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Nursing 2005: Clinical Pathophysiology > Nursing 2005: Cardiovascular Disorders: (part 1) Disorders of Blood Flow and Oxygenation > Flashcards

Nursing 2005: Cardiovascular Disorders: (part 1) Disorders of Blood Flow and Oxygenation Flashcards

1
Q

Systolic phase (S1)

A
  • one contraction
  • ventricle contraction
  • mitral and tricuspid valves close
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2
Q

Stroke volume

A

.- amount of blood pumped out during systole

  • 70 cc average
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3
Q

Ejection fraction

A
  • ejects 66% of blood
  • Estimated by echocardiography
    • stroke vol/end- diastolic vol
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4
Q

Diastole (S2)

A
  • ventricles fill = relax
  • aortic and pulmonary valves close
  • end of diastole
  • atrial contract
  • most supply goes to the heart because its relaxed
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5
Q

Frank-Starling Law

A
  • length tension of preload to myocardial contractility
  • contraction of heart increases if muscle fibers are stretched
  • increase contractility if ventricles fill
  • generated by vol
  • over stretched = fatigue of muscles overtime
  • inc contractility if inc in ventricle filling
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6
Q

Laplace law

  • dilation = ?
A
  • amount of tension in the wall that the ventricle produces depends on its size
  • dilation = decreases ability to eject blood and to contract
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7
Q

Cardiac output

A
  • amount of blood pumped out of the heart in 1 minute
  • CO = HR x Stroke volume
  • normal heart rate 70-80 beats/min
  • 5-6 liters/min
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8
Q

What are the factors affecting cardiac output?

A
  1. Preload
  2. After load
  3. Heart rate
  4. Contractility
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9
Q
  1. Preload
  • determined by
  • inc preload
A
  • pressure generated in left ventricle at the end of diastole = end diastole pressure
  • more blood in ventricles = higher the preload
  • increase preload =
  • increase force of contraction = increase cardiac output
  • inc force of contraction = inc cardiac output
  • High preload is good for a healthy heart, but not for people with heart disease d/t weak heart
  • determined by:
    • amount of venous return entering ventricle after diastole
    • blood left in ventricle after systole
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10
Q
  1. Afterload
  • inc
  • dec
A
  • resistance that the left ventricle has to pump blood to eject it
    • after contraction
  • decrease after load = heart pumps easily
  • inc in after load= harder for heart to pump because it has to work harder
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11
Q
  1. Heart rate
A
  • autonomic nervous sys
  • average 70 beats/min
  • slight increase in HR = increase cardiac output
  • as HR increases = stroke vol decreases –> decreases cardiac output
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12
Q
  1. Contractility
A
  • heart changes force of contraction
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13
Q

Inotropic agents

A
  • affects force of contraction

+ = inc contractility

Ex: epinephrine

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14
Q

Anatropic agents

A
  • = dec force of contraction

Ex: meds that the heart has to work hard , use of alcohol

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15
Q

Arteriole blood Pressure

A
  • measure of pressure exerted by blood against arterial system
  • SBP (systolic blood pressure) = ventricles contract
  • DBP (diastolic blood pressure) = ventricles relax
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16
Q

How do you calculate blood pressure?

A

SBP/DBP

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17
Q

What is normal bp?

A

120/70

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18
Q

Pulse pressure

A
  • difference between SBP and DBP
  • normal 1/3 of SBP

Ex: what is the pulse pressure of 120/80

120/1/3= 40

  • high = arteriosclerosis
  • low = heart failure
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19
Q

Mean Arteriole Pressure (MAP)

A

Average pressure in arteries throughout cardiac cycle

  • MAP = DBP + 1/3 Pulse Pressure
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20
Q

What are the main factors that influence BP?

A
  1. Cardiac output
  2. Systemic vascular resistance (SVR)
    - force opposing the movement of blood in small arteries and arterioles
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21
Q

What are the mechanisms that regulate BP?

A
  1. Nervous system
  • Baroreceptors
  • hormones
  1. Renal system
  2. Endocrine system
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22
Q
  1. Nervous system

A. Baroreceptors

B. hormones

A

A. Baroreceptors
- stim NS

  • specialized nerve ells in arch of aorta and arteries
  • sensitive to pressure and stretching
  • shut down sympathetic = enhance
  • parasympathetic = dec BP

B. hormones

  • stimulate NS
  • dec in BP = parasympathetic = inc BP
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23
Q
  1. Renal system
A
  • no Na excretion and ECF
  • renin -> angiotensinogen -> angiotensin 1 -> angiotensin 2 -> aldosterone inc
  • water and sodium tension is cause by aldosterone
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24
Q
  1. Endocrine
A
  • ADH is released

- inc ECF vol -> inc BP

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25
Q

Hypertension

  • Incidence
  • d/t
A
  • failure of a system = high BP
  • sustained elevation of arterial BP
  • SBP= > 140
  • DBP = >90
    • repeated readings when monitored = HTN
  • inc afterload d/t pressure and constriction
  • strains heart and blood vessels
    • cardiovasc problems and organ failure
  • no symptoms
  • Incidence
    • depends on ethnicity = blacks more susceptible
    • men >60
    • people with diabetes
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26
Q

What is the significance of HTN?

A
  • heart works harder

- more strain on the heart and blood vessels

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27
Q

Primary HTN

A
  • cause = unknown
  • genetic of environmental factors
  • 95% of cases
  • ages 30-50
  • diet:
    • high in sodium
    • low mag, low cal
    • smoking
    • stress
    • alcohol
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28
Q

Secondary HTN

A
  • caused by systemic disease process that inc systemic vascular resistance or cardiac output

ex: renal disease = d/t kidney failure, hormone problem, meds that inc bp
- can be treated and eliminated

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29
Q

Isolated Systolic HTN

A 
- sustained in elevation
  SBP= >160
  DBP= < 90
- diastolic pressure would be low or normal
-seen in elderly d/t weakened vessels
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30
Q

What are the pathophysiology of HTN

A
  • high pressure stim thickening and strengthening to handle stress
  • smooth muscles grow larger = lumens narrow
  • injury = imflam = inc permeability
    • which substances can enter vessel walls
    • causes more thickening, vasoconstriction, inc resistance
  • changes lining of vessels to let calcium in d/t thickening
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31
Q

What are the long term clinical manifestations?

A
  1. heart
    - failure d/t afterload
    - CAD, angina, MI
  2. brain
    - aneurysm, stroke
  3. kidneys
    - renal faulure
  4. retina
    - lack of o2 = blind
    - sclerosis
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32
Q

What are the types of treatment for HTN?

A
  • lifestyle modification
  • diet
  • exercise
  • weight reduction
  • meds if treatments above don’t work
33
Q

Aneurysm

A
  • localized dialation or outpuching of vessel wall or chamber of heart
  • caused by arteriosclerosis and HTN
  • develop in diff parts of body
  • weak blood vessles = dilation of vessel wal
  • stretch of vessel d/t pressure in diff parts of the arter
33
Q

What is the risk factor of aneurysm?

A
  • busting due to high pressure
34
Q

What are the common areas of aneurysm

A
  • cerebral artery = hemorrhage in brain
35
Q

What are the types of aneurysms?

A
  1. True

2. False

37
Q

What are false aneurysms?

A
  • not entire blood vessel, injury

- bleeding is contained

38
Q

What what true aneurysm? What are the 2 types?

A
  • all layers of artery have bulges

a. fusiform
- all around the artery that bulges out

b. saccular
- only one side is bulged

39
Q

Aneurysms in the abdominal aorta

A
  • 3/4 of aneurysms occur here
  • no symptoms
  • as it gets bigger = hard to breathe and swallow
  • poor survival rate if detected late
40
Q

Aneurysms in the cerebral

A
  • stroke
  • s/s:
  • headaches
  • vision problems
41
Q

What can be used to treat aneurysms?

A
  • meds to dec bp and vol to prevent bursting of vessels
  • surgery if spotted early enough
  • replace vessel with a graft to make a new blood vessel
42
Q

Thrombus

A
  • blood vessel attached to a vessel wall
  • inc clotting in body d/t injury or trauma
  • creates clots
43
Q

Thrombus:

1. Arteries

A
  • cause damage to lining of blood vessel = clot
  • where it is loc it affects tissue
  • causes askemia = dec blood flow
44
Q
  1. Veins
A
  • blood clot in legs or pelvic region = deep vein thrombosis
  • pooling of blood = immobile people because lack of blood flow
  • clots can break and travel through other parts of the body = bad
45
Q
  1. Heart
A
  • pooling of blood in heart d/t lack of pumping= clot because attached to valve
  • clots can break and travel to other parts of the body
46
Q

What are the treatments for thrombus?

A
  • anticoagulants to prevent clots
    • blood thinner
  • prevent new ones from developing
    ex: herparin, coumadin
47
Q

Embolism

A
  • obstruction of vessel by embolus = a clump of matter
  • parts can break off and travel through circulation
  • ex: air, fat, bacteria
48
Q

When an emboli becomes lodged in a vessel what can happen?

A
  • ischemia = dec blood supply
  • infarction = death of tissue d/t obstruction
  • life threatening:
    • coronary = heart attack
    • cerebral arteries = stroke
    • lungs = pulmonary embolism
49
Q

Atherosclerosis

A
  • abnormal thickening and hardening of arteries

ex: in femoral and coronary arteries

50
Q

What does it do to the artery walls?

A
  • deposits of cholesterol, lipids, and fibrous tissue within wall of artery
51
Q

Atherosclerosis Stages:

  1. fatty steak
A
  • lipid filled smooth muscle cell

- worsens with age

52
Q
  1. raised fibrous plaque
A
  • d/t chronic injury that activates platelets
  • release growth factor and thickening of artery wall
  • fibrous plaque develops
  • platelets accumulate= blood clot
  • narrowing/occlusion
    ex: high cholesterol, smoking, HTN
53
Q
  1. Complicated lesion
A
  • necrotic damage and fibrous tissue
  • rigid, hard
  • occlusion = slows blood flow
54
Q

What are the clinical manifestations of atherosclerosis?

A
  • ischemia (dec blood flow)- > infarction (tissue death)
  • dec oxygen ->blood flow = ischemia
  • inc bp = HTN
Coronary = MI
Cerebral = stroke
Systemic = HTN
55
Q

What are the treatments for atherosclerosis?

A
  • lifestyle changes
  • diet exercise stop smoking
  • all in order to increase ipids
56
Q

Coronary Artery Disease (CAD)

A
  • impairment of pumping heart

- main cause of death in US

57
Q

What are the risk factors for CAD?

  1. Unmodifiable
A
  1. age
    - over 65 years old
  2. gender
    - men are more susceptible
  3. family history
    - even healthy people can develop CAD
58
Q
  1. Modifiable
A
  1. elevated serum lipid levels
    - atherosclerosis, LDL (cholesterol)
  2. HTN
  3. cigarette smoking.
    - nicotine = vasoconstriction and inc bp
  4. sedentary lifestyle
    - exercise = higher HDL, lower LDL
    - dec bp
  5. obesity
    - high LDL
59
Q

Angina

A
  • transient chest pain due to myocardial ischemia
  • not enough blood flow to heart and oxgen
  • short term= 3-5 min
60
Q

Myocardial ischemia

A
  • imbalance of need of o2 and the supply of oxygen = angina
61
Q

Mayocardial ischemia:

A. decrease supply

A
  1. dec in BP
  2. dec in blood volume
  3. inc in HR
    - shorter time diastole
  4. inc in coronary vasc resist
62
Q

B. Increase need

A
  1. inc in BP
  2. inc in HR
  3. inc in ventricular volume
63
Q

Dilation of vessels with heart disease

A
  • its fully dilated and can’t dilate anymore because it is already over stretched
64
Q

What is the most common cause for mayocardial ischemia?

A
  • exercise because the lack of oxygen and needing more of with with not enough supply
65
Q

Types of Angina

  1. Stable
A
  • most common
  • chest pain intermittent
  • same pattern of onset, duration and intensity.
  • Pain relieved with med or rest
  • Can be controlled
66
Q
  1. Unstable
A
  • progressive inc in frequency, duration and intensity of symptoms.
  • Unpredictable, advanced ischemia.
  • associated w/ inc stenosis of vessels.
  • Can occur from exercise and rest
  • causes a heart attack = myocardial infarction
67
Q
  1. Prinzmetal
A
  • cyclic short bursts of pain at rest
  • Unpredictable, spasms of coronary arteries
  • not blockage, it’s a spasm
  • assoc w/ REM sleep d/t electrolyte issue
68
Q

What are the clinical manifestations of myocardial ischemia?

A
  • chest, leg, arm pain
  • similar to MInfartion attack
  • causes anxiety
  • constrictive, squeezing, heavy, choking sensation
  • severe indigestion or burning
69
Q

How to diagnose MIschemia?

A
  1. EKG (Electrocardiogram)
    - measure electrolyte production of heart
    - angina shows depressed ST segment
  2. exercise stress test
    - on a bike or treadmill to diagnosing to see ST segment
  3. nuclear imaging studies (thallium)
    - injected with radio active isotope to scan heart
  4. coronary angiogram: (x)
    - femoral artery scan
    - ingest a dye and scan to see
70
Q

What kind of treatments are used for MIschemia?

A
  • Meds = nitroglycerin
    • to reduce myocardial oxygen requirements
    • decreases BP = decrease HR
71
Q

Myocardial Infarction

A
  • heart attack
  • irreversible hypoxia and cell death because of prolonged ischemia
  • destroyed d/t lack of blood flow
  • ischemia can happen for 20 min in heart, if longer causes cell injury
72
Q

What is the patho for MInfarction?

  1. cell injury

a. anaerobic
b. electrolytes
c. catecholamine release

A
  • lack of oxygen

A. anaerobic metabolism:

  • lack of o2 to heart
  • not produce enough energy for heart
  • lactic acid builds and affects heart

B. electrolytes
- potassium controls contractility and it is effected

C. catecholamine release

  • epinephrine and norepinephrine and causes imbalance
  • irregular heart rate
73
Q
  1. Cell death
A
  • irreversible hypoxia, enzymes
  • releases enzymes into circulation when it dies
  • can be measured
74
Q
  1. Structural and func changes
A
  • depends on area and size
75
Q
  1. Repair
A
  • cell death = inflammatory response = scar tissue

- scar tissues doesn’t let the heart pump as efficiently

76
Q

What are the clinical manifestations of MInfarction?

A
  1. pain - severe and not relieved w/ nitroglycerin
    - last for more than 20 min
  2. Nausea, vomit (n/v)
  3. cool, pale clammy skin
  4. fever
    - d/t inflam response
  5. Cardiovascular (cv)
    - weakness of heart, it’s output
    - effect perfusion
77
Q

What are the complications of MInfarction?

A
  1. dysrhythmias- abnormal heart rate

2. heart failure- dec output

78
Q

What are the types of diagnostic tests for MInfarction?

A
  1. EKG
    - inc ST waves
  2. echocardiogram
    - ultrasound
  3. cardiac enzyme levels
    - released enzymes can be measured
  4. troponin
79
Q

What are the types of treatments for MIfarction?

A
  1. EKG monitoring.
  2. O2
  3. aspirin
    - prevent platelets for clumping
  4. pain relief = morphine
  5. anticoagulants
    - stop clotting
  6. meds to decrease work of heart
    - vasodilators to dec bp

Nursing 2005: Clinical Pathophysiology (9 decks)

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