Lecture 9 - Cardiovascular System 2 Flashcards

Blood flow

1
Q

What are hemodynamics

A

A collection of mechanisms that influence the dynamic circulation of blood

  • diff rates/min in diff areas
  • greater activity requires greater blood flow
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2
Q

What are the 2 control mechanisms of hemodynamics

A
  1. Maintenance of circulation

2. Vary volume and distribution of blood

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3
Q

What causes fluids to flow in circulation

A

Pressure gradients from high to low

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4
Q

How does heart circulate blood

A

By changing pressure

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5
Q

What is a local pressure gradient known as

A

Perfusion pressure

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6
Q

Characteristics of arterial BP

A
  • needs high pressure to keep blood flowing

- arterial BP is directly proportional to arterial blood volume

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7
Q

What are 2 important factors in arterial BP

A
  1. Cardiac output

2. Peripheral resistance

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8
Q

What does cardiac output influence

A

Amount of blood entering arteries

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9
Q

What does peripheral resistance influence

A

Amount of blood leaving arteries

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10
Q

Cardiac output formula

A

CO = SV x HR

CO= amount of blood that flows out of a ventrical/min
Sv = volume/ beat
Hr = beat/min
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11
Q

What is impacted by changes in SV or HR

A

CO, BP and arterial blood volume in the same direction

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12
Q

What is cardiac reserve

A

Amount that CO can increase above normal expressed as %

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13
Q

What is the typical resting cardiac output

A

5000 ml/min or 5L/min

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14
Q

What is inotropic factors

A

Factors caused by changes in myocardial contraction

Mechanical, chemical or neural (like length of myocardiac fibers at start of contraction)

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15
Q

What is Starlings law

A

Longer fibers make strong contractions up to a point (350 mL)

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16
Q

What is End Distal Volume (EDV)

A

More blood returned, more stretched fibers, stronger contractions
-too much blood will result in lowered elasticity

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17
Q

What does Norepinephrine do

A

Increases contractility of the heart

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18
Q

Where does Norepinephrine come from

A

Sympathetic nerve fibers or adrenal glands

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19
Q

What is ejection fraction

A

Ratio of SV to EDV

(SV/EDV x 100%),-55%

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20
Q

What is afterload

A

Work necessary to pump blood into arteries

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21
Q

What is mean pressure

A

Usually about (2 x diastolic + systolic) ÷3

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22
Q

What is result in increase of CO or PR

A

Increase in blood volume and thus increase in arterial BP

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23
Q

What typically controls chronotropic factors

A

Sinoatrial node

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24
Q

What affects stroke volume

A

Inotropic factors
Ejection fraction
Afterload

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25
Q

What affects CO through what heart rate factors

A
Chronotropic factors ( timing)
Other reflexes
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26
Q

What typically controls chronotropic factors

A

Sinoatrial node (SA node)

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27
Q

What innervates SA node to correct beat

A

Sympathetic (Nor) nerves

Vagus (ACh) nerves

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28
Q

How do nerves send impulses to SA node to change timing

A

Cardiac Pressoreflexes

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29
Q

How does cardio pressoreflexes work

A

Send info to cardiac control centers in medulla
- starts a negative feedback loop that responds to increased pressure from barorecptors in:
Carotid sinus reflex
Or Aortic reflex

  • receptors in SA node get message to increase CO or decrease
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30
Q

What are other reflexes that affect heart rate

A
Emotions
Exercise 
Hormones 
Blood temp
Pain
Acceleration typically from epinephrine 
Nerves : sympathetic causes increase, parasympathetic causes decrease
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31
Q

Where are baroreceptors located

A

Common carotid

Aorta

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32
Q

What would be variable, sensor, integrator, effector of CO feedback loop

A
Variable = BP
Sensor = baroreceptors 
Integrator= cardioregulatory centers in medulla oblongata 
Effector= SA node
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33
Q

What is peripheral resistance

A

Resistance to flow from friction between blood and walls of vessels
- how hard the blood is pushing against walls of vessel

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34
Q

Where does peripheral resistance develop from

A
The viscosity (thickness) of blood and small diameter of arterioles and capillaries.
- creates a "back up in blood traffic" which helps maintain pressure
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35
Q

What can too much peripheral resistance “back up in blood traffic” cause

A

In extreme

Chronic hypertension or high BP, and plaque build up.

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36
Q

What causes blood viscocity to increase

A

Mainly proportion RBC (hematocrit level)
Also
-proteins and other dissolved molecules

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37
Q

What is vasomotor mechanism

A

A way to decrease blood viscosity -> decrease peripheral resistance

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38
Q

How does vasomotor mechanism work

A

Contraction or dilation of arterioles to change resistance to flow
- vasoconstriction/ vasodilation
This will change arterial runoff and total peripheral resistance

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39
Q

Why do small changes to vessel size have large impact on blood flow

A

Because blood is quartic

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40
Q

Where is vasomotor motor control mechanisms controlled from

A

Medulla (vasomotor / vasoconstrictor center)

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41
Q

What happens when vasomotor center is activated

A

Causes constriction of blood reservoirs

- this venoconstriction increases amount of blood moving

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42
Q

Where are main reservoirs that vasomotor center constricts

A

Skin and abdominal organs (venous plexuses and sinuses)

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43
Q

How does vasomotor pressoreflexes from BP work

A
  • same system as cardiac pressoreflexes
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44
Q

What happens with vasomotor pressoreflexes when sudden BP increase

A
  • sudden increase in arteriole BP stimulates aortic and carotid baroreceptors which results in arterioles and venules of blood reservoir dilating
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45
Q

What happens with vasomotor pressoreflexes when BP decreases

A

Decrease in arterial BP results in stimulation of vasoconstrictor centers, causing vascular smooth muscle to constrict

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46
Q

What do chemoreceptors do

A

Detect changes in chemical composition

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47
Q

What do baroreceptors do

A

Detect stretch

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48
Q

What do chemoreceptors in aorta and carotid detect that affect vasomotor control mechanisms

A

Hypercapnia -> excessive CO2

Hypoxia -> diminished O2 (less sensitive)

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49
Q

How does chemoreceptor reflex work

A

Sends signal to vasomotor center which causes constriction of arterioles

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50
Q

What is medulla ischemic reflex

A

If flow to medulla low (ischemic)
The chemoreceptors in medulla signal vasomotor center to greatly restrict arterioles and venous centers so more blood flows to medulla

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51
Q

What else can influence medullary signaling

A

Hypothalamus and cortex if emotions like fear or anger are high

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52
Q

Can local tissue affect vasodilation

A

Yes in things like active hyperemia (increased movement/excercise)

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53
Q

What are 3 major things that influence amount of blood returned to heart by veins

A

Reservoirs
Gravity
Total blood volume

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54
Q

What is the stress- relaxation effect

A

Due to elasticity of venous walls
Low pressure shrink reservoirs and high pressure expands reservoirs
Which helps to maintain blood flow

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55
Q

What is gravity effect of venous blood

A

Pulls blood to legs when upright as walls are too elastic to resist
- has no effect if lying down

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56
Q

What is Orthostatic effect

A

When you stand from lying down blood all tries to go down to feet worse in elderly can cause syncope

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57
Q

What overcomes Orthostatic effect

A

Use of venous pumps, back up valves, and movement that keep pressure gradient

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58
Q

What facilitates venous pumps

A

Respirations and skeletal muscles

They increase pressure gradient between peripheral and central veins

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59
Q

How does respiration facilitate venous pump

A
  • contraction of diaphragm on inspiration increases thoracic cavity volume, decreases pressure of vena cava , atria
  • diaphragm pumps blood up as inspire and expire (deeper respirations intensify effects)
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60
Q

How do skeletal muscles help venous pumps

A

Muscle contractions serve as booster pumps by squeezing blood up
- one way valves prevent backflow as muscle contraction moves it up with each contraction

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61
Q

Where is retention of water mainly done

A

Kidneys

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62
Q

What is total blood volume affect on vous pumps

A

Greater total volume -> more blood returned (pressure gradient)

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63
Q

How is movement of blood accomplished with increased total blood volume

A

By movement of water through retention

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64
Q

What happens if kidneys retaining too much water

A

Could cause high BP as too much blood constantly returning to heart

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65
Q

How is total blood volume affected by capillary exchange

A

Movement of fluid between plasma (blood) and interstitial fluid (fluid between cells in system)

66
Q

Starling’s law re: capillary exchange affected total blood volume

A
  • osmosis promotes fluid flow into plasma due to large colloids that cannot migrate through capillaries; small in arterioles, reverse in venules
  • hydrostatic pressure gradient, fluid leaves high pressure in arterioles to low pressure in tissue, large in arterioles, less in venules
  • 90 % water retained 10% returned to lymph
67
Q

What is hydrostatic pressure

A

Pressure generated when a force is applied to water (pushing force)

68
Q

What is osmotic pressure

A

Pressure due to gradient generated across a semi-permeable membrane (pulling force)

69
Q

What are 4 ways to control total blood volume

A

ADH Mechanism
Renin-Angiotensin-Aldosterone (RAAS) system
ANH Mechanism
Balance of Regulation

70
Q

What is ADH mechanism

A

Anti diuretic hormone released by pituitary gland to reduce amount of water lost in kidneys
- by increasing absorption of water from urine thus increasing blood volume

71
Q

What is renin-angiotension-aldosterone (RAAS) system

A

Renin released when kidney detects BP low

  • promotes release of aldosterone from adrenal glands
  • aldosterone promotes sodium retention
  • promotes water retention by osmosis if ADH active
  • angiotensin ll promotes vasoconstriction sending blood back up
72
Q

What does angiotensin converting enzyme (ACE) do

A

Limits angiotensin ll and can combat high BP (hypertension)

73
Q

What is ACE inhibitor

A

Usually med to control high BP / hypertension

74
Q

What is ANH Mechanism

A

Atrial natriuretic hormone secreted by pericytes in atria in response to overstretching

  • if atria chronically overstretched by high venous return to heart will release this hormone
  • ANH reduces water in plasma by increasing sodium loss in kidneys and water loss by osmosis
75
Q

What is balance of regulation

A

ANH opposes ADH and RAAS

- multiple systems increase precision of volume regulation

76
Q

How does sphygmomanometer work

A

Approximates air pressure equal to BP
- cuff wrapped around arm over brachial artery
- air added until exceeds BP
- pressure reduced until it approximates BP
- vessel will open, blood will spurt through making tapping sound that gets louder then muffled then dissapeared
- tapping sound approximates systolic BP
- lowest pressure where sounds are heard is diastolic BP
(Sounds called korotkoff sounds heard between 120 and 80mmHg -> first sounds when you start to open artery until fully open)

77
Q

Other ways to measure BP

A

Directly with catheter or connecting a cannula to a nanometer

78
Q

Ideal BP

A

120/80

79
Q

What is systolic BP

A

Force of L ventricle contraction

80
Q

What is diastolic BP

A

Resistance of blood vessel

81
Q

What is difference between SBP &DBP

A

Pulse pressure

82
Q

What is normal ranges of MAP

A

70 to 110 mmHg at rest

83
Q

What is enough MAP to supply brain, kidneys, other vitals

A

6 mmHg

84
Q

Pressure of veins is practically uniform because

A

Blood enters them at a steady pressure from arterioles elastic movement

85
Q

How does blood leave vessels

A

Spurts from arteries

Drains from veins

86
Q

Hypotensive range

A

<90 SBP <60DBP

87
Q

Desirable range BP

A

90 -119 SBP

60-79 DBP

88
Q

Prehypertension range

A

120 - 139 SBP

80-89 DBP

89
Q

Stage 1 hypertension

A

140-159 SBP

90-99 DBP

90
Q

What is minute volume of blood

A

Volume of blood circulating through body per minute

91
Q

What determines minute volume of blood

A

Magnitude of BP gradient and peripheral resistance

92
Q

What is poisuilles law minute volume equasion

A

Minute volume = pressure gradient / resistance
Or
Minute volume = (MAP - central venous pressure) / resistance

93
Q

Breakdown of poisuilles law

A

Increase in peripheral resistance mathematically reduces minute volume but biologically reduces arterial runoff -> increases blood in arteries-> increases arterial pressure

94
Q

When is blood velocity greatest

A

When pressure is greatest

95
Q

What reduces conduction velocity

A

Larger surface area makes effects more diffuse. Less conduction volume because it is split amongst larger surface

96
Q

What is the pulse

A

Alternate expansion and recoil of elastic artery

97
Q

What 2 factors are responsible for a pulse that can be felt

A
  1. Intermittent interjections of blood into the aorta from the heart, leading to alternating increase and decrease in pressure in that vessel
  2. Elasticity of artery walls, allowing the vessel to expand and contract with alterations in BP
98
Q

What would cause you to not fee pulse

A

Constant pressure or rigid material

99
Q

What starts a new pulse wave

A

Each ventricular systole (as it moves through arteries it dissipates until it disappears in capillaries)

100
Q

What produces dicrotic notch in pulse wave

A

Produced by closure of aortic valve and noticeable in carotid but not radial

101
Q

What is noticeable about pulse the further distance from heart

A

More delay

102
Q

How does pulse wave conserve energy

A

By shifting energy from contractions into elastic arterial walls

103
Q

What are 9 pulse locations

A
Radial
Temporal
Common carotid
Facial
Brachial
Femoral
Popliteal
Posterior tibeal 
Dorsalis pedis
104
Q

Where is radial pulse

A

Wrist

105
Q

Where is temporal pulse

A

In front of ear, above outer edge of eye

106
Q

Where is common carotid pulse

A

Along anterior edge of sternocleidomastoid and lower margin of thyroid cartilage

107
Q

Where is facial pulse felt

A

Lower margin of lower jawbone, in line with mouth

108
Q

Where is brachial pulse felt

A

In the bend of elbow along inner margin of biceps

109
Q

Where is femoral pulse felt

A

In groin where it passes over the pelvic bone

110
Q

Where is popliteal pulse felt

A

Behing knee

111
Q

Where is posterior tibeal pulse felt

A

Behind medical malleosus (inner ankle)

112
Q

Where is dorsalis pedis felt

A

Dorsum of foot

113
Q

What are 6 pressure points for bleeding

A
  1. Temporal
  2. Facial
  3. Common carotid (same as pulse with pressure on spinal column)
  4. Subclavian (behind medial 3rd of clavicle, pressing against first rib)
  5. Brachial (few inches above elbow, pressing against humerus)
  6. Femoral (same as pulse)
114
Q

What is key note about apply pressure to pressure points

A

Pressure must be applied at the pressure point above the lesion between the heart

115
Q

What is anemia

A

RBC disorder

Not enough Hgb to carry enough O2 for the production of ATP

116
Q

What causes anemia

A

Bleeding
Destructive mechanism for RBC
Incapacity of the red bone marrow

117
Q

What is polycythemia

A

Excess RBCs which cause increased viscosity of blood and decreased circulation

118
Q

What is aplastic anemia

A

Abnormally low RBCs from destruction of red bone marrow

119
Q

What is pernicious anemia

A

Low RBCs from vitamin B12 deficiency due to lack of intrinsic factor

120
Q

What is folate deficiency anemia

A

Usually from vitamin B9 deficiency, common in alcoholism

121
Q

What can cause changes in hemoglobin

A

Hyperchromic or hypochromic

  • inadequate iron in diet leads to iron deficiency anemia
  • pregnancy, wound healing, nutritional deficiency
122
Q

What is hemolytic anemia

A

Various inherited conditions

Like sickle anemia, thalassemia

123
Q

What are some WBC disorders

A

Multiple myeloma
Leukemia
Infectious mononucleosis (mono

124
Q

What is multiple myeloma

A

Cancer of b Lymphocytes, creates defective antibodies

125
Q

What is leukemia

A

Cancer of WBCs, marked leukocytes
Cell counts in excess of 100000/mm3
Acute vs chronic, lymphocytic vs myeloid

126
Q

What is infectious mononucleosis

A

Caused by a virus found in saliva

Atypical WBCs with large body and nucleus

127
Q

What are clotting disorders

A

1 Thrombosis
- formation of clot in unbroken blood vessel
- dislodged clot is embolus or embolism
2 Hemophilia
- failure to produce proteins for clot formation
- x-linked inherited disorder

128
Q

Heart valve disorders

A

Rheumatic heart disease
Mitral valve prolapse
Aortic regurgitation

129
Q

What is rheumatic heart disease

A

Inflammation of cardiac valves and other tissues (rheumatic fever) stemming from delayed inflammatory response to streptococcal infection

130
Q

What is mitral valve prolapse

A

Flaps extend back into atrium causing leak

131
Q

What is aortic regurgitation

A

Blood returns to left ventricle after ejection, increasing load on LV leading to myocardial ischemia

132
Q

Myocardium disorders

A

Coronary artery disease
Myocardial infarction
Angina pectoris
Cardiomyopathy

133
Q

What is coronary artery disease

A

Reduced blood flow to coronary arteries from atherosclerosis

134
Q

What is myocardial infarction

A

Death of myocytes (muscles cells)

Basically heart attack

135
Q

What is angina pectoris

A

Pain caused by decrease for a moment or irrigation of myocardium
- temporary lack of O2 which weakens myocardial cells
(Often precursor to myocardial infarction)

136
Q

What is cardiomyopathy

A

Abnormal enlargement of the heart

137
Q

What is dysrhythmia

A

Abnormal heart rhythm

138
Q

What is heart block

A

Interference stops SA node signals from reaching AV node

139
Q

Whay is bradycardia

A

Slow heart rhythm below 60 Bpm

140
Q

What is tachycardia

A

Rapid Heart rhythm above 100Bpm

141
Q

What is sinus dysrhythmia

A

Variation in heart rate during breathing cycle

142
Q

What is premature contractions

A

Contractions that occur before next set of expected contractions, can be atrial or ventricular, can lead to fibrillation

143
Q

What is atrial fibrillation

A

Common with mitral stenosis

144
Q

What is ventricular fibrillation

A

Immediately life threatening due to blood not reaching vital tissues

145
Q

What is heart failure

A

Inability to pump blood to sustain life

- a combination of previous disorders

146
Q

What is CHF

A

Left sided heart failure

147
Q

What is Cor pulmonade

A

Right sided heart failure

148
Q

What is arteriosclerosis

A

Thickening of walls due to calcium deposits

149
Q

What is aneurysm

A

Abnormally widened section of artery

- can form thrombus, embolus or burst- hemorrhage

150
Q

What is ischemia

A

Decreased blood supply to tissue, leads to necrosis

- necrotic tissue with bacterial action - gangrene

151
Q

What is varicose veins

A

Enlarged veins where blood pools

152
Q

What are Hemorrhoids

A

Varicose veins in anal canal

153
Q

What is phlebitis

A

Vein inflammation

154
Q

What is thrombophlebitis

A

Due to clot

155
Q

What is DVT

A

Clot in deep vein

156
Q

What is circulatory shock

A

Failure to deliver O2 to tissue, ultimately caused by reduced blood flow

157
Q

What is carcinogenic shock

A

Any type of heart failure

158
Q

What is hypovolemia shock

A

Loss of blood volume ex. Hemorrhage

159
Q

What is neurogenic shock

A

Widespread dilation of blood vessels from imbalance in ANS

  • sometimes called vasodilatory shock
  • damage to medulla, depressive drugs, stress
160
Q

What is anaphylactic shock

A

Acute allergic reaction , anaphylaxis

161
Q

What is septic shock

A

Complications of septicemia, where infectious agents release toxins into blood