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ACS > Mosby 15 > Flashcards

Mosby 15 Flashcards

1
Q

Effects on blood vasculature durign pregnancy

A

Vascular resistance decreases and peripheral vasodilatation

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2
Q

Cause of hypotension during preganancy

A

Compression of vena cava and venous return

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3
Q

What are vascular changes in elderly?

A

Calcifications leading to dilation and tortuosity

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4
Q

HPI for blood vasculature

A

Leg pain or cramps

Onset? Duration? Recent injurity/immobilization?

Character?

Burning feeling in toes/thigs/buttocks

Skin changes: cold, pallor, hair loss, sores, rednes, or warmth of vein, visible vein, darkened or ischemic skin

walking at night with leg pain

Swollen ankles

Onset and duration: present in the morning, appearing as the day progersses, sudden onset, insidious onset

RElated circumastance: recent airplane, travel to high elevations

Associated symptoms: onset of nocturia, increased frequncy of urination, increasing SOB

Treatment attempted

Rest, massage, heat, elevation

MEDs: heparin, warfarin diuuretics, antihypertensive, non prescrition (NSAID),

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5
Q

PMH for blood vasculature

A

Cardiac surgery / hospitalization, Congential Heart defect, vascular procedures

Acute rheumatic fever, unexplained fever, swollen joints, vasculitis

Chronic illness: hypertension, bleeding, hyperlipiedmia, DM, thyroid, storke, transiet ischemic attack, coronary artery disease, AF,

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6
Q

FH for blood vasculature

A

Cardiovascular system

HT

dyslipidemia

DM

Heart

Thrombosis

Peripheral vascular disease

Abdominal aortic aneurysm

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7
Q

SX for blood vasculature

A

Employment: physical demands, hazards: heat, chemicals, dust, stress

Tabacoo

Nutrition

Weight loss/gain

Exercise

Alcohol

Recreational drugs

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8
Q

History of infants for blood vasculature

A

Hemophilia

Renal disease

Coarctation of the aorta

Leg pain during exercise

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9
Q

Histor of pregnant women for blood vasculature

A

BP before pregnancy (and change)

Headaches, visual changes, nausea, vomiting, epigastric pain, right upper quadrant pain, oiligura, rapid onset edema, hyperreflexia, proteinuraia, too much brusiing

Legs: edema, aricositites, pain, discomfort

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10
Q

Preeclampsia

A

Pregnancy complication characterized by high blood pressure

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11
Q

Preeclampsia

Risk factors

A

40+ yo

First pregnancy

Preexisting chronic hypertension

Renal disease / DM

Familial history of preeclampsia

Previous preeclampsia

Obestiy

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12
Q

History in older adults

A

Leg edema: pattern, frequency, time of the day

Interference with normal activities

Ability to cope

Claudication - areaa involved, unilateral or bilateral, distance one can walk b4 onset, length of tiem required for relief

Meds for relief

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13
Q

Varicose veins

risk factors

A

Gender - women (during preganncy especally)

Genetic (irish or german, taking birth control)

Sedentary lifestyle

Age

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14
Q

Pulses

A

A Carotid

B Brachial

C Radial

D Femoral

E Popliteal

F Dorsalis pedis

G Posterior tibial

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15
Q

Pulse abnormalities

A

Alternating pulse (pulsus altenans) - left ventricular failure

Pulsus bisferiens - aortic stenosis combine with aortic insuficiency (percussion 1st and tidial wave)

Bigeminal pulse - disorder of rhythm, normal pulsation following premature contraction

Large bounding pulse - exercise, anxiety, fever, hyperthyrodism, aorti rigidity

Paradoxic pulse - premature cardiac contraction, tracheobrachail obstruction, bronchial asthma, emphysema, pericardial effusion, constrictive pericarditis

Water-hammer pulse - patent ductus arteriosus, aortic regurgtation

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16
Q

Allen test

A

Test for patency of the ulnary artery

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17
Q

Venous Hum vs. Carotid Artery Bruits

A

Venous Hum

median end of clavicle & anterior border of stechleidomastoid muscle

no clinical significant

confused w/ carotid vruit, patent ductus arteriosus, aortic regurgitation

Carotid Artery Bruits

Heard above medial end of clavicle and aterior margin of stenocledomastoid

Transmitted murmus: valvular aortic stenosis, ruptured chordate tendineae of mitrial valve, or severe aortic regurgitation

Stenosis disease in cervial arteries

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18
Q

Arterial Occlusion

Ps

A

Pallor

Pain

Pulselessness

Paresthesias

Paralysis

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19
Q

First symptoms of peripheral arterial disease (stenosis)

A

Pain - ischemia - claudication “dull w/ muscle cramp w/ exercise” that pain is distal to stenosis

20
Q

Evaluate during stenosis

A

◆Pulses (weak and thready, or possibly absent)
◆ Possible systolic bruits over the arteries that may extend through diastole
◆ Loss of expected body warmth in the affected area
◆ Localized pallor and cyanosis
◆ Collapsed superficial veins, with delay in venous filling
◆ Thin, atrophied skin; muscle atrophy; or loss of hair (particularly in the case of long-term
insufficiency)
◆ Long-term insufficiency also accentuates skin mottling and increases the likelihood of
ulceration, localized anesthesia, and tenderness
To judge the degree of stenosis and the potential severity of the arterial insufficiency, perform
the following steps:
◆ Have the patient lie supine.
◆ Elevate the extremity.
◆ Note the degree of blanching.
◆ Have the patient sit on the edge of the bed or examining table in order to lower the
extremity.

21
Q

Korotkoff sounds

A
22
Q

Conditions where BP is difficult to take

A

Cardiac dysrhythmias (infrequent odd beats ignored)

Aortic regurgitation (sound no dissapearing)

VEnous conestion (lower systolic/higher diastolic)

Valve replacement

23
Q

Jugular Venous Pressure

difficult cases

A

Obesity

Volume depletion

Right hear failure, tricuspid insufficiency, constrictive pericarditis, cardiac tamponade

24
Q

Jugular veins vs. Carotid artery

Waves

Respiration

Venous compression

Abdominal pressure (hepatojugular reflux)

A

3 vs. 1

Decreases on inspiration and increase on expiration / no effect

Elimiates / no effects

Increase prominence / no effect

25
Q

Venous Obstruction

Symptoms

A

Constant pain

Swelling and tenderness over the muscles

Engorgement of superficial veins

Erythema and/or cyanosis

26
Q

Venous Obstruction

signs

A

thrombosis, varicose veins, or edema

27
Q

Homan sign

A

Flex the patient’s knee slightly with one hand and, with the other, dorsiflex the foot.

The complaint of calf pain with this procedure is a positive sign and may indicate venous thrombosis

28
Q

Pitting edema levels

A

1+ Slight pitting, no visible distortion, disappears rapidly
2+ A somewhat deeper pit than in 1+, but again no readily detectable distortion, and it
disappears in 10 to 15 seconds
3+ Noticeably deep pit that may last more than a minute; the dependent extremity looks
fuller and swollen
4+ Very deep pit that lasts as long as 2 to 5 minutes, and the dependent extremity is grossly
distorted

29
Q

Inspection for varicose veins

A

Stand 10 times on toues

Dependent position

30
Q

Vessels disorders

Description

Pathophysiology

Subjective

Objective

A

DESCRIPTION

An inflammatory disease of the branches of the aortic arch including the temporal arteries

PATHOPHYSIOLOGY

Inflammatory infiltrates develop in the thoracic aorta and neighboring arterial structures
Arterial intimal thickening and thrombosis can lead to ischemia ofsupplied structures such as the masseter muscle, tongue, or optic nerve

SUBJECTIVE

Usually affects persons older than 50 years of age
Flulike symptoms (e.g., low-grade fever, malaise, anorexia) may be accompanied by polymyalgia involving the hips and shoulders
Headache in the temporal region on one or both sides, although the headache can occur in other regions
Ocular symptoms, including loss of vision, are common
Ischemia can also cause tongue pain and jaw claudication

OBJECTIVE

Area over the temporal artery can become red, swollen, tender, and nodular
Temporal pulse may be variously strong, weak, or absent

31
Q

Vessels Disorders: Arterial Aneurysm

Description

Pathophysiology

Subjective

Objective

A

DESCRIPTION

An aneurysm is a localized dilation, generally defined as 1.5 times the diameter of the normal artery, caused by a weakness in the arterial wall

PATHOPHYSIOLOGY

Usually the result of atherosclerosis; with family history, tobacco use, and hypertension playing important roles
Abdominal aneurysms are four times more common in men than in women

SUBJECTIVE

Generally asymptomatic until they dissect or compress an adjacent structure
With dissection, the patient may describe a severe ripping pain

OBJECTIVE

Pulsatile swelling along the course of an artery
Occurs most commonly in the aorta, although renal, femoral, and popliteal arteries are also common sites
A thrill or bruit may be evident over the aneurysm

32
Q

Vessels Disorders: Arteriovenous fistula

Description

Pathophysiology

Subjective

Objective

A

DESCRIPTION

An arteriovenous fistula is a pathologic communication between an artery and a vein

PATHOPHYSIOLOGY

May be congenital or acquired
Damage to vessels caused by catheterization is the most common acquired etiology
If the fistula is large, there may be significant arterial-to-venous shunting of blood

SUBJECTIVE

Patients may present with lower extremity edema, varicose veins, or claudication due to ischemia
If severe, high output cardiac failure can develop

OBJECTIVE

May result in an aneurysmal dilation
A continuous bruit or thrill over the area
of the fistula suggests its presence
Edema or ischemia may develop in the
involved extremity

33
Q

Vessels Disorders:Peripheral Arterial Disease

Description

Pathophysiology

Subjective

Objective

A

DESCRIPTION

Stenosis of the blood supply to the extremities by atherosclerotic plaques

PATHOPHYSIOLOGY

Most common cause is peripheral atherosclerosis
Diabetes, hypertension, dyslipidemia, and tobacco use are all risk factors
Can also be a result of vascular trauma, radiation therapy, or vasculitis

SUBJECTIVE

Intermittent claudication produces pain, ache, or cramp in the exercised muscle that is receiving an inadequate blood supply
The amount of exercise necessary to cause the discomfort is predictable (e.g., occurring each time the same distance is walked)

OBJECTIVE

Limb appears healthy, but pulses are weak or absent
Progressive stenosis results in severe ischemia, in which the foot or leg is painful at rest, is cold and numb, and has skin changes (e.g., dry and scaling, with poor hair and nail growth)
Edema seldom accompanies this disorder, but ulceration is common in severe disease, and the muscles may atrophy

34
Q

Vessels Disorders:Raynaud Phenomenon

Description

Pathophysiology

Subjective

Objective

A

DESCRIPTION

This is the exaggerated spasm of the digital arterioles (occasionally in the nose and ears) usually in response to cold exposure

PATHOPHYSIOLOGY

Primary Raynaud phenomenon occurs most commonly in young, otherwise healthy individuals, most commonly women, with no evidence of underlying cause
Secondary Raynaud phenomenon is associated with an underlying connective tissue disease such as scleroderma or systemic lupus erythematosus

SUBJECTIVE

Involved areas will feel cold and achy, which improves on rewarming
In secondary Raynaud, there can be intense pain and digital ischemia with necrosis at the tips

OBJECTIVE

With primary Raynaud phenomenon, there is a triphasic demarcated skin pallor (white), cyanosis (blue), and reperfusion (red) within the extremities The vasospasm may last from minutes to less than an hour
In secondary Raynaud, ulcers may appear on the tips of the digits and eventually the skin over the digits can appear smooth, shiny, and tight from loss of subcutaneous tissue

35
Q

Vessels Disorders:Arterial Embolic Disease

Description

Pathophysiology

Subjective

Objective

A

DESCRIPTION

Atrial fibrillation can lead to clot formation within the atrium; if the clot is unstable, emboli may be dispersed throughout the arterial system

PATHOPHYSIOLOGY

Emboli can also be caused by atherosclerotic plaques, infectious material from fungal and bacterial endocarditis, and atrial myxomas

SUBJECTIVE

Pain is the most common symptom
Paresthesias may also develop

OBJECTIVE

Occlusion of small arteries and necrosis of the tissue supplied by that vessel
With endocarditis, you can see splinter hemorrhages in the nail beds

36
Q

Vessels Disorders:Venous Thrombosis

Description

Pathophysiology

Subjective

Objective

A

DESCRIPTION

Thrombosis can occur suddenly or gradually and with varying severity of symptoms; it can be the result of trauma or prolonged immobilization

PATHOPHYSIOLOGY

Risk factors for venous thrombosis include prolonged immobilization, malignancy, trauma, use of birth control medication, and history of previous thrombosis

SUBJECTIVE

Tenderness along the iliac vessels or the femoral canal, in the popliteal space, or over the deep calf veins
Deep vein thrombosis in the femoral and pelvic circulations may be asymptomatic
Pulmonary embolism may occur without warning

OBJECTIVE

Swelling may be distinguished only by measuring and comparing the circumference of the upper and lower
legs bilaterally
There may be minimal ankle edema; low-grade fever; and tachycardia
Homan sign can be helpful but is not absolutely reliable in suggesting deep vein thrombosis

37
Q

Vessels Disorders: Hypertension

Description

Pathophysiology

Subjective

Objective

A

DESCRIPTION

Hypertension is one of the most common diseases in the world; it is often responsible for stroke, renal failure, and congestive heart failure

PATHOPHYSIOLOGY

Hypertension continues to be defined as a blood pressure consistently at 140/90 mm hg or higher
For essential hypertension, the pathogenesis remains poorly understood

SUBJECTIVE DATA

Essential hypertension is asymptomatic unless it is malignant, where patients may present with headache, visual symptoms, or encephalopathy

OBJECTIVE DATA

In addition to checking the blood pressure, you should assess for any end-organ damage that may be present

This includes papilledema and evidence of
heart failure

38
Q

Jugular Venous Pressure Disorders: Tricuspid Regurgitation

Description

Pathophysiology

Subjective

Objective

A

DESCRIPTION

The backflow of blood into the right atrium during systole; a mild degree of tricuspid regurgitation can be seen in up to 75% of the normal adult population

PATHOPHYSIOLOGY

Most commonly due to conditions that lead to dilation of the right ventricle (e.g., hypertension, pulmonary thrombosis)
Less frequently it can also result from primary valvular disease

SUBJECTIVE

With mild to moderate tricuspid regurgitation, there are typically no symptoms
With severe disease, you may see symptoms of right-sided heart failure such as ascites or peripheral edema

OBJECTIVE

The v wave is much more prominent and occurs earlier, often merging with the c wave (Fig. 15-20; see also Fig. 15-7)

A holosystolic murmur in the tricuspid region, a pulsatile liver, and peripheral edema

39
Q

Jugular Venous Pressure Disorders: Atrial Fibrillation

Description

Pathophysiology

Subjective

Objective

A

DESCRIPTION

This arrhythmia, seen more commonly in older adults, may result in decreased cardiac output and atrial thrombus formation
with subsequent embolization

PATHOPHYSIOLOGY

Typically occurs in patients with some underlying heart disease that results in the atrial pathology such as enlargement or elevated pressures

SUBJECTIVE

While many episodes are asymptomatic, patients may describe palpitations, lightheadedness, or dyspnea

OBJECTIVE

The a wave is absent and the pulse is irregularly irregular
There are only two venous pulsations for each arterial pulsation, and the time interval between v waves is variable

40
Q

Jugular Venous Pressure Disorders: Cardiac Tamponade

Description

Pathophysiology

Subjective

Objective

A

DESCRIPTION

The accumulation of fluid within the pericardial space leading to compression and dysfunction of the heart chambers

PATHOPHYSIOLOGY

Pericardial fluid can accumulates from a number of etiologies (e.g., infection, malignancy, autoimmune disease)
The pressure within this space increases such that it compresses the heart chambers, decreasing their volume, allowing less filling, and compromising cardiac output

SUBJECTIVE

The history will depend on the rapidity of the pericardial fluid collection; in acute settings, there may
be sudden onset chest pain and dyspnea
If more chronic in development, there may be the insidious development of symptoms of heart failure

OBJECTIVE

The Y-descent is abolished and the JVP is markedly elevated (15 to 25 cm H2O)
The JVP fails to fall with inspiration as it usually does and may actually increase (Kussmaul sign)
Pulsus paradoxus (decrease in systolic blood pressure greater than 10 mm Hg with inspiration) may be present (see Box 15-5, Fig. 14-23)
41
Q

Jugular Venous Pressure Disorders: Constrictive Pericarditis

Description

Pathophysiology

Subjective

Objective

A

DESCRIPTION

Results from chronic inflammation and subsequent scarring of the pericardium

PATHOPHYSIOLOGY

Chronic inflammation leads to pericardial thickening and inelasticity
This results in diminished cardiac filling and output

SUBJECTIVE

Symptoms of progressive cardiac insufficiency such as worsening of lower extremity edema or dyspnea

OBJECTIVE

The JVP is elevated, just as with cardiac tamponade, but there is a prominent Y-descent
Signs of severe right heart failure such as ascites and severe peripheral edema (Fig. 15-21) may develop

42
Q

Jugular Venous Pressure Disorders: Coarctation of the aorta (children)

Description

Pathophysiology

Subjective

Objective

A

DESCRIPTION

Coarctation of the aorta is a stenosis seen most commonly in the descending aortic arch near the origin of the left subclavian artery and ligamentum arteriosum

SUBJECTIVE

Most patients are asymptomatic unless severe hypertension or vascular insufficiency develops
In those settings, patients may develop symptoms of heart failure or vascular insufficiency of an involved upper extremity with activity

OBJECTIVE

Differences in systolic blood pressure readings when the radial and femoral pulses are palpated simultaneously

43
Q

Jugular Venous Pressure Disorders: Kawasaki Disease (children)

Description

Pathophysiology

Subjective

Objective

A

DESCRIPTION

An acute vasculitic illness of uncertain cause affecting young males more often than females; the critical concern is cardiac involvement in which aneurysms of a coronary artery may develop

PATHOPHYSIOLOGY

The etiology of the vasculitis is unknown
Immune-mediated blood vessel damage can result in both vascular stenosis and aneurysm formation

SUBJECTIVE

The symptoms are diffuse and typified by fever lasting a few days to several weeks
The effects of a systemic vasculitic illness, such as weight loss, fatigue, myalgias, as well as arthritis, may develop

OBJECTIVE

Findings may include conjunctival injection, strawberry tongue, and edema of the hands and feet
Lymphadenopathy and polymorphous nonvesicular rashes (Fig. 15-23)

44
Q

Preeclampsia-Eclampsia

A

DESCRIPTION

Preeclampsia-eclampsia defines a syndrome specific to pregnancy; it is determined by hypertension that occurs after the 20th week of pregnancy and the presence of proteinuria; eclampsia is preeclampsia with seizures when no other cause for the seizures can be found

PATHOPHYSIOLOGY

Theorized to result from a combination of vascular and immunologic abnormalities within the uretoplacental circulation

SUBJECTIVE DATA

May be diagnosed without proteinuria if other systemic symptoms are present (e.g., visual changes, headache, abdominal pain, pulmonary edema

OBJECTIVE

Sustained elevation of the blood pressure (systolic >160 mm Hg, diastolic > 110 mm Hg)

45
Q

Jugular Venous Pressure Disorders: Venous Ulcers (elderly)

Description

Pathophysiology

Subjective

Objective

A

DESCRIPTION

This results from chronic venous insuffiency in which lack of venous flow leads to lower extremity venous hypertension

PATHOPHYSIOLOGY

Obstruction of venous flow may
result from incompetent valves,
obstruction of blood flow, or loss of
the pumping effect of the leg muscles

SUBJECTIVE

Frequently asymptomatic in the early stages
Patients may describe a leg heaviness and discomfort progressing to edema and ulceration

OBJECTVIE

Ulcers are generally found on the medial or lateral aspects of the lower limbs
Induration, edema, and hyperpigmentation are common associated findings

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