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Cardiovascular System > Pathphysiology > Flashcards

Pathphysiology Flashcards

1
Q

What is the definition of shock?

A

A serious and life threatening condition resulting in tissue hypoperfusion

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2
Q

Is hypertensive shock similar to emotional shock?

A

No they should NOT be confused

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3
Q

What is the end result in every type of shock?

A

Hypotension

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4
Q

How do we calculate shock index?

A

Shock index = heart rate / systolic BP

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5
Q

What is the normal range for shock index?

A

0.5-0.8

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6
Q

What mechanism does shock operate on?

A

Positive feedback

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7
Q

What is the effect of inflammatory mediators being released and causing increased blood flow to an area?

A

The blood is being diverted and starving other areas of blood/oxygen and therefore those areas then release their own inflammatory mediators

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8
Q

What happens when the cells begin to suffer from hypoxia injury?

A

They begin to fail and the circulatory system collapse

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9
Q

How many different types of shock are there and what are they?

A

4 types
~ hypovolaemic
~ cardiogenic
~ distributive
~ obstructive

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10
Q

What is the problem associated with hypovolemic shock?

A

There is a fluid loss problem

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11
Q

What type of things can cause hypovolemic shock?

A

Dehydration, sickness, diarrhoea, haemorrhage (internal or external), burns and diabetic ketoacidosis

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12
Q

In hypovolemic shock is the sympathetic system working more or less? And what effect does this have?

A

Working more (more active) which leads to vasoconstriction to maintain BP

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13
Q

Are organs well or poorly perfused in hypovolemic shock, and why?

A

Poorly, because there is reduced blood flow

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14
Q

Is cardiogenic shock a fluid or blood loss problem?

A

No it’s a pumping problem

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15
Q

What happens to the heart during cardiogenic shock?

A

It fails to pump effectively

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16
Q

What can cause cardiogenic shock?

A

Large myocardial infarction,arrhythmias or heart failure

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17
Q

What happens to the sympathetic system during cardiogenic shock?

A

It is over active and therefore leads to vasoconstriction

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18
Q

Is the venous pressure high or low in cardiogenic shock, and what effect does this have?

A

High pressure, leading to fluid extraction and oedema

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19
Q

What causes distributive shock?

A

An inappropriate peripheral vasodilation that is causing pooling of blood or fluid in the tissues.

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20
Q

What are the 3 types of distributive shock?

A

Septic, neurogenic and anaphylaxis

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21
Q

What is happening during septic shock?

A

You have an ongoing release of inflammatory mediators in response to infective organisms

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22
Q

After adequate fluid resuscitation does sepsis persist or subside?

A

Persists

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23
Q

What happens during an anaphylaxis shock?

A

There’s a huge release if histamines

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24
Q

What happens during neurogenic shock?

A

There is a loss of nerve supply to the small vessels that prevent vasoconstriction

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25
Q

During distributive shock do you see an increase or decrease in SVR

A

Decrease because the vessels are dilated and you have caused hypovolemia

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26
Q

What type of shock is classified as a medical emergency?

A

Obstructive shock

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27
Q

What is obstructive shock?

A

When there is an obstruction to blood flow

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28
Q

Give 3 examples of things that could cause obstructive shock

A
  • cardiac tamponade
  • pulmonary embolus
  • aortic stenosis (an obstruction of the left ventricle flow tract)
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29
Q

During obstructive shock is the sympathetic system more or less active?

A

More active which leads to vasoconstriction

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30
Q

During obstructive shock are the organs well or poorly perfused?

A

Poorly as you have a reduced blood flow

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31
Q

In obstructive shock what does back pressure lead to?

A

Venous congestion

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32
Q

What are the two stages of shock?

A

Initial and refractory

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33
Q

What’s another way to describe initial shock?

A

Compensated shock

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34
Q

What’s another way of describing refractory shock?

A

Decompensated shock

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35
Q

Describe why lactic acid builds up in compensated shock

A

The hypoperfusion of tissues leads to anaerobic respiration starting and so you get the build up of lactic acid

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36
Q

Does irreversible cells damage occur in compensated or decompensated shock?

A

Decompensated shock

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37
Q

What are the 4 things you need to do when you are treating a patient in hypotensive shock?

A
  • keep the patient warm
  • seek senior help immediately
  • try to identify the cause (must be reserved for successful treatment)
  • give 100% oxygen and give IV normal saline
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38
Q

How much saline should an adult receive in hypotensive shock?

A

1000ml stat

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39
Q

How much saline should a frail or elderly patient receive in hypotensive shock?

A

500ml

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40
Q

How much saline should a patient suspected of cardiogenic shock receive?

A

500ml

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41
Q

How much saline should a child receive in hypotensive shock?

A

Should be calculated on their body weight (20mg/kg)

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42
Q

What classifies a patient to be in hypertensive shock?

A

A sudden BP increase of 180/110 or more

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43
Q

What blood pressure do you usually see in patients who are in a hypertensive emergency?

A

220/120

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44
Q

What do you need to ensure you assess for if you suspect a patient is in a hypertensive emergency?

A

End organ damage

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45
Q

What is the most common cause of a hypertensive emergency?

A

Idiopathic hypertension

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46
Q

What are the secondary causes of a hypertensive emergency?

A
  • pregnancy
  • renal disease
  • phaeochromocytoma
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47
Q

If you think a patient might have a hypertensive emergency but after assessment show now signs of end organ failure what are they then categorised as?

A

A hypertensive urgency

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48
Q

How should you treat a patient in a hypertensive emergency?

A
  • Take regular BP measurements
  • Gain IV access and carry out routine bloods
  • ABCDE as required
  • Seek senior help
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49
Q

Why do you have to slowly titrate the BP of patients in a hypertensive emergency?

A

Because if you drastically decrease the BP the body will not like that as much as it doesn’t like the high BP and will then go into a different type of shock

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50
Q

How do we usually treat a hypertensive urgency?

A

With oral medication

51
Q

What is the mneumonic that we use to consider all the possible causes of pain?

A

VINDICATE

52
Q

What does VINDICATE stand for?

A

V- vascular
I- Infection
N- Neoplasm
D- Degenerative or drugs
I- Iatrogenic or intoxication
C- Congenital
A-Autoimmune
T-Trauma
E-Endocrine

53
Q

What is the mnemonic that we use to assess pain?

A

SOCRATES

54
Q

What does SOCRATES stand for?

A

S-Site
O-Onset
C-Characteristics
R-Radiates
A-Association
T-Time course
E-Exacerbation/relieving factors
S-Severity

55
Q

What are the 3 main vascular causes of chest pain?

A

~ Acute coronary syndrome
~ Pulmonary embolism
~ Acute aortic syndrome

56
Q

What happens during aortic dissection?

A

There is a tear in the aorta from the tunica media to the tunica adventicia

57
Q

What type of pain is an aortic dissection usually described as?

A

A tearing pain

58
Q

Where might the pain radiate in an aortic dissection?

A

The back and sometimes in the abdomen too

59
Q

How can we look to diagnose an aortic dissection?

A

~ Difference in BP in each limb
~ Widened media sternum seen on the chest x-ray
~ Aortic regurgitation (in type A)

60
Q

How do we confirm an aortic dissection?

A

Contrast CT

61
Q

How do we treat a type 1 aortic dissection?

A

Surgically

62
Q

Where is a type 1 aortic dissection?

A

The ascending arch of the aorta

63
Q

Where is a type 2 aortic dissection?

A

The descending limb or arch of the aorta

64
Q

How do we treat a type 2 aortic dissection?

A

Medically

65
Q

What’s the most common drug used to treat a type 2 aortic dissection?

A

Labetalol

66
Q

What are the 2 different types of infection that can cause chest pain?

A

~ Pericarditis
~ Myocarditis

67
Q

What is an infection in the pericardium called?

A

Pericarditis

68
Q

What is pericarditis?

A

Inflammation of the membrane surrounding the heart (pericardium)

69
Q

Will you see a change in an ECG when the patient has pericarditis?

A

Yes, you will see ST elevation

70
Q

Will the ST elevation in an ECG of a patient with pericarditis and myocarditis be the same as the ST elevation in an MI?

A

No, the ST elevation will be saddle shaped unlike in an MI

71
Q

What chest sounds would you hear if the patient has pericarditis?

A

You would hear a high pitched scratching, which is the pericarditis friction rub

72
Q

What is the first line treatment for pericarditis?

A

NSAIDs (unless elderly or GI problems)

73
Q

What is myocarditis?

A

An infection of the heart causing inflammation in the myocardium

74
Q

What usually makes chest pain worse when you have pericarditis?

A

Lying on your back or deep breathing

75
Q

When will pain ease when a patient has pericarditis?

A

When they hold their breath

76
Q

What is a common medical history of a patient with myocarditis?

A

A recent viral or bacteria infection

77
Q

What different blood levels will a patient with myocarditis have?

A

Raised CRP, ESR and trops

78
Q

What’s a long term complication of myocarditis?

A

Chronic heart failure

79
Q

What is costocondritis?

A

The inflammation and swelling of the cartilage between the rib and the breast bone

80
Q

When is pain aggregated in costocondritis?

A

During deep breathing

81
Q

Where can the pain radiate in costocondritis?

A

To the arm and shoulder

82
Q

Where can pathologies be seen due to hypertension?

A

Heart, vessels, brain

83
Q

What leads to left ventricular failure?

A

Long standing hypertrophy

84
Q

What is the biggest cause of arteriosclerosis?

A

Atheroma

85
Q

What causes an aneurysm?

A

Focal dilation of an artery which leads to an enlargement of the plaque

86
Q

What replaces the muscle and elastic fibres, which causes an aneurysm?

A

Collagen

87
Q

Is collagen capable of elastic recoil and contractions?

A

No

88
Q

What does atheroma affect?

A

Large and medium sized vessels

89
Q

Can you get atheroma in veins?

A

No, just high pressure vessels

90
Q

Where does atheroma begin?

A

In the tunica intima

91
Q

If atheroma progresses from the tunica intima where will it go?

A

Tunica media

92
Q

How can we remember the risk factors of atheroma?

A

A- arterial hypertension
T- tobacco
H- hereditary
E- endocrine
R- reduced physical activity
O- obesity
M- male gender
A- age

93
Q

What are the 4 stages of atheroma that can be seen by the naked eye?

A

~ Fatty streak
~ Lipid plaque
~ Fibrolipid plaque
~ Complicated atheroma

94
Q

How do the blood lipids enter the intima in atheroma?

A

through the damaged endothelium

95
Q

What are the two ways in which atheroma can be fatal?

A

Formation of plaque fissure and the development of a thrombosis

96
Q

What’s the definition of palpatation?

A

Unpleasant awareness of forceful, rapid or orregular beating of heart

97
Q

How might palpitations be described?

A

Pounding, fluttering or flip-flopping

98
Q

What is the time limit a to when we become really concerned about palpitation?

A

If they are lasting longer than 5 minutes

99
Q

What is the heart doing during premature atrial complex and premature ventricular complex?

A

It is sorting out the problem itself and putting the heart back into the normal rhythm

100
Q

What does AVNRT stand for?

A

Atrio ventricular node reentry tachycardia

101
Q

What happens to the QRS complex during AVNRT?

A

They become narrowed and look very thin

102
Q

Where is a P wave visible during AVNRT?

A

Immediately after the QRS complex

103
Q

What is happening during AVNRT?

A

The AV node is working constantly as it has an additional pathway and so the constant loop of electrical activity causes the heart to beat faster

104
Q

How can we manage AVNRT?

A

~ Vagal Manoeuvres
~ Adenosine
~Cardioversion
~ Catheter ablation
~ Beta blockers, calcium channel blockers

105
Q

What does AVRT stand for?

A

Atrio ventricular reentry tachycardia

106
Q

What is the most common example of an AVRT?

A

Wolff Parkinson White Syndrome?

107
Q

What is the accessory pathway in WPW known as?

A

The bundle of Kent

108
Q

What side of the heart is affected by type A WPW?

A

Left side

109
Q

What side of the heart is affected by type B WPW?

A

Right side

110
Q

What is a clear indication on an ECG that a person is suffering from WPW syndrome?

A

Delta wave presence

111
Q

What are the two types of life threatening tachycardias?

A

Ventricular tachycardia and ventricular fibrillation

112
Q

What are the two types of VT?

A

Focal VT and Re-entant VT

113
Q

What is the problem during Focal VT?

A

The cells become irritated and they begin to over fire

114
Q

What is the problem during Re-entrant VT?

A

There is scaring on the heart tissue and this causes electrical loop abnormalities

115
Q

What causes ventricular fibrillation?

A

Prolonged ventricular tachycardia

116
Q

Why is ventricular fibrillation so dangerous?

A

Because you have very small blood flow, if any to the body

117
Q

What are the 5 things that you must do when you are assessing a patient who is presenting with palpitations?

A
  1. Take a history
  2. Physical exam
  3. 12 lead ECG
  4. Lab tests
  5. Further monitoring
118
Q

What investigative tests should you carry out when you have a patient presenting with palpitations?

A

12 lead ECG
ECHO
Blood tests including FBC, U and Es, TFT (thyroid function test) and CRP

119
Q

What is the first thing you should doo when you are presented with a patient that has palpitations?

A

Carry out your ABCDE approach

120
Q

What are the two different classes of heart failure?

A

~Chronic or acute
~Preserved or reduced ejection fraction

121
Q

When you are in heart failure what is your body doing to try and help the issue that is occuring?

A

The body tries to compensate to try and retain cardiac output

122
Q

What is classified as a reduced ejection fraction?

A

Less than 35%

123
Q

How would you describe acute heart failure?

A

The sudden inability of the heart to maintain an adequate cardiac output and blood pressure

Cardiovascular System (8 decks)

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