Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PCE Study > Cardiopulmonary > Flashcards

Cardiopulmonary Flashcards

1
Q

What is valve heart disease?

A

VALVE HEART DISEASE

  • failure of valve to open completely thereby impede forward-flow (stenosis)
  • regurgitations (insufficiency) = fail valve to close = reverse blood flow

-Either mitral valve or aortic valve
Aortic stenosis is most common valvular abnormality = resistance to flow is higher

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is dilated cardiomyopathy?

A

DILATED CARDIOMYOPATHY

  • (systolic dysfunction)
  • heart with increased mass = increased difficulty w/ pumping
  • risks: third trimester, alcohol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is hypertrophic cardiomyopathy?

A 
HYPERTROPHIC CARDIOMYOPATHY
- (diastolic dysfunction)
- hypertrophied heart, abnormalities in filling
- young athletes at risk of dying
S/S
- chest pain & SOB, sudden
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Diffentiate between aortic stenosis and mitral stenosis

A

Aortic stenosis: calcification due to age or lipid accumulation
- Consequences: heart murmur, hypertrophy, angina, syncope

Mitral Stenosis
- Signs: Small stroke volume and pulse pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is cardiac temponade?

A

CARDIAC TAMPONADE

  • compression of the heart due to blood or fluid buildup in the pericardial sac
  • may occasionally be the result of puncture wound through the heart during a procedure

SYMPTOMS
o jugular distension
o hypotension
o muffled heart sounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Differentiate between arteriosclerosis and athersclerosis

A

Arteriosclerosis= stiffening of the arteries; thickening and loss of elasticity - hardening of arteries

Atherosclerosis = plaques into lumen and weakened underlying artery;

  • Atheromas (plaques, cholesterol or lipids) form within the intima of artery
  • Consequences: heart attack, stroke, aortic aneurism, PVD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is an aneurism

A

Localized abnormal dilation of the wall of a blood vessel; all aneurisms may rupture

Causes: atherosclerosis, trauma, congenital defects, infections, weakening of vessel wall
Most common site: abdominal aortic aneurysm (AAA)

RESULT = AORTIC DISSECTION

  • Tear in inner wall of aorta = causes blood to flow btw layers of aorta wall = forces layers apart
  • S/S = chest or abdominal pain, dissecting aneurism (tear w/in wall of blood vessel)

Need to prevent rupture! May need surgical intervention if large

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Define myocardial ischemia and infarct

  • what part of the heart is most affected
  • Signs and symptoms
  • What hormones are released
  • What is a physical attribute that can increase risk of MI
  • Exercise consideration for post MI
A

MYOCARDIAL ISCHEMIA AND INFARCTION
Infarction = necrosis develops distal to occlusion of an artery
MI: “heart attack”; death of heart muscle due to ischemia
 Most frequent location = LEFT VENTRICLE d/t occlusion of left coronary artery
 S&S: chest pain, dyspnea, rapid pulse, profuse sweating
 Release of troponin and creatine kinase
 Increased risk of MI with higher (above >0.9) waist-to-hip ratio
 Post MI upper limit for exercise intensity based on S&S; teminated exs is downsloping ST segment depression
 Post MI exs: RPE <13 and HR <120 bpm or resting HR plus 20 bpm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a terrible triad?

- What part of a ECG correlates with the different levels

A

Terrible Triad: (3 I’s)
1) Ischaemia = Inverted T waves, poor blood supply and hypoxia, occurs w/i seconds of onset and is REVERSIBLE

2) Injury = Abnormal ST segment
- Elevated ST segment: myocardial tissue injured during MI; occurs in 20-40mins, IS REVERSIBLE
- Depressed ST segment: inj to myocardial tissue, can occur during angina, is reversible

3) Infarction = Abnormal Q waves and QS complexes, can also be tall R waves
- Tissue necrosis, NOT REVERSIBLE, occurs 2hrs after onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is an electrocardiogram?

- What are the normal findings for each segment

A

ELECTROCARDIOGRAM (EKG): measures the summation of AP’s of cardiac cells; electrical activity precedes muscle
Normal results:
o P wave = atrial depolarization
o QRS = ventricular depolarization
o ST segment = pause in EKG time before ventricular repolarization; myocardium is depolarized
o T – ventricular repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Differentiate between the different heart blocks

A

HEART BLOCKS:
1st degree AVblock= caused by prolonged conduction in AV node; P-wave normal

2nd degree AV block (2 types, mobitz 1 and 2)

  • MOBITZ type 1: block occurs at occurs at AV node and is transient; PR lengthens until totally blocked then NO QRS follows a P causing a missed beat
  • MOBITZ type 2: block occurs at bundle branches/bundle of His; abrupt drop of QRS, but PR interval normal

3rd degree AV block: block at AV node, bundle of His OR bundle branches; complete disassociation between atria and ventricles, this produces independent atrial and ventricIular rate (atrial faster)
- Bundle branch block: in bundle branches and QRS is longer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is congestive heart failure?

  • What are some physical and physiologic features of CHF
  • What are the 2 types
  • What should patients w/ CHF restrict
A

CONGESTIVE HEART FAILURE (CHF) -heart is unable to pump blood at a rate required by tissues of the body, OR it does so at elevated filling pressures

Marked by breathlessness and abnormal retention of sodium and water resulting in edema with congestion of lungs or peripheral circulation, or BOTH; presence of dyspnea & pink, frothy sputum

Two types: 1) systolic deterioration of contractile function; 2) diastolic: can’t accommodate ventricular blood vol

Patient with CHF should restrict SODIUM

End-stage CHF can be treated with cardiac transplantation
Post transplant: low to mod exs intensity, using longer warm-up and cool-down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Differentiate between L sided CHF and R sided CHF

A

LEFT-SIDED CHF
o Commonly associated with PULMONARY EDEMA, tachypnea, increase work of breathing, crackles on auscultation, cyanosis (if severe)
o Due to: damming of blood in pulmonary circulation; SOB when lying, nocturnal gasp of breath when sleeping, kidney and brain decreased perfusion
o Pulmonary edema is most often symptomatic of left ventricular failure

RIGHT-SIDED CHF
o S&S: PERIPHERAL EDEMA (ex. Ankle edema), pitting edema, ascites, jugular venous distension (distended neck veins); liver damage and enlarged spleen, dec flow in periphery, kidney and brain issues
o Common cause: L sided heart failure; damming of blood in periphery, congestion of the portal system:
 Systemic edema results from increased hydrostatic pressure from impaired venous return

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Cor Pulmonale?

A

Cor Pulmonale = failure of the R side of heart; due to chronic severe pulm HTN: emphysema and chronic bronchitis (COPD)

long-term increased BP in lung arteries + R ventricle

  • chronic severe pulmonary HTN –> emphysema, chronic bronchitis (COPD)
  • cystic fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is carotid pulse?

A

CAROTID PULSE: Pressure receptor (baroreceptors) are present in the carotid sinus & these receptors respond changes in BP. An increase in blood pressure that is sensed by these receptors will stimulate the parasympathetic system to decrease the rate & force of contraction of the heart in order to help lower the pressure. An increase in BP that is sensed by these receptors will stimulate the parasympathetic system to decrease the rate & force of contraction of the heart in order to help lower the pressure.

Repeated palpation in the carotid sinus area may stimulate an increase in BP & cause this reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is Angina Pectoris?

A

Angina pectoris: paroxysmal (short, sudden outbust) recurrent episodes of chest discomfort caused by transient myocardial ischemia; 3 overall patterns:

  • Stable (occurs with activity/excitement)
  • Unstable (brought on by less effort)
  • Prinzmetal (variant; occurs at rest and caused by coronary vasospasm)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the causes of Pneumonia?

- Causes

A

PNEUMONIA (primary or post-operative/preventive)
- inflammation of parenchyma of lungs (lung tissue)

CAUSES

  • bacterial, viral or fungal (NORMALLY – airborne pathogens)
  • inhalation of toxic chemicals (smoke, dust, gas)
  • aspiration

impaired consciousness = alcohol abuse, after surgery, neuro disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the two main types of Pneumonia

A

TYPES
Typical
- Sudden symptom onset  usually bacterial cause
- Fever, sputum, physical consolidation signs

Atypical
- No symptoms, little sputum, min chest signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the signs and symptoms and treatment of Pneumonia?

A 
S/S
o most preceded by upper respiratory infection --> followed by sudden + sharp chest pain
o productive green sputum
o Tachypnea = Incr rate of breathing
o SOB
Rx
o antibacterials/antibiotics
o airway clearance techniques
o antifungals (if fungal infection)
o oxygen support
o positioning

HOSPITAL ACQUIRED PNEUMONIA HAS A HIGHER MORTALITY RATE THAN COMMUNITY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What would you expect to find on objective Ax of someone w/ pneumonia?

What are some secretion clearance techniques?

What are some preventative measures?

A

O/E there will be: BRONCHIAL BREATH SOUNDS & DECREASED AIR ENTRY over the lobe affected.

Appropriate secretion mobilization techniques include: PERCUSSION, VIBRATION, HUFFING, SHAKING. Also include appropriate POSTURAL DRAINAGE position.

PREVENTION: vaccine, Rx of influenza, mobility (keep lungs clear of sputum), prevent aspiration (HOB at 30), universal precautions and overall health

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is atelectasis?

- What are the 3 main causes?

A

ATELECTASIS (primary or post-operative/preventive)
Collapse of normally expanded and aerated lung tissue at any structural level involving all or part of the lung; can be patchy, segmental or lobar distribution

Can be due to:

1) blockage of bronchus/bronchiole, lung is prevented from expanding due to: paralysis, diaphragmatic disorders, mucous or airway obstruction, hypoventilation
2) compression due to pneumothorax, pleural effusion, space-occupying lesion (tumor) which prevents alveoli from expanding
3) post-anesthetic - effects of anaesthesia and prolonged recumbency, breathing at low lung volumes

22
Q

What are signs and symptoms of atelectasis?

A

S/S
o CXR = shifting of lung structures toward collapse = if entire lobe, may show shadow
o Quiet breath sounds
o Dyspnea
o Tachypnea
o Cyanosis = low O2 saturation = skin’s blue

23
Q

What is the treatment for atelectasis?

A 
RX
o identify underlying cause
o suctioning if d/t secretions
o chest tube if d/t pneumo/hemo thorax or
extensive pleural effusion
24
Q

What is ARDS?

  • Risk factors
  • Key features for CXR
  • Signs and symptoms
  • Treatment
A

ARDS: acute respiratory failure with severe hypoxemia as a result of pulmonary or systemic problem
Lung injury characterized by increased permeability on alveolar capillary membrane; leakage of fluid and blood into lung interstium and alveoli - inflammatory reaction; alveolar edema and collapse

RF/Causes: severe trauma; aspiration; embolism; indirect- happen after viral infection or pneumonia

Key feature on x-ray = WHITE OUT

S&S: incr RR, shallow breathing, severe dyspnea, cyanosis, acc muscle use

Rx: PEEP to keep airways open, tackle underlying cause, PRONE position, intubation and ventilatory assistance

25
Q

What is SARS?

- Symptoms

A

SARS – Severe Acute Respiratory Syndrome
- viral respiratory illness that is caused by SARS coronavirus

S/S

  • Flu-like = fever, myalgia, cough, sore throat, lethargy
  • Can lead to pneumonia
26
Q

What is IRDS

  • Risk factors
  • Medical management
A

IRDS: occurs in infants whose lungs have not fully developed; lack surfactant (helps lungs inflate with air and keeps the sacs from collapsing)

Risks: prematurity, c-section, multiple preggers, blue baby, stop breathing, grunts

Rx: deliver artificial surfactant

27
Q

Differentiate between hypoxic and hypercapnic respiratory failure

A 
HYPOXEMIC RESP FAILURE
Gas exchange failure = arterial hypoxemia = Decr blood O2, no increase in CO2
DUE TO:
- Pneumonia
- ARDS
- obstructive lung disease
- pulmonary embolism
HYPERCAPNIC RESP FAILURE
\++ CO2 in the blood = decr blood O2
DUE TO
- Decr ventilation = d/t drugs decr resp control
- acute upper/lower airway obstruction
- weak/ impaired respiratory mm
- SCI
28
Q

What are the main causes of Asthma?

A

Main categories:
1) Extrinsic - allergic or atopic – allergy to specific trigger; mast cells release mediators which cause bronchospasm and hypersecretion; usually CHILDHOOD onset

2) Intrinsic - non allergic- no known allergic cause/trigger; hypersensitivity to bacteria, virus, drugs, cold air, exs, stress; usually ADULT onset
3) Occupational – related to exposure of workplace irritants

29
Q

What is COPD?

A

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
Chronic resp condition characterized by progressive airway obstruction that is not fully reversible. Paraenchymal inflammation and decr elastic recoil AND airway inflammation and remodeling lead to:

Decr expiratory flow, hyperinflation and gas exchange abnormalities

Incr in airway resistance & Premature collapse of the airways upon exhalation, which leads to more air enters on inspiration than exits on expiration, air trapping & poor gas exchange; causes hyperventilation and large lung volumes leading to shortened inspiratory muscles

Age of onset middle aged to older adults

Mostly caused by smoking; other RF are occupational exposures, biomass smoke, genetic susceptibility

30
Q

What is the pharmacological Mx of COPD

A

 Rx: pharmacological focuses on: 1) smooth mm relaxation, 2) reduce airway inflammation
o Decr airway inflammation with CORTICOSTEROIDS
o Smooth muscle relaxation with BRONCHODILATORS
 Sympathomimetic meds (ex Ventalin/Albuterol) reduce airway resistance by decreasing bronchospasm. Adverse reactions = increased BP and tachycardia; also tremor, anxiety, nervousness, weakness
 Theophylline: bronchodilator to reverse airway obstruction. toxicity: irregular HR, jittery, gastric upset, can cause arrhythmias and seizures

31
Q

Pulmonary function test of patient with COPD will typically show.

A

o increased functional residual capacity
o increased total lung capacity
o increased residual volume
o Forced expiratory volume in one second that is less than 80% of the vital capacity

32
Q

What is emphysema?

  • What is the impact of this on the respiratory system?
  • How is it diagnosed?
A

Emphysema aka parenchymal destruction - destruction of air spaces distal to the terminal bronchiole with destruction of alveolar septa which causes merging of alveoli into larger air spaces

This reduces the surface area for gas exchange; loss of airways and capillaries as well

Impact: hyperventilation (pt breaths at high lung volumes) - puts the diaphragm at mechanical disadvantage (it’s flattened)

Dx via Diffusing Capacity lung fxn test (measures exchange of gas across the alveoli, using CO

33
Q

What is bronchitis?

  • What are the signs and symptoms?
  • What impact does this have on pulmonary function?
A

Small airway remodeling
Chronic Bronchitis = productive cough, lasting for 3 months/year for 2 consecutive years

S&S: long term irritation of the trachea/bronchi, increased mucus production, decreased vital capacity

Impact on lung fxn: airway wall increased, thus smaller airway to move air in; increase in mucous also reduces size of lumen; damage to cilia increases infection susceptibility; increase in airway smooth mm contraction can cause increase in bronchoconstriction

34
Q

What is bronchiectasis?

  • What would you expect to hear on ausc?
  • Treatment?
A

Bronchiectasis - irreversible destruction (necrosis) and dilation of the airways associated with chronic bacterial infection; excess mucus production; Hx of repeated resp infections; can be caused by CF, TB, and endobronchial tumors; eventually alveoli replaced with scar tissue due to chronic inflamm

Ausc: coarse crackles over affected lobes

Rx: bronchodilators, antibiotics, regular secretion clearance

35
Q

What is RESTRICTIVE PULMONARY DISEASE (AKA INTERSTITIAL LUNG DISEASE)

A

Characterized by a loss of lung compliance; typically have an increase in scarring aka Pulmomary Fibrosis
Stiff, less compliant lungs (not airway obstruction); 2/3 are idiopathic, 1/3 from inhaling known particles

S&S: dyspnea, severe O2 desaturation, finger clubbing, scarring on CT, dry/painful cough, rapid/shallow breathing; on Lung Fxn test: small lung volumes, decr FEV1 and FVC,

Tx: O2 therapy, lung transplant, pulmonary rehab

Paralysis of respiratory muscles
Weakness of the diaphragm would cause decreased distension of the epigastric area & may result in a compensatory increase in upper chest expansion to improve ventilation

36
Q

What is tuberculosis?

A

Infectious, inflamm systemic disease that affects lungs and may disseminate to involve kidneys, growth plates, meninges, avascular necrosis of hip jt, lymph nodes and other organ.

Travels via airbourne particles

37
Q

What are the signs and symptoms of TB

- What is the medical management?

A

S&S: productive cough 3+wks, wt loss, fever, night sweats, fatigue, bronchial breath sounds

TB skin test: inject in forearm: determine of body’s immune response has been activated by TB before

medical management: 10 drugs

When active: pt should be in a private, negative-pressured room; pt should wear a mask when leaving room
PT: thorough history and self protection (masks etc)

38
Q

What is a pleural effusion?

  • What are the 2 types?
  • What are the symptoms?
A

EFFUSION = excess fluid in body cavities
Pleural effusion - accumulation of fluid in the pleural space due to disease - this can impair breathing by limiting expansion of the lungs. Two types:
1) transudate: high fluidity and low protein (thin and clear fluid); commonly due to heart fail
2) exudate: low fluidity and high protein/cells (thick and pus) formation of fluid by inflammation or disease of pleura; caused by infection or cancer of the pleura - opaque

Symptoms: SOB, chest pain, percussion: dull, decreased or ABSENT breath sounds, may hear a pleural rub; may cause mediastinal shift to opposte side

39
Q

What is pulmonary edema?

  • Signs and symptoms?
  • Treatment
A

Pulmonary edema - increased fluid in extravascular spaces of the lungs; may be increased hydrostatic pressure due to heart or kidney failure (pushes fluid out of vessels) or increased alveolar permeability (drug induced, ARDS, inhalation of noxious gas)

Signs and symptoms

  • Presents as stiffer lungs - inc work of breathing, and dyspnea
  • Classic symptom: cough that produces a frothy pink tinged sputum
  • On auscultation: FINE CRACKLES; CXR: fluffy looking white areas

Rx: Oxygen, vasodilators to decr venous load, diuretics to decr fluid overload

40
Q

What is cystic fibrosis?

A

Cystic fibrosis - inherited recessive genetic disorder of chloride and sodium transport across the epithelium of the resp, digestive and genital tracts (ie., all exocrine glands); results in defective Cl- excretion and Na+ absorption = THICK MUCUS and scarring and formation of cysts in the affected body organs

Can get: recurrent chest infections, consolidation, atelectasis and thickened bronchial walls

41
Q

How is CF diagnosed?

A

Diagnose with fam history, sweat test - chloride content of sweat, 2 copies of abnormal gene; obstruction on lung function test; CXR (linear opacities, thickened bronchial walls, consolidation, atelectasis)

42
Q

Whats are the effects of CF on the body?

A

Respiratory symptoms most common; also get: finger clubbing, breathlessness, delayed puberty and skeletal maturity, infertility in males, symptomatic steatorrhea, diabetes mellitus, liver disease, OP

Chronic bacterial infections and progressive loss of lung function leads to resp failure and early death

43
Q

What is the role of physio for CF?

A

Tx: airway clearance techniques (aggressive bronchial drainage, chest vibration, percussion), bronchodilators, aggressive antibiotics, exercise, use of acapella device, Active Cycle of Breathing, autogenic drainage

Most critical part of Tx = chest PT/postural drainage (require secretion removal once or twice/day!)

44
Q

What is a pneumothorax?

  • Signs and symptoms
  • Differentiate between spontaneous and tension pneumothorax
  • What is the role of physio?
A

Pneumothorax – collapse of the lung d/t air gathering in the pleural space; can be due to puncture

S&S: chest P, SOB, diminished breath sounds, hyperresonant percussion; CXR = hyperlucent lung

  • Spontaneous pneumothorax- spont rupture of air containing space of lungs
  • Tension Pneumothorax – can be quickly fatal! Increased pressure on heart that can stop beating. Need to remove seal or quick insertion of chest tube

Rx: If mod: aspirate w/ catheter needle; if severe: chest tube insertion connected to suction

45
Q

What is peripheral artery disease (PAD)/ peripheral vascular disease (PVD)?
- Signs and symptoms

A

PAD: Account for 95% of arterial occlusive disease; artherosclerosis is the underlying cause.
Pathologic conditions of blood vessels that supply extremities and major abdominal organs

Artherosclerotic obstruction of iliac, femoral, and politieal arteries in the legs; feel pain during physical activity, most often in the calf/feet.

S&S: occur distal to site of narrowing or obstruction; intermittent claudication, acute ischemia (pallor, pain paralysis, pulseless), ulceration and gangrene, skin is shiny, thin, hairless, cool to touch, decr vital capacity

Outcome: decreased mobility d/t pain and loss of function or limb

46
Q

What is are the tests and treatment for PAD/ PVD?

A

TESTS: rubor test, girth measurement, volumetric measurement, reactive hyperemia, ischemia test

Tx: walking, short duration, 2-3 times/day (walk to maximum tolerable pain, then rest)

47
Q

What is throbophlebitis?

A

THROMBOPHLEBITIS = When associated with the formation of blood clots (thrombosis)

  • Partial or complete occlusion of a vein by a thrombus with secondary inflammation
  • Can be superficial or deep

THROMBOSIS: caused by endothelial cell damage (ex catheters), poor blood flow (prolonged sitting), and hypercoagulability
- Tx: Heparin (rapid onset), Warfarin (slower onset, used as long-term prophylaxisis
PHEBLITIS = inflammation of a vein, usually in the legs

48
Q

What is a DVT?

  • Risk factors
  • Signs and symptoms
  • Physical tests and scans
  • What is the most appropriate thing to do post Sx prevent DVT
  • What is the role of physiotherapy in treating DVT
A

DEEP VEIN THROMBOSIS (DVT) – Risk: can become pulm emboli

RF: venous stasis, venous damage, hypercoagulation, obesity, smoking, genetic susceptibility

S&S: dull ache, tightness/pain in calf (d/t thrombus in calf vein); swelling, may have fever, TOP, P w/ DF

Appropriate Test = HOMAN’S SIGN (pain on DF of foot)
Rapid screening with Doppler Ultrasonography

Most appropriate to prevent DVT post-surgery = ANKLE PUMPS

PT Tx: deep breathing exs, frequently turn from side to side in bed, active flexion/ext of the toes, ankles, knees and hips

49
Q

What is chronic venous insufficiency?

  • Cause
  • Symptoms
A

CHRONIC VENOUS INSUFFICIENCY- inadequate venous return over a prolonged period; abnormal circulatory condition characterized by decreased return of the venous blood from the legs to the trunk of the body

Cause: DVT, trauma, obstruction by tumor,

Symptoms of discoloration with mild atrophic changes in the nails, mild swelling of the foot/ankle, thickening brown/bluish skin and ulcers; skin is thin, and cyanotic; minimal dull aching pain

50
Q

What is arterial insufficiency?

A

ARTERIAL INSUFFIFIENCY - may not be able to sustain blood flow against gravity
Presents with severe pain, decr/absent pulses, skin is cool, pale and shiny

Elevation can cause vasodilation/hyperemia (caused by local mechanisms) which occurs in response to ischemia; can cause pain as well

Ankle Brachial Index of 0.5-0.8 indicates decr arterial perfusion and compression therapy is CONTRAINDICATED

51
Q

What is orthostatic hypotension

A

Orthostatic hypotension from bed rest occurs as a result of decreased venous tone, which will lead to a pooling of blood in the LE upon standing. The pooling of blood in the LE will reduce the amount of blood returning to the heart decreasing ventricular filling & ultimately decreasing cardiac output. This results in drop in BP with resultant dizziness. With pooling of blood in the LE, the hydrostatic pressure would increase. To compensate for the decrease in CO, the sympathetic system would stimulate the heart

52
Q

What are the signs and symptoms of orthostatic hypotension?

  • How is it diagnosed clinically
  • What is the optimal positioning for orthostatic hypotension?
A

S&S: dizziness, light headedness, fatigue, blurred vision, muscle weakness, syncope

Dx: drop in BP is measured: SBP >20 mmHg OR DBP >10 mmHg

Optimal position is SUPINE if pt demonstrates signs

  • If severe, use tilt table with progressive vertical positioning to assist with standing
  • Tolerance can be improved by meds, regular PA and being upright

PCE Study (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions