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CVP > Unit 3 > Flashcards

Unit 3 Flashcards

1
Q

Cardiac output is determined mainly by

A

Venous return

CO= VR (Also CO = SV X HR)

SV = stoke volume
HR = heart rate
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2
Q

Factors that influence VR

A

Body metabolism (local flow and autoregulation) - VR is a summation of all local blood flows

Age

Body size

Gender (heart size)

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3
Q

Factors affecting heart rate

A

Autonomic innervation
Hormones
Fitness levels
Age

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4
Q

Factors affecting stroke volume

A 
Heart size
Fitness levels
Gender
Contractility
Duration of contraction
Preload (EVD)
Afterload (resistance)
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5
Q

Stroke volume =

A

SV = EVD - ESV

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6
Q

Cardiac index increases from age ___-___

It decreases after age

A

0 - 10ish

10ish

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7
Q

CO will match VR via the following mechanisms:

A 
Frank sterling’s mechanism (effects force of contraction)
Bainbridge Reflex (effects rate of contraction)
SA node stretch (effects rate of contraction)
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8
Q

Normal CO limit (at rest)

A

5 L/min

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9
Q

Maximum CO it can achieve

A

13 L/min

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10
Q

Cardiac output curve demonstrates:

A

The effectiveness of cardiac function at different levels of right atrial pressure (which reflects venous return)

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11
Q

Hyper-effective heart causes (More than normal amount of CO)

A

Sympathetic stimulation

Hypertrophy

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12
Q

Hypo-effective heart causes (less than normal amount of CO)

A

Hypertension
Sympathetic inhibition
Any heart pathology

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13
Q

Factors that decrease peripheral resistance

These can cause:

A

Beriberi (Thiamin deficiency)
Arteriorvenous fistula
Hyperthyroidism
Anemia

Cause pathologically HIGH cardiac output

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14
Q

Abnormal connection between an artery and vein

A

Arteriovenous fistula

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15
Q

Inability to hold O2 in the blood

A

Anemia

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16
Q

Too much fluid in the cardiac sac

A

Cardiac tamponade

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17
Q

Cardiac factors that can cause pathologically low CO

A

Myocardial infarction
Severe valve disease
Myocarditis
Cardiac tamponade

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18
Q

Peripheral factors cause it pathologically low CO

A

Decreased blood volume (hypovolemia)
Acute venous dilation (SNS suppression)
Large vein obstruction
Decreased metabolic rate of tissues (hypothyroidism)

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19
Q

When cardiac output falls too low, it is called:

A

Circulatory shock

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20
Q

Venous return curve plateau is due to

A

Low atrial pressures leading to vein collapse

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21
Q

The higher the right atrial pressure, the _____ venous return will be

A

Less

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22
Q

Venous return curve- mean systemic filling pressure

A

The venous return becomes 0 when the right atrial pressure rises to mean systemic filling pressure

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23
Q

If first atrial pressure is in the negatives, what happens to venous return

A

Increases until it gets to plateau

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24
Q

What happens to CO when sympathetic stimulation increases

A

It increases as right atrial pressure increases

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25
Q

What happens to CO and VR curves during exercise? What happens to right atrial pressure?

A

Increase

Does not really change—- should never really change!!!!

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26
Q

If resistance increases, what happens to VR?

A

It decreases

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27
Q

What happens to VR if systemic filling pressure (Psf) increases?

A

It increases

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28
Q

Normal systemic filling pressure

A

7

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29
Q

2 ways to increase delivery (X) of a substance

Fick’s Principle

A

1- increase it’s concentration [x]

2- increase flow into a tissue (Q)

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30
Q

Equation of Fick’s principle

A

X = Q [x]

X = delivery

Q = flow into a tissue

[x] = concentration

Just know what calculation is for, don’t worry about the math

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31
Q

What does Fick’s principle calculate?

A

Cardiac output by solving for Q

Q = X/[x]

[x] can be measured by [x]art - [x]vein

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32
Q

How can you apply Fick’s principle?

A

By measuring oxygen uptake from the lungs, and blood gas measurements

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33
Q

If a tissue is metabolically active, it will have an increase demand for”

A

Oxygen

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34
Q

Most important determinant for how much blood flow is needed in a spot

A

Local-autoregulation

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35
Q

To maintain blood pressure when tissues require a lot of blood, ________ system steps in to help. Why?

A

Nervous

To increase heart rate via sympathetic NS (norepinephrine)

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36
Q

Sympathetic (norepinephrine) uses ______ receptors.

Which so adrenal (epinephrine) use?

A

Alpha

Beta

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37
Q

Mass sympathetic discharge increases:

A

HR and cardiac contractility

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38
Q

In mass sympathetic discharge, what happens to arterioles

A

They are contracted all over the body except muscles that are working, coronary blood vessels, and cerebral blood vessels

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39
Q

During mass sympathetic discharge, what happens to capacitance vessels and reservoirs?

A

They contract to increase mean systemic filling pressure

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40
Q

a result of mass sympathetic discharge

A

Increase in arterial pressure

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41
Q

What can cause increase in anterior pressure? (AKA BP)

Which causes higher BP?

A

Stress
Whole body exercises.

Stress— there is little muscle activity so there is no vasaodilation, so higher BP

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42
Q

Increase arterial pressure increases:

A

Blood flow directly and indirectly (stress-relaxation of arteries decreases peripheral resistance.)

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43
Q

Average blood flow at rest

A

3-4 ml/min/100g of muscle tissue

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44
Q

When skeletal muscle contracts, what happens?

A

Muscles shorten and widen. They squish the blood vessels.

This causes the blood flow go down

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45
Q

Average blood flow during exercise

A

50-80 ml/min/100g of muscle tissue

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46
Q

Left coronary artery and branches supply

A

The anterior and left lateral portions of the left ventricle

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47
Q

Right coronary artery and branches supplies

A

Most of the right ventricle and posterior part of the left ventricle

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48
Q

During systole, coronary blood flow (INCREASES/DECREASES)

What about diastole?

A

Systole decreases

Diastole increases

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49
Q

Blood vessels on outside of the heart.

A

Epicardial coronary arteries

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50
Q

Cardiac arteries within the heart that cannot be seen on the outside

A

Subendocardial arteries

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51
Q

What arteries in the heart are affected more by the “squish” effect? Impacted more by pressure

A

Subendocardial arteries

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52
Q

Local autoregulation of coronary blood flow is determined by

A

Local muscle cells’ metabolism; most likely by adenosine secretion in presence of low O2

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53
Q

Some epicardial arteries contain ______ receptors. Why?

A

Alpha 1 vasoconstrictor receptors

Thought to help prevent backflow during heavy exercise in the epicardial arteries

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54
Q

Coronary mostly contain _________ receptors

A

Beta2 adrenergic receptors, so general tendency is vasodilation

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55
Q

Parasympathetic coronary innervation

A

Very little direct innervation.

Though since Ach slows heart rate, autoregulation leads to decreased blood flow

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56
Q

Structure of the blood brain barrier

A

Continuous capillaries- endothelial cells with tight junctions and lack fenestrae - low amount of vesicular transport

Astrocyte foot processes

Pericytes

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57
Q

Function of the blood brain barrier

A

Low permeability to most water soluble substances

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58
Q

Blood brain barrier needs special carrier systems to transport:

A

Glucose, amino acids, etc

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59
Q

% of the hearts energy is derived from fatty acids at rest

A

70

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60
Q

When must the heart rely more on glucose/glycolysis? What can this cause?

A

Under anaerobic or ischemic conditions.

Results in lactic acid which can cause pain

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61
Q

How is adenosine made? What happens with this in the cardiac cell?

A

ATP degrades to ADP -> AMP -> Adenosine

Diffuses out of the cardiac muscle cell and is a potent vasodilator

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62
Q

Excessive loss of adenosine can lead to:

A

Cardiac muscle death

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63
Q

About 1/2 of the heart’s adenosine can be lost in”

A

30 min of ischemia

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64
Q

A slow process of plaque formation

A

Artherosclerosis

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65
Q

In artherosclerosis, what happens to cholesterol

A

Large quantities become deposited beneath the endothelium, scar tissue forms (fibrosis), then calcifies (plaque)

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66
Q

Partial or total blockage of coronary arteries leads to:

A

Ischemia

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67
Q

A sudden process with Thrombus and/or embolus

A

Acute coronary occlusion

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68
Q

A penetrating artherosclerotic plaque that can cause a blood clot to form which quickly occluded an artery

A

Thrombus

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69
Q

A thrombus that has broken loose from the site of origin and flows to another site where it lodges

A

Embolus

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70
Q

Congestive heart failure

A

Failure of the heart to pump enough blood to satisfy the needs of the body

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71
Q

Heart failure is characterized by:

A

A reduced cardiac output and damming up of the venous circulation

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72
Q

Heart failure is due to:

A

Either systolic OR diastolic dysfunction

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73
Q

Progressive loss of contractile function of the heart muscle.

A

Systolic dysfunction

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74
Q

Inability of heart to expand enough to fill the ventricles properly

A

Diastolic dysfunction

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75
Q

Which congestive heart failure is more common

A

Systolic dysfunction

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76
Q

Heart failure care also be classified as:

A

Left sided or right sided

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77
Q

Causes of left heart failure:

These cause:

A

Ischemic heart disease
Hypertension
Valve diseases
Myocardial diseases

This cause the left ventricle to hypertrophy and/or dilate

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78
Q

Left sided CHF leads to:

A

Pulmonary congestion and edema

Decreased renal perfusion leading to water and salt retention

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79
Q

Symptoms of CHF

A

Dyspnea (feeling of not getting enough air)
Orthopnea (Breathing effected differently depending on different positions)
Cough

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80
Q

Causes of right sided heart failure

A

Left sided heart failure

Cor pulmonale (heart problem secondary to a lung problem. So lungs started this, like cystic fibrosis)

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81
Q

Pure right sided heart failure leads to

A

Systemic and portal vein congestion

Hepatomegaly and spenomegaly

Peripheral edema

Kidney congestion leading to water and salt retention

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82
Q

What happens to a patient in severe CHF

A

The pt will manifest with both right and left heart failure symptoms

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83
Q

Acutely damaged heart, CO output at 4mmHg right atrial pressure

A

2ish l/min

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84
Q

If the heart is not too damaged from CHF, whaat happens to the excess fluid retention

A

It actually helps cardiac output by increasing venous return. (Compensated heart failure)

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85
Q

What happens w/ excess fluid in a heart severely damaged by CHF

A

Retention can overwhelm the heart and lead to severe edema and death (decompensated heart failure)

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86
Q

Aspects of compensated heart failure

A

CO will be normal
Right atrial pressure is ELEVATED
NO further renal salt and water retention occurs
Heart MAY recover over weeks and months

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87
Q

Aspects of decompensated heart failure

A

Excessive fluid retention
Overstretching of the heart (weakens it further)
Pulmonary edema (w/ decreased oxygenation)
Renal failure

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88
Q

Right atrial pressure at critical cardiac output level for normal fluid balance

This indicates decompensated heart disease.

A

5-11 mm Hg

Caused by fluid retention raising the rt atrial pressure over a period of days

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89
Q

The kidney needs a min CO of ______ L/min for normal fluid balance

A

5

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90
Q

Renal contribution to progressive decompensated heart failure:

Decreased _____ _____

Activation of:

A

Decreased glomerular filtration

Activation of renin angiotensin-aldosterone system

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91
Q

What hormone may slow the progression of heart failure

A

Atrial natriuretic hormone

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92
Q

Max percentage that the CO can increase above the normal level

A

Cardiac reserve

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93
Q

Cardiac reserve for normal adult

A

300-400%

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94
Q

Cardiac reserve for athlete

A

500-600%

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95
Q

Cardiac reserve for moderate coronary artery disease

A

150-200%

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96
Q

Cardiac reserve for compensated heart failure

A

As little as 0%

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97
Q

Cardiac reserve for decompensated heart failure

A

Less than 0%

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98
Q

1st heart sound (__)
Closure
Duration
Pitch

A 
S1
Closure of AV valves
Duration of .14 seconds
Lower pitch 
“Lub”
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99
Q

2nd heart sound (__)
Closure
Duration
Pitch

A

S2
Closure of semilunar valves
.11 seconds
Higher pitch

“Dub”

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100
Q

3rd heart sounds
Happens during:
Caused by:
Frequency

A 
During middle third of diastole
Caused by inrushing of blood into ventricles
Low frequency (may be audible)
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101
Q

4th heart sound
During:
Caused by:
frequency:

A

During atrial systole
Caused by inrushing of blood
Very low frequency—- very unlikely to hear without any machines

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102
Q

Range of sounds that can be heard is between:

This is in relation to:

A

40-520 cycles/second

Threshold of audibility

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103
Q

Where is auscultation of aortic area checked?

A

2nd rt intercostal space

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104
Q

Where is auscultation of pulmonic area checked?

A

2nd left intercostal space

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105
Q

Where is auscultation of Erb’s point checked?

A

3rd left intercostal space

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106
Q

Where is auscultation of tricuspid area checked?

A

5th left intercostal space

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107
Q

Where is auscultation of mitral area checked?

A

5th intercostal space at mid-clavicular line

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108
Q

Erb’s Point

A

Spot to hear the best sounds.

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109
Q

Aortic Murmur heard during systole

A

Aortic stenosis

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110
Q

Aortic Murmur heard during diastole

A

Aortic regurgitation

111
Q

Mitral Murmur heard during systole

A

Mitral regurgitation

112
Q

Mitral murmur heard during diastole

A

Mitral stenosis

113
Q

Type of murmur that is continuous, although louder during systole

A

Patent ductus arteriosus

114
Q

Circulatory shock

A

Generalized inadequacy of blood flow throughout the body to the extent that the body tissues are damaged

115
Q

Cardinal features of circulatory shock inculde:

A

Decrease in CO

Decrease in BP

116
Q

In circulatory shock, body tissues, including the CV system, begin to:

A

Deteriorate leading to death within hours or days.

it is self perpetuating

117
Q

Causes of circulatory shock via cardiogenic shock

A

MI
Toxicity
Valve dysfunction
Arrhythmias

Something is wrong with the heart

118
Q

Factors that decrease venous return, causing circulatory shock

A

Diminished blood volume

Decreased vascular tone

Venous obstruction

119
Q

Stages of circulatory shock

A

Non-progressive

Progressive

Irreversible

120
Q

Non-progressive stage of circulatory shock

A

Compensated stage- where the body’s own compensatory mechanisms will lead to recovery without outside help

121
Q

Progressive stage of circulatory shock

A

Where shock becomes self-perpetuating until death- is reversible with treatment

122
Q

Irreversible stage of circulatory shock

A

Severe shock that is refractory to treatment

123
Q

Types of circulatory shock

A

Hypovolumic / hemorrhagic shock

Neurogenic shock

Anaphylactic shock

Septic shock

124
Q

Shock characterized by decreased systemic filling pressure and therefore decreased venous return. CO and BP then also decrease

A

Hypovolumic/hemorrhagic shock

125
Q

Hypovolumic/hemorrhagic shock- Non-progressive/compensated stage

What happens at 30 sec?

10 min-1hr?

1-48 hours?

A

30 sec- Baroreceptor reflexes (increase SNS response)

Within 10 min to 1 hour- Reverse stress-relaxation response
Renin-angiotensin system activation
Vasopressin (ADH)

Within 1-48 hrs- Absorption of water from interstitial spaces
Increased thirst.

126
Q

Progressive stage of hypovolumic/hemorrhagic shock

A

Hallmarked by progressive deterioration of the CV system (positive feedback loops)

127
Q

Progressive stage of hypovolumic/hemorrhagic shock features:

A 
Cardiac depression
Vasomotor failure (CNS depression)
Blockage of small vessels “slugged blood”
Increased capillary permeability (late)
Release of toxins 
Cellular deterioration
Acidosis (carbonic and lactic acid)
128
Q

Review slide 64

A

Review slide 64

129
Q

Irreversible stage of hypovolumic/hemorrhagic shock:

A

Too much tissue damage

Too many destructive enzymes and toxins have been released into the tissues

Too much acidosis

Depletion of high-energy phosphates in the body (creatine phosphate, ATP)

130
Q

Other former of hypovolumic shock other than hemorrhagic

A

Intestinal obstruction

Severe burns

Dehydration (sweating, diarrhea, vomiting, nephrotic kidney disease)

131
Q

Neurogenic shock-
Hallmarked by:

Causes

A

Hallmarked bu an increased vascular capacity (loss of vasomotor tone)

Causes- Deep general anesthesia
Spinal anesthesia
Brain damage

132
Q

Shock caused by an allergic response to an antigen in the circulation

A

Anaphylactic shock

133
Q

In anaphylactic shock, basophils and mast cells release:

This causes:

A

Histamine

Venous dilation
Arteriole dilation
Increased capillary permeability

134
Q

Blood poisoning, AKA

A

Septic shock

135
Q

Septic shock is caused by

A

A blood borne bacterial infection in which the bacteria has been disseminated throughout the body

136
Q

Damage of septic shock is due to

A

Infection itself, or due to bacterial endotoxin release

137
Q

Features of septic shock

A

High fever,
Vasodilation
Sludging of blood
Disseminated intravascular coagulation

138
Q

Treatment of shock

A

Blood or plasma transfusion

Dextran

Sympathomimetic drugs

Oxygen therapy

Glucocorticoids

139
Q

RBC, AKA

A

Erythrocytes

140
Q

RBC lack:

A

Nucleus, ER, mitochondria

141
Q

Size of RBS

A

8 micrometers in diameter

They are biconcave discs

142
Q

Concentration of RBC in the blood

A

Approx 5 million/cc

143
Q

RBC contains

A

Hemoglobin (O2 transport. And buffer)
And
Carbonic anhydrase

144
Q

Process of making blood cells

A

Hematopoietic

145
Q

Hematopoiesis takes place:

A

Bone marrow at birth- mostly axial skeleton

146
Q

Hematopoeisis involves what cell types?

A

PHSC cells (Pluripotent hematopoietic stem cells)
CFU-S (Colony-forming unit-spleen)- (Myeloid stem cell)
LSC (lymphoid stem cell)

147
Q

CFU-S cells can form

A

CFU-GM
CFU-B/CFU-E
CFU-M

148
Q

LSC cells can form

A

T lymphocytes and

B lymphocyte

149
Q

Genesis of RBC:

A

Proerythroblast
Reticulocyte
Erythrocytes

150
Q

For regulation of RBC production, ______ is secreted by __________ in response to low O2 levels in the blood

A

Erythropoietin (EPO)

Kidneys

151
Q

EPO stimulates:

A

EBC production in the bone marrow

152
Q

Factors that decrease oxygenation

A 
Low blood volume
Anemia
Low hemoglobin 
Poor blood glow
Pulmonary disease
153
Q

Hemoglobin composition

A

Heme- Iron containing protoporphyrin ring structure

Globin- Polypeptide, alpha, beta, gamma or delta

154
Q

Most common types of hemoglobin

A

HbA - Adult Hg = Alpha2/beta2

HbF- Fetal Hb- Alpha2/Gamma2

155
Q

Iron is absorbed from the:

A

GI tract

156
Q

Iron binds to ________ to form:

A

Apotransferrin

Forms transferrin which carries the ion in the blood

157
Q

Iron, leased to tissues, will bind to ______ to form:

A

Apoferritin

Forms ferritin which is the storage form of iron in cells

158
Q

What happens when ferritin stores are maximized

A

An insoluble form of iron storage is hemosiderin

159
Q

Iron excreted from plasma daily

A

0.6 mg

160
Q

Amount of iron lost daily in menses

A

0.7 mg Fe

161
Q

Dead hemoglobin enters _______
What happens here?

What is excreted?

A

Macrophages

Hemoglobin is degraded, free iron is released

Bilirubin is excreted

162
Q

How is iron lost

A

In feces
Bleeding
Menstrual loss

163
Q

Avg RBC life span

A

120 days

164
Q

Why does the metabolism of RBS weaken?

A 
So that:
Cell membrane becomes less pliable
Membrane transport of ions decreases
Heme iron goes into the ferric form
Oxidation of proteins
165
Q

RBCs rupture where?

A

In the peripheral circulation, or especially in the spleen

166
Q

What phagocytoses damaged RBC?

A

Kupffer cells

167
Q

Hemoglobin is broken down into ____ and _____ which then break down into _____ and _______

A

Heme
Globin

Bilirubin
amino acids

168
Q

Deficiency of hemoglobin

A

Anemia

169
Q

Classification of anemia is based on

A

RBC size (Normocytic, Macrocytic, microcytic)

170
Q

Anemia classification if based on

A

Hemoglobin content
Normochromic
Hypochromic

171
Q

CBC, AKA

A

Complete blood count

172
Q

What aspects of the CBC indicate anemia?

A

Low RBC, HCT (hematocrit), and HGB

173
Q

MCV in CBC indicates

A

Average cell size

174
Q

MCHC and MCH indicates

A

Hemoglobin content per cell

175
Q

Problem with CBC

A

It cannot detect abnormalities in shape of cells

176
Q

Types of anemia’s

A

Hemorrhagic

Aplastic

Megablastic

177
Q

Cbl, aka cobalamin =

A

B12

178
Q

Hemorrhagic anemia

A

Had a bleeding episode, so anemic until you have a transfusion or make new RBC

Blood cells lost- normocytic and normochromic

179
Q

Aplastic anemia

A

Bone marrow not growing RBC- could be genetic, a drug that kills the bone marrow, etc

Generally normocytic and normochronic

180
Q

Megaloblastic anemias

A

Macrocytic, normochromic

Anemia of folate deficiency
Or
Anemia of B12 deficiency

Pernicious anemia

181
Q

Anemia B12 deficiency with special mechanism

A

Pernicious anemia

182
Q

B12 and HC come together to bind,_______ is resp to transport the B12 into the blood

A

Intrinsic factor (IF)

183
Q

An autoimmune disease keeping us from making intrinsic factor (IF), making it difficult to absorb B12

A

Pernicious anemia

184
Q

Hemolytic anemia’s

A

Normocytic, normochromic
Shorter lifespan, so lose them faster

Hereditary spherocytosis

Sickly cell anemia

Erythroblastosis fetalis

185
Q

Anemia of iron deficiency

A

Microcytic, hypochromic

186
Q

Abnormal hemoglobin, causing Hemoglobin S

Shapes distorts in absence of O2`

A

Sickle cell anemia

187
Q

Erythroblastosis fetalis

A

Mother with Rh- blood type with an Rh+ blood type baby. No problem bc moms blood and babies blood don’t mix.

When baby is born and placenta bleeds into the uterine wall. Some of the blood comes in contact with the moms immune system. Causes her to make anti-Rh antibodies.

Antibodies can cross the placenta and attack another baby

188
Q

Hereditary sperocytosis

A

Non spheared blood cells

189
Q

Symptoms of general anemia

A

Fatigue
Weakness
Dizziness
Paleness of skin

190
Q

High RBC count

A

Polycythemia

191
Q

What is real active to polycythemia

A

Intravascular volume depletion

- loss of fluid concentrates blood cells

192
Q

Absolute polycythemia

A

Actual increase in RBC production

193
Q

Primary polycythemia

A

Genetic defect involving bone barrow

194
Q

Secondary polycythemia

A

Consequence of hypoxia, drugs, high altitude, sleep apnea, COPD, etc

195
Q

2 most important blood groups antigens

A

ABO blood group- possible blood types

Rh (rhesus blood group)- gene located on chromosome 1

196
Q

What happens if wrong blood types are mixed

A

An immune reaction takes place

197
Q

During early childhood, we make antibodies against:

A

Gut bacteria that have similar antigens to the A and B, unless they are present on your own blood (self vs non-self principle)

198
Q

So, type A RBC have antibodies against

A

B types

199
Q

People only make anti-rh antibodies if:

A

They are Rh negative and they are exposed to Rh positive blood in their life.

200
Q

Review slide 94 chart

A

Review slide 94

201
Q

Most common blood type

A

O+

202
Q

Rarest blood type

A

AB-

203
Q

Hemostasis =

A

Prevention of blood loss

204
Q

Steps of hemostasis

A

Vascular spasm

Platelet plug formation

Fibrin clot formation

Retraction

205
Q

Vascular spasm

A

Constriction of blood vessels reducing the rate of blood loss.

206
Q

What can cause vascular spasm?

A

Pain, vascular wall damage, or thrombocytes A2

207
Q

Platelet plug formation

A

Activated platelets forming a weak plug

208
Q

Fibrin clot formation (coagulation)

A

A series of clotting factors are involved in forming a clot

209
Q

Retraction in homeostasis

A

“Shrinking” of a clot material to approximate edges of would together

210
Q

Platelets are formed where?

A

In bone marrow from megakaryocytes

211
Q

What do platelets contain?

A

Actin and myosin

212
Q

What do platelets store?

A

Calcium

213
Q

Platelets synthesize:

A

ATP, ADP, prostaglandins, fibrin-stabilizing factor, thrombocytes A2, and growth factors

214
Q

Platelets have _____ ______ that stick to exposed ______

A

Surface glycoproteins

Collagen

215
Q

Lifespan of platelets

A

12 days

216
Q

Primary hemostasis-

A

Platelet plug formation

217
Q

What happens when platelets encounter damaged blood vessel wall?

A

Platelets swell and send out pseudopods that stick to the vessel wall

218
Q

After platelets swell and send out pseudopods that stick to the vessel wall, what happens?

A

Contractile proteins contract

This causes release of factors including ADP and thromboxane A2; these factors activate other platelets, and promote vascular spasm

219
Q

What happens to newly activated platelets

A

They stick to the growing plug

220
Q

Secondary hemostasis

A

Coagulation, clot formation

Platelet plugs are strengthened by the clotting process

221
Q

Clotting factors for 2ndary hemostasis

A 
1- Fibrinogen
2- prothrombin
3- Tissue factor
4- Calcium
5- label factor
6- obsolete factor
7- stable factor
8- anti-hemophilia factor
9- Christmas factor
10- Stuart-prower factor
11- Plasma thromboplastin
12- Hangeman Factor
12- Fibrin stabilizing factor
222
Q

Hemostasis clotting cascade

A

Intrinsic and extrinsic pathways ——> common pathway

223
Q

Final common pathway for clotting

A

Prothrombin

Activated by prothrombin activator

Ends with cross-linked fibrin fibers

224
Q

Extrinsic pathway for clotting

A

Tissue trauma -> Tissue factor -> prothrombin activator

225
Q

See slide 103

A

Slide 103

226
Q

Review slide 104

A

Slide 104

227
Q

Prothrombin time states:

A

The lower the concentration of clotting factors such as prothrombin, the longer it takes for blood to clot

228
Q

What test is used to help detect and diagnose a bleeding disorder?

A

Prothrombin Time (PT)

229
Q

Prothrombin time test can also be used to monitor:

A

How well an anticoagulation medication is working to prevent blood clots

230
Q

Contraction of platelets tighten the clot and pull the edges of the wound together

A

Clot retraction

231
Q

What are ways to prevent unwanted clotting?

A

Keeping an intact blood vessel wall

Glycocalyx

Thrombomodulin

232
Q

What effect does glycocalyx have?

A

It repels platelets and clotting factors

233
Q

What effect does thrombomodulin have?

A

Inhibits thrombin

Activated the anticoagulant “protein C” which in turn inactivates factors V and VIII

234
Q

Purpose of anticoagulants

A

To limit the size of the clot

235
Q

Types of anticoagulants

A

Heparin

Antithrombin

236
Q

What does heparin bind with

A

Antithrombin

237
Q

What does antithrombin bind with

A

Thrombin

238
Q

What is heparin used in surgery for?

A

To prevent blood clots

239
Q

Lysis of blood clots is done by

A

Plasminogen activator (tissue plasminogen activator, TPA)

240
Q

Plasminogen activator is released by what?

A

By damaged tissues over time as they heal

241
Q

Plasminogen activator converts _____ to _____.

When?

A

Plasminogen

Plasmin

When the concentration of the activator is great enough

242
Q

What does plasmin digest?

A

Fibrin clot

243
Q

Plasminogen can be used to:

A

Digest thrombi (abnormal clots)

244
Q

Bleeding disorders

A

Vitamin K deficiency

Liver damage/disease

Hemophilia

thrombocytopenia

245
Q

Factors that need vitamin K for their synthesis by the liver

A

Factors II, VII, IX, and X

246
Q

What is the source of many clotting factors?

A

The liver

247
Q

What causes hemophilia?

A

Inheritance of a faulty factor VIII gene.

It is an X-Linked trait

248
Q

Lack of platelets (petechial rash = red spots visible on the skin)

A

Thrombocytopenia

249
Q

Abnormal clots that form on roughened endothelial surfaces (atherosclerosis, infection, trauma)

A

Thrombi

250
Q

Thrombi that have broken loose from their attachment and may large elsewhere in the circulation

A

Emboli

251
Q

Unwanted clots may be dissolved clinically how?

A

By administering plasminogen activator

252
Q

Nerves used for circulation regulation

A

Sympathetic (norepinephrine)

Adrenal (epinephrine)

253
Q

Attempt by the body to restore blood supply to ischemic tissue

A

Collateral circulation

254
Q

What happens in collateral. Circulation during plaque formation?

A

Angiogenesis may occur

255
Q

What happens after acute occulsion of the collateral circulation?

A

Angiogenesis is too slow to restore blood flow acutely,

However, vasodilation os collateral vessels may prevent some cardiac muscle death

256
Q

Ischemic heat disease includes:

A

Angina pectoris

Coronary artery disease

Myocardial infarction

Sudden cardiac death

257
Q

Chest pain

A

Angina pectoris

258
Q

2 types of angina

A

Chronic stable angina

Unstable angina

259
Q

Angina is often a prelude to _____ if not treated

A

MI

260
Q

Myocardial infarction results from

A

An acute coronary occlusion- muscle has little or no blood flow

261
Q

What happens to the affected area of a MI?

A

It ceases to function and may die

262
Q

MI most commonly affects what part of the heart?

A

Left ventricle

263
Q

Causes of death due to MI:

A

Decreased cardiac output

Pulmonary edema and kidney failure

Fibrillation

Cardiac rupture

264
Q

Decreased CO usually occurs when?

A

When more than 40% of the left ventricle is infarcted

265
Q

Systolic stretch exacerbates the decrease in:

A

CO

266
Q

How does MI cause pulmonary edema and kidney failure?

A

Results from the backlog of blood in the body’s venous system

267
Q

Fibrillation may result from:

A

Leakage of K+ from infarcted area

Formation of an “injury current” (ischemic muscle cannot repolarize effectively)

Sympathetic reflexes

Bulging weak muscle sets up “circus movements”

268
Q

Cardiac rupture happens (OFTEN/RARELY)

A

Rarely

269
Q

An infarct area of the heart has a central area of:

And a peripheral area of:

A

Dead cardiac myocytes

Non-functional but living myocytes

270
Q

Dead fibers from MI are replaced by what?

A

Scar tissue

271
Q

What happens to nonfunctional fibers after recovery of MI?

A

They either die, or recover (if reversible) when clot is dissolved, or collateral circulation is adequate

272
Q

What happens to scar tissue on the affected MI area over time?

A

It retracts (shrinks)

Normal tissue hypertrophied over time to compensate for tissue lost

273
Q

Lifestyle treatments for ischemic heart disease

A

Lose weight

Eat a diet low in saturated fat and cholesterol

Exercise

274
Q

Other treatments for ischemic heart diseases

A

Nitroglycerin (vasodilator)

Beta blockers

TPA (tissue plasminogen activator)

Bypass surgery

Angioplasty

CVP (4 decks)

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