Cardiovascular & Pulmonary Systems

Question 1

VTE - Clinical Definition

What is venous thromboembolism (VTE)?

Answer 1

Venous thromboembolism (VTE) is a venous disorder that is considered a subcategory of peripheral vascular disease. Venous thromboembolism refers to both deep vein thrombosis (DVT) and pulmonary embolism (PE). Venous thromboembolism results in venous insuffiency, or inadequate drainage of venous blood from the extremities or major organs, excluding the heart and brain.

Deep vein thrombosis (DVT) refers to partial or complete occlusion of a deep vein by a thrombus with secondary inflammatory reaction in the wall of the vein (i.e., thrombophlebitis).

Pulmonary embolism refers to the lodging of an embolus in a pulmonary artery with subsequent obstruction of the blood supply to the lung parenchyma, the portion of the lungs involved in gas exchange.

References:

• Goodman and Fuller (4th ed.), p.633 (“Peripheral Vascular Disease”), 646 (“Deep Vein Thrombosis and Pulmonary Embolism”), 849 (“Pulmonary Embolism and Infarction–Definition and Incidence”)​
• See “Cardiopulmonary” flashcards.

Question 2

DVT - Clinical Presentation

What are the hallmark signs and symptoms of deep vein thrombosis (DVT)?

Answer 2

*Adapted from Wells Clinical Decision Rule for DVT (see Table 12-22):

• Entire lower-extremity edema. Due to leakage of fluids into the interstitial space as a result of (1) venous pooling or (2) the inflammatory process following mechanical injury to the venous walls (e.g., intravenous injections, fractures, or dislocations)
• Unilateral calf edema (more than 3 mm larger than uninvolved side). Due to involvement of the deep veins in the calf (e.g., posterior tibial vein). See above for rationale for lower-extremity edema.
• Unilateral pitting edema in the lower extremity. See above for rationale for lower-extremity edema.
• Localized tenderness in the center of the posterior calf (posterior tibial vein), the popliteal space (popliteal vein), or the anterior thigh or groin (femoral vein). Due to increased interstitial pressure secondary to lower-extremity edema that stimulates nearby afferent nerve endings
• Collateral superficial veins (nonvaricose) in the lower extremity. Dilated collateral superficial veins may become visible or palpable due to the back up of venous blood associated with deep vein thrombosis.

References:

• Goodman and Fuller (4th ed.), p.647 (collateral veins), 649 (“DVT–Clinical Manifestations”), 650 (Table 12-22)
• Merk Manual: Deep Vein Thrombosis (https://www.merckmanuals.com/professional/cardiovascular-disorders/peripheral-venous-disorders/deep-venous-thrombosis-dvt)

Question 3

PE - Clinical Presentation

What are the hallmark signs and symptoms of pulmonary embolism (PE)?

Answer 3

• Sudden pleuritic chest pain that increases with breathing. Due to pulmonary infarction
• Dyspnea and tachypnea. Due to the stimulation of a reflex response caused by pulmonary edema (*see Vander’s [15th ed.], p.478 [“Reflexes from J Receptors”])
• Persistent cough or hemoptysis. Due to pulmonary edema
• Tachycardia. Due to the compensatory activation of the sympathetic nervous system in response to inadequate cardiac output
• Excessive sweating. Due to activation of the sympathetic nervous system (*see previous bullet point)
• Cyanosis. Due to decrease in the flow of oxygenated blood throughout the body
• Lightheadedness or loss of consciousness. Due to decrease in flow of oxygenated blood to the brain
• Anxiety, restlessness, apprehension. May be due to the onset of aforementioned signs and symptoms
• Death. Due to the resulting failure of the lungs and heart to maintain adequate gas exchange and circulation in the body

References:

• Goodman and Fuller (4th ed.), p.649 (“Clinical Manifestations”)
• See “Specific NPTE Study Topics” Word doc.

Question 4

DVT - PT Implications

What are the major indications, contraindications, guidelines, or protocols for treating deep vein thrombosis (DVT)?

Answer 4

• Instruct the patient on elevating the legs. Patients with lower extremity DVTs should elevate the legs just above the level of the heart to faciliate venous return via the gravitational force on blood flow, which thereby (1) prevents the formation of new thrombi by reducing the likelihood of the development of venous stasis, and (2) decrease symptoms related to DVT (e.g., pain and tenderness) by decreasing lower-extemity edema.
• Acute care considerations
  
  • If a patient is suspected of having a DVT but the medical diagnosis is pending, hold on initiating physical therapy until after the diagnosis is confirmed and an adequate anticoagulant has been administered (e.g., warafin with an INR of 2.0 to 3.0). This can help to reduce the risk of PE.
  • After thrombosis of a deep calf vein, patients should wear a compressive or elastic stocking in the involved lower extremity to reduce the risk of progression of DVT to PE. In addition to its role in facilitating venous return by increasing venous pressure, the compressive force applied by the stocking causes the venous wall to become applied to the thrombus, thereby keeping the thrombus in its location and preventing movement inside the vein when upright and ambulating. Without the external compressive force of the stocking, once the person stands, increased hydrostatic pressure causes venous distention and permits the thrombus to become free floating inside the vessel.
  • Patients with DVTs will often be on anticoagulant (“blood-thinners”) therapy (e.g., warafin), so it is important to monitor for and immediately report signs and symptoms of excessive bleeding (e.g., subcutaneous bruising, blood in the urine, back pain).
• Homan’s sign was a clinical test that was used in the past to assess for DVTs. It is no longer considered a sensitive or specific test for ruling in or out DVT.
  
  • Homan’s sign is positive if there is deep-seated pain in the posterior leg or calf when the ankle is passively dorsiflexed with the patient supine. Squeezing the calf or deep palpation may be done as follow-up tests if results are unclear. Pain associated with DVT should resolve quickly.
• Doppler duplex ultrasonography (aka, “Doppler study”) is a medical test that uses sound waves to visualize the flow of blood through blood vessels. A Doppler study is often used to detect and diagnose deep vein thrombosis.

References:

• Goodman and Fuller (4th ed.), pp.651-653 (“Special Implications for the Therapist”)
• For more information about Doppler duplex ultrasound, see MedlinePlus: Duplex Ultrasound (https://medlineplus.gov/ency/article/003433.htm).
• For more information about Homan’s sign, see “Screening for DVT” from Case Integration I.

Question 5

CVI - Clinical Definition

What is chronic venous insufficiency (CVI)?

Answer 5

Chronic venous insufficiency (CVI) (aka, postphlebitic syndrome, venous stasis) is a venous disorder that is considered a subcategory of peripheral vascular disease. Chronic venous insufficiency refers to inadequate venous return over a long period of time that occurs as the result of damaged or destroyed venous valves secondary to deep vein thrombosis, varicose veins, or injury to the veins.

References:

• Goodman and Fuller (4th ed.), p.633 (“Peripheral Vascular Disease”), 655 (“Definition and Incidence;” “Etiologic Factors and Pathogenesis”)

Question 6

CVI - Clinical Presentation

What are the hallmark signs and symptoms of chronic venous insufficiency (CVI)?

Answer 6

• Progressive lower-extremity edema
• Venous insufficiency ulcers (aka, stasis ulcers). Due to inadequate venous circulation. The specific mechanism by which venous insufficiency ulcers happens is not well understood.
• Depending on the etiologic factor, may present with additional signs and symptoms associated with deep vein thrombosis or varicose veins

Reference:

• Goodman and Fuller (4th ed.), p.656 (“Clinical Manifestations”)

Question 7

CVI - PT Implications

What are the major indications, contraindications, guidelines, or protocols for treating chronic venous insufficiency (CVI)?

Answer 7

• Instruct the patient on elevating the legs. Patients with CVI should elevate the legs just above the level of the heart to faciliate venous return via the gravitational force on blood flow, which thereby (1) prevents thrombus formation by reducing the likelihood of the development of venous stasis, and (2) decreases lower-extremity edema.
• Compression therapy (e.g., bandages, gradient compression stockings, pumps) is the gold standard for treatment of CVI, especially when venous insufficiency ulcers are present. The goal is to increase venous pressure and thereby promote venous return.
  
  • Compression therapy is contraindicated if the ankle-brachial index (ABI) value is less than 0.8, which is a value associated with impaired arterial perfusion.
• Avoid whirlpool treatments beyond an initial one or two treatments. The increased blood volume and dependent position (underlying causes of wound) can make the lower extremity edema worse.

Reference:

• Goodman and Fuller (4th ed.), p.652 (“DVT–Prevention and Intervention”), 656-657 (“Chronic Venous Insufficiency–Special Implications for the Therapist”)

Question 8

Venous Insufficiency Ulcers

What is a venous insufficiency ulcer?

Answer 8

A venous insufficiency ulcer (aka, stasis ulcer) is a wound that develops as a result of inadequate drainage of venous blood from the extremities or major organs, excluding the heart and brain. A venous insufficiency ulcer has the following characteristics:

• Location: Proximal to the medial malleolus
  
  • Note: The posterior tibial vein is located just posterior to the medial malleolus and runs alongside the posterior tibial artery.
• Ulcer bed: Wet with fibrinous material and moderate to heavy drainage
• Appearance: Shallow and irregular margins, margins are either flat or have a slightly steep elevation, margins vary from small to nearly encircling the leg
• Surrounding skin: Hemosiderin staining or lipodermatosclerosis
  
  • Hemosiderin staining refers to yellow or brown pigmented skin due to hemosiderin deposition from the breakdown of red blood cells.
  • Lipodermatosclerosis refers to the hardening of the skin due to inflammation of the subcutaneous adipose tissue. Lipodermatosclerosis is associated with the “inverted champagne bottle” appearance of the distal leg.

References:

• Goodman and Fuller (4th ed.), p.642 (Table 12-21)
• Folder: DMGMC → Wound and Burn Care Unit → Lab Materials → Wound ID and Dressing Lab → Wound ID and Dressing Lab Presentation (PDF p. 2)
• Folder: DMGMC → Wound and Burn Care Unit → Lecture Materials → Wound Care Lecture HO (PDF pp. 37-38, 41)

Question 9

PAD - Clinical Definition

What is peripheral arterial disease (PAD)?

Answer 9

Peripheral arterial disease (PAD) (aka, arteriosclerosis obliterans, occlusive disease, chronic occlusive arterial disease, obliterative arteriosclerosis) is an arterial disorder that is considered a subcategory of peripheral vascular disease. Peripheral arterial disease is characterized by the thickening and loss of elasticity of the arterial walls that causes the partial or total obliteration (i.e., filling out) of the lumen of an artery. The result is arterial insufficiency, or inadequate arterial blood flow to the extremities or major organs, excluding the heart and brain.

References:

• Goodman and Fuller (4th ed.), p.633 (“Peripheral Vascular Disease”), 638-639 (“Arteriosclerosis Obliterans [Peripheral Arterial Disease]–Definition and Overview”)
• O’Sullivan et al. (7th ed.), p.532 (“Arterial Insufficiency and Ulceration”)

Question 10

PAD - Risk Factors

What are the characteristics of the demographic population that is at risk for developing peripheral arterial disease (PAD) (e.g., gender, age, past medical history)?

Answer 10

Gender: Male

• Men have an increased prevalence of coronary artery disease as compared with women. Sex hormones may contribute to this difference (*from Goodman and Fuller [4th ed.], p.553). (*Note: Coronary artery disease is an atherosclerotic disease process).

Past medical history: (*The following are direct or primary risk factors for the development of atherosclerosis.)

• **Tobacco smoking** and hypertension
  
  • The arterial wall damage that leads to the pathogenesis of atherosclerosis can be caused by harmful substances in the blood (e.g., as with tobacco smoking) or by physical wear and tear (e.g., as a result of hypertension) (*from Goodman and Fuller [4th ed.], p.556).
• Diabetes mellitus
  
  • The chronic hyperglycemia of diabetes mellitus results in an acceleration of atherosclerosis (*from Goodman and Fuller [4th ed.], pp.510-511).

*Note: Because obesity is associated with diabetes mellitus and hypertension, obesity is considered a secondary risk factor for the development of atherosclerosis.

• Type 2 diabetes mellitus is often associated with obesity (*from Goodman and Fuller [4th ed.], p.33 [Box 2-4, “Clinical Manifestations”]).
• The excess weight associated with obesity makes the heart work harder to pump blood throughout the body, resulting in increased intravascular volumes that can predispose the individual to the development of hypertension (*see Goodman and Fuller [4th ed.], p.550, 577 [Box 12-8]).

Reference:

• See also Goodman and Fuller (4th ed.), p.550 (Table 12-3).

Question 11

PAD - Etiology

What causes peripheral arterial disease (PAD)?

Answer 11

Peripheral arterial disease is caused by atherosclerosis, or the thickening of the arterial wall in which plaques or fatty deposits form in the inner layer or tunica intima of the arteries. Atherosclerosis narrows the lumen of arterial blood vessels, resulting in arterial insufficiency and the development of peripheral arterial disease.

References:

• Goodman and Fuller (4th ed.), p.549 (“Atherosclerosis”), 639 (“Etiologic and Risk Factors,” “Pathogenesis”)
• O’Sullivan et al. (7th ed.), p.532 (“Arterial Insufficiency and Ulceration”)

Question 12

PAD - Clinical Presentation

What are the hallmark signs and symptoms of peripheral arterial disease (PAD)?

Answer 12

• Intermittent claudication. Due to ischemia of the lower extremity muscles
• Pallor of the distal portion of the lower extremity when the foot is elevated (aka, elevation pallor). Due to gravity further decreasing arterial blood flow and exacerbating the effects of the baseline arterial insufficiency (e.g., further decrease in arterial blood flow, increase in pain due to ischemia)
• Pronounced redness of the distal portion of the lower extremity when in the dependent (“hanging down”) position (e.g., sitting at the edge of bed) (aka, dependent rubor). Due to gravity assisting arterial blood flow through the region of arterial insufficiency
  
  • When the feet are in the dependent position (e.g., when sitting at the edge of the bed), the pain associated with ischemia will decrease as a result of the increase in arterial blood flow.
• Pain in the lower extremities at rest (aka, resting pain). Indicates significant muscle ischemia due to severe obstruction of the affected arteries
• Arterial insufficiency ulcers. Due to impaired wound healing as a result of decreased arterial blood flow through the affected region
• Neuropathic ulcers. Observed in individuals with peripheral arterial disease secondary to diabetes mellitus. Due to further exacerbation of wound healing and arterial insufficiency as well as onset of peripheral neuropathy that causes a loss of sensation
• Gangrene. Due to impaired arterial blood flow that causes tissue death
• Decreased or absent peripheral pulses. Due to impaired arterial blood flow through the affected region

References:

• Goodman and Fuller (4th ed.), p.640 (Figure 12-30), 642 (Table 12-21)
• TherapyEd NPTE Study Guide, Table 3-13, p. 208

Question 13

Arterial Insufficiency Ulcers

What is an arterial insufficiency ulcer?

Answer 13

An arterial insufficiency ulcer is a wound that develops as a result of inadequate arterial blood flow to the extremities or major organs, excluding the heart and brain. An arterial insufficiency ulcer has the following characteristics:

• Location: Frequently occurs distally and over bony prominences (e.g., malleoli)
• Ulcer bed: Dry necrotic base
• Appearance: Well circumscribed with a sharply demarcated border
• Surrounding skin: Pale, shiny and dry, loss of hair, cool temperature
  
  • Note: Shiny and dry skin is due to decreased moisture content in the skin as a result of impaired arterial blood flow.

References:

• Goodman and Fuller (4th ed.), p.642 (Table 12-21)
• Folder: DMGMC → Wound and Burn Care Unit → Lab Materials → Wound ID and Dressing Lab → Wound ID and Dressing Lab Presentation (PDF p. 2)
• Folder: DMGMC → Wound and Burn Care Unit → Lecture Materials → Wound Care Lecture HO (PDF pp. 37-38, 41)

Question 14

Neuropathic Ulcers

What is a neuropathic ulcer?

Answer 14

A neuropathic ulcer (aka, diabetic ulcer) is a wound that develops as a result of repetitive, unrecognized trauma due to complications associated with peripheral arterial disease and peripheral neuropathy. A neuropathic ulcer has the following characteristics:

• Location: Frequently on the plantar surface of the foot at sites of pressure (e.g., metatarsal heads, heel, toes)
• Ulcer bed: Variable depth, ranging from partial thickness to severe ulcer involving the tendon, fascia, joint capsule, or the bone itself
• Appearance: Surrounding callus (aka, callus rim), round or punched out, prolonged bacterial infection may be associated with underlying osteomyelitis (i.e., inflammation of bone)
• Surrounding skin: Frequently callused and dry (i.e., anhydrous skin)
  
  • Note: Anhydrous skin is typically due to autonomic nerve dysfunction secondary to the neuropathy associated with diabetes mellitus.

References:

• Goodman and Fuller (4th ed.), p.642 (Table 12-21)
• Folder: DMGMC → Wound and Burn Care Unit → Lab Materials → Wound ID and Dressing Lab → Wound ID and Dressing Lab Presentation (PDF p. 2)
• Folder: DMGMC → Wound and Burn Care Unit → Lecture Materials → Wound Care Lecture HO (PDF pp. 37-38, 41)

Question 15

PAD - PT Implications

What are the major indications, contraindications, guidelines, or protocols for treating peripheral arterial disease (PAD)?

Answer 15

• When PAD is suspected, screen using assessments of arterial perfusion (i.e., ankle-brachial index) and peripheral pulse.
  
  • Ankle-brachial index: See “ABI - Clinical Definition” flashcard.
  • Peripheral pulse assessment: Posterior tibial pulse (primarily) and dorsalis pedis (aka, pedal) pulse (secondarily)
• Instruct the patient to keep the legs in the dependent (‘hanging down”) position (e.g., when sitting at the edge of the bed) to help alleviate pain due to ischemia.
• Exercise has numerous benefits for patients with PAD (*see Goodman and Fuller [4th ed.], p.645 [“Prescriptive Exercise”]). Instruct patients in a progressive conditioning program, including walking for fixed periods, even if the initial length of walking time is only 1 minute. The most effective program includes brisk treadmill walking at a pace that is comfortable for the individual until intermittent claudication begins, followed by immediate rest and continued walking when the pain subsides.

References:

• Folders: DMGMC → Prosthetics Unit → Lecture Materials → Lecture Powerpoints and PDFs → “DM, Foot Ulcers, and Amputations” PowerPoint lecture (slides 6-13)
• Goodman and Fuller (4th ed.), pp.644-646 (“Special Implications for the Therapist”)

Question 16

What is the ankle-brachial index (ABI)?

What are the interpretations of ABI values?

Answer 16

The ankle-brachial index (ABI) is a measure of arterial perfusion available to physical therapists that compares the systolic blood pressures (BPs) in the arm and leg. The ABI is represented as a ratio of ankle systolic BP to brachial systolic BP. The purpose of the ABI is to determine the presence of arterial occlusive diseases such as peripheral arterial disease.

Interpretation of ABI values: With increasing degrees of arterial narrowing, there is a progressive fall in systolic blood pressure distal to the sites of involvement. If the arteries are unobstructed, the ratio of ankle to brachial systolic BPs should be close to 1.0. If the arterial blood flow to the lower extremity is decreased, the ABI ratio will be less than 1.0.

• A normal ABI is greater than 0.9.
• An ABI of less than 0.8 (i.e., lower systolic BP in the legs as compared with that in the arms) is considered abnormal and is associated with claudication or pathology.
• An ABI of less than 0.4 is associated with ischemic rest pain and tissue necrosis.
• Compression therapy is contraindicated if the ABI value is less than 0.8.

Note: Calcification of the blood vessels as a result of diabetes mellitus can make arteries non-compressible and contribute to a falsely high ABI (i.e., the ABI ratio appears normal but is actually abnormal—”a false negative”).

References:

• Goodman and Fuller (4th ed.), p.645
• DMGMC Lecture PowerPoint, “1_DM, Foot Ulcers, & Amputations”

Question 17

Dorsalis Pedis Pulse

Describe how you would palpate the dorsalis pedis (aka, pedal) pulse.

Answer 17

On the dorsal aspect of the foot with the ankle slightly dorsiflexed to reduce the tension on the dorsum of the foot, the peripheral pulse from the dorsalis pedis artery can be palpated on the lateral aspect of the extensor hallucis longus tendon near the base of the first metatarsal bone (i.e., near the center of the long axis of the foot). The extensor hallucis longus tendon can be identified by having the patient extend the great toe as well as the other toes.

References:

• Physical Rehabilitation, p. 49, Box 2.4
• Clinically Oriented Anatomy, p. 625, Figure B5.27

Question 18

Posterior Tibial Pulse

Describe how you would palpate the posterior tibial pulse.

Answer 18

With the ankle in slight inversion to reduce the tension on the medial aspect of the ankle, the pulse from the posterior tibial artery can be palpated between the posterior surface of the medial malleolus and the medial border of the calcaneal (aka, Achilles) tendon.

References:

• Physical Rehabilitation, p. 49, Box 2.4
• Clinically Oriented Anatomy, p. 608, Figure B5.25

Question 19

CAD - Clinical Definition

What is coronary artery disease (CAD)?

Answer 19

Coronary artery disease (CAD) (aka, coronary heart disease [CHD], ischemic heart disease) is a pathological disorder of the myocardium that is characterized by ischemia and subsequent infarction due to atherosclerosis of the coronary arteries.

References:

• Goodman and Fuller (4th ed.), p.548 (“Ischmic Heart Disease, Coronary Heart Disease, Coronary Artery Disease”)
• O’Sullivan et al. (7th ed.), p.469 (“Introduction and Epidemiology of Heart Disease”)

Question 20

CAD - Risk Factors

What are the characteristics of the demographic population that is at risk for developing coronary artery disease (CAD) (e.g., gender, age, past medical history)?

Answer 20

Gender: Male

• Men have an increased prevalence of coronary artery disease as compared with women. Sex hormones may contribute to this difference (*from Goodman and Fuller [4th ed.], p.553). (*Note: Coronary artery disease is an atherosclerotic disease process).

Past medical history: (*The following are direct or primary risk factors for the development of atherosclerosis.)

• **Tobacco smoking** and hypertension
  
  • The arterial wall damage that leads to the pathogenesis of atherosclerosis can be caused by harmful substances in the blood (e.g., as with tobacco smoking) or by physical wear and tear (e.g., as a result of hypertension) (*from Goodman and Fuller [4th ed.], p.556).
• Diabetes mellitus
  
  • The chronic hyperglycemia of diabetes results in an acceleration of atherosclerosis (*from Goodman and Fuller [4th ed.], pp.510-511).

*Note: Because obesity is associated with diabetes mellitus and hypertension, obesity is considered a secondary risk factor for the development of atherosclerosis.

• Type 2 diabetes mellitus is often associated with obesity (*from Goodman and Fuller [4th ed.], p.33 [Box 2-4, “Clinical Manifestations”]).
• The excess weight associated with obesity makes the heart work harder to pump blood throughout the body, resulting in increased intravascular volumes that can predispose the individual to the development of hypertension (*see Goodman and Fuller [4th ed.], p.550, 577 [Box 12-8]).

Reference:

• See also Goodman and Fuller (4th ed.), p.550 (Table 12-3).

Question 21

CAD - Clinical Presentation

What are the hallmark signs and symptoms of coronary artery disease (CAD)?

Answer 21

• Angina pectoris (aka, angina)
  
  • Refers to chest pain or discomfort that is related to ischemia of the myocardium (*see stable angina in “Types of Angina” flashcard)
    
    • Substernal pain is most common.
  • Can be associated with radiation or referral of pain to the left shoulder as well as the arms, neck, jaw, throat, teeth, or upper back (e.g., between the shoulder blades)
  • Angina can be precipitated by the three E’s (eating, physical exertion, and emotional stress) or cold weather.
  • Activity, chest wall palpation, breathing, and position changes will not produce changes in anginal pain.
  • On a continuous ECG monitoring strip, an early indicator of myocardial ischemia is an inverted T-wave as a result of prolonged ventricular repolarization.
• Myocardial infarction (MI)
  
  • Signs and symptoms associated with unstable angina (*see “Types of Angina” flashcard), including:
    
    • Nitroglycerin, rest (i.e., cessation of activity causing the anginal attack), and reduced activity do not relieve the anginal pain within 20 minutes.
    • Radiation pattern, severity of pain, and severity and duration of symptoms changes or worsens within the treatment session
  • On a continuous ECG monitoring strip, can be associated with (1) elevation or depression of the S-T segment; or (2) a prominent, pathological Q wave

References:

• Goodman and Fuller (4th ed.), p.557 (“Common sequelae of atherosclerosis affecting coronary arteries include…”)
• See “Specific NPTE Study Topics” Word doc.

Question 22

Types of Angina

Differentiate between the three types of angina: stable angina, unstable angina, and variant (Prinzmetal) angina.

Answer 22

Stable angina

• Generally occurs during physical effort (i.e., increases with physical exertion)
• Characterized by substernal (usually non-radiating) pain lasting between 5 and 15 minutes after relief from the initiating trigger
• Reflects progressive arterial stenosis and ischemia
• Decreases after (1) taking sublingual nitroglycerin tablets, or (2) cessation of the activity causing the angina

Unstable angina

• Occurs during physical exertion, psychological stress, at rest, or in sleep
• As compared with stable angina, episodes are more frequent, each episode usually lasts more than 15 minutes, and pain may be more severe.
• **Medical red flag!**
  
  • Usually indicates progression of CAD and increased risk for myocardial infarction (MI)
  • Requires hospitalization and intravenous nitrates
  • Unstable angina is less responsive to treatment with rest and sublingual nitroglycerin tablets.

Variant (Prinzmetal) angina

• Occurs while the individual is at rest, usually during waking and at the same hour (e.g., early morning)
• Unaffected by physical exertion
• Pain is intense and prolonged.
  
  • Can be relieved with sublingual nitroglycerin tablets or rest
• Characterized by dysrhythmias
• Caused by combination of stenosis and coronary artery spasm (aka, coronary vasospasm)
  
  • Can be treated with calcium channel blockers

References:

• Frownfelter and Dean (5th ed.), p.80
• DMCC Lecture PowerPoint, “Ischemia,” slide 5

Question 23

CAD - PT Implications

What are the major indications, contraindications, guidelines, or protocols for treating coronary artery disease (CAD)?

Answer 23

• Exercise guidelines for a patient with angina pectoris:
  
  • The patient with a history of angina should first be cleared by his or her general practitioner or cardiologist for physical therapy treatment.
  • The onset of an anginal attack requires an immediate cessation of the activity causing the angina (e.g., exercise). If currently prescribed, administration of nitroglycerin or another anti-anginal medication is recommended.
  • If the anginal attack is resolved with rest or nitroglycerin, continue treatment with reduced activity with close monitoring. If signs and symptoms of a myocardial infarction (MI) is present (*see flashcards), stop treatment and immediately contact medical services.
  • Some people with CAD have higher levels of systolic blood pressure that exceed peak exercise values. A proper cool-down after vigorous exercise is therefore important to prevent such an occurrence.
• Considerations for medications used to treat angina pectoris:
  
  • Vasodilator medications such as the ones described below cause vasodilation of the coronary arteries, thereby improving blood flow to the heart. Vasodilation of the coronary arteries may also relieve coronary artery spasm (aka, coronary vasospasm).
    
    • Nitroglycerin (aka, nitrostat) is a vasodilator medication that is metabolically converted into nitric oxide in the body. (Nitric oxide is a gas that acts on the immediately adjacent vascular smooth muscle as a vasodilator.)
      
      • Sublingual nitroglycerin tablets are fast-acting. Therefore, patients should be SITTING and not standing when taking nitrates because of the sudden drop in blood pressure (hypotension) that can occur as a result of taking nitroglycerin. Orthostatic hypotension may also occur.
    • Calcium-channel blockers are vasodilator medications that block the entry of calcium into vascular smooth muscle, where calcium ions normally facilitate contraction by initiating actin-myosin interaction.
      
      • Orthostatic hypotension and peripheral edema can be issues for patients taking calcium-channel blockers.
  • Beta (β) blockers are medications that bind to β-1 receptors on the myocardium and block the effects of norepinephrine and epinephrine on the heart. The subsequent reductions in heart rate and arterial blood pressure results in a reduction in the rate pressure product, an index of myocardial oxygen consumption and an estimate of myocardial work. The reduction in RPP therefore helps to reduce angina pectoris by reducing the heart’s oxygen demands.
    
    • Beta-blockers cause a reduction in resting and exercise heart rate. Anyone taking these medications may not be able to achieve a target heart rate above 90 beats/min. Therefore, using symptoms (e.g., angina, diaphoresis, shortness of breath, dizziness, pallor, isolated [arm or leg] or overall fatigue) and rating perceived exertion (RPE) may be a more appropriate means of monitoring. Avoid increases of more than 20 beats/min over the resting rate for individuals taking beta-blockers.

References:

• Goodman and Fuller (4th ed.), p.567
• See “Specific NPTE Study Topics” Word doc.
• Ciccone (5th ed.), p.327 (“Calcium Channel Blockers–Adverse Effects), 339 (“Calcium Channel Blockers”), 369 (“Beta Blockers”)
• DMCC lectures: “Cardiac Anatomy and Physiology” (slide 60 on RPP), “Ischemia” (slide 29 on beta-blockers)
• Klabunde (2nd ed.), pp.29-30 (“premature depolarizations”)
• Paz et al. (5th ed.), p.36, 52 (Table 3A.2)
• For more about ectopic foci, see CV Physiology: Ectopic Foci (https://cvphysiology.com/Arrhythmias/A017#:~:text=Ectopic%20foci%20are%20abnormal%20pacemaker%20sites%20within%20the,They%20can%20occur%20within%20the%20atria%20or%20ventricles).

Question 24

PVC and Contraindications

What is a premature ventricular contraction (PVC)? What quality and frequency of PVCs is a contraindication for further activity?

Answer 24

A premature ventricular contraction (PVC) is the most common form of arrythmia, and it originates from ectopic foci in the ventricle. On a continuous ECG strip, premature ventricular contractions appear as extra and early QRS complexes that interrupt the established heart rhythm. Premature ventricular contractions can either be unifocal (i.e., originates from one ectopic foci, all PVCs look the same) or multifocal (i.e., originates from more than one ectopic foci, PVCs will look different).

The quality and frequency of the PVCs will determine whether to continue or stop treatment.

• Continue treatment: PVCs are unifocal; less than six PVCs per minute
• Stop treatment: PVCs are multifocal; there are more than six PVCs per minute, or PVCs appear as a pair (i.e., ventricular couplet)
  
  • More likely to progress to ventricular tachycardia (aka, “v-tach”)

References:

• Paz et al. (5th ed.), p.52 (Table 3A.2)
• DMCC Lecture: “ECG” (slide 72)

Question 25

Obstructive Lung Disease - Clinical Definition

What is obstructive lung disease?

Answer 25

Obstructive lung disease is a pathological condition of the lungs that is characterized by reduced airflow due to an obstruction.

Examples of obstructive lung diseases include:

• Chronic obstructive pulmonary disease (COPD) (i.e., chronic bronchitis, emphysema)
• Bronchiectasis
• Cystic fibrosis
• Asthma

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 26

Obstructive Lung Disease - Clinical Presentation

What are the hallmark signs and symptoms of obstructive lung disease?

Answer 26

• Increased residual volume (i.e., “too much air in the lungs;” hyper-inflated lungs with loss of elastic recoil)
• Increased airway resistance
• Increased difficulty expiring air rapidly through the narrowed airways
• Characterized by early inspiratory crackles upon auscultation
• Digital clubbing due to hypoxemia

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 27

Obstructive Lung Disease - PT Implications

What are the major indications, contraindications, guidelines, or protocols for treating obstructive lung disease?

Answer 27

• Patients with obstructive lung diseases tend to work harder to expire air because of the primary issue of increased airway resistance. It is therefore recommended that these patients optimize their breathing pattern by expiring air slowly and deeply using relaxed pursed-lip breathing.
  
  • Rationale: Relaxed pursed-lip breathing decreases the velocity or flow rate at which the air travels through the airways, thereby decreasing airway resistance as well as increasing the amount of air expired out. Relaxed pursed-lip breathing also creates a back pressure that helps to keep the airways from prematurely collapsing during expiration.
• Patients with obstructive lung diseases tend to experience an increase in the work of breathing because of overuse of their accessory inspiratory muscles (e.g., sternocleidomastoid, pectoralis minor) and the associated increase in energy and oxygen utilization to fuel those accessory inspiratory muscles. In conjunction with relaxed pursed-lip breathing, patients with mild obstructive lung diseases should be instructed to relax their accessory inspiratory muscles and perform diaphragmatic breathing (aka, deep breathing, belly breathing) to reduce the work of breathing through increased use of the diaphragm during inspiration.
  
  • Note: Diaphragmatic breathing is NOT recommended for patients with moderate or severe obstructive lung diseases due to the structural changes in the shape of the diaphragm (i.e., low and flat diaphragm) from significant lung hyperinflation.
• Patients with chronic airflow limitations (e.g., COPD) can adapt to baseline hypercapnia and thus can become dependent on their hypoxic drives (i.e., stimulation of ventilation through decreases in PaO2 levels) instead of rising PaCO2 levels to increase ventilation. As a result, low-flow supplemental oxygen is usually administered to these patients to avoid abolishing their O2-dependent drive to breathe.
  
  • Note: When increasing the amount of supplemental oxygen delivered to these patients, monitor the patient’s respiratory rate and breathing pattern. An increase in PaO2 may reduce the ability of the hypoxic drive to “drive” ventilation for these patients, resulting in hypoventilation that further exacerbates hypercapnia and increases the risk of death.

References:

• Pursed-lip breathing
  
  • Goodman and Fuller (4th ed.), p.794 (“Pursed-lip breathing helps slow the respiratory rate and prevent airway collapse during exhalation.”)
  • Frownfelter and Dean (5th ed.), p.359 (“Pursed-Lips Breathing”)
• ​Diaphragmatic breathing
  
  • Goodman and Fuller (4th ed.), p.794 (“Diaphragmatic breathing may be helpful to those with mild disease…”)
  • Frownfelter and Dean (5th ed.), p.359 (“Considerations in Teaching Breathing Control to Patients with Primary Versus Secondary Pulmonary Dysfunction”)
  • DMCC Lecture: Pulmonary Pathophysiology (slide 32)
• Hypoxic drive:
  
  • Frownfelter and Dean (5th ed.), p.480 (“Patients with chronic airflow limitation can adapt to high PaCO2 levels and thus can become dependent on their hypoxic drives to breathe. Therefore lowflow supplemental oxygen is administered to these patients to avoid abolishing their O2-dependent drive to breathe.”)
  • Goodman and Fuller (4th ed.), p.795 (“Some people with COPD retain carbon dioxide and have a depressed hypoxic drive requiring low oxygen levels to stimulate the respiratory drive.”)
  • DMCC Lecture: Pulmonary Anatomy and Physiology (slide 65)
• See “Specific NPTE Study Topics” Word doc.

Question 28

Restrictive Lung Disease - Clinical Definition

What is restrictive lung disease?

Answer 28

Restrictive lung disease is a pathological condition of the lungs that is characterized by a limitation in lung expansion.

Examples of restrictive lung disease include:

• Pulmonary fibrosis
• Atelectasis
• Sarcoidosis
• Pneumonia

In addition to the progression of various lung diseases, restrictive lung disease can develop as a result of:

• Structural abnormalities (e.g., kyphosis, scoliosis, chest wall injury or deformity)
• Neurologic or neuromuscular disorders (e.g., Guillain-Barré syndrome, muscular dystrophy, traumatic brain injury, spinal cord injury, amyotrophic lateral sclerosis, myasthenia gravis)

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 29

Restrictive Lung Disease - Clinical Presentation

What are the hallmark signs and symptoms of restrictive lung disease?

Answer 29

• Decreased residual volume (i.e., “too little air in the lungs;” hypo-inflated lungs)
• Decreased lung compliance
• Increased difficulty with inspiring air
• Impaired respiratory movements because of abnormalities in the lung tissue (e.g., progressive scarring or fibrosis of the lungs), the pleura, the chest wall (e.g., chest wall injury or trauma), or the neuromuscular machinery (e.g., head or spinal cord injury)
• Characterized by late inspiratory crackles upon auscultation
• Digital clubbing due to hypoxemia

References:

• See “Specific NPTE Study Topics” Word doc.
• Goodman and Fuller (4th ed.), p.812 (“Clinical Manifestations”)

Question 30

Restrictive Lung Disease - PT Implications

What are the major indications, contraindications, guidelines, or protocols for treating restrictive lung disease?

Answer 30

• Patients with restrictive lung diseases tend to work harder to inspire air because of the primary issue of limited lung expansion. It is therefore recommended that these patients optimize their breathing pattern by inspiring air quickly using short, shallow breaths.
  
  • ​Breathing in quickly is a compensation strategy for patients with restrictive lung diseases who have limited lung expansion. The strategy allows for patients to inspire an adequate volume of air.
• A person with restrictive lung disease will be more adversely affected by the restriction in lung expansion in the supine position due to the additional weight of gravity on the chest wall when breathing. Routine positioning (especially upright positioning) is therefore required.

References:

• See “Specific NPTE Study Topics” Word doc.
• Goodman and Fuller (4th ed.), p.812 (“Special Implications for the Therapist”)

Question 31

Sarcoidosis - Clinical Definition

What is sarcoidosis?

Answer 31

Sarcoidosis is a systemic disease of unknown cause that is characterized by lumps called granulomas that are formed by groups of immune cells. These granulomas present diffusely throughout the body and can involve any organ in the body but most often involves the lungs and lymph nodes. In sarcoidsosis of the lungs, the granulomas can progress to pulmonary fibrosis and restrictive lung disease.

References:

• Goodman and Fuller (4th ed.), p.840 (“Sarcoidosis”)
• Frownfelter and Dean (5th ed.), p.95 (“Sarcoidosis”)

Question 32

Pulmonary Fibrosis - Clinical Definition

What is pulmonary fibrosis?

Answer 32

Pulmonary fibrosis (aka, interstitial lung disease) is a general term that refers to a variety of lung disorders in which ongoing epithelial damage leads to progressive scarring (fibrosis) of the lungs. Fibrosis irreversibly distorts and shrinks the lung lobe at the alveolar level and causes a marked loss of lung compliance, resulting in the limitation of lung expansion that is characteristic of restrictive lung diseases. Most cases of pulmonary fibrosis are idiopathic.

Reference:

• Goodman and Fuller (4th ed.), p.812 (“Definition and Overview;” “Etiologic and Risk Factors”), 813 (“Pathogenesis and Clinical Manifestations”)

Question 33

Pulmonary Fibrosis - Risk Factors

What are the characteristics of the demographic population that is at risk for developing pulmonary fibrosis (e.g., gender, age, past medical history)?

Answer 33

Age: 50-70 years

Past medical history:

• Recent active lung disease (e.g., cystic fibrosis)
• Chest radiation therapy
  
  • Pulmonary fibrosis can develop in patients who are undergoing radiation of the chest as part of cancer treatment. As radiation dose increases, the frequency of pulmonary fibrosis increases.

Reference:

• Goodman and Fuller (4th ed.), p.812 (“Eitologic and Risk Factors”) 813 (“Special Implications for the Therapist”)
• asd

Question 34

Pulmonary Fibrosis - Clinical Presentation

What are the hallmark signs and symptoms of pulmonary fibrosis?

Answer 34

• Progressive dyspnea
• Nonproductive (dry) cough
• Pulmonary function tests
  
  • Decreased total lung capacity
  • Decreased forced vital capacity
  • Decreased forced expiratory volume in 1 sec (FEV1)
• Restrictive lung disease signs and symptoms (*see flashcard)

Reference:

• Goodman and Fuller (4th ed.), p.812 (“Definition and Overview”)

Question 35

CF - Clinical Definition

What is cystic fibrosis (CF)?

Answer 35

Cystic fibrosis (CF) is a congenital (inherited) genetic disorder of the exocrine glands that is primarily characterized by dehydrated and increased thickening of mucous gland secretions. In the lungs, the dehydration results in thickened dry and gooey secretions that (1) predispose the lungs to infection and (2) result in the mechanical obstruction of the airways that is characteristic of obstructive lung diseases.

*Note: Cystic fibrosis is strongly associated with bronchiectasis, or the destruction of the bronchial walls. The recurrent bacterial infections combined with mucus hypersecretion in the lungs can lead to bronchiectasis.

References:

• Goodman and Fuller (4th ed.), p.821 (“Definition and Overview”), 822 (“Pathogenesis”)
• Frownfelter and Dean (5th ed.), p.310 (“Cystic Fibrosis”)

Question 36

CF - Clinical Presentation

What are the hallmark signs and symptoms of cystic fibrosis?

Answer 36

• Chronic cough and purulent sputum production
• Increased anterior-posterior (A-P) diameter of the chest (i.e., “barrel chest”) due to hyperinflation of the lungs
• Obstructive lung disease signs and symptoms (*see flashcard)

Reference:

• Goodman and Fuller (4th ed.), p.824 (“Pulmonary”)

Question 37

Pneumonia - Clinical Definition

What is pneumonia?

Answer 37

Pneumonia is an acute lung disorder that is characterized by inflammation, damage, and fibrosis of the lung parenchyma in response to offending organisms or agents (e.g., upper respiratory viral infection such as influenza) when the immune system is compromised. Pneumonia results in limitations in lung expansion that is characteristic of restrictive lung diseases.

Pneumonia can be caused by:

• Aspiration of food, fluids, or vomit (aspiration pneumonia)
• Inhalation of toxic or caustic chemicals, smoke, dusts, or gases
• Bacterial infection (bacterial pneumonia)
• Viral infection (viral pneumonia)
• Fungal infection (fungal pneumonia)

Reference:

• Goodman and Fuller (4th ed.), p.779 (“Overview and Etiologic Factors”), 780 (“Pathogenesis”)

Question 38

Pneumonia - Clinical Presentation

What are the hallmark signs and symptoms of pneumonia?

Answer 38

• Sudden and sharp pleuritic chest pain aggravated by chest movement
• Decreased chest excursion on the affected side
• Hacking, productive cough with rust-colored or green purulent sputum
• Restrictive lung disease signs and symptoms

References:

• Goodman and Fuller (4th ed.), p.780 (“Clinical Manifestations”)

Question 39

Asthma - Clinical Definition

What is asthma?

Answer 39

Asthma refers to chronic airway inflammation caused by airway hyperresponsiveness to allergens or irritants. The inflammation process associated with asthma primarily results in (1) intermittent attacks of bronchospasm, (2) mucosal edema, (3) hypertrophy of the mucosal membrane, and (4) production of thick, tenacious mucus. Asthma results in reduced airflow due to obstruction of the airways, which is characteristic of obstructive lung diseases.

Asthma can be divided into two main types according to causative factors:

• Extrinsic (allergic or atopic) asthma is the result of an allergy to specific triggers (e.g., pollen, dust, molds, smoke, automobile exhaust, or animal dander).
• Intrinsic (nonallergic) asthma has no known allergic cause or trigger and is most often secondary to chronic or recurrent infections.

References:

• Goodman and Fuller (4th ed.), p.799 (“Definition and Overview”), 800 (“Etiologic Factors”)
• DMCC Lecture: Pulmonary Pathophysiology (slide 40)

Question 40

Asthma - Clinical Presentation

What are the hallmark signs and symptoms of asthma?

Answer 40

• Sensation of chest constriction described as “chest tightness” or a sense of suffocation
• Inspiratory and expiratory wheezing
• Coughing may be initially dry but can become more productive of a thick, tenacious sputum.

Reference:

• Goodman and Fuller (4th ed.), pp.801-802 (“Clinical Manifestations”)

Question 41

Asthma - PT Implications

What are the major indications, contraindications, guidelines, or protocols for treating asthma?

Answer 41

• Patients with asthma should use their metered-dose inhaler before exercise in conjunction with a warm-up activity in order to avoid bronchospasm with higher workload exercise.
• If a patient experiences an acute asthma attack, place the patient in an upright sitting position, and encourage diaphragmatic and pursed-lip breathing to reduce the work of breathing. If the client has a metered-dose inhaler available, provide whatever assistance is necessary for that person to self-administer the medication.
  
  • Bronchodilators are medications that stimulate beta (β) 2 receptors on the smooth muscle of the bronchi and bronchioles and subsequently induces relaxation of these structures. Patients usually take two doses (i.e., “puffs”) when using the metered-dose inhaler. The first dose induces dilation of the bronchi, and the second dose dilates the bronchioles.

Reference:

• Goodman and Fuller (4th ed.), p.805

Question 42

COPD - Clinical Definition

What is chronic obstructive pulmonary disease (COPD)?

Answer 42

Chronic obstructive pulmonary disease (COPD) refers to a prolonged and progressive airflow limitation and includes chronic bronchitis, emphysema, or a combination of the two.

References:

• Goodmand and Fuller (4th ed.), p.789 (“Definition”)
• See “Specific NPTE Study Topics” Word doc.

Question 43

COPD - Risk Factors

What are the characteristics of the demographic population that is at risk for developing chronic obstructive pulmonary disease (COPD) (e.g., gender, age, past medical history)?

Answer 43

Gender: Male

Age: 55-60 years

Past medical history:

• Current or past **tobacco smoker**
• Exposure to environmental irritants (e.g., air pollution, chemical and dust exposure, second-hand smoke)

Question 44

Chronic Bronchitis - Clinical Definition

What is chronic bronchitis?

Answer 44

Chronic bronchitis refers to prolonged inflammation of the inner lining of the bronchi and bronchioles that results in swollen mucous membranes and the production of thick sputum secondary to mucus hypersecretion. The inflammation-induced changes obstructs the airways and results in the reduced airflow that is characteristic of obstructive lung diseases.

Reference:

• Goodman and Fuller (4th ed.), p.796 (“Risk Factors and Pathogenesis”)

Question 45

Emphysema - Clinical Definition

What is emphysema?

Answer 45

Emphysema refers to abnormal permanent enlargement of air spaces distal to the terminal bronchiole, accompanied by destruction of their walls as well as airway collapse and trapping of inspired air due to the loss of elasticity in the distal airways. This results in the airflow limitation that is characteristic of obstructive lung diseases.

• The most common type of emphysema is called centrilobular emphysema, which is characterized by inflammatory destruction of the respiratory bronchioles.

References:

• Goodman and Fuller (4th ed.), p.796 (“Definition and Overview”)
• See “Specific NPTE Study Topics” Word doc.

Question 46

Chronic Bronchitis - Clinical Presentation

What are the hallmark signs and symptoms of chronic bronchitis?

Answer 46

“Blue Bloater” (*see image below)

• Wheezing and sputum-producing cough. Occurs as part of the body’s response to clear the airways of excessive mucus
• Cyanosis. Due to hypoxemia
• Excessive weight gain. Due to (1) impaired nutrition from neglect, and (2) decreased activity level due to the excessive energy cost needed to complete activities of daily living
• Hypercapnia. Due to obstruction of the airways that results in a decrease in alveolar ventilation and a subsequent increase in PaCO2 levels (i.e., increased CO2 retention) (*see Goodman and Fuller [4th ed.], p.796 [“Clinical Manifestations”])
• Frequent infections. Due to mucus hypersecretion and impaired ciliary removal of the excess mucus
• Chronic cor pulmonale. Due to pulmonary arterial hypertension caused by hypoxemia and the associated vasoconstriction of the pulmonary arterioles
  
  • Peripheral edema. Due to chronic cor pulmonale

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 47

Emphysema - Clinical Presentation

What are the hallmark signs and symptoms of emphysema?

Answer 47

_“Pink Puffer” (*see image below)_

• Excessive weight loss and muscle wasting. Due to impaired nutrition, increase in tumor necrosis factor-α production (*see Goodman and Fuller [4th ed.], p.728), and increased energy cost to complete the work of breathing due to significant reliance on the accessory inspiratory muscles
  
  • Patient will often be in the sitting tripod position in order to maximize use of the accessory inspiratory muscles.
• Pink complexion (among white individuals). Due to having normal to near-normal PaCO₂ and PaO₂ levels as compared with a patient with chronic bronchitis. May also be due to the increased effort required to complete the work of breathing
  
  • Patients with emphysema have relatively normal arterial blood gas values because of compensatory hyperventilation via the pursed-lip breathing pattern.
• Pursed-lip breathing pattern and hyperventilation. Occurs as a way to “blow off excess CO₂” (i.e., the excessive trapping of air within the lungs) and decrease the elevated level of PaCO₂
• “Barrel-chest” appearance. Due to excessive trapping of air within the lungs that eventually cause lung hyperinflation (*see DMCC lecture on pulmonary pathophysiology [slide 20])
  
  • Can be associated with decreased or absent breath sounds due to severe hyperinflation of the lungs (*from Frownfelter and Dean [5th ed.], p.206 [“Abnormal Breath Sounds”])

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 48

Atelectasis - Clinical Definition

What is atelectasis?

Answer 48

Atelectasis refers to the partial collapse of normally expanded and air-filled lung parenchyma that involves all or part of the lung. Atelectasis results in limtations in lung expansion, which is characteristic of restrictive lung diseases.

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 49

Atelectasis - Risk Factors

What are the characteristics of the demographic population that is at risk for developing atelectasis (e.g., gender, age, past medical history)?

Answer 49

Past medical history:

• Prolonged bed rest in the supine position and immobilization associated with hospitalization or severe illness
  
  • Hypoventilation, which decreases the secretion of surfactant as well as ventilation of the gravity-dependent lung parenchyma (e.g., alevoli)
  • Physical compression of the lung tissues (e.g., obesity—compression of the lungs by excessive abdominal weight when in supine)

Question 50

Atelectasis - Clinical Presentation

What are the hallmark signs and symptoms of atelectasis?

Answer 50

• Reduced or absent breath sounds over the involved area
  
  • Due to reduced or absent ventilation of the lung secondary to hypoventilation
• Whispered pectoriloquy over the involved area (i.e., increased resonance when whispering “one, two, three” or “nine, nine, nine”) (*see Goodman and Fuller [4th ed.], p.795; Frownfelter and Dean [5th ed.], p.207)
  
  • Due to increase in lung density secondary to significant collapse of the involved lung
• Chest X-ray: Increased density over the involved areas with a shift of the trachea and mediastinum toward the collapsed lung tissue

​

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 51

Bronchiectasis - Clinical Definition

What is bronchiectasis?

Answer 51

Bronchiectasis is a progressive condition characterized by destruction of the bronchial walls and the development of abnormal dilation and distortion of medium-sized bronchi and bronchioles as the result of chronic inflammatory changes associated with infection. Other inflammatory changes such as the increase in mucus production, airway plugging, and bronchospasm cause the reduced airflow that is characterstic of obstructive lung diseases.

*Note: Bronchiectasis is strongly associated with cystic fibrosis (*see flashcard). Cystic fibrosis causes half of all cases of bronchiectasis.

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 52

Bronchiectasis - Clinical Presentation

What are the hallmark signs and symptoms of bronchiectasis?

Answer 52

• Persistent coughing with large amounts of purulent sputum production (worse in the morning)
  
  • The breath and sputum may become foul-smelling with progression of bronchiectasis.

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 53

GBS and DMD - Cardiopulmonary Considerations

What are cardiopulmonary considerations for Guillain-Barré syndrome (GBS) and Duchenne muscular dystrophy (DMD)?

Answer 53

Patients with neurological, neuromuscular, or musculoskeletal conditions that are associated with respiratory muscle weakness (e.g., GBS, DMD) will have weak, ineffective coughing mechanisms and inadequate control of respiratory secretions. Appropriate interventions to improve airway clearance include manual-assistive cough techniques (e.g., costophrenic assist) and other airway clearance techniques.

Costophrenic assist is a manual technique that actively assists a patient with forceful expiration and coughing through manual faciliation of the movements of the abdomen and intercostals when these respiratory muscles are weak or paralyzed. (For information about how to perform the costophrenic assist, see Frownfelter and Dean [5th ed.], pp.342-343.)

References:

• See Youtube video, “Costophrenic assist” (https://www.youtube.com/watch?v=qgVHfWS0t7E)
• Physiopedia: Assisted Coughing (https://www.physio-pedia.com/Assisted_Coughing)

Question 54

Prophylactic Respiratory Care

What is prophylactic respiratory care?

Answer 54

Prophylactic respiratory care (aka, bronchopulmonary hygiene) refers to a therapeutic regimen that helps to prevent the development of respiratory complications as a result of immobilization. Prophylactic respiratory care in physical therapy can include:

• Postural drainage. Frequent position changes associated with postural drainage helps to promote drainage of secretions (e.g., mucus plugs) in all lung segments.
  
  • Postural drainage is one of various airway clearance techniques that can be used to improve clearance of the airways.
• Upright positioning and mobilization. The upright position (i.e., sitting, standing) promotes lung and chest wall expansion by reducing the effects of gravity on chest and lung compliance. As a result, lung volumes and capacities are maximized in the upright position. The upright position also allows for optimal use of the abdominal muscles to assist with forceful expiration as during coughing. Mobilization (especially early ambulation) helps to promote drainage in all lung segments.
  
  • Note: The effect of gravity on the body in the supine position forces the patient to work harder to recruit the abdominal muscles when coughing. In the upright position, the abdominal muscles are more easily recruited because the effects of gravity are lessened (i.e., it is easier to perform trunk flexion in sitting or standing as compared with supine).
• Coughing. Patients who have increased secretions and fluids that the mucociliary escalator cannot clear on its own should be instructed on coughing as a means to facilitate clearance of the airways. Coughing will help clear the airways down to the segmental bronchi. (*For more details, see Frownfelter and Dean [5th ed.], pp.337-341).
  
  • Note: To minimize postoperative pain during deep-breathing and coughing exercises, teach the patient the pillow splinting technique. The technique involves holding a pillow firmly over the incision. Pain is reduced with the pillow splinting technique because the incision and sensitive skin surrounding the incision are prevented from moving when completing deep-breathing or coughing exercises.
• Deep breathing. Deep breathing is beneficial because it promotes the ciliary clearance of secretions, stabilizes the alveoli by redistributing surfactant, and permits collateral ventilation of the alveoli through the Kohn pores that helps re-expand collapsed alveoli. Deep breathing can be accomplished through use of an incentive spirometer or instruction on breath control techniques (e.g., diaphragmatic breathing).
  
  • Note #1: Deep breathing helps to loosen pulmonary secretions, making it easier for the secretions to be removed by the mucociliary escalator.
  • Note #2: Because the surfactant in the alveoli will begin to disappear within 24 to 36 hours, it is very important that patients who are at high-risk for developing atelectasis be educated on deep breathing.
• Mechanical suctioning (e.g., nasotracheal suctioning) can be used as a last resort for clearing the airways when all other options are not effective.

References:

• See “Specific NPTE Study Topics” Word doc.
• For more about incentive spirometry, see Frownfelter and Dean (5th ed.), p.496; MedlinePlus: Using an incentive spirometer (https://medlineplus.gov/ency/patientinstructions/000451.htm).

Question 55

Ventilation and Respiration

Differentiate between ventilation and respiration.

Answer 55

Respiration refers to the exchange of oxygen and carbon dioxide between the organism and the environment via the lungs. In other words, respiration refers to the actual gas exchange that occurs in the alveoli.

Ventilation refers to the mechanical movement of air between the atmosphere and the alveoli. In other words, ventilation refers to the movement of air through the lungs that is basic to respiration.

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 56

Digital Clubbing

What is digital clubbing?

Answer 56

Digital clubbing (aka, clubbing) refers to thickening and widening of the terminal phalanges of the fingers and toes. Digital clubbing results in a painless, club-like appearance recognized by the loss of the angle between the nail and the nail bed.

Lung diseases (e.g., chronic obstructive pulmonary disease [COPD], pulmonary fibrosis) are a major cause of clubbing due to impaired tissue perfusion secondary to hypoxemia.

Reference:

• Goodman and Fuller [4th ed.], pp.775-776 (“Clubbing”)

Question 57

Postural Drainage - Clinical Definition

What is postural drainage?

Answer 57

Postural drainage (aka, bronchial drainage) is a passive technique in which the patient is placed in positions that allow gravity to assist with the drainage of secretions from specific bronchopulmonary segments. Postural drainage is accomplished by positioning the patient so that the angle of the lung segment to be drained allows gravity to have its greatest effect. The patient should be encouraged to take deep breaths and cough after each position and, if possible, again after the treatment is completed.

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 58

Postural Drainage - Precautions and Contraindications

What are the hallmark precautions and contraindications to be aware of for postural drainage?

Answer 58

• Post-neurosurgery. For patients with recent craniotomies, Trendelenberg (“head-down”) bed positions are contraindicated due to the increase in intracranial pressures in those positions.
• Potential decrease in SpO2
• Neonates. Avoid placing neonates in the Trendelenberg (“head-down”) bed position. The position can increase the likelihood of the neonate experiencing gastroesophageal reflux.
• End-stage lung disease. Due to risk for hemoptysis, or coughing up of blood

Reference:

• Frownfelter and Dean (5th ed.), p.315 (“General Precautions and Contraindications to Postural Drainage Positioning”), 316 (Box 21-2)

Question 59

Postural Drainage - Inferior Lobes of the Lungs

Describe the positions used to perform postural drainage for the various bronchopulmonary segments of the lower (aka, inferior) lobes of the lungs.

Answer 59

*Note: The Trendelenburg (heads-down) position is the ideal position when completing postural drainage of the inferior lobes. Alternative positions include elevating the pelvis above the level of the thorax using a therapy ball, pillows, and so on.

Right inferior lobe (*acronym for bronchopulmonary segments is “LAMPS”)

• Lateral: Trendelenburg, left-sidelying
• Anterior: Trendelenburg, supine
• Medial: Trendelenburg, right-sidelying
• Posterior: Trendelenburg, prone
• Superior: Prone only

Left inferior lobe (*acronym for bronchopulmonary segments is “ALPS”)

• Anterior: Trendelenburg, supine
• Lateral: Trendelenburg, right-sidelying
• Posterior: Trendelenburg, prone
• Superior: Prone only

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 60

Postural Drainage - Superior Lobes of the Lungs

Describe the position used to perform postural drainage for the various bronchopulmonary segments of the upper (aka, superior) lobes of the lungs.

Answer 60

To drain the apical segments of the superior lobes, have the patient positioned in long-sitting. Leaning forward will also facilitate drainage of the apical segments.

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 61

Percussion - Clinical Definition

What is percussion?

Answer 61

Percussion (aka, chest clapping) is a manual technique that involves applying a rhythmical force against the thorax with cupped hands for the purpose of dislodging or loosening bronchial secretions from the airways so they may be removed by suctioning or expectoration. The proposed mechanism of action of percussion is the transmission of a wave of energy through the chest wall into the lung. This wave loosens secretions from the bronchial wall and moves them proximally, where ciliary motion and cough (or suction) can remove them. This technique is performed during both the inspiratory and expiratory phases of breathing and has been shown to be effective in secretion removal when combined with postural drainage.

Reference:

• Frownfelter and Dean (5th ed.), pp.315-316 (“Percussion”)

Question 62

Percussion - Precautions and Contraindications

What are the hallmark precautions and contraindications for percussion?

Answer 62

• Post-operative pain. Percussion is not well tolerated by many patients postoperatively without adequate pain control.
• Osteoporosis and coagulopathy. Percussion is contraindicated because of (1) risk of fracturing the weak, fragile osteoporotic bones; and (2) risk for excessive bleeding due to impaired blood-clotting ability.
• Potential fall in SpO2
  
  • Can be eliminated with concurrent thoracic expansion exercises and pauses for breathing control

Reference:

• Frownfelter and Dean (5th ed.), p.313 (Box 21-1), 317 (“Advantages and Disadvantages of Percussion”)

Question 63

Vibration and Shaking - Clinical Definitions

What is vibration and shaking?

Answer 63

Vibration and shaking are manual techniques that are used in conjunction with postural drainage to facilitate removal of secretions from the airways. Vibration and shaking are only performed during the expiratory phase of breathing.

Vibration involves delivering a gentle, high-frequency force and pressure to the chest wall through a sustained co-contraction of the caregiver’s upper extremities.

Shaking is more vigorous than vibration and involves delivering a bouncing maneuver (aka, “rib springing”) through a concurrent, compressive force to the chest wall.

Reference:

• Frownfelter and Dean (5th ed.), p.317 (“Vibration and Shaking”)

Question 64

Vibration and Shaking - Precautions and Contraindications

What are the hallmark precautions and contraindications for vibration and shaking?

Answer 64

• Shaking or vibration may be better tolerated than percussion, especially in the postsurgical patient.
• Osteoporosis and coagulopathy. Vibration and shaking are contraindicated because of (1) risk of fracturing the weak, fragile osteoporotic bones; and (2) risk for excessive bleeding due to impaired blood-clotting ability.
• Potential fall in SpO2
  
  • Can be eliminated with concurrent thoracic expansion exercises and pauses for breathing control

Reference:

• Frownfelter and Dean (5th ed.), p.313 (Box 21-1), 317 (“Advantages and Disadvantages of Percussion”), 318 (“Advantages and Disadvantages of Vibration and Shaking”)

Question 65

Cardiac Rehab - Clinical Definition

What is cardiovascular rehabilitation?

Answer 65

Cardiovascular rehabilitation (aka, cardiac rehab) is a comprehensive interdisciplinary management program that includes physical activity and exercise, education, and behavioral change designed to improve the physical and emotional status of individuals with cardiovascular dysfunction or their risk factors. The goal of cardiac rehab is to maintain or return an individual with cardiovascular and pulmonary dysfunction to full participation in life with a high level of life satisfaction.

Cardiac rehab consists of four phases:

• Phase I refers to inpatient care (medical and surgical) and a predischarge exercise test.
  
  • **Cardiovascular training is not an objective during phase I.** Examples of phase I objectives include (1) minimizing deconditioning effects of bedrest and relative inactivity; and (2) patient education concerning heart disease, risk factors, exercise and home program, and self-monitoring.
• Phase II refers to a supervised exercise program lasting 3 to 6 months. Phase II usually takes place in a community center where the patients can be monitored during exercise and education by the rehabilitation professions can be ongoing.
  
  • The focus on cardiovascular training begins in Phase II.
• Phase III refers to the maintenance phase, during which the patient is responsible for exercising mostly at home. This phase lasts from 6 to 12 months.
• Phase IV refers to an unsupervised community program. The patient is usually ready for this phase within 9 to 12 months.

References:

• Frownfelter and Dean (5th ed.), p.378 (Box 24-1), 393-394 (“Phases”)
• DMCC Lecture: Cardiac Rehabilitation

Question 66

Cardiac Rehab - Phase I Contraindications

What are contraindications to the continuation of physical activity during phase I of cardiovascular rehabilitation?

Answer 66

• Diastolic blood pressure (DBP) ≥ 110 mm Hg
• Decrease in systolic blood pressure (SBP) > 10 mm Hg during exercise with increasing workload
• Significant ventricular or atrial arrhythmias with or without associated signs/symptoms
• Second- or third-degree AV block
• Signs/symptoms of exercise intolerance including angina, marked dyspnea, and electrocardiogram (ECG) changes suggestive of ischemia

Reference:

• ACSM (10th ed.), p.227 (Box 9.3)

Question 67

Carotid Pulse

Describe how you would palpate the carotid pulse.

Answer 67

The carotid pulse can be palpated on either side of the anterior neck between the trachea and the medial border of the sternocleidomastoid (SCM) muscle. The SCM muscle can be identified by having the patient tilt the head to one side (i.e., cervical lateral flexion) and turn the head to the opposite side (i.e., cervical rotation). The muscle is palpated from its origins at the mastoid process and superior nuchal line to its insertions at the manubrium of the sternum and the medial aspect of the clavicle (i.e., sternal end of the clavicle).

Reference:

• Physical Rehabilitation, p. 49, Box 2.4
• Folder: Anatomy → “Overview of Muscle OINAs” Word doc

Question 68

Carotid Pulse Monitoring

When assessing pulse rate (i.e, heart rate), repeated palpation of the carotid pulse will result in what effect? Explain your reasoning.

Answer 68

Repeated palpation of the carotid pulse places excessive manual pressure on the carotid sinus baroreceptors, causing stimulation of the carotid sinus baroreceptors and subsequently a reflexive decrease in pulse rate (i.e., heart rate) and arterial blood pressure.

The reflexive decrease is due to activation of the baroreceptor reflex. Physiologically, the baroreceptor reflex is activated as follows: increased blood volume (as during exercise) → increased blood pressure → increased stretch and stimulation of the arterial baroreceptors → decreased pulse rate (i.e., heart rate) and arterial blood pressure.

References:

• Physical Rehabilitation, p. 49, Box 2.4
• Specific NPTE Study Topics (Word doc): “Review of Concepts” → “Baroreceptor Reflex” section

Question 69

Cool-Down Exercise Period

Explain the importance of the cool-down exercise period.

Answer 69

During a cool-down period, the skeletal muscle pump is used to facilitate venous return and prevent the venous pooling that precedes post-exercise hypotension. When a cool-down period is not completed, decreased venous return as well as increased venous pooling and increased risk for developing post-exercise hypotension occurs as a result of the absence of the skeletal muscle pump. Individuals are also more likely to complain of experiencing muscle stiffness (i.e., “muscle tightness”), which is caused by the buildup of metabolites in the blood during venous pooling.

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 70

Vital Signs - Normal Ranges for Adults

What are the normal ranges for vital signs in a healthy adult?

Answer 70

• Heart rate (HR): 60-100 beats per minute
• Respiratory rate (RR): 12-20 breaths per minute
• Blood pressure (BP)
  
  • Systolic BP less than 120 mm Hg
  • Diastolic BP less than 80 mm Hg
• Oxygen saturation (SpO2): 95-100%
  
  • It is clinically acceptable to maintain oxygen saturation at 90% or higher. A drop below 90% is of concern.
  • Note: Because oxygen consumption increases proportionately with exercise, a patient may desaturate if oxygen transport is compromised to the extent that it is unable to compensate or respond appropriately to increased demand. For example, if a patient is on oxygen at rest and the SpO2 is 90%, he or she may desaturate because the red blood cells need to give up more oxygen to supply the exercising muscle.

References:

• O’Sullivan et al. (7th ed.), p.29 (Table 2.1), 33 (“Observation”)
• Frownfelter and Dean (5th ed.), p.674 (“Special Monitoring Considerations for Patients on Oxygen”)

Question 71

Acute Compartment Syndrome - Clinical Definition

What is acute compartment syndrome?

Answer 71

Compartment syndrome (aka, myofascial compartment syndrome) is a condition in which the circulation within a closed fascial compartment is compromised by an increase in interstitial pressure within the compartment. This causes necrosis of muscles and nerves and eventually of the skin because of excessive swelling.

Acute compartment sydrome refers to the abrupt and recent onset of compartment syndrome, usually following a traumatic event such as a bone fracture. Acute compartment syndrome is a **medical emergency** because of the potential for permanent loss of function or limb if the condition is left untreated. Patients with acute compartment syndrome require immediate surgical intervention (i.e., emergent fasciotomy that allows for surgical decompression of the involved fascial compartment).

References:

• Paz et al. (5th ed.), p.189 (“Compartment Syndrome”)
• See “Specific NPTE Study Topics” Word doc.

Question 72

Acute Compartment Syndrome - Etiology

What causes acute compartment syndrome?

Answer 72

Traumatic events (e.g., fractures, crush injuries, penetrating injuries)

• Fractures of long bones such as the tibia, ulna, and radius are the most common cause.
• Rationale: Fractures and other traumatic events can cause excessive bleeding and subsequently increase the interstitial pressure within the fascial compartment.

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 73

Acute Compartment Syndrome - Risk Factors

What are the characteristics of the demographic population that is at risk for developing acute compartment syndrome (e.g., gender, age, past medical history)?

Answer 73

Circumferential burn injuries

• Rationale: Swelling associated with a burn injury (aka, burn edema) occurs as a result of the leakage of fluid from damaged blood vessels into the surrounding tissues. Burn edema can increase the interstitial pressure within the fascial compartment.

Excessively constrictive circumferential wraps, dressings, cast, or other unyielding immobilizer

• Rationale: External compression that is excessive can reduce the volume capacity of the fascial compartment and subsequently increase the interstitial pressure within the compartment.

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 74

Acute Compartment Syndrome - Clinical Presentation

What are the hallmark signs and symptoms of acute compartment syndrome?

Answer 74

The five “P’s”:

1. Pain
   
   • Sharp, deep, and throbbing pain that is disproportionate to that expected from the injury
   • Passive stretching of the muscles within the affected compartment increases the pain.
   • The involved extremity is tense and tender when palpated.
2. Paresthesia
   
   • Occurs distal to the affected fascial compartment
   • Can progress to a loss of sensation
3. Pulselessness of the peripheral pulses
4. Pallor, indicating tissue ischemia
   
   • Pallor can be associated with observation of reduced perfusion of the distal extremity during capillary refill test.
     
     • The capillary refill test involves squeezing the nail bed of the toes and noting the amount of time it takes for the pink color to return to the nail bed. Capillary refill is delayed if the pink color does not return to the nail bed within 2 seconds after release of the pressure (*from Magee [6th ed.], p.1112).
5. Paralysis of muscles within the involved fascial compartment
   
   • Anterior (volar) compartment of the forearm
     
     • Muscles: Pronator teres, flexor carpi radialis, palmaris longus, flexor carpi ulnaris, flexor digitorum superficialis, flexor digitorum profundus, flexor pollicis longus, and pronator quadratus
     • Nerve: Median nerve
       
       • Exceptions: Flexor carpi ulnaris and the medial head of the flexor digitorum profundus are innervated by the ulnar nerve. Flexor pollicis longus and pronator quadratus are innervated by the anterior interosseous nerve, a branch off of the median nerve.
     • Arterial supply: Radial and ulnar arteries
   • Anterior compartment of the lower leg
     
     • Muscles: Tibialis anterior, fibularis tertius, extensor digitorum longus, and extensor hallucis longus
     • Nerve: Deep fibular nerve
     • Arterial supply: Anterior tibial artery
   • Deep posterior compartment of the lower leg
     
     • Muscles: Tibialis posterior, popliteus, flexor digitorum longus, flexor hallucis longus
     • Nerve: Tibial nerve
     • Arterial supply: Primarily the posterior tibial artery

Other signs: In severe acute compartment syndromes, other objective signs include a swollen extremity with smooth, shiny, or red skin. If acute compartment syndrome is left untreated or is inadequately treated, the muscles and nerve undergo ischemic necrosis, and a limb contracture usually follows (e.g., Volkmann contracture).

• Volkmann contracture (aka, Volkmann ischemic contracture) is associated with anterior (volar) compartment syndrome of the forearm and is the result of the replacement of necrotic muscle and nerve tissue with fibrous tissue. Volkmann contracture is a permanent flexion contracture of the wrist and fingers, resulting in a claw-like appearance of the hand.

References:

• See “Specific NPTE Study Topics” Word doc.
• Paz et al. (5th ed.), p.189 (“Compartment Syndrome”)
• Moore et al. (8th ed.), p.217 (Table 3.10)

Question 75

Acute Compartment Syndrome - PT Implications

What are the major indications, contraindications, guidelines, or protocols for treating acute compartment syndrome?

Answer 75

• Elevation of the affected limb must be discontinued, and the limb should be placed no higher than the heart level.
  
  • Excessive elevation of the affected limb will allow gravity to further decrease arterial blood flow and subsequently exacerbate the tissue ischemia.
• Circumferential wraps, dressings, cast, or any other unyielding immobilizer must be removed to reduce the excessive compression on the extremity.
• Following emergent fasciotomy, be aware of the patient’s ROM precautions.

Reference:

• Paz et al. (5th ed.), p.189 (“Physical Therapy Considerations”)

Question 76

HF - Clinical Definitions

What is heart failure (HF)?

Answer 76

Heart failure (HF) refers to a condition in which the heart is unable to pump enough blood to supply the body’s needs (i.e., “low-output problem”). Failure may occur on both sides of the heart or may predominantly affect the right or left side.

• Strictly classified, left-sided heart failure is referred to as congestive heart failure (CHF). Congestive heart failure occurs when the left ventricle is unable to adequately pump blood forward to the body (*think impairment in forward blood flow from the heart).
• Right-sided heart failure occurs when the right ventricle is unable to adequately pump blood to the lungs (*think back-up of blood). In contrast to cor pulmonale, right-sided heart failure indicates that the underlying cause of the condition is a cardiac pathology (e.g., left-sided heart failure, vascular dysfunction, congenital heart disease).
• Biventricular heart failure occurs when both sides of the heart are unable to adequately pump blood. Biventricular heart failure usually occurs as a progression of left-sided heart failure that eventually involves the right side of the heart. Biventricular heart failure can present with signs and symptoms of both left-sided and right-sided heart failure.

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 77

HF - Etiologic and Risk Factors

What are the etiologic and risk factors for heart failure (HF)?

Answer 77

• Hypertension, coronary artery disease, diabetes mellitus
  
  • Hypertension that is either idiopathic (i.e., no known cause) or due to a condition that narrows the lumen of arterial vessels (e.g., atherosclerosis from coronary artery disease or diabetes mellitus) increases the work the ventricles must do to eject blood (i.e., increased afterload).
• Cardiac ischemia or myocardial infarction
  
  • Structural damage to the myocardium due to decreased coronary blood flow (e.g., cardiac ischemia) or death of myocardial tissue (e.g., myocardial infarction) causes either an impairment or loss of the ventricle’s ability to contract and eject blood. As a result, more blood remains in the ventricle at the end of each contraction (i.e., increased end-diastolic volume).

Reference:

• See “Specific Study Topics” Word doc.

Question 78

HF - Clinical Presentation

What are the hallmark signs and symptoms of heart failure (HF)?

Answer 78

• General
  
  • Tachycardia. Due to compensatory activation of the sympathetic nervous system to maintain normal cardiac output
• Left-sided heart failure (aka, congestive heart failure)
  
  • Pulmonary edema (aka, pulmonary congestion). Due to backup of blood from the left ventricle to the pulmonary veins in the lungs
  • Dyspnea. Due to the stimulation of a reflex response caused by pulmonary edema
  • Coughing up of pink and frothy sputum. Due to blood and fluid in the lungs as a result of pulmonary edema
  • Fatigue and muscle weakness. Due to decrease in flow of oxygenated blood to the body, especially skeletal muscle
• Right-sided heart failure
  
  • Peripheral edema. Due to backup of blood into the systemic venous vessels –> venous pooling –> increased filtration of fluids into the interstitial space. The resultant edema is usually symmetric and occurs in the dependent or peripheral parts of the body (especially the lower extremities—e.g., legs, feet), where venous pressure is the highest.
    
    • May present as pitting edema
  • Jugular vein (venous) distension. Characterized by bulging of the jugular veins
  • Abdominal pain. Secondary to enlargement of the liver as the liver becomes congested with venous blood (*note that the liver is most susceptible to venous congestion because the hepatic veins are located most proximally
    along the inferior vena cava)
    
    • May be associated with right-upper quadrant pain. (Note that the right-upper quadrant contains the liver.)
    • Can progress to ascites
  • Cyanosis (especially of the nail beds). Due to venous congestion and subsequent reduction in peripheral blood flow

Question 79

HF - PT Implications

What are the major indications, contraindications, guidelines, or protocols for treating heart failure (HF)?

Answer 79

General

• Education on upright positioning (e.g., supine with head of bed elevated to 60-90 degrees, upright sitting) with legs in a dependent position as much as possible
  
  • Supine positions can exacerbate the signs and symptoms of heart failure by increasing venous return. The position described above helps to decrease venous return, alleviating signs and symptoms.

Left-sided heart failure (aka, congestive heart failure)

• Education on tripod positions in sitting or standing to facilitate use of accessory inspiratory muscles (especially the pectoralis minor) and decrease severity of dyspnea

Right-sided heart failure

• Monitor for signs of increasing peripheral edema.
  
  • Circumferential girth measurements and pitting edema assessments of the lower extremities, especially the legs and feet

Reference:

• See “Specific NPTE Study Topics” Word doc.

Question 80

Cardiopulmonary Standardized Outcome Measures

Describe what the purposes of the following cardiopulmonary standardized outcome measures are.

Answer 80

• The 6-Minute Walk Test (6-MWT) or 2-Minute Walk Test (2-MWT) examines walking endurance and exercise (aerobic) capacity as individuals cover as far a distance as possible over 6 minutes or 2 minutes, respectively.
• The 10-Meter Walk Test (10-MWT) examines walking speed (aka, gait velocity, gait speed) as individuals walk 10 meters (32.8 feet) without assistance.
• The Timed-Up-And-Go (TUG) test examines fall risk. The test evaluates time (in seconds) required for individuals to rise from chair, walk 3 meters, turn around, walk back to the chair, and sit down.
• The 2-Minutes Step Test (aka, 2-Step Exercise Test) examines endurance and exercise (aerobic) capacity and is the clinical standard for assessing exercise-induced ischemia. In this test, the subject is asked to step in place for 2 minutes.
• Maximum VO2 assessment examines the maximum rate of oxygen consumption as measured during incremental exercise.
  
  • VO2 max treadmill test examines functional cardiovascular capacity.
• A submaximal exercise test on a cycle ergometer estimates VO2 max and assesses aerobic power.

​

References:

• O’Sullivan et al. (7th ed.), pp.246-247 (Table 7.9)
• See “Specific NPTE Study Topics” Word doc.