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Cardiovascular System > Session 12 - Shock > Flashcards

Session 12 - Shock Flashcards

1
Q

What is the main cause of peripheral vascular disease?

A

-Partial occlusion of arteries due to atheromatous plaque

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2
Q

What is intermittent claudication?

A
  • Intermittent calf pain due to limited bloodflow at rest causing downstream vasodilation
  • Upon exercise vessels cannot dilate anymore and BF cannot be increased resulting in the accumulation of toxic metabolites
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3
Q

How does peripheral vascular disease present in the veins?

A
  • Varicose veins

- Deep vein thrombosis

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4
Q

At what point does coronary artery occlusion become problematic?

A

->70% occlusion

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5
Q

At what point does coronary occlusion produce pain on rest?

A

-90%

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6
Q

What is the difference between stable angina and unstable angina?

A

-Unstable angina can be present at rest

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7
Q

How does unstable angina present differently from MI?

A
  • Does not radiate as much

- Limited duration and smaller obstruction

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8
Q

What is the usual cause of progression from stable angina to unstable angina?

A

-Disruption of atherosclerotic plaque and thrombus formation

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9
Q

How is unstable angina separable from NSTEMI clinically?

A

-No detectable necrosis in unstable angina ie no cardiac enzymes or troponin elevation

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10
Q

What is the difference between NSTEMI and STEMI?

A
  • STEMI is full thickness of myocardial wall

- NSTEMI is more limited

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11
Q

How is an STEMI different from STEMI on ECG?

A

-NSTEMI has ST depression

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12
Q

Describe the ECG changes of a STEMI

A
  • ST elevation
  • Pathological Q waves
  • Twave inversion
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13
Q

When is a Q wave pathological?

A

-Greater then 1mm in width and 2 small squares in height

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14
Q

Define cardiac arrest

A

-Unresponsiveness associated with a lack of pulse due to the heart stopping or ceasing to pump effectively

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15
Q

What is asystole?

A

-Loss of electrical and mechanical activity

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16
Q

What is ventricular fibrillation?

A

-A form of cardiac arrest where there is asynchronous contraction of ventricles

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17
Q

What are the main causes of ventricular fibrillation?

A
  • Following an MI
  • Electrolyte imbalance
  • Some arrythmias
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18
Q

Name an arrhythmia which develops to ventricular fibrillation

A

-Long QT syndrome and Torsades de pointes

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19
Q

What are the modes of treatment for cardiac arrect?

A
  • Basic life support -> chest compressions and external ventilation
  • Advanced life support -> defibrillation
  • Adrenaline
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20
Q

How does defibrillation work in ventricular fibrillation?

A
  • Electrical current delivered to the heart
  • Depolarises all the cells and puts them into refractory period
  • Allows coordinated electrical activity to restart
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21
Q

How does adrenaline help treat cardiac arrest?

A
  • Increases total peripheral resistance

- Enhances myocardial function

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22
Q

What is the equation to calculate MABP?

A

-COxTPR

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23
Q

What are the two groups of causes of shock?

A
  • Decrease CO

- Decrease TPR

24
Q

Define shock

A

-Circulatory collapse when the arterial blood pressure is too low to maintain adequate perfusion

25
Q

What are the three causes of decreased CO leading to shock?

A
  • Mechanical -> pump cannot fill
  • Pump failure
  • Loss of blood volume
26
Q

What is the main cause of a decrease in peripheral resistance?

A

-Excessive vasodilation

27
Q

Name the 3 types of shock due to falls in CO

A
  • Cardiogenic shock
  • Mechanical shock
  • Hypovalaemic shock
28
Q

Define cardiogenic shock

A

-Acute failure of the heart to maintain cardiac output

29
Q

What are the main causes of cardiogenic shock?

A
  • Following MI due to damage to LV
  • Serious arrhythmias
  • Acute worsening HF
30
Q

How is the CVP effected in cardiogenic shock?

A

-Can be normal or raised as heart fills but fails to pump effectively

31
Q

What are the main issues in cardiogenic shock?

A
  • Drop in arterial BP
  • Poor perfusion to coronary arteries -> makes pump failure worse
  • Poor perfusion to kidneys -> oliguria
32
Q

What are the main causes of mechanical shock?

A
  • Cardiac tamponade

- Pulmonary embolism

33
Q

What is a cardiac tamponade?

A
  • Blood or fluid build up in pericardial space

- Restricts filling of the heart -> limits end diastolic volume

34
Q

What are the clinical features of mechanical shock?

A
  • High central venous pressure

- Low arterial blood pressure

35
Q

Is the electrical activity of the heart effected in mechanical shock?

A

-No

36
Q

Describe the effect of a pulmonary embolus occluding a large pulmonary artery

A
  • Pulmonary artery pressure high
  • RV cannot empty
  • High CVP
  • Reduced flow to left heart
  • Limits filling of heart
37
Q

How could you tell the difference clinically between mechanical shock caused by cardiac tamponade and that caused by PE?

A
  • PE will have chest pain and dyspnoea

- Cardiac tamponade will have muffled heart sounds

38
Q

What is hypovolaemic shock?

A

-Shock caused by a reduced blood volume

39
Q

What is the most common cause of hypovolaemic shock?

A

-Haemorrhage

40
Q

Over what % loss does hypovolaemic shock occur?

A

-20%

41
Q

What are the clinical signs of hypovolaemic shock?

A
  • Tachycardia
  • Weak pulse
  • Pale skin
  • Cold, clammy extremities
42
Q

Besides haemorrhage, name 2 other causes of hypovolaemic shock

A
  • Severe burns

- Severe diarrhoea or vomiting and loss of Na+

43
Q

What decompensative mechanism occurs in hypovolaemic shock?

A
  • Peripheral vasoconstriction impairs tissue perfusion
  • > tissue damage due to hypoxia
  • > release of chemical mediator causes vasodilation and TPR falls
  • > AP falls dramatically
  • > Vital organs no longer pefused
44
Q

What is distributive shock?

A

-Shock caused by profound peripheral vasodilaiton

45
Q

Name 2 types of distributive shock

A
  • Anaphylactic

- Toxic

46
Q

What causes toxic shock?

A
  • Septicaemia caused by endotoxins being released by circulating bacteria causes profound vasodilation
  • Dramatic fall in TPR followed by a fall in AP as CO cannot compensate
47
Q

What are the clinical signs of toxic shock?

A
  • Tachycardia

- Warm, red extremities

48
Q

How is CO attemted to be increased in toxic shock?

A
  • Drop in AP detected by baroreceptors
  • Increased sympathetic output
  • Heart rate and SV increased
49
Q

In toxic shock, if vasoconstriction is stimulated by the sympathetic nervous system, why does vasodilation occur?

A

-Vasoconstrictor effect overridden by mediators of vasodilation

50
Q

What is the cause of anaphylactic shock?

A
  • Severe allergic reaction causes release of histamine from mast cells
  • Histamine is a powerful vasodilator which causes a dramatic fall in TPR
  • Dramatic drop in BP which cannot be overcome by sympathetic response
51
Q

Why do people in anaphylactic shock have difficulty breathing?

A

-Mediators also cause bronchoconstriction and laryngeal oedema

52
Q

What are the clinical signs of anaphylactic shock?

A
  • Difficulty breathing
  • Collapsed
  • Rapid heart rate
  • Warm red extremities
53
Q

Define hypertension

A

-Consistent BP over 140/90

54
Q

What are the three key sites of BP regulation?

A
  • Kidneys
  • Heart
  • Vasculature
55
Q

What are the possible consequences of longstanding hypertension?

A
  • LV hypertrophy and risk of HF
  • Risk of arterial disease
  • > coronary arteries (MI/angina)
  • > cerebral (stroke)
  • > renal (kidney failure)
56
Q

What are the two main causes of poor regional perfusion?

A
  • Arterial occlusion

- Venous congestion

Cardiovascular System (19 decks)

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