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(SG) condensed phase 2a > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

define angina pectoris

A

Central chest tightness

/ pain caused by myocardial ischaemia

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2
Q

define MI

A

Death of heart tissue due to an ischaemic event

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3
Q

name 4 types of angina

A

stable

unstable

decubitus

prinzmetal’s

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4
Q

how does angina clinically present

A

Tightness or heaviness in chest on exertion/rest/emotion/cold/heavy meals.

May radiate to one or both arms, neck, jaws or teeth.

Other Symptoms: Dyspnoea, nausea, sweatiness, faintness

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5
Q

what is stable angina like?

A

Induced by effort

Relieved by rest

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6
Q

what is unstable angina like?

A

Increasing severity/frequency

Minimal exertion

^^risk of MI

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7
Q

when do you get decubitus angina pain?

A

Pain when lying flat

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8
Q

when does prinzmetal’s angina occur?

A

During rest

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9
Q

what is the pathophysiology of angina (apart from prinzmetal)?

A

Atheroma obstructing or narrowing coronary vessels

(rarely; others such as anaemia)

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10
Q

what is the pathophysiology of prinzmetal’s angina like?

A

Coronary artery spasm

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11
Q

what causes angina?

A

Atheroma

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12
Q

what is the diagnostic test for angina? And usual findings?

A

ECG: usually normal, some ST depression, flat or inverted T waves

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13
Q

what is the treatment for angina?

A

Modify risk factors

aspirin

B Blockers

Nitrates (isosorbide mononitrate or GTN spray)

Long-acting calcium channel blocker

K+ channel activator

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14
Q

what is angina linked to?

A

MI risk

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15
Q

Define myocardial infarction?

A

Death of heart tissue due to an ischaemic event

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16
Q

Name 2 types of Myocardial Infarction?

A

STEMI

NSTEMI

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17
Q

What is the clinical presentation of MI?

A

Crushing chest pain, radiating to the left arm.

Sweating, nausea, vomiting, dyspnoea, fatigue, and/or palpitations.

Signs: Fever, hypo/hypertension, 3rd/4th heart sound, signs of congestive heart failure.

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18
Q

What is STEMI MI like?

A

ST elevated. Medical emergency.

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19
Q

What is NSTEMI MI like?

A

Non-ST elevated. Medical emergency.

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20
Q

What is the cause of MI?

A

Atheroma.

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21
Q

What are the Diagnostic Tests for MI?

A

Dont delay treatment.

ECG: ST elevation (if STEMI), initially peaked T waves and then T wave inversion, New Q waves, New conduction defects. FBC: Rules out anaemia.

Cardiac enzymes: Troponins T and I are markers for cardiac damage.

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22
Q

Treatment for MI?

A

Thrombolytic (aspirin).

Percutaneous transluminal coronary angioplasty.

Possibly CABG, if PCI fails.

Follow up clopidogrel (antiplatelet) for 30 days.

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23
Q

Complications of MI?

A

Ischaemic: Recurrent infarct. Post - infarction angina.

Mechanical: Left ventricular dysfunction -> Heart failure. Ventricular septal rupture (life threatening). Free wall rupture -> Pericardial bleed -> Cardiac tamponade. False aneurysm in ventricular wall. Acute mitral regurgitation (caused by ischaemic damage to papillary muscle).

Arrhythmias: Ventricular tachycardia, ventricular fibrillation and total AV block. Bradycardia.

Thrombotic/Embolus: Thrombus can form in ventricular wall. DVT and PE possible, but low risk.

Pericarditis: Common after anterior infarct. Dressler’s syndrome (presents as pericarditis).

Depression: 20% of patients following MI.

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24
Q

What is MI linked to?

A

Shock

Heart failure

Pericardiitis

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25
Q

Define Cardiac Failure?

A

Cardiac output inadequate for the body requirements.

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26
Q

Name 2 types of cardiac failure?

A

Left

Right

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27
Q

What is the clinical presentation of left cardiac failure?

A

Dyspnoea

Tachypnea

Crackles in the lungs (base -> the rest).

Wheezing

Cyanosis (late occurring)

Frothy pink sputum.

Signs: Laterally displaced apex beat, ‘gallop’ rhythm. Heart murmurs possible.

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28
Q

What is the clinical presentation of right cardiac failure?

A

Peripheral Oedema

Ascites

Liver

Enlargement

Raised JVP.

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29
Q

What is the pathophysiology of left cardiac failure?

A

Blood backs up into the pulmonary circulation.

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30
Q

What is the pathophysiology of right cardiac failure?

A

Blood backs up into the systemic circulation.

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31
Q

Aetiology of cardiac failure?

A

Systolic: Ischaemic heart disease, MI, cardiomyoptahy.

Diastolic: Tamponade, constrictive pericarditis, systemic hypertension.

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32
Q

Diagnostic tests for cardiac failure?

A

ECG

CXR (Bat wing alveolar oedema, Kerley B lines, cardiomegaly, dilated prominent upper lobe vessels,
pleural effusion) and BNP.

If abnormal -> Echocardiography

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33
Q

Treatment for cardiac failure?

A

Stop smoking

eat healthily and exercise.

Chronic: Loop and potassium sparing diuretics for fluid overload, ACEI, Beta-blockers

Acute: Oxygen, monitor ECG, diamorphine, furosemide, GTN spray LOON: Loop, Oxygen, Opioid Nitrates

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34
Q

Define valvular heart disease?

A

Disease process affecting the valves of the heart.

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35
Q

What are the 4 types of valvular heart disease?

A

Mitral stenosis

Mitral regurgitation

Aortic stenosis

Aortic regurgitation

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36
Q

What is the clinical presentation of mitral stenosis?

A

Pulmonary hypertension -> dyspnoea,

pink frothy sputum,

left atrial dilatation,

right ventricular hypertrophy,

palpitations.

Malar flush due to low CO. Opening snap and diastolic murmur.

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37
Q

What is the clinical presentation of mitral regurgitation?

A

Variable haemodynamic effects.

Pansystolic murmur,

Mid-systolic click and late systolic murmur in mitral prolapse.

Deviated apex beat.

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38
Q

What is the clinical presentation of aortic stenosis?

A

Ejection systolic murmur.

Left ventricular hypertrophy.

(SAD)

Syncope

Angina

Dyspnoea

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39
Q

What is the clinical presentation of aortic regurgitation?

A

Early diastolic murmur.

Wide pulse pressure,

collapsing pulse,

angina,

left ventricular failure.

Austin flint murmur: Fluttering of anterior mitral valve cusp due to regurgitant stream.

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40
Q

What is mitral stenosis like?

A

Mid-diastolic murmur.

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41
Q

What is mitral regurgitation like?

A

Pansystolic murmur.

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42
Q

What is aortic stenosis like?

A

Early systolic murmur.

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43
Q

What is aortic regurgitation like?

A

Early diastolic murmur.

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44
Q

What is the pathophysiology of mitral stenosis?

A

Inflammation -> Mitral valve thickened/calcified obstructing normal flow.

Raised LA pressure -> LA hypertrophy and dilatation -> palpitations.

Raised LA pressure -> pulmonary hypertension -> RV hypertrophy and failure.

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45
Q

What is the pathophysiology of mitral regurgitation?

A

Mitral valve fails to prevent reflux of blood.

Regurgitation into the LA -> increased LA pressure -> increased pulmonary pressure -> pulmonary oedema.

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46
Q

What is the pathophysiology of aortic stenosis?

A

Aortic valve thickened/calcified obstructing normal flow.

Obstructed LV outflow -> Increased LV pressure -> Compensatory LV hypertrophy -> Relative ischaemia -> Angina, arrythmia and LV failure -> Reduced cardiac output.

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47
Q

What is the pathophysiology of aortic regurgitation?

A

Aortic valve fails to prevent reflux of blood.

LV hypertrophy to maintain cardiac output -> Reduced diastolic blood pressure -> relative ischaemia.

Eventually leads to left ventricular failure.

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48
Q

Aetiology of mitral stenosis?

A

Rheumatic valvular disease (usually Strep pyogenes).

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49
Q

Aetiology of mitral regurgitation?

A

Dilation of mitral valve annulus.

Mitral valve prolapse.

Infective endocarditis.

Rheumatiic valvular disease.

Marfan’s and Ehler-Danlos

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50
Q

Aetiology of aortic stenosis?

A

Calcific degeneration. Rheumatic valvular disease.

Congenital bicuspid valve.

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51
Q

Aetiology of aortic regurgitation?

A

Aortic root dilation.

Infective endocarditis

Rheumatic fever

Some rheumatological disorders.

Ascending aortic dissection possible.

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52
Q

Epidemiology of aortic stenosis?

A

Most common valvular condition requiring surgery.

Mostly in the elderly.

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53
Q

What are the diagnostic tests for mitral stenosis?

A

Echocardiography.

ECG: AF, LA enlargement, RV hypertrophy.

Echocardiography: Definitive diagnosis; measure mitral orifice .

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54
Q

What is the diagnostic test for mitral regurgitation?

A

Echocardiography

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55
Q

What is the diagnostic test for aortic stenosis?

A

Echocardiography.

ECG: LV hypertrophy.

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56
Q

What is the diagnostic test for aortic regurgitation?

A

Echocardiography.

ECG: LV hypertrophy

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57
Q

What is the treatment for mitral stenosis?

A

Diuretics (furosemide), rate control + anticoagulation. Valvotomy.

Excise segments of valve, or valve replacement.

Infective endocarditis prophylaxis (amoxicillin?)

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58
Q

What is the treatment for mitral regurgitation?

A

Repair preferred over replacement.

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59
Q

What is the treatment for aortic stenosis?

A

Valve replacement,

Balloon valvuloplasty,

Transcatheter aortic valve replacement,

Surgical valvuloplasty

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60
Q

What is the treatment for aortic regurgitation?

A

Treat underlying cause.

Possibly vasodilators or inotropes.

Diuretics.

Valve replacement.

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61
Q

What are the complications of valvular heart disease?

A

Valve replacements can cause clotting.

Anticoagulants prescribed with them.

Endocardititis.

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62
Q

What is aortic stenosis linked to?

A

Left sided heart failure.

Sudden death.

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63
Q

What is aortic regurgitation linked to?

A

Left sided heart failure.

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64
Q

Define Atrial fibrillation

A

Irregularly irregular ventricular pulse and loss of association between cardiac apex beat and radial pulsation.

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65
Q

Define Heart block

A

Disrupted electrical impulses

-> bradycardia

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66
Q

Types of Heart block

A

First degree.

Second degree: Mobitz I.

Second degree: Mobitz II.

Third degree - (complete).

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67
Q

How does Atrial fibrillation clinically present?

A

Breathlessness,

palpitations,

syncope,

chest discomfort,

stroke/TIA.

Irregularly irregular pulse.

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68
Q

How does First degree heart block clinically present?

A

Bradycardia.

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69
Q

How does Second degree: Mobitz I heart block clinically present?

A

Bradycardia.

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70
Q

How does Second degree: Mobitz II heart block clinically present?

A

Bradycardia.

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71
Q

How does Third degree heart block clinically present?

A

If site of block is His-Purkinje system:

Stokes-Adams attacks (dizziness and blackouts).

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72
Q

Pathophysiology of Atrial fibrillation

A

Artial activity is chaotic and mechanically ineffective.

Stagnation of blood in the atria

-> thrombus formation and a risk of embolism

-> stroke.

Reduction in cardiac output -> Heart failure.

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73
Q

Pathophysiology of First degree heart block

A

Delayed atrioventricular conduction.

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74
Q

Pathophysiology of Second degree heart block

A

Some atrial impulses fail to reach the ventricles.

75
Q

Pathophysiology of Third degree heart block

A

All atrial activity fails to conduct to ventricles.

Ventricular contractions maintained by spontaneous escape rhythm from below site of the block; His bundle: narrow complex QRS relatively reliable.

His-Purkinje: gives rise to broad QRS complex unreliable

76
Q

Cause of Atrial fibrillation

A

Hypertension,

coronary artery disease,

valvular heart disease (particularly mitral valve stenosis),

cardiac surgery.

77
Q

Cause of Heart block

A

Coronary artery disease,

cardiomyopathy and (in elderly) fibrosis of conducting tissue.

78
Q

Epidemiology of Atrial fibrillation

A

Most common sustained arrhythmia.

Males.

79
Q

Diagnostic test for Atrial fibrillation

A

ECG: variability in the R-R intervals, absent p waves.

80
Q

Diagnostic test for First degree heart block

A

ECG: Prolonged PR interval >200 ms.

81
Q

Diagnostic test for Second degree: Mobitz I heart block

A

ECG: Progressively increasing P-R intervals

-> dropped QRS.

82
Q

Diagnostic test for Second degree: Mobitz II heart block

A

ECG: Sustained P-R intervals

-> occasional dropped QRS.

83
Q

Diagnostic test for Third degree heart block

A

ECG: Complete dissociation of P from QRS.

84
Q

Treatment of Atrial fibrillation

A

Control arrhythmia; rate: Beta blockers,

Calcium antagonists rhythm: cardioversion.

Thromboprophylaxis to prevent strokes. Treat underlying cause.

85
Q

Treatment of First degree heart block

A

None needed.

86
Q

Treatment of Second degree: Mobitz I heart block

A

Managed with monitoring,

may need pacemaker.

87
Q

Treatment of Second degree: Mobitz II heart block

A

Managed with monitoring,

may need pacemaker.

88
Q

Treatment of Third degree heart block

A

His bundle: May respond to atropine,

if not -> pacemaker His-Purkinje: permanent pacemaker.

89
Q

Define Supraventricular tachycardia

A

Rapid heart rhythm originating at or above the AV node.

90
Q

Define Bundle branch block

A

Heart block before the bundle branches.

91
Q

Types of Supraventricular tachycardia

A

Re-entrant.

Automatic.

92
Q

Types of Bundle branch block

A

Left.

Right.

93
Q

How does Supraventricular tachycardia clinically present?

A

Paroxysmal attacks.

Maybe minimal.

Syncope, and palpitations.

Tachycardia.

94
Q

How does Bundle branch block - left - clinically present?

A

Usually asymptomatic.

Possible syncope.

95
Q

How does Bundle branch block - right - clinically present?

A

Usually asymptomatic.

Possible syncope.

96
Q

Pathophysiology of Supraventricular tachycardia

A

The gating mechanism of the AV node is being bypassed.

In reentrant, a bypass tract exists to go around the node (Wolff-Parkinson-White syndrome)

and in automatic, an impulse is created that never encounters the AV node.

97
Q

Pathophysiology of Bundle branch block - left

A

Left bundle branch no longer conducts an impulse and the two ventricles do not receive an impulse simultaneously (first right then the left).

This creates the second R wave in the left ventricular leads (I, AVL and V4-V6) and a slurred S wave (V1 and V2).

98
Q

Pathophysiology of Bundle branch block - right

A

Right bundle branch no longer conducts an impulse and the two ventricles do not receive an impulse simultaneously (first left then the right).

This creates the second R wave (V1) and a slurred S wave (V5 and V6).

99
Q

Cause of Supraventricular tachycardia

A

Drugs,

alcohol,

caffeine,

congenital,

stress,

smoking.

100
Q

Cause of Bundle branch block - left

A

Cardiac pathology; ischarmic heart disease,

left ventricular hypertrophy,

aortic valve disease

and following cardiac surgery.

101
Q

Cause of Bundle branch block - right

A

Pulmonary embolus,

RV hypertrophy,

ischaemic/congenital heart disease.

102
Q

Epidemiology of Supraventricular tachycardia

A

RF: Previous MI,

Mitral valve prolapse,

rheumatic heart disease,

pericarditis.

103
Q

Epidemiology of Bundle branch block - right

A

Can be in normal healthy individuals.

104
Q

Diagnostic test for Supraventricular tachycardia

A

ECG: P waves may not be visible.

Pre-excitation on resting ECG

+ rapid and paroxysmal regular palpitations

-> re-entrant.

Short PR interval.

105
Q

Diagnostic test for Bundle branch block - left

A

ECG: Secondary R in I, AVL, V4-V6.

Slurred S in V1 and V2.

106
Q

Diagnostic test for Bundle branch block - right

A

ECG: Secondary R in V1 and a slurred S wave in V5 and V6.

107
Q

Treatment of Supraventricular tachycardia

A

Haemodynamically unstable: Cardioversion.

Haemodynamically stable: carotid massage.

108
Q

Treatment of Bundle branch block - left

A

May require pacemaker.

109
Q

Treatment of Bundle branch block - right

A

Treat underlying condition.

110
Q

Define Aortic aneurysm

A

Permanent

> 50% dilation of the aorta.

111
Q

Types of Aortic aneurysm

A

Abdominal (Unruptured).

Abdominal (Ruptured).

Thoracic (Unruptured).

Thoracic (Ruptured).

112
Q

How does an Abdominal (Unruptured) aortic aneurysm clinically present?

A

Usually asymptomatic.

Incidental finding.

Possible pain in back (Severe lumbar pain indicator of imminent rupture).

Pulsatile abdominal swelling.

113
Q

How does an Abdominal (Ruptured) aortic aneurysm clinically present?

A

Consider if Hypotensive w/ unusual abdominal symptoms.

Pain in back (sudden, severe).

Syncope, shock, collapse.

114
Q

How does a Thoracic (Unruptured) aortic aneurysm clinically present?

A

Usually asymptomatic.

Incidental finding.

Possible pain in chest, neck, etc, related to location.

Aortic regurgitation.

Symptoms relating to compression of structures (cough, etc).

115
Q

How does a Thoracic (Ruptured) aortic aneurysm clinically present?

A

Acute pain.

Collapse, shock, sudden death.

116
Q

Thoracic (Unruptured) aortic aneurysm - note

A

Possibility of rupturing.

Risk proportional to diameter.

117
Q

Pathophysiology of an Abdominal (Ruptured) aortic aneurysm

A

Spontaneous occurrence from unruptured aneurysm.

118
Q

Pathophysiology of a Thoracic (Unruptured) aortic aneurysm

A

Inflammation.

Proteolysis.

Reduced survival of smooth muscle cells.

119
Q

Pathophysiology of a Thoracic (Ruptured) aortic aneurysm

A

Spontaneous occurrence from unruptured aneurysm.

120
Q

Cause of Abdominal (ruptured and unruptured) aortic aneurysm

A

Most no specific cause.

Very few: Trauma, infection.

Risk Factors: Atherosclerotic damage. Family history. Smoking. Hypertension. COPD.

121
Q

Cause of thoracic (ruptured and unruptured) aortic aneurysm

A

Strong genetic link.

Infection possible. Trauma.

Connective tissue disorders.

Risk Factors: Smoking, hypertension, Family history, Atherosclerotic damage. COPD.

122
Q

Diagnostic test for Abdominal (Unruptured) aortic aneurysm

A

Ultrasound.

123
Q

Diagnostic test for Abdominal (Ruptured) aortic aneurysm

A

None, medical emergency.

124
Q

Diagnostic test for Thoracic (Unruptured) aortic aneurysm

A

ECG,

Ultrasound,

Lung function tests,

Blood tests: FBC, clotting screen, renal function.

125
Q

Diagnostic test for Thoracic (Ruptured) aortic aneurysm

A

ECG,

CT scan with contrast.

126
Q

Treatment of Abdominal (Unruptured) aortic aneurysm

A

Surgical repair / Insertion of supportive stents.

127
Q

Treatment of Abdominal (Ruptured) aortic aneurysm

A

Immediate surgical repair (50% mortality).

128
Q

Treatment of Thoracic (Unruptured) aortic aneurysm

A

Surgical repair / Insertion of supportive stents.

129
Q

Treatment of Thoracic (Ruptured) aortic aneurysm

A

Immediate surgical repair.

130
Q

Complications of Abdominal (Unruptured) aortic aneurysm

A

Rupture into the retroperitoneal space.

131
Q

Complications of Abdominal (Ruptured) aortic aneurysm

A

Death.

132
Q

Complications of Thoracic (Unruptured) aortic aneurysm

A

Rupture.

133
Q

Complications of Thoracic (Ruptured) aortic aneurysm

A

Death.

134
Q

Sequelae of - Abdominal (Unruptured) aortic aneurysm

A

Peripheral vascular disease.

135
Q

Sequelae of - Thoracic (Unruptured) aortic aneurysm

A

Pressure on adjacent structures.

Aortic dissection.

136
Q

Define Aortic dissection

A

Tear in the tunica intima

-> blood between layers of aortic wall.

137
Q

Define Peripheral vascular disease.

A

Narrowing of arteries distal to the aortic arch.

138
Q

How does aortic dissection clinically present?

A

Phase 1: Initial event; severe ‘ripping’ pain and pulse loss. The bleeding then stops. Diastolic murmur.

Phase 2: Pressure builds, and causes a rupture, either into pericardium (tamponade), mediastinum or pleural space.

Pain often migrates as dissection progresses.

139
Q

How does peripheral vascular disease clinically present?

A

Varying symptoms:

Asymptomatic -> Intermittent claudication (on exercise)

-> rest pain (critical limb ischaemia)

-> skin ulceration and gangrene.

Signs: Absent femoral, popliteal or foot pulses.

Cold white legs.

140
Q

Aortic dissection - note

A

Most common sites are within 2-3cms of the aortic valve,

or distal to the left subclavian artery in descending aorta.

141
Q

Pathophysiology of aortic dissection

A

Starts with a tear in the intima of the aortic lining.

This allows column of blood to enter the aortic wall under pressure.

This forms a haematoma with separates the intima from the adventitia and creates a false lumen, variable distance in either direction.

142
Q

Pathophysiology of peripheral vascular disease

A

Atherosclerosis causing stenosis of arteries.

143
Q

Cause of aortic dissection

A

Genetic link. Atherosclerotic.

Inflammatory. Trauma.

Risk Factors: Connective tissue disorders. Hypertension.

Cocaine use. Aortic aneurysm. Smoking. Hypercholesterolaemia.

144
Q

Cause of peripheral vascular disease

A

Atherosclerotic damage.

Risk Factors: Classical atheroma risk factors.

145
Q

Diagnostic test for aortic dissection

A

ECG: 20% will have evidence of ischaemia/MI.

Ultrasound: Indicates site/extent.

MRI: Confirmation.

CXR: Appears normal (poor indicator)

146
Q

Diagnostic test for peripheral vascular disease

A

ECG: 60% of claudication patients have evidence of coronary artery disease.

Doppler ultrasonography: Confirm diagnosis.

Site, degree and length.

147
Q

Treatment of aortic dissection

A

Stentgraft.

Surgery if the dissection shows to be progressing.

148
Q

Treatment of peripheral vascular disease

A

Modify risk factors.

149
Q

Complications of aortic dissection

A

Rupture (80% mortality).

Cardiac tamponade -> Syncope and hypotension.

150
Q

Complications of peripheral vascular disease

A

Acute limb ischaemia

-> Amputation, gangrene, infection, poor healing, ulceration.

151
Q

Define Shock

A

Inability of the heart to adequately perfuse tissues.

152
Q

Types of Shock

A

Hypovolaemic: Haemorrhagic

Hypovolaemic: Septic

Hypovolaemic: Neurogenic

Hypovolaemic: Anaphylactic

Cardiogenic

153
Q

How does Hypovolaemic: Haemorrhagic shock clinically present?

A

Anxiety, blue lips/fingernails,

low urine output,

shallow breathing,

sweating,

dizziness,

confusion,

weak pulse,

low BP, high HR.

154
Q

How does Hypovolaemic: Septic shock clinically present?

A

Low BP,

dizziness,

confusion,

diarrhoea,

cold clammy skin,

tachypnoea,

fever.

155
Q

How does Hypovolaemic: Neurogenic shock clinically present?

A

Instantaneous hypotension, warm flushed skin,

Priaprism,

bradycardia.

Note contrast to other shocks

156
Q

How does Hypovolaemic: Anaphylactic shock clinically present?

A

Itching,

sweating,

diarrhoea,

vomiting,

erythema,

urticaria,

oedema,

wheeze,

cyanosis,

tachycardia, hypotension.

157
Q

How does Cardiogenic shock clinically present?

A

Chest pain, nausea, dyspnoea,

profuse sweating,

confusion/disorientation, palpitations, syncope.

Signs: Pale mottled skin.

Slow capillary refill. Hypotension.

Tachycardia/bradycardia, ^JVP,

Peripheral oedema.

158
Q

Hypovolaemic: Haemorrhagic shock - note

A

As a result of a bleed.

Possibly internal, if no external signs.

Medical emergency.

159
Q

Hypovolaemic: Septic shock - note

A

As a result of an infection.

Medical emergency.

160
Q

Hypovolaemic: Neurogenic shock - note

A

Sympathetic innervation lost due to CNS damage.

Sympathetic tone lose leads to pooling of blood in extremities.

161
Q

Hypovolaemic: Anaphylactic shock - note

A

Type I IgE-mediated hypersensitivity reaction.

Precipitant examples: Drug, latex, fish, stings, eggs.

162
Q

Cardiogenic shock - note

A

Failure of the pump action of the heart.

Sustained hypotension for >30 mins,

Tissue hypoperfusion.

Mortality rate variable: Up to 50%.

163
Q

Pathophysiology of Hypovolaemic: Haemorrhagic shock

A

Lower blood volume

-> lower stroke volume

-> lower CO

-> Reduced perfusion.

164
Q

Pathophysiology of Hypovolaemic: Septic shock

A

Bacterial infection can damage blood vessels

causing them to leak fluid into the surrounding tissues.

165
Q

Pathophysiology of Hypovolaemic: Neurogenic shock

A

Trauma causes a sudden loss of background sympathetic stimulation to blood vessels.

This causes sudden vasodilation and therefore a sudden drop of blood pressure.

166
Q

Pathophysiology of Hypovolaemic: Anaphylactic shock

A

Release of histamine and other agents causes:

capillary leak, wheeze, cyanosis, oedema and urticaria.

167
Q

Pathophysiology of Cardiogenic shock

A

Cardiac dysfunction

-> inability to perfuse vital organs and tissues.

This leads to acute hypoperfusion and hypoxia of tissues and organs despite adequate intravascular volume.

168
Q

Cause of Hypovolaemic: Haemorrhagic shock

A

Bleeding (in turn caused by trauma etc).

Burns also possible (loss of fluid).

169
Q

Cause of Hypovolaemic: Septic shock

A

Sepsis.

170
Q

Cause of Hypovolaemic: Neurogenic shock

A

Damage to the CNS.

Spinal cord above T6.

171
Q

Cause of Hypovolaemic: Anaphylactic shock

A

Hypersensitivity reaction.

172
Q

Cause of Cardiogenic shock

A

Acute MI (most often).

Other intrinsic heart problem possible (arrythmias, PE, Cardiac tamponade).

Risk Factors: History of infarction.

Diabetes. Peripheral vascular disease.

173
Q

Epidemiology of Hypovolaemic: Haemorrhagic shock

A

Worse prognosis in the elderly.

174
Q

Diagnostic test for Hypovolaemic: Haemorrhagic shock

A

Bloods: Electrolytes

Ultrasound: Visualise organs.

175
Q

Diagnostic test for Hypovolaemic: Septic shock

A

FBC: leukocytosis, low platelets.

U&E: raised urea and creatinine.

176
Q

Diagnostic test for Hypovolaemic: Neurogenic shock

A

Physical examination.

FBC, U&E, CT scan to assess condition.

177
Q

Diagnostic test for Cardiogenic shock

A

U&Es: Assess renal function.

FBC: Exclude anaemia.

Echocardiogram: Assess cause.

178
Q

Treatment of Hypovolaemic: Haemorrhagic shock

A

Stop bleeding.

Give oxygen.

Acquire IV early; supply fluids.

179
Q

Treatment of Hypovolaemic: Septic shock

A

Oxygen therapy.

Vasopressors,

Take cultures,

Acquire IV early; supply fluids,

Antibiotics.

180
Q

Treatment of Hypovolaemic: Neurogenic shock

A

Inotropic (dopamine),

Vasopressin,

Vasopressors.

181
Q

Treatment of Hypovolaemic: Anaphylactic shock

A

Adrenaline, chlorphenamine + hydrocortisone.

If wheeze, treat for asthma.

182
Q

Treatment of Cardiogenic shock

A

If MI, revascularisation immediately, with thrombolysis.

183
Q

Complications of Hypovolaemic: Haemorrhagic shock

A

Death,

organ failure (kidneys),

gangrene,

heart attack.

184
Q

Complications of Hypovolaemic: Septic shock

A

Recurrence,

cardiomyopathy,

acute kidney injury.

(SG) condensed phase 2a (9 decks)

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