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
2
Q
Stroke volume
A
.- amount of blood pumped out during systole
- 70 cc average
3
Q
Ejection fraction
A
- ejects 66% of blood
- Estimated by echocardiography
- stroke vol/end- diastolic vol
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
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
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
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
8
Q
What are the factors affecting cardiac output?
A
- Preload
- After load
- Heart rate
- Contractility
9
Q
- 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
10
Q
- 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
11
Q
- 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
12
Q
- Contractility
A
- heart changes force of contraction
13
Q
Inotropic agents
A
- affects force of contraction
+ = inc contractility
Ex: epinephrine
14
Q
Anatropic agents
A
- = dec force of contraction
Ex: meds that the heart has to work hard , use of alcohol
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
16
Q
How do you calculate blood pressure?
A
SBP/DBP
17
Q
What is normal bp?
A
120/70
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
19
Q
Mean Arteriole Pressure (MAP)
A
Average pressure in arteries throughout cardiac cycle
- MAP = DBP + 1/3 Pulse Pressure
20
Q
What are the main factors that influence BP?
A
- Cardiac output
- Systemic vascular resistance (SVR)
- force opposing the movement of blood in small arteries and arterioles
21
Q
What are the mechanisms that regulate BP?
A
- Nervous system
- Baroreceptors
- hormones
- Renal system
- Endocrine system
22
Q
- 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
23
Q
- Renal system
A
- no Na excretion and ECF
- renin -> angiotensinogen -> angiotensin 1 -> angiotensin 2 -> aldosterone inc
- water and sodium tension is cause by aldosterone
24
Q
- Endocrine
A
- ADH is released
- inc ECF vol -> inc BP
25
Hypertension
- Incidence
- d/t
- 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
26
What is the significance of HTN?
- heart works harder
| - more strain on the heart and blood vessels
27
Primary HTN
- cause = unknown
- genetic of environmental factors
- 95% of cases
- ages 30-50
- diet:
- high in sodium
- low mag, low cal
- smoking
- stress
- alcohol
28
Secondary HTN
- 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
29
Isolated Systolic HTN
```
- sustained in elevation
SBP= >160
DBP= < 90
- diastolic pressure would be low or normal
-seen in elderly d/t weakened vessels
```
30
What are the pathophysiology of HTN
- 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
31
What are the long term clinical manifestations?
1. heart
- failure d/t afterload
- CAD, angina, MI
2. brain
- aneurysm, stroke
3. kidneys
- renal faulure
4. retina
- lack of o2 = blind
- sclerosis
32
What are the types of treatment for HTN?
- lifestyle modification
- diet
- exercise
- weight reduction
- meds if treatments above don't work
33
Aneurysm
- 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
What is the risk factor of aneurysm?
- busting due to high pressure
34
What are the common areas of aneurysm
- cerebral artery = hemorrhage in brain
35
What are the types of aneurysms?
1. True
| 2. False
37
What are false aneurysms?
- not entire blood vessel, injury
| - bleeding is contained
38
What what true aneurysm? What are the 2 types?
- all layers of artery have bulges
a. fusiform
- all around the artery that bulges out
b. saccular
- only one side is bulged
39
Aneurysms in the abdominal aorta
- 3/4 of aneurysms occur here
- no symptoms
- as it gets bigger = hard to breathe and swallow
- poor survival rate if detected late
40
Aneurysms in the cerebral
- stroke
- s/s:
- headaches
- vision problems
41
What can be used to treat aneurysms?
- 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
Thrombus
- blood vessel attached to a vessel wall
- inc clotting in body d/t injury or trauma
- creates clots
43
Thrombus:
| 1. Arteries
- cause damage to lining of blood vessel = clot
- where it is loc it affects tissue
- causes askemia = dec blood flow
44
2. Veins
- 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
3. Heart
- 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
What are the treatments for thrombus?
- anticoagulants to prevent clots
- blood thinner
- prevent new ones from developing
ex: herparin, coumadin
47
Embolism
- obstruction of vessel by embolus = a clump of matter
- parts can break off and travel through circulation
- ex: air, fat, bacteria
48
When an emboli becomes lodged in a vessel what can happen?
- ischemia = dec blood supply
- infarction = death of tissue d/t obstruction
- life threatening:
- coronary = heart attack
- cerebral arteries = stroke
- lungs = pulmonary embolism
49
Atherosclerosis
- abnormal thickening and hardening of arteries
| ex: in femoral and coronary arteries
50
What does it do to the artery walls?
- deposits of cholesterol, lipids, and fibrous tissue within wall of artery
51
Atherosclerosis Stages:
1. fatty steak
- lipid filled smooth muscle cell
| - worsens with age
52
2. raised fibrous plaque
- 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
3. Complicated lesion
- necrotic damage and fibrous tissue
- rigid, hard
- occlusion = slows blood flow
54
What are the clinical manifestations of atherosclerosis?
- ischemia (dec blood flow)- > infarction (tissue death)
- dec oxygen ->blood flow = ischemia
- inc bp = HTN
```
Coronary = MI
Cerebral = stroke
Systemic = HTN
```
55
What are the treatments for atherosclerosis?
- lifestyle changes
- diet exercise stop smoking
* all in order to increase ipids
56
Coronary Artery Disease (CAD)
- impairment of pumping heart
| - main cause of death in US
57
What are the risk factors for CAD?
1. Unmodifiable
1. age
- over 65 years old
2. gender
- men are more susceptible
3. family history
- even healthy people can develop CAD
58
2. Modifiable
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
Angina
- transient chest pain due to myocardial ischemia
- not enough blood flow to heart and oxgen
- short term= 3-5 min
60
Myocardial ischemia
- imbalance of need of o2 and the supply of oxygen = angina
61
Mayocardial ischemia:
A. decrease supply
1. dec in BP
2. dec in blood volume
3. inc in HR
- shorter time diastole
4. inc in coronary vasc resist
62
B. Increase need
1. inc in BP
2. inc in HR
3. inc in ventricular volume
63
Dilation of vessels with heart disease
- its fully dilated and can't dilate anymore because it is already over stretched
64
What is the most common cause for mayocardial ischemia?
- exercise because the lack of oxygen and needing more of with with not enough supply
65
Types of Angina
1. Stable
- most common
- chest pain intermittent
- same pattern of onset, duration and intensity.
- Pain relieved with med or rest
- Can be controlled
66
2. Unstable
- 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
3. Prinzmetal
- 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
What are the clinical manifestations of myocardial ischemia?
- chest, leg, arm pain
- similar to MInfartion attack
- causes anxiety
- constrictive, squeezing, heavy, choking sensation
- severe indigestion or burning
69
How to diagnose MIschemia?
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
What kind of treatments are used for MIschemia?
- Meds = nitroglycerin
- to reduce myocardial oxygen requirements
- decreases BP = decrease HR
71
Myocardial Infarction
- 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
What is the patho for MInfarction?
1. cell injury
a. anaerobic
b. electrolytes
c. catecholamine release
- 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
2. Cell death
- irreversible hypoxia, enzymes
- releases enzymes into circulation when it dies
- can be measured
74
3. Structural and func changes
- depends on area and size
75
4. Repair
- cell death = inflammatory response = scar tissue
| - scar tissues doesn't let the heart pump as efficiently
76
What are the clinical manifestations of MInfarction?
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
What are the complications of MInfarction?
1. dysrhythmias- abnormal heart rate
| 2. heart failure- dec output
78
What are the types of diagnostic tests for MInfarction?
1. EKG
- inc ST waves
2. echocardiogram
- ultrasound
3. cardiac enzyme levels
- released enzymes can be measured
4. troponin
79
What are the types of treatments for MIfarction?
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
