Cardiovascular & Pulmonary Systems Flashcards
VTE - Clinical Definition
What is venous thromboembolism (VTE)?
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.
DVT - Clinical Presentation
What are the hallmark signs and symptoms of deep vein thrombosis (DVT)?
*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)
PE - Clinical Presentation
What are the hallmark signs and symptoms of pulmonary embolism (PE)?
- 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.
DVT - PT Implications
What are the major indications, contraindications, guidelines, or protocols for treating deep vein thrombosis (DVT)?
- 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.
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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).
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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.
CVI - Clinical Definition
What is chronic venous insufficiency (CVI)?
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”)
CVI - Clinical Presentation
What are the hallmark signs and symptoms of chronic venous insufficiency (CVI)?
- 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”)
CVI - PT Implications
What are the major indications, contraindications, guidelines, or protocols for treating chronic venous insufficiency (CVI)?
- 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.
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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”)
Venous Insufficiency Ulcers
What is a venous insufficiency ulcer?
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:
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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
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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)

PAD - Clinical Definition
What is peripheral arterial disease (PAD)?
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”)
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)?
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).
PAD - Etiology
What causes peripheral arterial disease (PAD)?
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”)
PAD - Clinical Presentation
What are the hallmark signs and symptoms of peripheral arterial disease (PAD)?
- 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
Arterial Insufficiency Ulcers
What is an arterial insufficiency ulcer?
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
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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)

Neuropathic Ulcers
What is a neuropathic ulcer?
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)
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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)

PAD - PT Implications
What are the major indications, contraindications, guidelines, or protocols for treating peripheral arterial disease (PAD)?
- 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”)
What is the ankle-brachial index (ABI)?
What are the interpretations of ABI values?
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”
Dorsalis Pedis Pulse
Describe how you would palpate the dorsalis pedis (aka, pedal) pulse.
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

Posterior Tibial Pulse
Describe how you would palpate the posterior tibial pulse.
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

CAD - Clinical Definition
What is coronary artery disease (CAD)?
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”)
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)?
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).
CAD - Clinical Presentation
What are the hallmark signs and symptoms of coronary artery disease (CAD)?
-
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.
- Refers to chest pain or discomfort that is related to ischemia of the myocardium (*see stable angina in “Types of Angina” flashcard)
-
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
- Signs and symptoms associated with unstable angina (*see “Types of Angina” flashcard), including:
References:
- Goodman and Fuller (4th ed.), p.557 (“Common sequelae of atherosclerosis affecting coronary arteries include…”)
- See “Specific NPTE Study Topics” Word doc.
Types of Angina
Differentiate between the three types of angina: stable angina, unstable angina, and variant (Prinzmetal) angina.
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
CAD - PT Implications
What are the major indications, contraindications, guidelines, or protocols for treating coronary artery disease (CAD)?
-
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.
-
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.)
-
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.
-
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).
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).
PVC and Contraindications
What is a premature ventricular contraction (PVC)? What quality and frequency of PVCs is a contraindication for further activity?
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)








