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Semester 2 > CVS Session 12 > Flashcards

CVS Session 12 Flashcards

1
Q

What diseases are associated with arterial occlusion?

A

Peripheral artery disease

Coronary artery disease

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2
Q

What diseases are associated with venous congestion?

A

Varicose veins

DVT

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3
Q

What causes the pain experienced in intermittent claudication?

A

Build up of metabolites

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4
Q

Which veins in the leg are assisted by musculaneous pump?

A

Deep

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5
Q

When do varicose veins become symptomatic?

A

Perfusion is reduced leading to venous ulcer

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6
Q

Which veins of the leg are affected in varicose veins?

A

Superficial

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7
Q

Stasis of blood in which vessels presents with a tender, swollen calf in the affected limb?

A

Calf, popliteal, femoral or iliac veins

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8
Q

If a patient with DVT becomes breathless and experiences chest pain, what has most likely happened?

A

Pulmonary embolism

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9
Q

What is experienced with >70% occlusion of the coronary arteries?

A

Symptoms of ischaemic heart disease on exercise

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10
Q

When does blood flow through the LCA largely occur?

A

During diastole

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11
Q

What happens when there is >90% occlusionsion in a coronary artery?

A

Ischaemia at rest

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12
Q

What are the S/S of ischaemic heart disease?

A

Central chest pain that radiates to neck and left arm and is brought on by exercise, relieved by rest

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13
Q

What is defined as a positive exercise stress test?

A

Chest discomfort or ST depression seen on ECG

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14
Q

What is the primary action of nitrate treatment in ischaemic heart disease?

A

Venodilation to increase preload of the heart

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15
Q

What treatments are used to decrease the workload of the heart and act on vasculature to decrease afterload?

A

Calcium channel antagonists

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16
Q

What is the numerical definition of hypertension?

A

Arterial B.P. > 140/90

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17
Q

What complications can follow from prolonged hypertension?

A

LVH –> heart failure

Arterial disease of the coronary, cerebral, kidney and retinal arteries as well as the aorta

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18
Q

What lifestyle changes can be recommended to control hypertension?

A

Weight loss
Exercise
Decrease dietary salt intake

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19
Q

How does the radiation of chest pain in unstable angina compare to that in MI?

A

More limited

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20
Q

What is the role of troponin?

A

Regulate excitation-contraction coupling

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21
Q

Which patients tend to not feel chest pain in MI?

A

Diabetics

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22
Q

What causes MI patients to display pallor and sweating?

A

Strong sympathetic reaction

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23
Q

How does necrosis of the myocardial wall differ between NSTEMI and STEMI?

A

NSTEMI: not full wall
STEMI: full wall

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24
Q

What biomarkers can be used to detect MI?

A

CK-MB

Troponin T and I

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25
Q

How does the ECG waveform progress in STEMI?

A

ST elevation –> R decreases and pathological Q wave forms –> T wave inversion and Q wave deepens –> ST normal and T inverted –> ST and T normal, Q wave persists

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26
Q

How long after MI are R wave changes seen on an ECG?

A

Horus

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27
Q

When is T wave inversion seen on ECG following a STEMI?

A

Days 1-2

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28
Q

How is a pathological Q wave defined?

A

> 1 mm width

>2 small squares depth

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29
Q

How long does it take for the ST to return to normal on an ECG following a STEMI?

A

Days

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30
Q

How long does it take for the T wave to return to normal on an ECG following STEMI?

A

Weeks

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31
Q

What is cardiac arrest?

A

Unresponsiveness associated w/lack of pulse

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32
Q

What are the two broad causes of cardiac arrest?

A

Asystole

Ventricular fibrillation

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33
Q

What is asystole?

A

Loss of electrical and mechanical activity in the heart

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34
Q

What is the most common cause of cardiac arrest?

A

Ventricular fibrillation

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35
Q

What three things can cause ventricular fibrillation and therefore lead to cardiac arrest?

A

MI
Electrolyte imbalance
Arrhythmias

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36
Q

Give two examples of arrythmias which may lead to cardiac arrest.

A

Long QT

Torsades de Pointes

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37
Q

What are the three treatments used in cardiac arrest?

A

Basic life support
Advanced life support
Adrenaline

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38
Q

What is basic life support?

A

Chest compression and external ventilation giving ~20% of cardiac output

39
Q

How does defibrillation treat cardiac arrest?

A

Depolarises all cells and puts them into refractory period allowing for a coordinated restart

40
Q

How does a pharmacological dose of adrenaline act when treating cardiac arrest?

A

Activates alpha-1 receptors to increase heart function and decrease TPR

41
Q

What is generalised shock?

A

Acute condition of inadequate blood flow throughout the body

42
Q

What leads to circulatory shock?

A

A catastrophic fall in arterial blood pressure due to decreased cardiac output or decreased TPR beyond the heart coping capacity

43
Q

What equation describes mean arterial blood pressure?

A

CO x TPR (flow x resistance)

44
Q

What equation describes cardiac output?

A

HR x SV

45
Q

What causes the TPR to decrease to a level that the heart cannot cope with?

A

Extensive systemic vasodilation

46
Q

Which three types of shock result from decreased cardiac output?

A

Mechanical (obstructive)
Cardiogenic
Hypovolaemic

47
Q

Which types of shock arise from decreased TPR?

A

Toxic

Anaphylactic

48
Q

What is cardiogenic shock?

A

Pump failure

49
Q

What can cause cardiogenic shock?

A

Damage to L. ventricle following MI
Ventricular tachycardia
Severe bradycardia
Acute worsening of heart failure

50
Q

How may central venous pressure be altered in cardiogenic shock?

A

May not be (sorry) or can be increased

51
Q

What causes the large decrease in arterial pressure in cardiogenic shock?

A

The heart fills but cannot pump effectively

52
Q

What exacerbates the problem of cardiogenic shock?

A

Poor perfusion of coronary arteries

53
Q

What is the affect on the kidneys of cardiogenic shock?

A

Poor perfusion –> oliguria

54
Q

Which two pathologies can cause mechanical shock?

A

Cardiac tamponade

Pulmonary embolism

55
Q

How does cardiac tamponade cause mechanical shock?

A

Blood/fluid in pericardial space exerts pressure on heart and prevents proper relaxation and filling

56
Q

What is limited in mechanical shock?

A

End diastolic volume

57
Q

What happens to the central venous pressure in mechanical shock?

A

Increases

58
Q

What happens to the arterial blood pressure in mechanical shock?

A

Decreases

59
Q

Why is SV altered in mechanical shock?

A

Heart attempts to beat faster due to continued electrical activity so SV decreases

60
Q

How does pulmonary embolism cause mechanical shock?

A

Massive PE –> occlusion of large pulmonary artery –> R ventricle cannot empty properly –> CVP increases –> decreased bloodflow to L heart

61
Q

How does the left atrial pressure change in mechanical shock?

A

Decreases

62
Q

How does the arterial blood pressure change in mechanical shock?

A

Decreases

63
Q

What else may be seen in a patient with mechanical shock due to pulmonary embolism in addition to the S/S of shock?

A

S/S of PE: chest pain and dyspnoea

64
Q

How does shock lead to multi-organ failure?

A

Decrease in arterial BP is sufficient enough to cause decrease in tissue perfusion

65
Q

What is hypovolaemic shock?

A

When blood volume is reduced so that cardiac output cannot be maintained

66
Q

What is the most common cause of hypovolaemic shock?

A

Haemorrhage

67
Q

What can cause plasma loss which leads to hypovolaemic shock?

A

Severe burns
Diarrhoea
Vomiting
Looks of sodium ions

68
Q

At what percentage of bloodloss does hypovolaemic shock become symptomatic?

A

20-30%

69
Q

At what percentage of blood volume loss is the serious shock response seen?

A

30-40%

70
Q

What does the severity of hypovolaemic shock depend on?

A

Amount and speed of bloodloss

71
Q

How are baroreceptors activated in haemorrhage?

A

Decreased venous pressure –> decreased CO –> arterial B.P. drops

72
Q

What effects does activation of the baroreceptors have in hypovolaemic shock?

A

Increased sympathetic stimulation: increased heart rate, increased contractility, peripheral vasoconstriction and venoconstriction

73
Q

What is internal transfusion?

A

Body’s mechanism of increasing blood volume in hypovolaemic shock

74
Q

How does internal transfusion work?

A

Increased TPR reduces downstream capillary hydrostatic pressure so fluid moves in to capillaries

75
Q

What are the S/S of hypovolaemic shock?

A

Tachycardia
Weak pulse
Pale skin
Cold, clammy extremities

76
Q

What does decompensation lead to?

A

Multi-system failure

77
Q

What is the progression of decompensation?

A

Hypoxic tissue damage –> vasodilators released, build up and overtake SNS –> increased TPR and decreased B.P. –> vital organs not perfumed

78
Q

Which are the two types of nonvolaemic shock?

A

Toxic (septic)

Anaphylactic

79
Q

What is nonvolaemic shock?

A

Normal blood volume but circulatory volume increases

80
Q

How do endotoxins seen in septic shock cause nonvolaemic shock?

A

Overcome SNS to cause vasodilation –> severely decreased TPR –> arterial pressure drops –> vital organs unperfused

81
Q

How can endotoxins from circulating bacteria cause hypovolaemic shock in septicaemia?

A

Cause capillaries to become leaky

82
Q

What is the vasoconstriction response from activated baroreceptors overridden by in septic shock?

A

Vasodilation mediators

83
Q

What is seen in the vasculature in the later stages of toxic shock?

A

Vasoconstriction

84
Q

What are the S/S of toxic shock?

A

Tachycardia
Warm and red extremities
Strong pulse

85
Q

Which type of shock is acutely life threatening?

A

Anaphylactic

86
Q

What causes the large decrease in arterial pressure seen in anaphylactic shock?

A

In sever allergic reaction mast cells release powerful vasodilators such as histamine and other mediators which decrease TPR

87
Q

How is cardiac output increased in anaphylactic shock?

A

Increased SNS

88
Q

Why does the increase in cardiac output seen in anaphylactic shock not restore systemic perfusion?

A

It is not enough to match the systemic vasodilation

89
Q

What do mediators released by mast cells cause in addition to vasoconstriction which makes the patient breathless and the situation acutely life threatening in anaphylactic shock?

A

Bronchoconstriction

Laryngeal oedema

90
Q

What are the S/S of anaphylactic shock?

A

Difficulty breathing
Collapsed
Increased HR
Red, warm extremities

91
Q

Why is adrenaline given to treat anaphylactic shock?

A

To activate more alpha-1 receptors than the body can with endogenous NA and adrenaline

92
Q

What two problems with the vasculature can cause poor perfusion?

A

Venous congestion

Arterial occlusion

93
Q

Which two types of shock are considered as distributive shock?

A

Sepsis

Anaphylaxis

Semester 2 (45 decks)

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