atrial 400–700; ventricular 100–160	No P waves, irregularly irregular; rate vs rhythm control; anticoagulation for stroke risk.
Atrial flutter	Atrial 240–340	Sawtooth F waves (II, III, aVF, V1); same stroke risk as Afib; ablation 95% success.
AVNRT / AVRT	150–190 (can > 200)	Vagal maneuvers → adenosine 6 mg (then 12 mg, 12 mg); ablation 95% curative.
VT	> 100 (wide QRS > 120 ms)	Unstable → cardioversion per ACLS; nonsustained → β-blockers; amiodarone/sotalol/mexiletine.
VF	Chaotic	Immediate defibrillation; epinephrine 1 mg; amiodarone 300 mg; magnesium 2 g if torsades.
Mobitz I	—	Progressive PR until a dropped beat; often no treatment.
Mobitz II	—	PR fixed before dropped beat; urgent pacemaker referral.
3rd-degree block	Ventricular 40–60	AV dissociation; urgent pacemaker; atropine 0.5 mg q3–5 min (max 3 mg) if poor perfusion.

WPW + Afib

Never block the node

Wide, bizarre QRS; ventricular rates up to 200–300 bpm, can degenerate to VF. Avoid AV nodal blockers (can cause 1:1 accessory-pathway conduction). Use procainamide or amiodarone if stable; immediate cardioversion if unstable.

PVCs

When to worry

Benign if infrequent/unifocal. More concerning if > 6 per minute, multifocal, bigeminal/trigeminal, in pairs, or landing on the downslope of the T wave (R-on-T → VT/VF). First-line treatment for symptomatic PVCs: β-blockers.

Antiarrhythmic agents (Table 21.1)

Filter class

Class IA — Na channel

Disopyramide · Procainamide · Quinidine

Atrial + ventricular arrhythmias, but infrequently used (significant toxicity); all may cause new/worse dysrhythmias
Procainamide: agranulocytosis, SLE, hypotension, hepatotoxicity, QT prolongation
Quinidine: GI upset, hemolytic anemia, thrombocytopenia, hepatotoxicity, QT

Class IB — Na channel

Lidocaine · Mexiletine

Ventricular arrhythmias (PVC, VT, VF); cannot treat atrial arrhythmias
Lidocaine: hypotension, nausea, blurred vision, methemoglobinemia, confusion, seizure, tremors
Mexiletine: nausea/vomiting, dizziness, tremor, blurred vision

Class IC — Na channel

Flecainide · Propafenone

Do not use in structural heart disease
Flecainide: palpitations, nausea, dizziness, blurred vision, fatigue
Propafenone: chest pain, edema, constipation, altered taste, agranulocytosis, heart failure

Class II — β-blockers

Acebutolol · Atenolol · Esmolol · Metoprolol · Propranolol

Primarily for rate control
Atrial tachyarrhythmias; Afib (control ventricular rate)
Hypotension, bradycardia, 2nd/3rd-degree heart block, fatigue

Class III — K channel

Amiodarone · Dofetilide · Ibutilide · Sotalol · Dronedarone

Atrial + ventricular arrhythmias; all may cause new/worse dysrhythmias
Amiodarone: thyroid dysfunction, pulmonary fibrosis, hepatotoxicity, photosensitivity, blue/gray skin, optic neuritis
Dofetilide/ibutilide/sotalol: QT prolongation
Dronedarone: doubles death risk in symptomatic heart failure

Class IV — Ca channel

Diltiazem · Verapamil

Primarily for rate control
Atrial tachyarrhythmias; Afib rate control; PSVT
Peripheral edema, hypotension, bradycardia, 2nd/3rd-degree block, constipation

Unstable Afib with rapid ventricular response → immediate DCCV.
Favor rhythm control: newly diagnosed/paroxysmal, symptomatic, young, no HTN/HF, HFrEF (restores "atrial kick"). Favor rate control: asymptomatic/persistent, older, HTN, failed rhythm control.
Before cardioversion of unknown duration or > 48 hr: TEE to rule out LAA thrombus. Anticoagulate ≥ 4 weeks after cardioversion (atrial stunning). If anticoagulated ≥ 3 weeks uninterrupted, TEE is not needed.
Catheter ablation with pulmonary vein isolation: 75% success, often needs more than one.

CHA₂DS₂-VASc points

2 pts: age ≥ 75, stroke/TIA
1 pt: heart failure or LVEF ≤ 40%, hypertension, diabetes mellitus, vascular disease, age 65–74, female sex
Anticoagulate when ≥ 2 in men or ≥ 3 in women; aspirin for score 0–1.

Table 21.5 — NOAC guidelines (nonvalvular Afib)
NOAC	Class	Normal dose	Renal dose
Rivaroxaban	Xa inhibitor	20 mg daily	CrCl > 50: 20 mg daily; 15–50: 15 mg daily; < 15: contraindicated
Apixaban	Xa inhibitor	5 mg BID	2.5 mg BID if 2 of 3: Cr ≥ 1.5, age ≥ 80, weight ≤ 60 kg
Dabigatran	Thrombin inhibitor	150 mg BID	CrCl > 30: 150 mg BID; 15–30: 75 mg BID; < 15/HD: not recommended
Edoxaban	Xa inhibitor	60 mg daily	CrCl > 95: contraindicated; > 50–95: 60 mg; 15–50: 30 mg; < 15/HD: not recommended

NOACs are not for moderate–severe mitral stenosis or mechanical valves; avoid in severe liver dysfunction; assess renal function first.
Reversal: idarucizumab (dabigatran); andexanet alfa (rivaroxaban, apixaban, edoxaban).
HAS-BLED (HTN, abnormal renal/liver function, stroke, bleeding, labile INR, elderly, drugs/alcohol): score 0–1 low, 2 moderate, ≥ 3 high bleeding risk.
Watchman LAA occlusion for those who cannot tolerate long-term anticoagulation; aspirin + warfarin ≥ 45 days post-implant, then dual antiplatelet 3–6 months.

The anticoagulation threshold

CHA₂DS₂-VASc ≥ 2 (men) or ≥ 3 (women) → anticoagulate. NOACs are not for moderate–severe mitral stenosis or mechanical valves.

Remember

Cardiomyopathy (Ch. 20)

Dilated = systolic (HFrEF) · Hypertrophic = diastolic (HFpEF), β-blockers · Restrictive = diastolic, rigid walls. Most common: dilated.

The one-sentence version of Week 3

Open the artery on a clock, culture the valve before you treat it, and know the rhythm's first move.

Self-Check

Rapid-fire review

Answer out loud first, then reveal. Fifteen questions across all seven chapters.

Differentiate UA, NSTEMI, and STEMI using cardiac enzymes and the ST segment.

UA — new onset or change in pattern/frequency of symptoms, no enzyme elevation, may show ST depression with transient T inversion. NSTEMI — elevated enzymes but no ST elevation (may show ST depression or T inversion). STEMI — elevated enzymes + ST elevation, with chest pain not relieved by NTG.

Name the four types of angina, and the ECG change seen in Prinzmetal versus stable angina.

Stable (predictable, exertional, ST depression), Prinzmetal/variant (coronary spasm, at rest up to 30 min, ST elevation), unstable (crescendo, > 20–30 min), and microvascular/syndrome X (positive stress test, normal angiogram).

A patient arrives with a STEMI. What are the two reperfusion time targets?

Door-to-fibrinolytic ≤ 30 minutes and door-to-balloon (angioplasty) ≤ 90 minutes. Fibrinolysis is preferred if PCI is not available within 90 minutes; the greatest benefit is within 1–3 hours of pain onset.

Give the alteplase dose for STEMI, and the weight-based tenecteplase (TNKase) doses.

Alteplase: 15 mg bolus, then 50 mg over 30 min, then 35 mg over 1 hour (max 100 mg). TNKase: single IV bolus over 5 seconds, max 50 mg — < 60 kg → 30 mg; 60–70 kg → 35 mg; 70–80 kg → 40 mg; 80–90 kg → 45 mg; > 90 kg → 50 mg.

List the absolute contraindications to fibrinolytic therapy.

Active bleeding · major trauma or surgery < 3 months ago · history of hemorrhagic stroke, intracranial aneurysm, or tumor · ischemic stroke within 3 months · severe uncontrolled HTN (SBP > 180 or DBP > 110) · pregnancy · aortic dissection · acute pericarditis.

Which cardiac enzyme rises first, and which is 100% specific for myocardial necrosis?

Myoglobin rises first (2–3 hr; within 1–2 hr). Troponin I is 100% specific for myocardial necrosis. Troponin (T or I) is the preferred biomarker; serial enzymes are drawn every 6–8 hr.

State the three hs-CRP risk strata.

Low risk < 1 mg/L · average risk 1–3 mg/L · high risk > 3 mg/L. Higher hs-CRP predicts future coronary events and higher mortality after UA/MI.

What is Beck's triad, and what is the gold-standard test for cardiac tamponade?

Jugular venous distention · narrowing pulse pressure · distant heart tones. The echocardiogram is the gold standard to confirm the diagnosis; treatment is pericardiocentesis plus symptomatic shock management.

In pericarditis, which ECG finding is highly diagnostic, and what is the preferred NSAID?

The depressed PR interval is highly diagnostic (along with concave "smiling-face" ST elevation in multiple leads). The preferred NSAID is ibuprofen 600 mg PO TID; aspirin 650 mg q8h × 2 weeks is preferred in post-MI pericarditis. Add colchicine (weight-based) and monitor for tamponade.

What is the empiric endocarditis regimen while cultures are pending, and what is the most important diagnostic test?

Empiric vancomycin dosed to a trough of 15–20 mcg/mL, covering Gram-positives (S. aureus, viridans streptococci, enterococci); add ceftriaxone 1–2 g IV q12h if HACEK/Gram-negative risk. The most important test is blood cultures × 3 from three different sites.

A patient has a mechanical mitral valve. What is the INR target, and how do you bridge?

Mechanical valves require therapeutic INR > 2.5–3.5. All mitral valve prostheses require postoperative anticoagulation; bridge with IV unfractionated heparin or LMWH until the therapeutic INR is reached.

What are the classic physical findings of aortic stenosis, and in what percentage do angina and syncope occur?

Harsh, systolic murmur at the 2nd right intercostal space radiating to the neck/apex · pulsus parvus et tardus · S4 · displaced LV impulse · softer S2 = more severe AS. Angina occurs in ~70% and syncope in ~20% of patients.

Which rhythm shows sawtooth F waves in II, III, aVF, and V1 with an atrial rate of 240–340, and what is its stroke risk?

Atrial flutter. It carries the same stroke risk as atrial fibrillation. Ablation of the reentrant circuit has a 95% success rate and is becoming first-line.

WPW presenting with atrial fibrillation — what must you avoid, and why?

Avoid AV nodal blockers — blocking the AV node can cause 1:1 conduction through the accessory pathway (heart rate > 300 bpm), because the accessory pathway lacks the AV node's decremental properties. Use procainamide or amiodarone if stable; immediate electrical cardioversion if unstable.

Using CHA₂DS₂-VASc, when do you anticoagulate for atrial fibrillation, and what is the warfarin INR goal?

Anticoagulate at ≥ 2 in men or ≥ 3 in women (aspirin for 0–1). The warfarin INR goal for Afib is 2–3. NOACs are preferred by many but are not for moderate–severe mitral stenosis or mechanical valves.

References

Sources

Every statement above comes from the assigned Week 3 reading — seven chapters of Practice Considerations for Adult-Gerontology Acute Care Nurse Practitioners.

Chapters

King, J. (2021). Angina and acute myocardial infarction. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 14).

Melander, S., Fellin, R., & Tien, E. (2021). Inflammatory cardiac diseases. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 17).

Wadas, T. M. (2021). Valvular disease. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 19).

Lakin, T. M., Hoy, H. M., & Fellin, R. (2021). Pulmonary hypertension and pulmonary vascular disorders. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 28).

Melander, S. (2021). Cardiomyopathy. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 20).

Wadas, T. M. (2021). Peripheral vascular disease. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 16).

Carlston, F. (2021). Arrhythmias. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 21).

Selected sources cited in the reading

O'Gara, P. T., Kushner, F. G., Ascheim, D. E., Chung, M. K., de Lemos, J. A., Ettinger, S. M., . . . Zhao, D. X. (2013). 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: Executive summary. Circulation, 127(4), 529–555.

O'Connor, R. E., Al Ali, A. S., Brady, W. J., Ghaemmaghami, C. A., Menon, V., Welsford, M., & Shuster, M. (2015). 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care: Part 9: Acute coronary syndromes. Circulation, 132(Suppl. 2), S483–S500.

Baddour, L. M., Wilson, W. R., Bayer, A. S., Fowler, V. G., Jr., Tleyjeh, I. M., Rybak, M. J., . . . Taubert, K. A. (2015). Infective endocarditis in adults: Diagnosis, antimicrobial therapy, and management of complications. Circulation, 132(15), 1435–1486.

Nishimura, R. A., Otto, C. M., Bonow, R. O., Carabello, B. A., Erwin, J. P., III, Fleisher, L. A., . . . Thompson, A. (2017). 2017 AHA/ACC focused update of the 2014 AHA/ACC guideline for the management of patients with valvular heart disease. Journal of the American College of Cardiology, 70(2), 252–289.

Klinger, J. R., Elliott, C. G., Levine, D. J., Bossone, E., Duvall, L., Fagan, K., . . . Badesch, D. B. (2019). Therapy for pulmonary arterial hypertension in adults: Update of the CHEST guideline and expert panel report. Chest, 155(3), 565–586.

Al-Khatib, S. M., Stevenson, W. G., Ackerman, M. J., Bryant, W. J., Callans, D. J., Curtis, A. B., . . . Page, R. L. (2017). 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Circulation, 138(13), e272–e391.

January, C. T., Wann, L. S., Calkins, H., Chen, L. Y., Cigarroa, J. E., Cleveland, J. C., Jr., . . . Yancy, C. W. (2019). AHA/ACC/HRS focused update of the 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation. Circulation, 140(2), e125–e151.

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