Cardiopulmonary System Flashcards
1.15: Peripheral Pulse Monitoring
Q#1: What artery are you palpating when assessing the carotid pulse?
Q#2: Describe how you would palpate the carotid pulse.
ANSWER #1: The carotid artery
ANSWER #2: 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).
REFERENCES:
- -Physical Rehabilitation, p. 49, Box 2.4
- -Folder: Anatomy → “Overview of Muscle OINAs” Word doc
1.15: Peripheral 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: 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.
REASONING: 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
1.15: Peripheral Pulse Monitoring
Q#1: What artery are you palpating when assessing the radial pulse?
Q#2: Describe how you would palpate the radial pulse.
ANSWER #1: The radial artery
ANSWER #2: The radial pulse can be palpated at the distal radius at the base of the thumb, lateral to the tendon of the flexor carpi radialis. The flexor carpi radialis tendon can be palpated by placing the wrist in flexion and radial deviation. The tendon will appear in line with the base of the second metacarpal bone.
REFERENCES:
- -Physical Rehabilitation, p. 49, Box 2.4
- -Folders: ECS I → Lecture Videos → Palpation → Wrist-Hand Region Palpation → “Tendons on Flexor Surface of Wrist Palpation” video
1.15: Peripheral Pulse Monitoring
FILL IN THE BLANK: The most common site for peripheral pulse monitoring is the _____ pulse.
Explain your reasoning.
ANSWER: Radial
REASONING: Out of all of the other pulse sites, the radial pulse site is the most easy to locate and access for peripheral pulse monitoring.
REFERENCE: Physical Rehabilitation, p. 49, Box 2.4
1.15: Peripheral Pulse Monitoring
Q#1: What artery are you palpating when assessing the temporal pulse?
Q#2: Describe how you would palpate the temporal pulse.
ANSWER #1: The frontal branches of the superficial temporal artery
ANSWER #2: The temporal pulse can be palpated on either side of the head over the temporal bone, lateral and superior to the eye.
REFERENCES:
- -Physical Rehabilitation, p. 49, Box 2.4
- -C. Anatomy app
1.15: Peripheral Pulse Monitoring
Q#1: What artery are you palpating when assessing the brachial pulse?
Q#2: Describe how you would palpate the brachial pulse.
ANSWER #1: The brachial artery
ANSWER #2: The brachial pulse can be palpated on the medial aspect of the biceps brachii tendon within the antecubital fossa. The elbow should be slightly flexed and supported to avoid contraction of biceps brachii muscle. The tendon of the biceps brachii muscle can be identified by having the patient complete resisted elbow flexion.
REFERENCE: Physical Rehabilitation, p. 49, Box 2.4
1.15: Peripheral Pulse Monitoring
Besides peripheral pulse monitoring, what is the brachial pulse most commonly used for?
ANSWER: To assess blood pressure using a blood pressure cuff (aka, sphygmomanometer)
REFERENCE: Physical Rehabilitation, p. 49, Box 2.4
1.15: Peripheral Pulse Monitoring
Q#1: What artery are you palpating when assessing the femoral pulse?
Q#2: Describe how you would palpate the femoral pulse.
ANSWER #1: The femoral artery
ANSWER #2: The femoral artery can be palpated inferior to the inguinal ligament, midway between the anterior superior iliac spine and the symphysis pubis.
REFERENCE: Physical Rehabilitation, p. 49, Box 2.4
1.15: Peripheral Pulse Monitoring
Q#1: What artery are you palpating when assessing the dorsalis pedis (aka, pedal) pulse?
Q#2: Describe how you would palpate the dorsalis pedis pulse.
ANSWER #1: The dorsalis pedis artery
ANSWER #2: On the dorsal aspect of the foot with the ankle slightly dorsiflexed to reduce the tension on the dorsum of the foot, the dorsalis pedis pulse 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
1.15: Peripheral Pulse Monitoring
Q#1: What artery are you palpating when assessing the posterior tibial pulse?
Q#2: Describe how you would palpate the posterior tibial pulse.
ANSWER #1: The posterior tibial artery
ANSWER #2: With the ankle in slight inversion to reduce the tension on the medial aspect of the ankle, the posterior tibial pulse 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
1.15: Peripheral Pulse Monitoring
What are the two best sites to monitor peripheral pulse rate among infants when the radial pulse is inaccessible?
ANSWER: The temporal and carotid pulses
REFERENCES:
–Physical Rehabilitation, p. 49, Box 2.4
1.15: Peripheral Pulse Monitoring
What two pulse sites are generally used to monitor for peripheral arterial disease?
ANSWER: The posterior tibial pulse (primarily) and dorsalis pedis (aka, pedal) pulse (secondarily)
REFERENCE:
–Folders: DMGMC → Prosthetics Unit → Lecture Materials → Lecture Powerpoints and PDFs → “DM, Foot Ulcers, and Amputations” PowerPoint lecture (slide 8)
1.47: Heart Failure, Clinical Definitions
Q#1: What is the clinical definition of heart failure? (*Hint: Low-output problem)
Q#2: What does congestive heart failure refer to?
Q#3: Dysfunction of the right ventricle of the heart can bet categorized as right-sided heart failure or cor pulmonale. What is the difference between right-sided heart failure and cor pulmonale?
Q#4: What is the difference between compensated and decompensated heart failure?
ANSWER #1: Heart failure is a general term that encompasses a group of clinical manifestations caused by the heart being unable to pump enough blood to supply the body’s needs. Failure may occur on both sides of the heart or may predominantly affect the right or left side.
ANSWER #2: Congestive heart failure strictly refers to left-sided heart failure.
ANSWER #3: When the underlying cause is a pulmonary pathology (e.g., pulmonary embolism, chronic obstructive pulmonary disease), the condition is called cor pulmonale. When the underlying cause is a cardiac pathology (e.g., left-sided heart failure), the condition is called right-sided heart failure.
ANSWER #4: Compensated heart failure occurs when systemic compensatory mechanisms help to achieve normal cardiac output either by increasing stroke volume or heart rate. Decompensated heart failure occurs when the heart is so severely damaged or weakened that compensatory mechanisms are no longer effective for achieving normal cardiac output. At this point, the disease progresses to end-stage heart failure, and a heart transplant is the only recourse.
REFERENCE: Specific NPTE Study Topics (Word doc): “Specific Topics From Practice Exams” → “Heart Failure” section
1.47: Heart Failure, Etiologic and Risk Factors
What are the most common etiologic and risk factors for heart failure?
Explain your reasoning.
ANSWERS:
o Etiologic factors: Hypertension, coronary artery disease, cardiac ischemia or myocardial infarction
• Rationale #1: 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).
• Rationale #2: 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).
o Risk factor: Diabetes mellitus
• Rationale: The chronic hyperglycemia of diabetes
results in the accelerated atherosclerosis, leading to hypertension and coronary artery disease (*from Pathology, pp. 510-511).
REFERENCE: Specific NPTE Study Topics (Word doc): “Specific Topics From Practice Exams” → “Heart Failure” section
1.47: Heart Failure, Categories
Heart failure is categorized from the perspectives of function (i.e., what heart function is failing) and structure (i.e., what heart structure is failing). Describe the categories of heart failure.
ANSWERS:
o Category—Function
• Heart failure with reduced ejection fraction (HFrEF, formerly known as systolic heart failure) = inefficient cardiac output due to impaired ventricular contractions during systole. Ejection fraction is less than 40%. (*Note: Normal EF is 50-75% at rest.)
• Heart failure with preserved ejection fraction (HFpEF, formerly known as diastolic heart failure) = inefficient cardiac output due to impaired ventricle filling during diastole. Ejection fraction is normal because most of the blood in the ventricles is being ejected (stroke volume), but the amount of blood that is initially present in the ventricles (end-diastolic volume) is low due to the ventricles being unable to fill appropriately.
o Category—Structure
• Left-sided heart failure = the left ventricle is unable to adequately pump blood forward to the body
• Right-sided heart failure = the right ventricle is unable to adequately pump blood to the lungs, causing a back-up of blood flowing into the heart
• Biventricular heart failure = both sides of the heart are unable to adequately pump blood
REFERENCE: Specific NPTE Study Topics (Word doc): “Specific Topics From Practice Exams” → “Heart Failure” section
1.47: Heart Failure, Pathophysiology
Describe the pathophysiology of the following categories of heart failure:
o Heart failure with reduced ejection fraction (HFrEF)
o Heart failure with preserved ejection fraction (HFpEF)
o Left-sided heart failure
o Right-sided heart failure
o Biventricular heart failure
ANSWERS:
o Heart failure with reduced ejection fraction (HFrEF)
• Cardiac ischemia or myocardial infarction →
structural damage to myocardium → impaired
ventricular contraction → more blood remains in the ventricle at the end of each contraction (i.e., increase in end-diastolic volume) → pathological eccentric hypertrophy to accommodate for volume overload → progressively excessive ventricular dilation and impaired ventricular contraction → back up of blood into structures behind the ventricle
o Heart failure with preserved ejection fraction (HFpEF) (*Note: Cor pulmonale has a similar pathophysiology. The pathophysiology of HFpEF only relates to left-sided heart failure.)
• Hypertension involving systemic arterial vessels
→ increased afterload → pathological concentric hypertrophy to accommodate for the pressure
overload → progressively excessive ventricular wall stiffness and loss of ventricular relaxation → impaired ventricular filling → back up of blood into structures behind the left ventricle
o Left-sided heart failure
• When the left ventricle is primarily involved in either HFrEF or HFpEF, blood will back up into the left atrium and pulmonary veins, leading to pulmonary edema (aka, pulmonary congestion), or the accumulation of blood in the interstitial spaces of the lung or in the air spaces themselves.
o Right-sided heart failure
• When the right ventricle is primarily involved in HFrEF, blood will back up into the right atrium and systemic venous vessels, leading to peripheral (dependent) edema.
o Biventricular heart failure
• Biventricular heart failure usually occurs as a progression of left-sided heart failure that eventually involves the right side of the heart.
REFERENCE: Specific NPTE Study Topics (Word doc): “Specific Topics From Practice Exams” → “Heart Failure” section
1.47: Heart Failure, Signs and Symptoms
Describe the signs and symptoms related to left-sided heart failure and right-sided heart failure.
ANSWERS:
o Left-sided heart failure
• Pulmonary edema. Due to backup of blood from the left ventricle to 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 decreased flow of oxygenated blood to the body, especially skeletal muscle
• Tachycardia. Due to compensatory activation of the sympathetic nervous system to maintain normal cardiac output
o Right-sided heart failure
• Peripheral edema. 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. Peripheral edema may present as pitting edema.
• Jugular vein (venous) distension. Characterized by bulging of the jugular veins
• Right-upper quadrant abdominal pain. Secondary to enlargement of the liver as the liver becomes congested with venous blood. (*Note: The liver is located in the right-upper quadrant of the abdomen. The liver is most susceptible to venous congestion because the hepatic veins are located most proximally along the inferior vena cava, closest to the right side of the heart.) Right-quadrant abdominal pain can progress to ascites, or abdominal swelling.
• Cyanosis (especially of the nail beds). Due to venous congestion and subsequent reduction in peripheral blood flow
• Tachycardia. Due to compensatory activation of the sympathetic nervous system to maintain normal cardiac output
REFERENCE: Specific NPTE Study Topics (Word doc): “Specific Topics From Practice Exams” → “Heart Failure” section
1.47: Heart Failure, Physical Therapy Implications
Describe the general and specific physical therapy implications for heart failure.
ANSWERS:
o General
• Monitor for tachycardia at rest. May be an indicator of transition into decompensated heart failure
• During activity, monitor for decreasing SpO2 due to impaired aerobic capacity or decreasing systolic blood pressure due to inadequate pump function.
• Educate the patient on upright positioning (e.g., supine with head of bed elevated to 60-90 degrees, or upright sitting) with legs in a dependent position as much as possible. Such a position alleviates the signs and symptoms of heart failure by decreasing venous return.
o Left-sided heart failure
• Educate the patient on using three-point (tripod) positions (e.g., sitting with both hands or elbows on the knees and leaning forward) to reduce dyspnea and allow ease of breathing. Such positions help to stabilize the coracoid process (i.e., the insertion point of the pectoralis minor), allowing the pectoralis minor to better elevate the ribs during inspiration
o Right-sided heart failure
• Evaluate for signs and symptoms of increasing peripheral edema.
– Circumferential girth measurements and pitting edema assessments of the lower extremities, especially the legs and feet
– Visual assessment of the right jugular vein to detect jugular vein distention. (*Note: The left internal jugular may be falsely elevated in some people.) Jugular vein pulsations are examined by inspecting the silhouette of the neck with the person reclining at a 45-degree angle.
– To determine liver involvement, monitor for right-upper quadrant abdominal pain and ascites.
– Monitor for cyanosis of the nail beds.
REFERENCE: Specific NPTE Study Topics (Word doc): “Specific Topics From Practice Exams” → “Heart Failure” section
2.12: Peripheral Vascular Disease, Clinical Definitions
Q#1: What is the clinical definition of peripheral vascular disease?
Q#2: Differentiate between peripheral arterial disease and peripheral vascular disease.
ANSWER #1: Peripheral vascular disease (PVD) is a general term that refers to any pathological condition that interferes with the arterial or venous blood flow to the extremities and the major abdominal organs, most often apparent in the intestines and kidneys. (*Note: Blood flow to the heart and brain is not included in the definition of PVD.) Peripheral vascular disease typically affects the legs more often than the arms, but upper extremity involvement is not uncommon.
ANSWER #2: In contrast to PVD, peripheral arterial disease (PAD; aka, arteriosclerosis obliterans) refers only to pathological conditions that interfere with arterial blood flow. (*Note: Arterial blood flow to the heart and brain is not included in the definition of PAD.)
REFERENCES:
- -Physical Rehabilitation, p. 532
- -Pathology Implications for the Physical Therapist, p. 633
2.12: Peripheral Vascular Disease, Categories
Peripheral vascular disease is organized based on the underlying pathological finding, either arterial or venous in origin. Describe the categories of peripheral vascular disease, and name and define the common conditions under these categories.
ANSWERS:
CATEGORY
o Arterial insufficiency: Any condition that causes inadequate arterial blood flow to a region or regions of the body. Peripheral vascular disease involving arterial insufficiency specifically refers to inadequate arterial blood flow to the extremities or major organs, excluding the heart and brain.
o Venous insufficiency: Any condition that causes inadequate drainage of venous blood from a region or regions of the body. Peripheral vascular disease involving venous insufficiency specifically refers to inadequate drainage of venous blood from the extremities or major organs, excluding the heart and brain.
COMMON CONDITIONS
o Peripheral vascular disease involving arterial insufficiency:
• Peripheral arterial disease (PAD; aka, arteriosclerosis obliterans). Refers to 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
o Peripheral vascular diseases involving venous insufficiency:
• Venous thromboembolism. Refers to both deep vein thrombosis (DVT) and pulmonary embolism (PE)
– Deep vein thrombosis is defined as partial or complete occlusion of a deep vein by a thrombus with secondary inflammatory reaction in the wall of the vein (thrombophlebitis).
– Pulmonary embolism is defined as 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.
• Varicose veins. Refers to an abnormal dilation of veins, leading to tortuosity (twisting and turning) of the vessel, incompetence of the valves, and a propensity to thrombosis along the inside of the vein.
• Chronic venous insufficiency (aka, postphlebitic syndrome and venous stasis). Refers to inadequate venous return over a long period of time
(*Note: Peripheral vascular disease also includes inflammatory and vasomotor disorders. For more information, see Pathology Implications, Box 12-13, p. 634; pp. 634-638; pp. 657-659.)
REFERENCES:
- -Physical Rehabilitation, pp. 532, 534
- -Pathology Implications, pp. 638, 646, 654-655, 849
- -Medscape: Varicose Veins and Spider Veins (https://emedicine.medscape.com/article/1085530-overview#a6)
2.12: Peripheral Vascular Disease, Etiologic and Risk Factors
For the categories of arterial and venous insufficiency, name the most common etiologic and risk factors.
Explain your reasoning.
ANSWERS:
o Peripheral vascular disease involving arterial insufficiency:
• Etiologic factor: Atherosclerosis
– Rationale: Atherosclerosis narrows the lumen of arterial blood vessels, resulting in arterial insufficiency.
• Risk factors: Tobacco smoking, diabetes mellitus, hypertension, male gender
– Rationale #1: 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 Pathology Implications, p. 556).
– Rationale #2: The chronic hyperglycemia of diabetes results in an acceleration of atherosclerosis (from Pathology, pp. 510-511).
– Rationale #3: Men have an increased prevalence of coronary artery disease as compared with women. Sex hormones may contribute to this difference (see Pathology Implications, p. 553). (Note: Coronary artery disease is an atherosclerotic disease process).
o Peripheral vascular diseases involving venous insufficiency:
• Etiologic factors: Thrombosis, embolism, inadequate valve function in the veins
– Rationale #1: Venous stasis, hypercoagulability, or injury to the venous wall (e.g., intravenous injections, fractures, dislocations, venous distension secondary to venous pooling) will result in thrombosis (see below). The thrombus or embolus can then interfere with venous blood flow as during venous thromboembolism.
–Rationale #2: Veins, particularly in extremities, contain one−way valves that permit blood flow toward the heart and prevent retrograde flow (from Cardiovascular Physiology, p. 110). These valves most commonly begin to fail as a result of excessive venous volume and pressure, leading to venous insufficiency. Inadequate valve function in the veins is associated with the pathogenesis of varicose veins and chronic venous insufficiency.
• Risk factors: Venous stasis, hypercoagulability, or vessel wall damage to a vein
– Rationale #1: In general, it is commonly held that at least two of these three aforementioned risk factors must be present for thrombi to form.
– Rationale #2: Venous stasis or thrombosis increases venous pressure and volume, resulting in distension of the veins that can damage the venous walls and contribute to impaired function of the valves.
– Note: Hypercoagulability may occur as a result of venous stasis (due to prolonged interaction of the platelets and clotting factors with the endothelium of the tunica intima), damage to the venous walls (e.g., intravenous injections, fractures, dislocations, venous distension secondary to venous pooling), or oral contraceptives (due to the increase in the amount of clotting factors in the circulation).
REFERENCES:
- -Pathology Implications for the Physical Therapist, pp. 549, 639, 647-649, 654-656
- -Differential Diagnosis for Physical Therapists, PDF p. 296
- -Medscape: Varicose Veins and Spider Veins (https://emedicine.medscape.com/article/1085530-overview#a1)
- -Venous Stasis. https://www.sciencedirect.com/topics/medicine-and-dentistry/venous-stasis
- -Specific NPTE Study Topics (Word doc): “Definition of Terms” → “Venous Stasis”
2.12: Peripheral Vascular Disease, Pathophysiology
Describe the pathophysiology of the following forms of peripheral vascular disease: o Peripheral arterial disease o Venous thromboembolism o Varicose veins o Chronic venous insufficiency
ANSWERS:
o Peripheral arterial disease
• Peripheral arterial disease is one expression of atherosclerosis: Injury to the inner layer (aka, tunica intima) of the arterial wall → low-density lipoproteins (LDLs) penetrate through the damaged tunica intima to form a fatty deposit called plaque → plaque grows outward then inward into the lumen → disruption of normal blood flow to the extremities and the major abdominal organs due to partial or complete obstruction of the artery.
o Venous thromboembolism
• Venous thromboembolism commonly begins with damage to the wall of the deep veins (especially major proximal deep veins such as the femoral veins, vena cavas, and axillary veins) → exposure of connective-tissue collagen fibers → the naked collagen acts like flypaper for platelets, causing platelets to adhere to, aggregate, and plug up the injured site → platelets attract the deposition of protein polymers (i.e., fibrin), leukocytes, and erythrocytes → venous insufficiency due to thrombosis when venous wall injury is in combination with venous stasis or hypercoagulability (resulting in deep vein thrombosis) → increase in venous pressure and volume distal to the site of occlusion → venous insufficiency due to embolism (resulting in pulmonary embolism)
o Varicose veins (most commonly involving superficial veins)
• Venous stasis or thrombosis → increase in venous volume and pressure → venous dilation → impaired valve function because the valve leaflets no longer meet → venous insufficiency due to varicose veins: increase in retrograde flow toward the congested limb and further decrease in venous return (see Pathology Implications, p. 654, Figure 12-35)
o Chronic venous insufficiency
• Damaged or destroyed venous valves secondary to thrombosis, varicose veins, or injury to the veins → chronic venous insufficiency
REFERENCES:
- -Specific NPTE Review Topics: “Review of Concepts” → “Atherosclerosis”
- -Pathology Implications for the Physical Therapist, pp. 639, 648-649, 654-656
- -Medscape: Varicose Veins and Spider Veins (https://emedicine.medscape.com/article/1085530-overview#a1)
