Cardiovascular, Pulmonary and Lymphatic Conditions and Rehabilitation

Most patients a physical therapist sees, whatever the referral says, carry some cardiovascular or pulmonary diagnosis: the hip fracture patient with heart failure, the knee replacement on a beta blocker, the stroke survivor with chronic obstructive pulmonary disease. The exam rewards the therapist who can dose exercise safely around these conditions, recognize decompensation early and know which precautions follow which procedure. This chapter covers the major heart, lung, peripheral vascular and lymphatic conditions and the rehabilitation built around each.

Section 1Coronary disease, heart failure and cardiac surgery

Coronary artery disease and the ischemic spectrum

Coronary artery disease (CAD) is atherosclerotic narrowing of the epicardial coronary arteries. Plaque builds over decades through endothelial injury, lipid deposition, macrophage infiltration and a fibrous cap. The clinical problem is a mismatch between myocardial oxygen supply and demand. Demand rises with heart rate, contractility and wall tension (afterload and preload), which is why the rate pressure product (heart rate times systolic pressure) tracks myocardial oxygen use and why a patient with fixed narrowing develops symptoms at a reproducible rate pressure product called the ischemic threshold.

The ischemic syndromes form a spectrum:

• Stable angina: chest pressure or tightness brought on by a predictable level of exertion, emotion, cold or a heavy meal, lasting a few minutes and relieved by rest or sublingual nitroglycerin. The plaque narrows the lumen but is not ruptured.
• Unstable angina: new onset angina, angina at rest, or angina that is increasing in frequency, duration or intensity (crescendo). A plaque has ruptured or eroded and a partial thrombus has formed, but troponin is not elevated. It is a medical emergency, not a reason to modify exercise.
• Myocardial infarction (MI): myocyte death proven by a rise and fall of cardiac troponin with symptoms or ECG change. A STEMI (ST elevation MI) usually reflects complete occlusion and full thickness (transmural) injury and needs emergency reperfusion. An NSTEMI has a troponin rise without ST elevation and usually involves subendocardial injury. Unstable angina, NSTEMI and STEMI together form the acute coronary syndromes.

Classic angina is retrosternal pressure radiating to the left arm, jaw or between the scapulae, with diaphoresis, dyspnea and nausea. Women, older adults and people with diabetes more often present atypically (fatigue, dyspnea, epigastric or jaw pain), and diabetic neuropathy can produce silent ischemia. Musculoskeletal chest pain is reproduced by palpation or movement and is not tied to exertional heart rate.

Troponin rises within about 3 to 4 hours, peaks near 24 hours and stays elevated for 7 to 14 days, so the trend matters more than one value. Programs hold mobility while troponin is rising and resume once it has peaked, with hemodynamic stability and no chest pain or new arrhythmia for about 8 hours.

Revascularization is by percutaneous coronary intervention (PCI, usually with a drug eluting stent) or coronary artery bypass grafting (CABG). After femoral PCI the leg stays straight for a few hours (commonly 2 to 6) and the groin is checked for bleeding before walking; radial access allows walking almost at once. Dual antiplatelet therapy raises bleeding risk.

Heart failure

Heart failure (HF) is a clinical syndrome in which the heart cannot pump enough blood to meet the body's needs, or can do so only at high filling pressures. It is classified by ejection fraction:

• HF with reduced ejection fraction (HFrEF), EF 40% or less: systolic dysfunction from a weak ventricle (ischemic cardiomyopathy after MI, dilated cardiomyopathy).
• HF with preserved ejection fraction (HFpEF), EF 50% or more: a stiff ventricle that fills poorly (diastolic dysfunction), typical of older adults with long standing hypertension, obesity and diabetes.
• HF with mildly reduced EF, 41% to 49%, sits between the two.

Normal EF is about 55% to 70%. Fluid backs up behind the failing side. A failing left ventricle congests the lungs: exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, basilar crackles, frothy cough, an S3, and fatigue from low output. A failing right ventricle backs fluid into the systemic veins: jugular venous distension, dependent pitting edema of the ankles and sacrum, liver congestion with right upper quadrant fullness, ascites, and weight gain. The most common cause of right sided failure is left sided failure. Right sided failure caused by lung disease and pulmonary hypertension is called cor pulmonale.

NYHA classes describe symptoms and can improve with treatment; ACC/AHA stages describe progression and never move backward.

HFrEF medical therapy combines an ACE inhibitor, ARB or neprilysin inhibitor combination, a beta blocker, spironolactone and an SGLT2 inhibitor, with loop diuretics for congestion. Expect orthostatic hypotension, potassium shifts and a blunted heart rate response.

Exercise training is safe and recommended in stable HF. Screen every session: a daily weight gain of about 2 to 3 pounds in a day or 5 in a week (programs vary slightly) suggests fluid retention. New dyspnea at rest, new crackles or S3, rising JVD, increasing edema or resting HR above about 120 mean no exercise that day. An exertional drop in systolic pressure of more than 10 mmHg despite rising workload means the ventricle cannot keep up: stop.

Prescribe long warm ups and cool downs, intervals when deconditioned, RPE 11 to 14, progression of duration before intensity, and light resistance work while exhaling on effort (no Valsalva maneuver).

Cardiac surgery and sternal precautions

CABG uses the left internal mammary (internal thoracic) artery, which has the best long term patency, usually to the left anterior descending artery, and saphenous vein or radial artery grafts to other vessels. Valve surgery repairs or replaces stenotic or regurgitant valves. Both are usually done through a median sternotomy, in which the sternum is split and wired together. The sternum takes about 6 to 8 weeks to unite, so sternal precautions protect it during that time.

Traditional sternal precautions, still the common exam answer, are:

• No lifting, pushing or pulling more than about 5 to 10 pounds.
• No pushing up with the arms from a chair or bed, and no pulling on bed rails or a walker to rise.
• No bilateral or resisted reaching overhead or behind the back, and no unilateral end range shoulder motion that stresses the sternum.
• Splint the chest with a pillow when coughing or sneezing.
• No driving for about 4 weeks (airbag and steering forces, plus medications).

Many hospitals now use a less restrictive approach (keep the upper arms close to the body and move within pain limits); the safe exam answer still avoids pushing up with both arms and heavy lifting. Signs of sternal instability are clicking, sternal movement with coughing, or wound drainage; risk rises with obesity, diabetes, COPD with heavy cough and osteoporosis. Mobilization starts on postoperative day 0 or 1; watch for atelectasis, new atrial fibrillation (peaking about days 2 to 3) and orthostasis.

Severe symptomatic aortic stenosis (angina, syncope, dyspnea) contraindicates exercise training until corrected, and sudden vasodilation can drop pressure dangerously. TAVR avoids sternotomy and allows faster mobilization.

Devices: pacemakers, ICDs, LVADs and transplant

A pacemaker code gives the chamber paced, chamber sensed and response (for example DDD); a fourth letter R means rate responsive. A fixed rate device cannot raise heart rate, so monitor RPE and blood pressure. After lead placement, limit ipsilateral shoulder elevation to about 90 degrees and avoid heavy lifting for about 4 to 6 weeks, and keep electrical stimulation and diathermy away from the device.

An implantable cardioverter defibrillator (ICD) paces or shocks ventricular tachycardia or fibrillation. Know its detection rate and keep exercise heart rate at least 10 to 20 beats below it to avoid an inappropriate shock. One shock in a patient who feels well: stop and notify the cardiologist; repeated shocks or symptoms: emergency care.

A left ventricular assist device (LVAD) pumps blood from the left ventricle to the aorta as a bridge to transplant or destination therapy. With continuous flow there is often no palpable pulse, so pressure is taken with Doppler and a manual cuff and read as a mean arterial pressure (typically about 70 to 90 mmHg). Protect the driveline, never disconnect both power sources, avoid submersion, and use RPE; low flow alarms with exercise often mean dehydration.

A transplanted heart is denervated: resting rate is high (often 90 to 110), heart rate rises slowly with exercise through circulating catecholamines and stays up afterward, and angina is usually absent. Use long warm ups and cool downs and RPE. Immunosuppression and steroids add infection, osteoporosis and myopathy risk.

Section 2Cardiac rehabilitation

Who qualifies and the phases

Cardiac rehabilitation combines exercise training, risk factor modification, education and psychosocial support, and it lowers mortality and readmissions. Qualifying diagnoses include MI, CABG, PCI, stable angina, valve surgery, transplant and stable HFrEF.

Programs are described in phases:

• Phase I, inpatient: from medical stability to discharge: counter bed rest, assess the response to self care and walking, teach, and plan discharge (about 1 to 4 METs).
• Phase II, early outpatient: supervised, often ECG monitored, typically up to 36 sessions over about 12 weeks, prescribed from an exercise test.
• Phase III, maintenance: community or home exercise for life (some texts add a phase IV).

Phase I progression and monitoring

Check vitals, telemetry, symptoms and labs before each activity. Common upper limits during phase I are an increase in heart rate of no more than about 20 beats per minute above resting after MI and about 30 above resting after cardiac surgery, with RPE of 13 or less (somewhat hard) on the 6 to 20 Borg scale. Normally systolic rises and diastolic stays within about 10 mmHg. Abnormal responses that mean stop and report:

• Angina, unusual dyspnea, dizziness, pallor, cyanosis, diaphoresis or confusion.
• Systolic pressure falling by more than 10 mmHg with activity, or failing to rise.
• Diastolic pressure above about 110 mmHg, or systolic well above the program limit.
• Heart rate rising beyond the limits above, or new arrhythmia (frequent or multifocal PVCs, runs of ventricular tachycardia, new atrial fibrillation, new heart block).
• ST segment change of about 1 mm or more on the monitor (horizontal or downsloping depression).

Exercise prescription in phase II and beyond

The prescription follows FITT (frequency, intensity, time, type) plus progression. A symptom limited graded exercise test gives peak heart rate, peak METs and, in some patients, the heart rate at which ischemia appears.

• Frequency: aerobic exercise on most days, at least 3 and ideally 5 or more days per week.
• Intensity: 40% to 80% of heart rate reserve (HRR) or of peak oxygen uptake, or RPE 12 to 16. If an ischemic threshold is known, set the upper limit at least 10 beats per minute below the heart rate at which ischemia (angina or 1 mm ST depression) appeared.
• Time: 20 to 60 minutes, which can be accumulated in shorter bouts in deconditioned patients, plus 5 to 10 minutes each of warm up and cool down.
• Type: rhythmic large muscle activity such as walking, cycling and arm ergometry; resistance training 2 to 3 days per week at about 40% to 60% of one repetition maximum, 10 to 15 repetitions.

The Karvonen method is the most tested calculation: Target HR = [(HRmax minus HRrest) times intensity] plus HRrest. Use the measured peak from an exercise test when available; 220 minus age is only an estimate and is meaningless on beta blockers. One MET is about 3.5 mL O2 per kg per minute; self care is 1 to 3 METs, walking at 3 mph about 3.3, and sexual activity about 3 to 5.

Medications that change the exercise response

Medications appear constantly in cardiac questions because they change what you measure. The essentials:

Education covers risk factors (smoking, hypertension, dyslipidemia, diabetes, obesity, inactivity, depression), self monitoring with RPE, symptom recognition, nitroglycerin use and adherence. Screen for depression after MI, and avoid early exercise in temperature extremes, after large meals or with isometric straining.

Section 3Obstructive and restrictive lung disease and pulmonary rehabilitation

Two patterns of disease

Lung diseases are grouped by what they do to airflow and volume. In obstructive disease the airways are narrowed or collapse on expiration, so air goes in but has trouble coming out. Expiratory flow falls, air is trapped, and residual volume and total lung capacity rise (hyperinflation). The defining spirometry finding is a reduced FEV1/FVC ratio, below 0.70 after a bronchodilator in COPD. In restrictive disease the lungs or chest wall cannot expand fully, so all volumes shrink (low total lung capacity, the defining finding, plus low FVC and vital capacity) while the FEV1/FVC ratio is normal or high because the stiff lungs empty quickly.

COPD

Chronic obstructive pulmonary disease is persistent, usually progressive airflow limitation caused mainly by cigarette smoke, with occupational dusts, biomass smoke and alpha-1 antitrypsin deficiency as other causes. Two overlapping processes are involved. Chronic bronchitis is defined clinically by a productive cough for at least 3 months in each of 2 consecutive years; mucus hypersecretion, airway inflammation and hypoxemia lead to cyanosis and right heart failure, giving the old "blue bloater" picture. Emphysema is destruction of alveolar walls with loss of elastic recoil, so small airways collapse on expiration; the classic "pink puffer" is thin, breathes through pursed lips, uses accessory muscles and leans forward on the arms. Severity of airflow limitation is graded by FEV1 percent predicted:

Hyperinflation flattens the diaphragm, putting it at a mechanical disadvantage, so accessory muscles take over. During exercise, rapid breathing leaves too little time to exhale and air builds up (dynamic hyperinflation), the main reason COPD patients stop exercising.

Long term oxygen is prescribed for resting SpO2 of 88% or lower (PaO2 55 mmHg or lower). The usual COPD target is SpO2 88% to 92%, because excess oxygen can worsen CO2 retention in some patients; titrate within the order, and never withhold oxygen from a patient in distress.

Asthma, cystic fibrosis and bronchiectasis

Asthma is airway inflammation with largely reversible obstruction (FEV1 improves 12% or more and 200 mL after bronchodilator). Exercise induced bronchoconstriction peaks 5 to 15 minutes after vigorous exercise; prevent it with a short acting beta agonist about 15 minutes before, a long warm up, and a scarf in cold air. Inability to speak in sentences, a quiet chest and cyanosis signal a severe attack and an emergency.

Cystic fibrosis is an autosomal recessive CFTR chloride channel defect: thick secretions, chronic infection (Pseudomonas), bronchiectasis, pancreatic insufficiency and salty sweat. Care centers on daily airway clearance and aerobic exercise; keep patients with CF at least about 6 feet apart, and add fluid and salt in heat. Bronchiectasis (permanent bronchial dilation with copious sputum) is also managed with airway clearance.

Restrictive lung disease

Interstitial lung disease (idiopathic pulmonary fibrosis, connective tissue disease, sarcoidosis, asbestos and silica) stiffens the lung and lowers diffusing capacity (DLCO), so patients desaturate quickly with exertion; use titrated oxygen, intervals and close SpO2 monitoring. Restriction also comes from chest wall deformity, obesity and neuromuscular weakness, where a falling vital capacity (toward about 15 to 20 mL/kg in Guillain Barre syndrome) warns of respiratory failure.

Pulmonary rehabilitation

Pulmonary rehabilitation does not improve FEV1 but improves exercise capacity, dyspnea and quality of life and reduces hospital use. Programs of about 8 to 12 weeks combine exercise, education, breathing strategies and psychosocial support.

• Endurance training: walking and cycling, 3 to 5 days per week, 20 to 60 minutes. Intensity is set by dyspnea (modified Borg 3 to 4, moderate to somewhat severe) or by 60% to 80% of peak work rate. Interval training lets severely limited patients accumulate more work.
• Strength training: large muscle groups of the legs and arms; upper extremity work matters because daily tasks with unsupported arms quickly provoke dyspnea when accessory muscles must stabilize the shoulder girdle.
• Inspiratory muscle training: resistive or threshold devices, often starting at about 30% of maximal inspiratory pressure, in patients with weak inspiratory muscles.
• Outcome: the 6 minute walk test (about 30 meters is a commonly cited important change in COPD).

Stop for SpO2 below about 88% that does not recover, severe dyspnea, chest pain or dizziness.

Breathing retraining

• Pursed lip breathing: inhale through the nose, exhale slowly through pursed lips for about twice as long as inspiration. The back pressure splints small airways open, slows respiratory rate, raises tidal volume and reduces air trapping. It is the most useful single technique in obstructive disease.
• Diaphragmatic breathing: the patient relaxes the upper chest and lets the abdomen rise during inspiration. It helps postoperative and anxious patients and asthma. In severe COPD with a flattened diaphragm it can increase the work of breathing and dyspnea, so use it selectively.
• Paced breathing coordinates breaths with activity: exhale during the effort phase (lifting, standing up, climbing a step).
• Positions to relieve dyspnea: forward lean sitting with forearms on the thighs or a table, standing leaning on a counter, and the tripod position. Leaning forward pushes abdominal contents up against the flattened diaphragm, restoring some dome, and fixes the shoulder girdle so accessory muscles work better.
• Segmental breathing and incentive spirometry encourage deep breaths and expansion of specific regions after surgery to prevent atelectasis.

Airway clearance

Airway clearance helps patients who produce excess or thick secretions (cystic fibrosis, bronchiectasis, some COPD, neuromuscular weakness with poor cough). Choose techniques the patient can do independently and will use.

Key drainage positions: upper lobe apical segments in sitting; right middle lobe and lingula supine with a quarter turn away from the involved side and the head lowered about 15 degrees; lower lobe superior segments prone flat; basal segments head down about 20 to 30 degrees (anterior in supine, lateral in sidelying on the opposite side, posterior in prone).

Section 4Peripheral vascular disease

Arterial versus venous disease

Peripheral artery disease (PAD) is limb atherosclerosis, strongly linked to smoking and diabetes, and most patients also have coronary disease. Intermittent claudication is a cramping muscle ache brought on by a predictable walking distance and relieved within minutes by standing still; pain sits one level below the narrowing (calf for femoral or popliteal, buttock and thigh for aortoiliac). Advanced disease causes forefoot rest pain at night, relieved by dangling the foot.

Chronic venous insufficiency follows valve incompetence or obstruction (often after DVT), producing venous hypertension, edema, brown hemosiderin staining, dermatitis and lipodermatosclerosis, with aching that worsens with standing and improves with elevation.

Bedside tests: pulse grading (0 absent to 2+ normal to 4+ bounding), capillary refill (normal under about 3 seconds), the elevation pallor and dependent rubor test, and venous filling time (more than 20 seconds suggests arterial disease).

The ankle brachial index

The ankle brachial index (ABI) compares systolic pressure at the ankle with that in the arm. With the patient supine and rested for about 5 to 10 minutes, measure brachial systolic pressure in both arms and ankle systolic pressure in the dorsalis pedis and posterior tibial arteries of each leg with a Doppler. For each leg, divide the higher ankle pressure by the higher of the two brachial pressures.

Claudication exercise

Supervised exercise therapy is a first line treatment for claudication and increases pain free and maximal walking distance as much as or more than revascularization in many patients. It works through better muscle oxidative capacity, improved endothelial function, collateral development and more efficient gait. The usual prescription:

• Mode: treadmill or track walking, because walking provokes and trains the affected muscles. Cycling or arm ergometry can supplement.
• Intensity: walk at a speed and grade that brings on claudication within about 3 to 5 minutes, continue until pain reaches moderate to moderately severe (about 3 to 4 on a 0 to 4 claudication scale), then rest until pain resolves completely, and repeat.
• Time: accumulate 30 to 45 minutes of walking (excluding rests), progressing toward 50 to 60 minutes.
• Frequency and duration: at least 3 sessions per week for at least 12 weeks.

Because PAD patients usually have coronary disease, monitor for angina, blood pressure response and dyspnea. Inspect the feet each session, especially in diabetes, and ensure footwear protects the skin. Smoking cessation is the single most important risk factor change.

Deep vein thrombosis and pulmonary embolism

Virchow triad: stasis (immobility, paralysis, travel), endothelial injury (surgery, trauma, lines) and hypercoagulability (cancer, pregnancy, estrogen, thrombophilia). Hip and knee surgery, hip fracture, major trauma and spinal cord injury carry the highest risk.

DVT signs are unilateral calf or leg swelling, pain or tenderness along the deep veins, warmth, erythema and pitting edema, but many DVTs are silent. Homans sign (calf pain on passive dorsiflexion) has poor sensitivity and specificity and should not be relied on. The Wells criteria estimate pretest probability:

In the two level version, a score of 2 or more means DVT is likely and 1 or less means unlikely; in the three level version, 0 is low, 1 to 2 moderate and 3 or more high probability. For a physical therapist, a likely score means hold lower extremity exercise and manual work on that limb and communicate with the physician the same day; diagnosis is by compression ultrasound and D-dimer.

Pulmonary embolism (sudden dyspnea, pleuritic chest pain, tachycardia, falling SpO2, hemoptysis) is an emergency: stop, support the patient and activate emergency response.

After a confirmed DVT, practice guidance supports early mobilization once therapeutic anticoagulation is reached (usually within about 24 hours with heparin products or direct oral anticoagulants; warfarin targets INR 2 to 3), because walking does not raise PE risk.

Also know Raynaud phenomenon (cold induced digital vasospasm, white to blue to red), Buerger disease (inflammatory small vessel occlusion in young smokers), and abdominal aortic aneurysm (pulsatile mass with deep abdominal or back pain in older male smokers; sudden pain with hypotension is rupture).

Section 5The lymphatic system and lymphedema

How the lymphatic system works

Lymphatics return filtered fluid and protein to the veins. Fluid enters blind ended initial lymphatics, then valved collectors whose segments (lymphangions) contract rhythmically, helped by muscle pumping and breathing. After regional nodes, the thoracic duct drains the legs, abdomen and left upper body into the left venous angle, and the right lymphatic duct drains the right arm and right side of the head and chest. Skin territories are separated by watersheds (trunk midline and a line near the umbilicus), and fluid can be moved across them through superficial anastomoses, the basis of manual lymph drainage.

Lymphedema: causes and staging

Lymphedema is protein rich interstitial fluid from lymphatic transport failure; the protein drives inflammation, fat deposition and fibrosis. Primary lymphedema is developmental: congenital, praecox (puberty to 35, the most common) or tarda (after 35). Secondary lymphedema follows damage: filariasis worldwide, and in the United States mainly cancer treatment (node dissection, radiation), trauma, venous disease and obesity. It can appear years after treatment.

Examination and measurement

History covers cancer treatment, node surgery and radiation, infections, onset and progression, and what makes swelling better or worse. Inspection notes skin color, folds, texture, wounds, and lymphorrhea (leaking lymph). Palpation assesses pitting and fibrosis. The Stemmer sign is positive when the examiner cannot lift a fold of skin at the dorsal base of the second toe or middle finger; a positive sign supports lymphedema, but a negative sign does not exclude it, especially early.

• Circumferential girth: tape measurements at fixed intervals (commonly every 4 cm, or at bony landmarks) on both limbs. A difference of about 2 cm or more at any point between limbs is a common threshold.
• Volume calculation: girths converted to volume with the truncated cone formula; a difference of about 200 mL or a 10% interlimb volume difference is commonly used to diagnose arm lymphedema, and smaller changes (around 3% to 5%) flag early change. Exact cutoffs vary by source.
• Water displacement (reference standard), perometry, and bioimpedance spectroscopy, which detects subclinical stage 0 fluid.

Lipedema is symmetric fat deposition in women that spares the feet with a negative Stemmer sign. Bilateral pitting edema suggests heart, kidney or liver disease. New swelling in a cancer survivor may be recurrence, and sudden unilateral swelling may be DVT; refer both.

Complete decongestive therapy

Complete decongestive therapy (CDT) is the standard treatment and has two phases.

• Phase 1, intensive (reduction): usually daily, 5 days per week for about 2 to 4 weeks or until the limb plateaus. It combines manual lymph drainage, multilayer short stretch compression bandaging worn about 23 hours a day, decongestive exercise in the bandages, and meticulous skin and nail care.
• Phase 2, self management (maintenance): the patient wears a fitted compression garment during the day, often bandages or a nighttime garment, performs self MLD and exercise, maintains skin care, and returns for remeasurement and new garments about every 6 months.

Manual lymph drainage (MLD) uses light, slow, rhythmic skin stretching (pressure of roughly 30 to 45 mmHg, enough to stretch the skin but not to compress underlying tissue). The sequence always starts proximally: clear the neck (terminus) and the healthy nodes and territories first, then move fluid from the trunk across watersheds toward working nodes, and only then work on the limb from proximal to distal, with strokes directed proximally. After left axillary dissection, left arm fluid is routed to the right axilla and left inguinal nodes.

Short stretch bandages have low resting and high working pressure: muscle contraction against the inelastic wrap pumps lymph, and resting pressure stays safe for night wear. They are applied with a distal to proximal gradient over padding. Garments (classes of about 20 to 30, 30 to 40 and 40 to 50 mmHg) are fitted only after reduction. Progressive resistance training, started light and supervised, is safe and does not worsen breast cancer related lymphedema. Intermittent pneumatic compression is an adjunct at low pressure after proximal clearing.

Precautions and education

Cellulitis (spreading redness, warmth, pain, fever) is common in lymphedematous limbs: stop MLD and compression and refer for antibiotics. Teach daily skin inspection, moisturizing and careful nail care. Avoiding blood pressure readings and needle sticks in the at risk arm has weak evidence but remains a reasonable precaution when another limb is available. Healthy weight lowers risk, and early reporting of heaviness allows treatment at stage 0 or I.

Words worth knowing