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7. CVS > 20. Shock and Review > Flashcards

20. Shock and Review Flashcards

1
Q

What are the two types of poor perfusion?

A

Regional poor perfusion, and generalised poor perfusion.

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2
Q

What can cause regional poor perfusion?

A

Arterial occlusion, or venous congestion.

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3
Q

What can cause generalised poor perfusion?

A

Insufficient cardiac output to meet the body’s needs.

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4
Q

What causes arterial occlusion?

A

Atheromatous plaques.

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5
Q

What gives the veins high capacitance?

A

Thin walls, low pressure, valves, external compression by skeletal muscle.

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6
Q

What are varicose veins?

A

Dilated, torturous superficial veins.

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7
Q

When are varicose veins a problem?

A

If they are severe and go over the medial malleolus, they can cause venous ulcers. Otherwise, they are just a cosmetic problem.

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8
Q

What are some common sites of deep vein thrombosis?

A

Calf veins, popliteal, femoral, and iliac veins.

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9
Q

What is the key symptom of DVT?

A

Tender swollen calves.

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10
Q

What is the main concern with DVT and how does this transpire?

A

Risk of pulmonary embolism. Part of the thrombus breaks off then travels through the inferior vena cava, through the right heart, into the pulmonary circulation where it lodges and causes an embolism.

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11
Q

What are the effects of 70% occlusion of coronary arteries by atheromatous plaques?

A

Compromised blood flow when O2 demand increases, e.g. in exercise where there will be a greater deficit between demand and supply as diastole (coronary blood flow time) is shortened.

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12
Q

What is the major symptom of 90% occlusion of coronary arteries by atheromatous plaques?

A

Pain at rest.

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13
Q

What is the symptom of ischaemic heart disease?

A

Angina, central chest pain radiating to neck and left arm.

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14
Q

Explain in detail how stable angina may be investigated.

A

By an exercise stress test. The ECG, heart rate and BP are monitored as a patient gradually increases exercise level on a treadmill. The test is stopped when the target heart rate is met, there are ECG changes, or the patient has chest pain.

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15
Q

What are pharmacological stress tests for testing stable angina?

A

The patient is given increasing doses of B-adrenoreceptor agonists, like dobutamine.

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16
Q

What are the treatments for stable angina?

A

Nitrates, B-blockers, and calcium channel antagonists.

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17
Q

What are the three conditions of acute coronary syndromes?

A

Unstable angina, NSTEMI, and STEMI.

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18
Q

What causes unstable angina?

A

Disruption of atherosclerotic plaque and thrombus formation. But there is a limited duration and extent of obstruction so there is some ischaemia but no necrosis.

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19
Q

What are the signs and symptoms of unstable angina?

A

ST depression, T wave inversion. Severe central pain, with less radiation than MI. Also rapid onset of pain at rest.

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20
Q

What are the symptoms of MI?

A

Acute, severe, central, crushing pain. May radiate to neck, left shoulder, and arm. Not relieved by rest.

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21
Q

What causes the sweating and pallor seen in patients with an MI?

A

Strong sympathetic reaction.

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22
Q

What causes MI?

A

Rupture of atheromatous plaque and formation of a thrombus. The thrombus detaches and propagates along the coronary arteries, blocking them - causing necrosis.

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23
Q

What is the difference between STEMI and NSTEMI regarding the extent of myocardial necrosis?

A

STEMI is full thickness of the myocardial wall, NSTEMI are more limited.

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24
Q

What are the typical ECG changes in STEMI?

A

ST elevation, Q waves, and T wave inversion.

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25
Q

How do the ECG changes with STEMI develop over time?

A

Acutely - ST elevation.
Hours later - ST elevation, depressed R wave, and Q wave begins.
Day 1-2 - T wave inversion, Q wave is deeper.
Days later - ST normalises, T wave still inverted.
Weeks later - ST and T normal, but Q wave persists.

26
Q

What is cardiac arrest?

A

An unresponsiveness associated with a lack of pulse. The heart has stopped pumping at all or has stopped pumping efficiently.

27
Q

What is asystole?

A

Loss of electrical and mechanical activity in cardiac arrest.

28
Q

What is pulseless electrical activity?

A

Dissociation between the electrical and mechanical activity of the heart. So there is a pulse on the ECG but not a physical one in cardiac arrest.

29
Q

What is ventricular fibrillation?

A

Uncoordinated electrical activity, the most common type of cardiac arrest often following MI.

30
Q

What is the protocol for treating cardiac arrest?

A

Basic life support - chest compression and external ventilation. Advanced life support - defibrillation, electrical current to the heart to depolarise all cells and put them into refractory period so coordinated electrical activity can restart. Adrenaline - enhance myocardial function and increases peripheral resistance.

31
Q

How does adrenaline increase peripheral resistance?

A

Acts on a1-adrenoceptors on peripheral vessels.

32
Q

What is haemodynamic shock?

A

An acute condition of inadequate blood flow throughout the body so the arterial blood pressure catostrophically falls.

33
Q

What is the key equation for all of CVS???

A

Mean arterial BP = CO x TPR

Remember: CO = HR x SV, therefore maBP = HR x SV x TPR.

34
Q

What can cause shock?

A

A fall in CO, or TPR beyond capacity of the heart to cope.

35
Q

What can cause a fall in CO?

A

Mechanical shock - pump cannot fill, cardiogenic shock - pump failure, or hypovolaemic shock - loss of blood volume.

36
Q

What can cause a fall in peripheral resistance?

A

Excessive vasodilation.

37
Q

What is the key equation for all of CVS???

A

Mean arterial BP = CO x TPR

Remember: CO = HR x SV, therefore maBP = HR x SV x TPR.

38
Q

What is cardiogenic shock?

A

Acute failure of the heart to maintain cardiac output, pump failure.

39
Q

What can cause cardiogenic shock?

A

MI - damage to left ventricle, serious arrhythmias, or acute worsening of heart failure.

40
Q

How does cardiogenic shock affect central venous pressure and arterial BP?

A

CVP - normal or raised.

aBP - dramatic drop.

41
Q

What is the result of cardiogenic shock?

A

Tissues are poorly perfused, in the coronary arteries, this exacerbates the problem, in the kidneys there is reduced urine production etc.

42
Q

Explain how cardiac tamponade causes mechanical shock.

A

There is blood or fluid build up within the pericardial space. This restricts filling of the heart so limits end diastolic volume and there is less blood to pump out of the heart.

43
Q

How does mechanical shock affect central venous pressure and arterial BP?

A

Higher central venous pressure, and lower arterial blood pressure.

44
Q

Explain how massive pulmonary emboli cause mechanical shock.

A

An embolus occludes a large pulmonary artery, so the pressure is high and the right ventricle can’t empty. This means central venous pressure is high so there is reduced return of blood to the left heart - limited filling. Left atrial pressure is low and so is arterial blood pressure, this is shock.

45
Q

What is hypovolaemic shock?

A

Reduced blood volume.

46
Q

How does the severity of hypovolaemic shock vary?

A

Related to amount and speed of blood loss.

47
Q

How does the body try to limit the effects of hypovolaemic shock?

A

The fall in venous pressure, cardiac output, and therefore arterial pressure, is detected by baroreceptors. This causes a compensatory response where there is increased sympathetic stimulation leading to tachycardia, increased force of contraction, peripheral vasoconstriction and venoconstriction. This all aims to increase stroke volume and therefore blood pressure.

48
Q

What is internal transfusion in hypovolaemic shock?

A

There is increase peripheral resistanve to reduce the capillary hydrostatic pressure. This leads to a net movement into the capillaries, by Starling’s forces.

49
Q

What are the signs of a patient with hypovolaemic shock?

A

Tahcycardia, weak pulse, pale skin, and cold, clammy extremities.

50
Q

What can cause hypovolaemic shock?

A

Haemorrhages, severe burns, or severe diarrhoea/vomiting/loss of Na+.

51
Q

What is decompensation in hypovolaemic shock?

A

Peripheral vasoconstriction (response to maintain BP) impairs tissue perfusion. There is tissue damage due to hypoxia, release of vasodilators, so TPR falls and so does BP. This means vital organs aren’t perfused and there can be multi system failure.

52
Q

What is the key equation for all of CVS???

A

Mean arterial BP = CO x TPR

Remember: CO = HR x SV, therefore maBP = HR x SV x TPR.

53
Q

What is distributive shock?

A

The volume of blood is constant, but profound peripheral vasodilation means there is a big drop in total peripheral resistance and BP.

54
Q

How does toxic shock arise?

A

Septicaemia, endotoxins are released by the circulating bacteria. These cause profound vasodilation, a dramatic fall in TPR, a fall in arterial pressure, impaired perfusion of vital organ and the capillaries become leaky which reduces blood volume.

55
Q

What are the body’s responses to toxic shock?

A

The decreased arterial pressure is detected by baroreceptors, which increase sympathetic output. But the vasoconstriction effect from SANS is overriden by the mediators of vasodilation. HR and SV are increased.

56
Q

What are the signs of toxic shock?

A

Tachycardia, and warm, red extremities.

57
Q

What is anaphylactic shock caused by?

A

A severe allergic reaction. There is a release of histamine from mast cells, which has a powerful vasodilator effect - causing a fall in TPR and thus maBP. This increases sympathetic response to increase CO but this won’t override vasodilatory effects. There is impaired perfusion of vital organs and mediators cause bronchoconstriction and laryngeal oedema which worsen breathing and the whole situation.

58
Q

How is anaphylactic shock treated?

A

Adrenaline to cause vasoconstriction via action at a1-adrenoceptors.

59
Q

What is hypertension?

A

Sustained increase in arterial blood pressure. Arterial BP >140/90mmHg.

60
Q

What are the three key sites for blood pressure regulation?

A

Kidneys (blood volume so SV), heart (CO), and vasculature (TPR).

61
Q

What are the consequences of hypertension?

A

Left ventricular hypertrophy - and risk of heart failure. Risk of arterial disease with their corresponding affects (e.g. in coronary arteries, risk of MI and angina).

62
Q

How is hypertension treated?

A

Non pharmacologically - weight loss, exercise etc. Pharmacologically - diuretics, vasodilators, and ACE inhibitors.

7. CVS (21 decks)

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