Cardiovascular Flashcards
1
Q
define angina pectoris
A
Central chest tightness
/ pain caused by myocardial ischaemia
2
Q
define MI
A
Death of heart tissue due to an ischaemic event
3
Q
name 4 types of angina
A
stable
unstable
decubitus
prinzmetal’s
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
5
Q
what is stable angina like?
A
Induced by effort
Relieved by rest
6
Q
what is unstable angina like?
A
Increasing severity/frequency
Minimal exertion
^^risk of MI
7
Q
when do you get decubitus angina pain?
A
Pain when lying flat
8
Q
when does prinzmetal’s angina occur?
A
During rest
9
Q
what is the pathophysiology of angina (apart from prinzmetal)?
A
Atheroma obstructing or narrowing coronary vessels
(rarely; others such as anaemia)
10
Q
what is the pathophysiology of prinzmetal’s angina like?
A
Coronary artery spasm
11
Q
what causes angina?
A
Atheroma
12
Q
what is the diagnostic test for angina? And usual findings?
A
ECG: usually normal, some ST depression, flat or inverted T waves
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
14
Q
what is angina linked to?
A
MI risk
15
Q
Define myocardial infarction?
A
Death of heart tissue due to an ischaemic event
16
Q
Name 2 types of Myocardial Infarction?
A
STEMI
NSTEMI
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.
18
Q
What is STEMI MI like?
A
ST elevated. Medical emergency.
19
Q
What is NSTEMI MI like?
A
Non-ST elevated. Medical emergency.
20
Q
What is the cause of MI?
A
Atheroma.
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.
22
Q
Treatment for MI?
A
Thrombolytic (aspirin).
Percutaneous transluminal coronary angioplasty.
Possibly CABG, if PCI fails.
Follow up clopidogrel (antiplatelet) for 30 days.
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.
24
Q
What is MI linked to?
A
Shock
Heart failure
Pericardiitis
25
Define Cardiac Failure?
Cardiac output inadequate for the body requirements.
26
Name 2 types of cardiac failure?
Left
Right
27
What is the clinical presentation of left cardiac failure?
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.
28
What is the clinical presentation of right cardiac failure?
Peripheral Oedema
Ascites
Liver
Enlargement
Raised JVP.
29
What is the pathophysiology of left cardiac failure?
Blood backs up into the pulmonary circulation.
30
What is the pathophysiology of right cardiac failure?
Blood backs up into the systemic circulation.
31
Aetiology of cardiac failure?
Systolic: Ischaemic heart disease, MI, cardiomyoptahy.
Diastolic: Tamponade, constrictive pericarditis, systemic hypertension.
32
Diagnostic tests for cardiac failure?
ECG
CXR (Bat wing alveolar oedema, Kerley B lines, cardiomegaly, dilated prominent upper lobe vessels,
pleural effusion) and BNP.
If abnormal -> Echocardiography
33
Treatment for cardiac failure?
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
34
Define valvular heart disease?
Disease process affecting the valves of the heart.
35
What are the 4 types of valvular heart disease?
Mitral stenosis
Mitral regurgitation
Aortic stenosis
Aortic regurgitation
36
What is the clinical presentation of mitral stenosis?
Pulmonary hypertension -> dyspnoea,
pink frothy sputum,
left atrial dilatation,
right ventricular hypertrophy,
palpitations.
Malar flush due to low CO. Opening snap and diastolic murmur.
37
What is the clinical presentation of mitral regurgitation?
Variable haemodynamic effects.
Pansystolic murmur,
Mid-systolic click and late systolic murmur in mitral prolapse.
Deviated apex beat.
38
What is the clinical presentation of aortic stenosis?
Ejection systolic murmur.
Left ventricular hypertrophy.
(SAD)
Syncope
Angina
Dyspnoea
39
What is the clinical presentation of aortic regurgitation?
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.
40
What is mitral stenosis like?
Mid-diastolic murmur.
41
What is mitral regurgitation like?
Pansystolic murmur.
42
What is aortic stenosis like?
Early systolic murmur.
43
What is aortic regurgitation like?
Early diastolic murmur.
44
What is the pathophysiology of mitral stenosis?
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.
45
What is the pathophysiology of mitral regurgitation?
Mitral valve fails to prevent reflux of blood.
Regurgitation into the LA -> increased LA pressure -> increased pulmonary pressure -> pulmonary oedema.
46
What is the pathophysiology of aortic stenosis?
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.
47
What is the pathophysiology of aortic regurgitation?
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.
48
Aetiology of mitral stenosis?
Rheumatic valvular disease (usually Strep pyogenes).
49
Aetiology of mitral regurgitation?
Dilation of mitral valve annulus.
Mitral valve prolapse.
Infective endocarditis.
Rheumatiic valvular disease.
Marfan's and Ehler-Danlos
50
Aetiology of aortic stenosis?
Calcific degeneration. Rheumatic valvular disease.
Congenital bicuspid valve.
51
Aetiology of aortic regurgitation?
Aortic root dilation.
Infective endocarditis
Rheumatic fever
Some rheumatological disorders.
Ascending aortic dissection possible.
52
Epidemiology of aortic stenosis?
Most common valvular condition requiring surgery.
Mostly in the elderly.
53
What are the diagnostic tests for mitral stenosis?
Echocardiography.
ECG: AF, LA enlargement, RV hypertrophy.
Echocardiography: Definitive diagnosis; measure mitral orifice .
54
What is the diagnostic test for mitral regurgitation?
Echocardiography
55
What is the diagnostic test for aortic stenosis?
Echocardiography.
ECG: LV hypertrophy.
56
What is the diagnostic test for aortic regurgitation?
Echocardiography.
ECG: LV hypertrophy
57
What is the treatment for mitral stenosis?
Diuretics (furosemide), rate control + anticoagulation. Valvotomy.
Excise segments of valve, or valve replacement.
Infective endocarditis prophylaxis (amoxicillin?)
58
What is the treatment for mitral regurgitation?
Repair preferred over replacement.
59
What is the treatment for aortic stenosis?
Valve replacement,
Balloon valvuloplasty,
Transcatheter aortic valve replacement,
Surgical valvuloplasty
60
What is the treatment for aortic regurgitation?
Treat underlying cause.
Possibly vasodilators or inotropes.
Diuretics.
Valve replacement.
61
What are the complications of valvular heart disease?
Valve replacements can cause clotting.
Anticoagulants prescribed with them.
Endocardititis.
62
What is aortic stenosis linked to?
Left sided heart failure.
Sudden death.
63
What is aortic regurgitation linked to?
Left sided heart failure.
64
Define Atrial fibrillation
Irregularly irregular ventricular pulse and loss of association between cardiac apex beat and radial pulsation.
65
Define Heart block
Disrupted electrical impulses
-> bradycardia
66
Types of Heart block
First degree.
Second degree: Mobitz I.
Second degree: Mobitz II.
Third degree - (complete).
67
How does Atrial fibrillation clinically present?
Breathlessness,
palpitations,
syncope,
chest discomfort,
stroke/TIA.
Irregularly irregular pulse.
68
How does First degree heart block clinically present?
Bradycardia.
69
How does Second degree: Mobitz I heart block clinically present?
Bradycardia.
70
How does Second degree: Mobitz II heart block clinically present?
Bradycardia.
71
How does Third degree heart block clinically present?
If site of block is His-Purkinje system:
Stokes-Adams attacks (dizziness and blackouts).
72
Pathophysiology of Atrial fibrillation
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.
73
Pathophysiology of First degree heart block
Delayed atrioventricular conduction.
74
Pathophysiology of Second degree heart block
Some atrial impulses fail to reach the ventricles.
75
Pathophysiology of Third degree heart block
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
Cause of Atrial fibrillation
Hypertension,
coronary artery disease,
valvular heart disease (particularly mitral valve stenosis),
cardiac surgery.
77
Cause of Heart block
Coronary artery disease,
cardiomyopathy and (in elderly) fibrosis of conducting tissue.
78
Epidemiology of Atrial fibrillation
Most common sustained arrhythmia.
Males.
79
Diagnostic test for Atrial fibrillation
ECG: variability in the R-R intervals, absent p waves.
80
Diagnostic test for First degree heart block
ECG: Prolonged PR interval >200 ms.
81
Diagnostic test for Second degree: Mobitz I heart block
ECG: Progressively increasing P-R intervals
-> dropped QRS.
82
Diagnostic test for Second degree: Mobitz II heart block
ECG: Sustained P-R intervals
-> occasional dropped QRS.
83
Diagnostic test for Third degree heart block
ECG: Complete dissociation of P from QRS.
84
Treatment of Atrial fibrillation
Control arrhythmia; rate: Beta blockers,
Calcium antagonists rhythm: cardioversion.
Thromboprophylaxis to prevent strokes. Treat underlying cause.
85
Treatment of First degree heart block
None needed.
86
Treatment of Second degree: Mobitz I heart block
Managed with monitoring,
may need pacemaker.
87
Treatment of Second degree: Mobitz II heart block
Managed with monitoring,
may need pacemaker.
88
Treatment of Third degree heart block
His bundle: May respond to atropine,
if not -> pacemaker His-Purkinje: permanent pacemaker.
89
Define Supraventricular tachycardia
Rapid heart rhythm originating at or above the AV node.
90
Define Bundle branch block
Heart block before the bundle branches.
91
Types of Supraventricular tachycardia
Re-entrant.
Automatic.
92
Types of Bundle branch block
Left.
Right.
93
How does Supraventricular tachycardia clinically present?
Paroxysmal attacks.
Maybe minimal.
Syncope, and palpitations.
Tachycardia.
94
How does Bundle branch block - left - clinically present?
Usually asymptomatic.
Possible syncope.
95
How does Bundle branch block - right - clinically present?
Usually asymptomatic.
Possible syncope.
96
Pathophysiology of Supraventricular tachycardia
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
Pathophysiology of Bundle branch block - left
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
Pathophysiology of Bundle branch block - right
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
Cause of Supraventricular tachycardia
Drugs,
alcohol,
caffeine,
congenital,
stress,
smoking.
100
Cause of Bundle branch block - left
Cardiac pathology; ischarmic heart disease,
left ventricular hypertrophy,
aortic valve disease
and following cardiac surgery.
101
Cause of Bundle branch block - right
Pulmonary embolus,
RV hypertrophy,
ischaemic/congenital heart disease.
102
Epidemiology of Supraventricular tachycardia
RF: Previous MI,
Mitral valve prolapse,
rheumatic heart disease,
pericarditis.
103
Epidemiology of Bundle branch block - right
Can be in normal healthy individuals.
104
Diagnostic test for Supraventricular tachycardia
ECG: P waves may not be visible.
Pre-excitation on resting ECG
+ rapid and paroxysmal regular palpitations
-> re-entrant.
Short PR interval.
105
Diagnostic test for Bundle branch block - left
ECG: Secondary R in I, AVL, V4-V6.
Slurred S in V1 and V2.
106
Diagnostic test for Bundle branch block - right
ECG: Secondary R in V1 and a slurred S wave in V5 and V6.
107
Treatment of Supraventricular tachycardia
Haemodynamically unstable: Cardioversion.
Haemodynamically stable: carotid massage.
108
Treatment of Bundle branch block - left
May require pacemaker.
109
Treatment of Bundle branch block - right
Treat underlying condition.
110
Define Aortic aneurysm
Permanent
>50% dilation of the aorta.
111
Types of Aortic aneurysm
Abdominal (Unruptured).
Abdominal (Ruptured).
Thoracic (Unruptured).
Thoracic (Ruptured).
112
How does an Abdominal (Unruptured) aortic aneurysm clinically present?
Usually asymptomatic.
Incidental finding.
Possible pain in back (Severe lumbar pain indicator of imminent rupture).
Pulsatile abdominal swelling.
113
How does an Abdominal (Ruptured) aortic aneurysm clinically present?
Consider if Hypotensive w/ unusual abdominal symptoms.
Pain in back (sudden, severe).
Syncope, shock, collapse.
114
How does a Thoracic (Unruptured) aortic aneurysm clinically present?
Usually asymptomatic.
Incidental finding.
Possible pain in chest, neck, etc, related to location.
Aortic regurgitation.
Symptoms relating to compression of structures (cough, etc).
115
How does a Thoracic (Ruptured) aortic aneurysm clinically present?
Acute pain.
Collapse, shock, sudden death.
116
Thoracic (Unruptured) aortic aneurysm - note
Possibility of rupturing.
Risk proportional to diameter.
117
Pathophysiology of an Abdominal (Ruptured) aortic aneurysm
Spontaneous occurrence from unruptured aneurysm.
118
Pathophysiology of a Thoracic (Unruptured) aortic aneurysm
Inflammation.
Proteolysis.
Reduced survival of smooth muscle cells.
119
Pathophysiology of a Thoracic (Ruptured) aortic aneurysm
Spontaneous occurrence from unruptured aneurysm.
120
Cause of Abdominal (ruptured and unruptured) aortic aneurysm
Most no specific cause.
Very few: Trauma, infection.
Risk Factors: Atherosclerotic damage. Family history. Smoking. Hypertension. COPD.
121
Cause of thoracic (ruptured and unruptured) aortic aneurysm
Strong genetic link.
Infection possible. Trauma.
Connective tissue disorders.
Risk Factors: Smoking, hypertension, Family history, Atherosclerotic damage. COPD.
122
Diagnostic test for Abdominal (Unruptured) aortic aneurysm
Ultrasound.
123
Diagnostic test for Abdominal (Ruptured) aortic aneurysm
None, medical emergency.
124
Diagnostic test for Thoracic (Unruptured) aortic aneurysm
ECG,
Ultrasound,
Lung function tests,
Blood tests: FBC, clotting screen, renal function.
125
Diagnostic test for Thoracic (Ruptured) aortic aneurysm
ECG,
CT scan with contrast.
126
Treatment of Abdominal (Unruptured) aortic aneurysm
Surgical repair / Insertion of supportive stents.
127
Treatment of Abdominal (Ruptured) aortic aneurysm
Immediate surgical repair (50% mortality).
128
Treatment of Thoracic (Unruptured) aortic aneurysm
Surgical repair / Insertion of supportive stents.
129
Treatment of Thoracic (Ruptured) aortic aneurysm
Immediate surgical repair.
130
Complications of Abdominal (Unruptured) aortic aneurysm
Rupture into the retroperitoneal space.
131
Complications of Abdominal (Ruptured) aortic aneurysm
Death.
132
Complications of Thoracic (Unruptured) aortic aneurysm
Rupture.
133
Complications of Thoracic (Ruptured) aortic aneurysm
Death.
134
Sequelae of - Abdominal (Unruptured) aortic aneurysm
Peripheral vascular disease.
135
Sequelae of - Thoracic (Unruptured) aortic aneurysm
Pressure on adjacent structures.
Aortic dissection.
136
Define Aortic dissection
Tear in the tunica intima
-> blood between layers of aortic wall.
137
Define Peripheral vascular disease.
Narrowing of arteries distal to the aortic arch.
138
How does aortic dissection clinically present?
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
How does peripheral vascular disease clinically present?
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
Aortic dissection - note
Most common sites are within 2-3cms of the aortic valve,
or distal to the left subclavian artery in descending aorta.
141
Pathophysiology of aortic dissection
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
Pathophysiology of peripheral vascular disease
Atherosclerosis causing stenosis of arteries.
143
Cause of aortic dissection
Genetic link. Atherosclerotic.
Inflammatory. Trauma.
Risk Factors: Connective tissue disorders. Hypertension.
Cocaine use. Aortic aneurysm. Smoking. Hypercholesterolaemia.
144
Cause of peripheral vascular disease
Atherosclerotic damage.
Risk Factors: Classical atheroma risk factors.
145
Diagnostic test for aortic dissection
ECG: 20% will have evidence of ischaemia/MI.
Ultrasound: Indicates site/extent.
MRI: Confirmation.
CXR: Appears normal (poor indicator)
146
Diagnostic test for peripheral vascular disease
ECG: 60% of claudication patients have evidence of coronary artery disease.
Doppler ultrasonography: Confirm diagnosis.
Site, degree and length.
147
Treatment of aortic dissection
Stentgraft.
Surgery if the dissection shows to be progressing.
148
Treatment of peripheral vascular disease
Modify risk factors.
149
Complications of aortic dissection
Rupture (80% mortality).
Cardiac tamponade -> Syncope and hypotension.
150
Complications of peripheral vascular disease
Acute limb ischaemia
-> Amputation, gangrene, infection, poor healing, ulceration.
151
Define Shock
Inability of the heart to adequately perfuse tissues.
152
Types of Shock
Hypovolaemic: Haemorrhagic
Hypovolaemic: Septic
Hypovolaemic: Neurogenic
Hypovolaemic: Anaphylactic
Cardiogenic
153
How does Hypovolaemic: Haemorrhagic shock clinically present?
Anxiety, blue lips/fingernails,
low urine output,
shallow breathing,
sweating,
dizziness,
confusion,
weak pulse,
low BP, high HR.
154
How does Hypovolaemic: Septic shock clinically present?
Low BP,
dizziness,
confusion,
diarrhoea,
cold clammy skin,
tachypnoea,
fever.
155
How does Hypovolaemic: Neurogenic shock clinically present?
Instantaneous hypotension, warm flushed skin,
Priaprism,
bradycardia.
Note contrast to other shocks
156
How does Hypovolaemic: Anaphylactic shock clinically present?
Itching,
sweating,
diarrhoea,
vomiting,
erythema,
urticaria,
oedema,
wheeze,
cyanosis,
tachycardia, hypotension.
157
How does Cardiogenic shock clinically present?
Chest pain, nausea, dyspnoea,
profuse sweating,
confusion/disorientation, palpitations, syncope.
Signs: Pale mottled skin.
Slow capillary refill. Hypotension.
Tachycardia/bradycardia, ^JVP,
Peripheral oedema.
158
Hypovolaemic: Haemorrhagic shock - note
As a result of a bleed.
Possibly internal, if no external signs.
Medical emergency.
159
Hypovolaemic: Septic shock - note
As a result of an infection.
Medical emergency.
160
Hypovolaemic: Neurogenic shock - note
Sympathetic innervation lost due to CNS damage.
Sympathetic tone lose leads to pooling of blood in extremities.
161
Hypovolaemic: Anaphylactic shock - note
Type I IgE-mediated hypersensitivity reaction.
Precipitant examples: Drug, latex, fish, stings, eggs.
162
Cardiogenic shock - note
Failure of the pump action of the heart.
Sustained hypotension for >30 mins,
Tissue hypoperfusion.
Mortality rate variable: Up to 50%.
163
Pathophysiology of Hypovolaemic: Haemorrhagic shock
Lower blood volume
-> lower stroke volume
-> lower CO
-> Reduced perfusion.
164
Pathophysiology of Hypovolaemic: Septic shock
Bacterial infection can damage blood vessels
causing them to leak fluid into the surrounding tissues.
165
Pathophysiology of Hypovolaemic: Neurogenic shock
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
Pathophysiology of Hypovolaemic: Anaphylactic shock
Release of histamine and other agents causes:
capillary leak, wheeze, cyanosis, oedema and urticaria.
167
Pathophysiology of Cardiogenic shock
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
Cause of Hypovolaemic: Haemorrhagic shock
Bleeding (in turn caused by trauma etc).
Burns also possible (loss of fluid).
169
Cause of Hypovolaemic: Septic shock
Sepsis.
170
Cause of Hypovolaemic: Neurogenic shock
Damage to the CNS.
Spinal cord above T6.
171
Cause of Hypovolaemic: Anaphylactic shock
Hypersensitivity reaction.
172
Cause of Cardiogenic shock
Acute MI (most often).
Other intrinsic heart problem possible (arrythmias, PE, Cardiac tamponade).
Risk Factors: History of infarction.
Diabetes. Peripheral vascular disease.
173
Epidemiology of Hypovolaemic: Haemorrhagic shock
Worse prognosis in the elderly.
174
Diagnostic test for Hypovolaemic: Haemorrhagic shock
Bloods: Electrolytes
Ultrasound: Visualise organs.
175
Diagnostic test for Hypovolaemic: Septic shock
FBC: leukocytosis, low platelets.
U&E: raised urea and creatinine.
176
Diagnostic test for Hypovolaemic: Neurogenic shock
Physical examination.
FBC, U&E, CT scan to assess condition.
177
Diagnostic test for Cardiogenic shock
U&Es: Assess renal function.
FBC: Exclude anaemia.
Echocardiogram: Assess cause.
178
Treatment of Hypovolaemic: Haemorrhagic shock
Stop bleeding.
Give oxygen.
Acquire IV early; supply fluids.
179
Treatment of Hypovolaemic: Septic shock
Oxygen therapy.
Vasopressors,
Take cultures,
Acquire IV early; supply fluids,
Antibiotics.
180
Treatment of Hypovolaemic: Neurogenic shock
Inotropic (dopamine),
Vasopressin,
Vasopressors.
181
Treatment of Hypovolaemic: Anaphylactic shock
Adrenaline, chlorphenamine + hydrocortisone.
If wheeze, treat for asthma.
182
Treatment of Cardiogenic shock
If MI, revascularisation immediately, with thrombolysis.
183
Complications of Hypovolaemic: Haemorrhagic shock
Death,
organ failure (kidneys),
gangrene,
heart attack.
184
Complications of Hypovolaemic: Septic shock
Recurrence,
cardiomyopathy,
acute kidney injury.
