Cardiovascular and Pulmonary Foundations: Physiology, Examination and Monitoring

Every exercise prescription is a request for more oxygen, and the heart, lungs and blood decide whether the body can meet it. On the licensing exam, cardiovascular and pulmonary questions rarely ask for physiology for its own sake: they ask whether a patient is safe to treat, when to stop, and what a number or rhythm means for the session in front of you. This chapter builds the physiology, monitoring, ECG, auscultation, imaging, pulmonary function, blood gas and laboratory knowledge that lets you answer those questions with confidence.

Section 1Cardiac and pulmonary physiology for the clinician

The cardiac cycle

The cardiac cycle has two main phases. During systole the ventricles contract: first with all valves closed (isovolumetric contraction), then, once ventricular pressure exceeds aortic and pulmonary pressure, with the semilunar valves open (ejection). During diastole the ventricles relax with all valves closed (isovolumetric relaxation), then the atrioventricular valves open and the ventricles fill, first passively and finally with the atrial kick, which supplies about 15 to 30 percent of filling and is lost in atrial fibrillation.

• S1 is closure of the mitral and tricuspid valves at the start of systole; S2 is closure of the aortic and pulmonic valves at the start of diastole.
• S3 (ventricular gallop, "Ken-tuc-ky") occurs in early diastole from rapid filling of a volume overloaded ventricle; it is a classic sign of heart failure in adults (normal in children and young athletes).
• S4 (atrial gallop, "Ten-nes-see") occurs just before S1 as the atrium pushes blood into a stiff ventricle (hypertension, hypertrophy, ischemia).
• Murmurs come from turbulent flow across stenotic or leaking valves. Aortic stenosis causes a systolic murmur and can produce exertional syncope, angina and dyspnea; severe symptomatic aortic stenosis is a contraindication to exercise.

The coronary arteries fill mainly during diastole, so tachycardia, which shortens diastole, reduces supply at the same time it raises demand. The right coronary artery usually supplies the right ventricle, the inferior wall, the SA node (in about 60 percent of people) and the AV node (in most), which is why inferior infarctions often cause bradycardia and heart block. The left anterior descending artery supplies the anterior wall and most of the septum, and the circumflex supplies the lateral wall.

Cardiac output and its determinants

Cardiac output (CO) is heart rate times stroke volume, about 4 to 8 L/min at rest (roughly 5 L/min). Stroke volume depends on three factors:

• Preload: ventricular stretch at the end of diastole (end diastolic volume). By the Frank Starling mechanism, more stretch produces a stronger contraction, up to a limit; a failing heart is on the flat part of the curve.
• Afterload: the resistance the ventricle must overcome, mainly arterial pressure and aortic valve resistance. Hypertension and aortic stenosis raise afterload.
• Contractility: the intrinsic force of contraction at a given preload, increased by sympathetic stimulation and inotropes such as dobutamine.

Ejection fraction (EF) is stroke volume divided by end diastolic volume; normal is about 55 to 70 percent. Heart failure with reduced EF is defined by an EF of 40 percent or less, and heart failure with preserved EF by 50 percent or more. Blood pressure equals cardiac output times total peripheral resistance. Mean arterial pressure (MAP) is approximately diastolic pressure plus one third of the pulse pressure; a MAP of at least about 65 mmHg is needed to perfuse vital organs.

Conduction

The sinoatrial (SA) node is the normal pacemaker, firing 60 to 100 times per minute. The impulse spreads through the atria to the atrioventricular (AV) node, which delays it (the PR interval) so the atria can finish emptying, then travels down the bundle of His, the right and left bundle branches and the Purkinje fibers. If higher pacemakers fail, lower tissues take over at slower intrinsic rates: AV junction about 40 to 60 per minute and ventricles about 20 to 40 per minute. Sympathetic stimulation raises rate and contractility; vagal (parasympathetic) stimulation slows the SA node and AV conduction.

Lung volumes and ventilation

Four volumes add up to total lung capacity, and capacities are sums of two or more volumes. Residual volume cannot be measured by simple spirometry (it requires body plethysmography or gas dilution), so neither can FRC or TLC.

Minute ventilation is tidal volume times respiratory rate, about 6 L/min at rest. Only the part that reaches perfused alveoli takes part in gas exchange: alveolar ventilation equals (tidal volume minus dead space) times rate. Anatomic dead space is about 150 mL (roughly 1 mL per pound of ideal body weight), so rapid shallow breathing wastes a larger share of each breath. Pursed lip and diaphragmatic breathing slow the rate and increase tidal volume, improving alveolar ventilation.

Inspiration is active (mainly the diaphragm, innervated by the phrenic nerve, C3 to C5, with the external intercostals); quiet expiration is passive elastic recoil. Accessory inspiratory muscles (sternocleidomastoid, scalenes, upper trapezius, pectorals) are recruited in distress and in hyperinflation, and forced expiration uses the abdominals and internal intercostals.

Ventilation and perfusion

In the upright lung, both ventilation and perfusion are greater at the bases than the apices, because gravity pulls blood down and the dependent alveoli are on a steeper, more compliant part of their pressure volume curve. Perfusion changes more steeply than ventilation, so the V/Q ratio is highest at the apex (about 3) and lowest at the base (about 0.6); the whole lung averages about 0.8. The two extremes of mismatch are:

• Dead space (ventilation without perfusion, V/Q approaching infinity), as in pulmonary embolism.
• Shunt (perfusion without ventilation, V/Q of zero), as in atelectasis, pneumonia filling alveoli or pulmonary edema. Hypoxemia from a true shunt responds poorly to supplemental oxygen.

Positioning uses gravity: in an adult with unilateral lung disease, placing the good lung down sends more blood and ventilation to the healthy lung and improves oxygenation. Exceptions include a lung abscess or pulmonary hemorrhage (keep the affected lung down so material does not spill into the good lung) and infants, in whom ventilation favors the uppermost lung.

Oxygen transport

Almost all oxygen in blood is bound to hemoglobin. Arterial oxygen content (CaO2) = (1.34 × Hb × SaO2) + (0.003 × PaO2), about 20 mL O2 per 100 mL of blood normally. Oxygen delivery = cardiac output × CaO2. The equation explains why anemia, low saturation and low cardiac output each limit exercise. The Fick equation states that oxygen consumption (VO2) = cardiac output × arteriovenous oxygen difference; training raises VO2max through both larger stroke volume and better extraction.

The oxyhemoglobin dissociation curve is S shaped. A PaO2 of 60 mmHg corresponds to an SaO2 of about 90 percent, at the shoulder of the curve; below that, small falls in PaO2 cause large falls in saturation. A right shift (lower affinity, easier unloading to tissues) is caused by increased temperature, increased CO2, acidosis (increased H⁺) and increased 2,3-BPG, all of which occur in exercising muscle. A left shift (higher affinity) occurs with alkalosis, hypothermia, carbon monoxide and fetal hemoglobin.

Section 2Vital signs and monitoring

Resting values

Measure blood pressure with the patient seated, back supported, feet flat, arm supported at heart level, after five minutes of rest, with a cuff whose bladder encircles about 80 percent of the arm. A cuff that is too small gives a falsely high reading. Do not take blood pressure in an arm with a PICC line, arteriovenous fistula, lymphedema risk after node dissection, or an arterial line. Orthostatic hypotension is a fall of at least 20 mmHg systolic or 10 mmHg diastolic within three minutes of standing, often with dizziness and a compensatory rise in heart rate; it is common after bed rest, with dehydration, diuretics, antihypertensives, Parkinson disease and spinal cord injury.

Normal and abnormal exercise responses

During graded aerobic exercise:

• Heart rate rises roughly linearly with workload (about 10 bpm per MET in an untrained person) until near maximum. Age predicted maximum is 220 minus age; the Tanaka formula, 208 minus 0.7 times age, is more accurate in older adults.
• Systolic blood pressure rises roughly 8 to 12 mmHg per MET (about 10), often reaching 160 to 220 mmHg at peak.
• Diastolic blood pressure stays about the same or changes by no more than about 10 mmHg, because peripheral resistance falls as muscle vessels dilate.
• Respiratory rate and tidal volume rise; SpO2 stays stable in healthy people.

Abnormal responses that signal a problem include a fall in systolic pressure of more than 10 mmHg as workload increases (suggesting the heart cannot raise output, as with ischemia or severe heart failure), a failure of systolic pressure to rise (flat response), a hypertensive response (systolic above 250 mmHg or diastolic above 115 mmHg is the usual stopping point), a rise in diastolic pressure of more than 10 mmHg, an excessive or inappropriately low heart rate response (chronotropic incompetence), and a fall in SpO2 below about 88 to 90 percent.

Intensity tools: heart rate reserve, RPE and METs

The Karvonen (heart rate reserve) method: target HR = [(HRmax minus HRrest) × intensity] + HRrest. Moderate intensity is about 40 to 59 percent of heart rate reserve and vigorous about 60 to 89 percent. For a 60 year old with a resting HR of 70: HRmax 160, reserve 90, and 50 percent intensity gives 45 + 70 = 115 bpm.

Beta blockers blunt resting and exercise heart rate (and blood pressure), so heart rate targets from age formulas are invalid; use RPE, a target from a medicated exercise test, or a heart rate rise above resting. The Borg RPE scale runs from 6 to 20 (roughly heart rate divided by 10 in healthy adults); 12 to 13 ("somewhat hard") is moderate intensity and 11 to 13 is a common target in cardiac rehabilitation. The Borg CR10 scale runs from 0 to 10, where 3 to 4 is moderate. The talk test is a practical check: at moderate intensity a person can talk but not sing. Dyspnea scales (0 to 4 or the modified Borg) and angina scales (1 to 4) guide symptom limited exercise.

One MET is the resting oxygen consumption, about 3.5 mL O2/kg/min. Self care is about 1 to 3 METs, walking at 3 mph about 3.3 METs, and stair climbing about 4 to 8 METs.

Rate pressure product

The rate pressure product (RPP, double product) is heart rate times systolic blood pressure. It is an index of myocardial oxygen demand. A patient with stable angina has symptoms at a fairly reproducible RPP, the ischemic threshold, so keeping exercise below that RPP prevents angina. Training lowers the HR and blood pressure at any submaximal workload, so the patient can do more work before reaching the threshold. Nitroglycerin and beta blockers raise the work achievable before angina by lowering demand.

Pulse oximetry

The pulse oximeter estimates arterial saturation from light absorption. It is unreliable with poor perfusion (cold hands, shock, vasoconstriction), motion, dark nail polish, and carbon monoxide poisoning, which produces falsely normal readings because carboxyhemoglobin is read as oxyhemoglobin. It can overestimate saturation in people with darker skin pigmentation. It says nothing about CO2; trust it only with a good waveform.

Lines, tubes and oxygen in acute care

Oxygen delivery devices differ in flow and fraction of inspired oxygen (FiO2). A nasal cannula runs at 1 to 6 L/min (each liter adds roughly 3 to 4 percent above room air's 21 percent, up to about 44 percent). A simple face mask uses 5 to 10 L/min (about 35 to 55 percent). A Venturi mask delivers a precise FiO2 (about 24 to 50 percent), useful in COPD. A nonrebreather mask with reservoir at 10 to 15 L/min delivers high concentrations (roughly 60 to 90 percent or more). High flow nasal cannula delivers heated humidified gas at up to about 60 L/min with FiO2 up to 100 percent. Oxygen is a prescribed drug: during exercise the therapist may adjust within the order (often to keep SpO2 at or above 90 percent, or the prescribed range) but not beyond it.

Section 3ECG basics for physical therapists

Waves, intervals and the paper

The electrocardiogram records the heart's electrical activity, not its pumping. On standard paper running at 25 mm/s, each small box is 1 mm, 0.04 seconds wide and 0.1 mV tall; each large box (five small boxes) is 0.20 seconds. Five large boxes equal one second.

To find the heart rate of a regular rhythm, divide 300 by the number of large boxes between two R waves (or 1,500 by the number of small boxes). The sequence 300, 150, 100, 75, 60, 50 gives the rate for R waves one to six large boxes apart. For an irregular rhythm, count the QRS complexes in a 6 second strip and multiply by 10.

Read systematically: rate, regularity, a P before every QRS, PR and QRS widths, then ST segments and T waves.

Rhythms the exam expects you to recognize

Heart blocks

• First degree AV block: PR interval longer than 0.20 s, every P conducted. Usually benign; common with beta blockers, calcium channel blockers and digoxin.
• Second degree type I (Wenckebach, Mobitz I): the PR interval lengthens progressively until a P wave is not followed by a QRS, then the cycle repeats. Usually at the AV node, often benign.
• Second degree type II (Mobitz II): a constant PR interval with sudden dropped QRS complexes. Below the AV node, can progress to complete block; do not exercise and notify the physician, as a pacemaker is often needed.
• Third degree (complete) heart block: P waves and QRS complexes are independent (AV dissociation), with a slow ventricular escape rhythm. It is a contraindication to exercise and usually requires a pacemaker.

A new bundle branch block (QRS 0.12 s or wider with a characteristic shape) during exercise is a relative reason to stop.

Ischemia and infarction

The ST segment is the key to ischemia:

• ST depression of 1 mm or more (horizontal or downsloping, measured about 80 ms after the J point) suggests subendocardial ischemia, the typical finding in exercise induced ischemia. More than 2 mm of horizontal or downsloping depression is a reason to stop exercise.
• ST elevation in contiguous leads suggests transmural injury, as in ST elevation myocardial infarction (STEMI), a medical emergency. New ST elevation of more than 1 mm during exercise in leads without Q waves is an absolute reason to stop.
• T wave inversion can reflect ischemia; pathologic Q waves (wide and deep) indicate an old, completed infarction.

Angina may be typical (pressure or squeezing behind the sternum that may radiate to the jaw, left arm or back, provoked by exertion and relieved by rest or nitroglycerin) or atypical. Women, older adults and people with diabetes more often present with dyspnea, fatigue, nausea, epigastric discomfort or no pain at all (silent ischemia). Stable angina occurs at a predictable workload; unstable angina (new, at rest, or worsening) is a contraindication to exercise and requires referral.

Pacemakers and implantable defibrillators

Pacemakers are described by a code: the first letter is the chamber paced, the second the chamber sensed, the third the response, and an R in the fourth position indicates rate responsiveness (the device raises the rate with activity). A paced beat shows a sharp spike before the P or QRS. Know the patient's programmed lower and upper rate limits; a patient with a fixed rate device depends on stroke volume to increase cardiac output, so monitor blood pressure and RPE. After implantation, the arm on the device side is commonly restricted from overhead motion (above about 90 degrees of flexion or abduction) and heavy lifting for about four to six weeks so the leads can anchor.

An implantable cardioverter defibrillator (ICD) detects VT or fibrillation and delivers pacing or a shock. Learn its detection rate and keep the exercise heart rate at least about 10 to 20 bpm below it, so sinus tachycardia during exercise does not trigger an inappropriate shock. If the patient receives a shock, stop, assess, and follow the facility protocol (more than one shock, or symptoms, needs emergency evaluation).

Section 4Auscultation, chest imaging and pulmonary function tests

Breath sounds

Auscultate with the diaphragm on bare skin as the patient breathes through an open mouth, comparing side to side. Normal sounds depend on location:

• Vesicular: soft and low pitched, heard over most of the lung periphery; inspiration is longer than expiration.
• Bronchovesicular: intermediate, heard over the mainstem bronchi (between the scapulae and near the sternum); inspiration and expiration about equal.
• Bronchial (tracheal): loud, high pitched and hollow, heard over the manubrium and trachea, with expiration longer than inspiration. Bronchial sounds heard over the periphery are abnormal and suggest consolidation, because solid lung transmits sound from the large airways.

Decreased or absent breath sounds occur with hyperinflation (emphysema), pneumothorax, pleural effusion, atelectasis with an obstructed airway, shallow breathing and obesity.

Voice sounds are increased over consolidation: egophony ("ee" heard as "ay"), bronchophony (spoken words louder and clearer) and whispered pectoriloquy (whispers heard clearly). The same rule applies to tactile fremitus and percussion: consolidation increases fremitus and is dull; air or fluid between lung and wall (pneumothorax, effusion) decreases fremitus, with effusion dull and pneumothorax or emphysema hyperresonant. The trachea shifts away from a tension pneumothorax or large effusion and toward lobar collapse or a pneumonectomy.

The chest radiograph

Dense structures absorb x rays and appear white (bone, fluid, consolidated lung, heart); air appears black. Patterns to know:

• Consolidation (pneumonia): white patch in a lobar or segmental pattern, often with air bronchograms (dark airways outlined by surrounding white alveoli).
• Pleural effusion: blunting of the costophrenic angle and a meniscus shaped fluid line on an upright film.
• Pneumothorax: a visible pleural line with no lung markings beyond it; tension pneumothorax shifts the mediastinum away.
• Atelectasis: increased density with volume loss, shifting fissures, the diaphragm or trachea toward the collapse.
• COPD (emphysema): hyperinflation with flattened diaphragms, increased anteroposterior diameter, increased retrosternal air, and a narrow vertical heart.
• Heart failure: cardiomegaly (cardiothoracic ratio over 0.5 on a posteroanterior film), vascular redistribution to the upper lobes, Kerley B lines, perihilar "bat wing" edema and effusions.

CT pulmonary angiography is the usual test for pulmonary embolism; a V/Q scan, showing a perfusion defect in a ventilated region, is the alternative.

Pulmonary function tests

Spirometry measures how much and how fast air can be exhaled after a maximal breath. The forced vital capacity (FVC) is the total volume exhaled forcefully; the FEV1 is the volume exhaled in the first second. Their ratio, FEV1/FVC, separates the two main patterns:

COPD severity by airflow limitation (the GOLD grades, applied when FEV1/FVC is below 0.70) uses FEV1 as a percent of predicted: grade 1 (mild) 80 percent or more, grade 2 (moderate) 50 to 79 percent, grade 3 (severe) 30 to 49 percent, and grade 4 (very severe) below 30 percent. In asthma, an increase in FEV1 of at least 12 percent and 200 mL after a bronchodilator shows significant reversibility. Peak expiratory flow, measured with a handheld meter, tracks asthma control at home. In neuromuscular disease, a falling FVC (and especially a fall from sitting to supine, which signals diaphragm weakness) helps time ventilatory support.

Arterial blood gases

Interpret in steps. (1) Look at the pH: acidosis or alkalosis? (2) Which component explains it? If PaCO2 moves in the opposite direction to pH (pH low, CO2 high), the cause is respiratory; if HCO3 moves in the same direction as pH (pH low, HCO3 low), the cause is metabolic. The mnemonic ROME captures this: Respiratory Opposite, Metabolic Equal. (3) Is there compensation? If the other component has moved to oppose the change, the disorder is partially compensated; if the pH has returned to normal, it is fully compensated (the pH usually stays on the side of the original problem). The lungs compensate within minutes to hours; the kidneys take days.

• Respiratory acidosis (hypoventilation): COPD exacerbation, sedation or opioids, neuromuscular weakness (GBS, ALS), obesity hypoventilation, chest wall restriction.
• Respiratory alkalosis (hyperventilation): anxiety, pain, early pulmonary embolism, early asthma attack, high altitude, overventilation on a ventilator.
• Metabolic acidosis: diabetic ketoacidosis, lactic acidosis, renal failure, severe diarrhea, some poisonings; the patient breathes deeply and rapidly (Kussmaul respiration) to blow off CO2.
• Metabolic alkalosis: vomiting, nasogastric suction, diuretics, excess antacids; often with low potassium.

Section 5Laboratory values and termination criteria

Why lab values matter to the therapist

Laboratory values tell you whether the body can tolerate activity: enough hemoglobin to carry oxygen, enough clotting function to prevent bleeding, enough glucose, stable electrolytes and no ongoing heart injury. Check the chart before each acute care session, look at the trend rather than one number, and always put the value next to the patient's symptoms and vital signs. Reference ranges vary slightly by laboratory; the values below are the commonly taught ones.

Hemoglobin and hematocrit

Hemoglobin determines oxygen carrying capacity. With anemia, the heart compensates by raising heart rate and cardiac output, so the patient reaches exercise limits sooner and may have exertional tachycardia, dyspnea, dizziness or angina. Older references used firm cutoffs, such as withholding exercise below 8 g/dL; current acute care guidance emphasizes the patient's symptoms, the trend and the medical plan rather than a single number. A practical teaching scheme: at or above about 10 g/dL, usual progression; about 8 to 10 g/dL, proceed with closer monitoring of symptoms and vital signs; below about 8 g/dL, activity is symptom limited and focused on essential mobility after discussion with the team; below about 7 g/dL, transfusion is commonly considered. A falling value over hours (active bleeding) is more worrisome than a stable low value in chronic anemia. Hematocrit is high in dehydration and polycythemia, which increase blood viscosity and clot risk.

Platelets and anticoagulation

Low platelets raise the risk of spontaneous bleeding, bruising and hemorrhage after minor trauma. Commonly taught activity tiers (sources differ slightly on the exact cutoffs):

• Above about 50,000: progressive exercise as tolerated; avoid high impact or contact activity when counts are below normal.
• About 20,000 to 50,000: light exercise, active range of motion and walking; no heavy resistance.
• Below about 20,000: essential activities and mobility only, after consulting the medical team; prevent falls, avoid resisted exercise and anything that raises bleeding risk. Some protocols use 10,000 as the threshold for spontaneous bleeding.

Watch for petechiae, bruising, bleeding and any new headache or neurologic change, and avoid firm manual pressure.

For patients on warfarin, the INR is the guide: a therapeutic range of 2.0 to 3.0 is expected and does not prevent activity. Many references advise holding or discussing activity when the INR is above about 4 (some say 3.5 to 5), and emphasize fall prevention at any elevated value. Direct oral anticoagulants (apixaban, rivaroxaban, dabigatran) are not monitored with INR. Unexplained bruising, black stools, or a new severe headache in an anticoagulated patient require prompt medical evaluation.

Glucose

Exercise lowers blood glucose by increasing muscle uptake, and the effect lasts for hours. For patients using insulin or sulfonylureas, check glucose before exercise:

• Below 70 mg/dL is hypoglycemia: do not start. Treat with the rule of 15 (15 g of fast carbohydrate such as 4 ounces of juice or glucose tablets, recheck in 15 minutes, repeat if still below 70), then eat a snack before resuming.
• 70 to about 100 mg/dL: give about 15 to 30 g of carbohydrate before exercise.
• About 100 to 250 mg/dL: exercise is appropriate.
• Above 250 mg/dL: check for ketones (especially in type 1 diabetes); if ketones are present, postpone exercise because it can worsen ketoacidosis. Without ketones, light to moderate exercise can proceed with caution if the person feels well and is hydrated. Many therapy references advise against exercise above about 300 mg/dL.

Hypoglycemia causes sweating, shakiness, tachycardia and hunger (masked by beta blockers), then confusion, slurred speech and seizures. Hyperglycemia causes thirst, polyuria and fatigue, and ketoacidosis adds fruity breath and Kussmaul respirations. Delayed hypoglycemia can occur hours after exercise, so teach patients to monitor that evening. Avoid injecting insulin into a limb that is about to be exercised heavily, because uptake speeds up.

Potassium, sodium and calcium

Hypokalemia (below 3.5 mEq/L), often from diuretics, vomiting or diarrhea, causes muscle weakness, cramps, fatigue, flattened T waves, U waves, PVCs and other arrhythmias, and increases digoxin toxicity. Hyperkalemia (above 5.0 mEq/L), often from kidney failure, potassium sparing diuretics or ACE inhibitors, causes weakness, peaked T waves, a widened QRS, bradycardia and risk of cardiac arrest. Exercise is generally deferred with significantly abnormal potassium or ECG changes until it is corrected. Hyponatremia (below 135) causes confusion, headache, lethargy and falls. Low calcium causes tetany and cramps; high calcium causes weakness, lethargy and kidney stones.

Cardiac markers

Troponin (I or T) is the most sensitive and specific marker of myocardial injury. It begins to rise within a few hours of injury (earlier with high sensitivity assays), peaks at about 12 to 24 hours or later, and stays elevated for about 7 to 14 days. A rising troponin means ongoing injury, and exercise beyond basic bedside activity is held until the team confirms the patient is stable; a troponin that has peaked and is trending down in a patient without symptoms usually allows progressive mobility per the cardiac protocol. CK-MB rises and falls faster and is less used. BNP (or NT-proBNP) is released by stretched ventricles and is elevated in heart failure.

Exercise contraindications and termination criteria

Absolute contraindications to exercise (commonly listed) include: acute myocardial infarction within about two days, unstable angina, uncontrolled symptomatic arrhythmias, symptomatic severe aortic stenosis, decompensated heart failure, acute pulmonary embolism or DVT that has not been treated, acute myocarditis or pericarditis, acute aortic dissection, and any acute systemic illness or fever. Relative contraindications include resting blood pressure above about 200/110 mmHg, significant electrolyte abnormalities, tachyarrhythmias or bradyarrhythmias, hypertrophic cardiomyopathy with outflow obstruction, high degree AV block, and conditions that limit cooperation.

For early inpatient cardiac rehabilitation, a traditional guide caps the heart rate rise at about 20 bpm above resting after myocardial infarction and about 30 bpm above resting after cardiac surgery, with an RPE of 13 or less, progressing as tolerated. After cardiac surgery through a median sternotomy, follow sternal precautions (traditionally no lifting more than about 5 to 10 pounds and no pushing up with the arms for about six to eight weeks; many programs now use activity based "keep your move in the tube" guidance).

Red flags that need medical attention

• Myocardial infarction: chest pressure lasting more than a few minutes, unrelieved by rest or nitroglycerin, with diaphoresis, nausea or dyspnea. Stop, call for help, and activate emergency services.
• Deep vein thrombosis: unilateral calf swelling, tenderness, warmth and pitting edema, especially after surgery or immobility; the Wells criteria estimate probability. Hold exercise of that limb and notify the physician.
• Pulmonary embolism: sudden dyspnea, pleuritic chest pain, tachycardia, tachypnea, falling SpO2, hemoptysis or syncope: emergency.
• Decompensated heart failure: weight gain of more than about 2 to 3 pounds in a day or 5 pounds in a week, worsening edema, orthopnea, paroxysmal nocturnal dyspnea, new S3 or crackles.
• Hypertensive crisis: blood pressure above 180/120 mmHg with headache, chest pain, vision change or neurologic signs.

Words worth knowing