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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
How does the ECG waveform progress in STEMI?
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
26
How long after MI are R wave changes seen on an ECG?
Horus
27
When is T wave inversion seen on ECG following a STEMI?
Days 1-2
28
How is a pathological Q wave defined?
>1 mm width | >2 small squares depth
29
How long does it take for the ST to return to normal on an ECG following a STEMI?
Days
30
How long does it take for the T wave to return to normal on an ECG following STEMI?
Weeks
31
What is cardiac arrest?
Unresponsiveness associated w/lack of pulse
32
What are the two broad causes of cardiac arrest?
Asystole | Ventricular fibrillation
33
What is asystole?
Loss of electrical and mechanical activity in the heart
34
What is the most common cause of cardiac arrest?
Ventricular fibrillation
35
What three things can cause ventricular fibrillation and therefore lead to cardiac arrest?
MI Electrolyte imbalance Arrhythmias
36
Give two examples of arrythmias which may lead to cardiac arrest.
Long QT | Torsades de Pointes
37
What are the three treatments used in cardiac arrest?
Basic life support Advanced life support Adrenaline
38
What is basic life support?
Chest compression and external ventilation giving ~20% of cardiac output
39
How does defibrillation treat cardiac arrest?
Depolarises all cells and puts them into refractory period allowing for a coordinated restart
40
How does a pharmacological dose of adrenaline act when treating cardiac arrest?
Activates alpha-1 receptors to increase heart function and decrease TPR
41
What is generalised shock?
Acute condition of inadequate blood flow throughout the body
42
What leads to circulatory shock?
A catastrophic fall in arterial blood pressure due to decreased cardiac output or decreased TPR beyond the heart coping capacity
43
What equation describes mean arterial blood pressure?
CO x TPR (flow x resistance)
44
What equation describes cardiac output?
HR x SV
45
What causes the TPR to decrease to a level that the heart cannot cope with?
Extensive systemic vasodilation
46
Which three types of shock result from decreased cardiac output?
Mechanical (obstructive) Cardiogenic Hypovolaemic
47
Which types of shock arise from decreased TPR?
Toxic | Anaphylactic
48
What is cardiogenic shock?
Pump failure
49
What can cause cardiogenic shock?
Damage to L. ventricle following MI Ventricular tachycardia Severe bradycardia Acute worsening of heart failure
50
How may central venous pressure be altered in cardiogenic shock?
May not be (sorry) or can be increased
51
What causes the large decrease in arterial pressure in cardiogenic shock?
The heart fills but cannot pump effectively
52
What exacerbates the problem of cardiogenic shock?
Poor perfusion of coronary arteries
53
What is the affect on the kidneys of cardiogenic shock?
Poor perfusion --> oliguria
54
Which two pathologies can cause mechanical shock?
Cardiac tamponade | Pulmonary embolism
55
How does cardiac tamponade cause mechanical shock?
Blood/fluid in pericardial space exerts pressure on heart and prevents proper relaxation and filling
56
What is limited in mechanical shock?
End diastolic volume
57
What happens to the central venous pressure in mechanical shock?
Increases
58
What happens to the arterial blood pressure in mechanical shock?
Decreases
59
Why is SV altered in mechanical shock?
Heart attempts to beat faster due to continued electrical activity so SV decreases
60
How does pulmonary embolism cause mechanical shock?
Massive PE --> occlusion of large pulmonary artery --> R ventricle cannot empty properly --> CVP increases --> decreased bloodflow to L heart
61
How does the left atrial pressure change in mechanical shock?
Decreases
62
How does the arterial blood pressure change in mechanical shock?
Decreases
63
What else may be seen in a patient with mechanical shock due to pulmonary embolism in addition to the S/S of shock?
S/S of PE: chest pain and dyspnoea
64
How does shock lead to multi-organ failure?
Decrease in arterial BP is sufficient enough to cause decrease in tissue perfusion
65
What is hypovolaemic shock?
When blood volume is reduced so that cardiac output cannot be maintained
66
What is the most common cause of hypovolaemic shock?
Haemorrhage
67
What can cause plasma loss which leads to hypovolaemic shock?
Severe burns Diarrhoea Vomiting Looks of sodium ions
68
At what percentage of bloodloss does hypovolaemic shock become symptomatic?
20-30%
69
At what percentage of blood volume loss is the serious shock response seen?
30-40%
70
What does the severity of hypovolaemic shock depend on?
Amount and speed of bloodloss
71
How are baroreceptors activated in haemorrhage?
Decreased venous pressure --> decreased CO --> arterial B.P. drops
72
What effects does activation of the baroreceptors have in hypovolaemic shock?
Increased sympathetic stimulation: increased heart rate, increased contractility, peripheral vasoconstriction and venoconstriction
73
What is internal transfusion?
Body's mechanism of increasing blood volume in hypovolaemic shock
74
How does internal transfusion work?
Increased TPR reduces downstream capillary hydrostatic pressure so fluid moves in to capillaries
75
What are the S/S of hypovolaemic shock?
Tachycardia Weak pulse Pale skin Cold, clammy extremities
76
What does decompensation lead to?
Multi-system failure
77
What is the progression of decompensation?
Hypoxic tissue damage --> vasodilators released, build up and overtake SNS --> increased TPR and decreased B.P. --> vital organs not perfumed
78
Which are the two types of nonvolaemic shock?
Toxic (septic) | Anaphylactic
79
What is nonvolaemic shock?
Normal blood volume but circulatory volume increases
80
How do endotoxins seen in septic shock cause nonvolaemic shock?
Overcome SNS to cause vasodilation --> severely decreased TPR --> arterial pressure drops --> vital organs unperfused
81
How can endotoxins from circulating bacteria cause hypovolaemic shock in septicaemia?
Cause capillaries to become leaky
82
What is the vasoconstriction response from activated baroreceptors overridden by in septic shock?
Vasodilation mediators
83
What is seen in the vasculature in the later stages of toxic shock?
Vasoconstriction
84
What are the S/S of toxic shock?
Tachycardia Warm and red extremities Strong pulse
85
Which type of shock is acutely life threatening?
Anaphylactic
86
What causes the large decrease in arterial pressure seen in anaphylactic shock?
In sever allergic reaction mast cells release powerful vasodilators such as histamine and other mediators which decrease TPR
87
How is cardiac output increased in anaphylactic shock?
Increased SNS
88
Why does the increase in cardiac output seen in anaphylactic shock not restore systemic perfusion?
It is not enough to match the systemic vasodilation
89
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?
Bronchoconstriction | Laryngeal oedema
90
What are the S/S of anaphylactic shock?
Difficulty breathing Collapsed Increased HR Red, warm extremities
91
Why is adrenaline given to treat anaphylactic shock?
To activate more alpha-1 receptors than the body can with endogenous NA and adrenaline
92
What two problems with the vasculature can cause poor perfusion?
Venous congestion | Arterial occlusion
93
Which two types of shock are considered as distributive shock?
Sepsis | Anaphylaxis

Semester 2 (45 decks)

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