Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

year 1 flash cards > clinical symposia - cardiovascular strand > Flashcards

clinical symposia - cardiovascular strand Flashcards

1
Q

what is a DVT and where fo they normally form?

A

deep vein thrombosis

  • formation of blood clot in deep vein
  • leg - femoral or popliteal vein
  • pelvis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

why are veins predisposed to clots?

A

low pressure, low flow velocity with valves to prevent backflow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how do veins move blood back to the heart?

A

against gravity

  • valves prevent backflow
  • contraction of skeletal muscles compresses veins (skeletal muscle pump)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how might a clot form in DVT?

A 
normal = laminar flow, rbc and platelets not in contact with endothelium
stasis = stagnation of flow, platelets in contact with endothelium, activated clotting factors not diluted by rapid flow, thrombus forms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

why does the leg swell in DVT?

A

thrombus causes a venous obstruction, leading to pooling of blood in the vein
increased hydrostatic pressure promotes fluid retention in tissue space (oedema)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the symptoms and signs of a DVT?

A 
warmth
redness
engorged superficial veins
unilateral swelling
pain tenderness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is a dependent oedema?

A

common in elderly patients with lack of motility
usually is symmetrical swelling
chronic
managed with compression stockings and elevation of limbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is cellulitis?

A

bacterial infection
usually unilateral
acute onset
accompanied with fever and general illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is nephrotic syndrome?

A

disease of kidneys causing severe proteinuria
lack of albumin in blood stream = fluid pools in interstitial space, severe oedema
accompanied with other kidney symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is Virchow’s triad?

A

thrombus is result of delicate interplay of

  • changes in blood flow
  • changes in blood vessel wall
  • changes in blood constituents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is an embolus?

A

material (blood clot, fat, air, amniotic fluid or foreign body) that is carried by the blood from one point in circulation to lodge at another point

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

why might a pulmonary embolus cause chest pain?

A

inflammation due to ischaemia/infarction in lung tissue sufficient to irritate parietal pleura (which has neve endings, intercostal nerve supply)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what score is used to asses DVT risk?

A

Wells score

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

why may a pulmonary embolus cause hypoxaemia?

A

ventialtion perfusion mismatch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what investigations could be done for a DVT?

A

d-dimer
doppler ultrasound - DVT
v/q scoring
CTPA - pulmonary embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is a d-dimer test?

A

fibrin break down product

very sensitive but not specific (can be caused by more than just a thrombus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is a doppler ultrasound?

A

will demonstrate presence or absence of clot

in high probability cases can do without performing d dimer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is v/q scanning?

A

not that common nowadays
nuclear medicine technique
radioactive uptake measured - can show areas of reduced perfusion (embolism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is CTPA?

A

computed tomography pulmonary angiogram
venus canula + IV contrast injected
pulmonary artery tree opacified - can see where embolus is

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is treatment for a DVT/ pulmonary embolism?

A

in 1st instance - injectable low molecular weight heparin (acts on factor II and factor Xa)
once confirmed - DOAC’s (direct oral anticoagulants) Xa inhibitors
if really bad = thrombolysis with TPA Ateplase to dissolve fibrin and remove clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

give 3 factor Xa inhibitors?

A

rivaroxaban
apixaban
edoxaban

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is angina?

A

crushing central chest pain that radiates to arms and jaws
precipitated by physical exertion and relived by rest or GTN spray
(also called chronic coronary syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the usual cause of angina?

A

myocardial ischaemia because of atherosclerosis or anaemia (not enough blood flowing through vessles)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what might decrease O2 supply?

A

coronary artery disease
coronary artery spasm
microvascular disease
anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what might increase O2 demand?

A 
exercise
tachycardia
hypertension
heavy meal
cold weather
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what happens during a heart attack?

A
  • most caused by coronary artery disease (narrowing due to gradual build up of atheroma (fatty material) within the walls)
  • if the atheroma becomes unstable, a piece may break off and lead to a blood clot forming
  • this clot can block the coronary artery, starving the heart of blood and oxygen, causing damage to the myocardium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is a myocardial infarction type I?

A

plaque rupture/erosion with occlusive thrombus or almost occlusive –> cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is myocardial infarction type II?

A

no plaque rupture/erosion, extreme form of angina - O2 supply and demand mismatch that’s severe enough to cause cell death

  • very severe anaemia
  • major haemorrhage
  • vasospasm (ie after cocaine)
  • non-atherosclerotic coronary destruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

how might ischaemia lead to heart failure?

A

impaired contraction of myocardium > abnormal electrical activity of heart cells > dangerous arrhythmia > heart failure if severe enough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what change in vichrows triad causes myocardial infarction ?

A

change in vessel wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what investigations would be performed for a MI?

A
  1. ECG most important (if ST elevation straight for emergency coronary angioplasty)
  2. coronary angiogram, echocardiography and serum troponin levels during admission
  3. MRI potentially but not for every patient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what artery supplies the inferior territory of the heart?

A

80% people is the right coronary artery

other 20% is left circumflex artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is troponin testing?

A

cardiac protein involved in interactions of actin and myosin
released in myocardial damage
three types = C I T (I and T highly specific to cardiac tissue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what are symptoms of MI?

A

diaphoresis (excessive sweating)
nausea
chest pain
breathlessness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is the treatment of MI?

A
  • pain relief with morphine, high flow O2, oral aspirin

- thrombolytic drugs replaced by primary percutaneous intervention (clot removed by tube in arm/ leg and stent placed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what preventative measures are there for MI?

A 
LIFESTYLE CHANGES
statins 
beta blockers 
antiplatlet agents
ACE inhibitors
GTN spray
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what do statins do?

A

inhibit HMG CoA reductase, reducing production of cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what do beta blockers do?

A

negatively chronotrophic = prolomg diastole, increasing coronary filling time
negatively inotropic = reduce myocardial O2 demand
reduce sympathetic overactivity - remodeling
prophylaxis against arrythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is GTN spray?

A

glyceral trinitrate

  • increase nitric oxide
  • peripheral vasodilation = decreased preload and offload of blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is a stroke

A

rapidly developing loss of brain function due to disturbance in blood supply to the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what are the 2 reasons why a stroke my occur

A
  • a blockage by thrombus or embolus: ischemic stroke

- haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is a cerebral ischema/infarction

A
  • blockage of blood vessel due to thrombus or emboli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

is a cerebral schema or haemorrhage more common?

A

ischemia- 80% strokes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

people with what kind of clinical features show cerebral ischemia

A

atrial fibrillation (irregular heartbeat)
heart attack
surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

how is a cerebral ischemia trigged

A

emboli from ruptured atherosclerotic plaque, usually from some type of intervention, ends up in carotid arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what is the main way we can prevent ischemic strokes

A

recognise risk factors early

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what causes a cerebral haemorrhage

A

rupture blood vessel when an aneurysm or out-pouching of blood vessel ruptures = bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what is the deadliest type of stroke

A

cerebral haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

how do we prevent cerebral haemorrhages

A

controlling high BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what is a TIA and what is it also known as

A

result of temporary disruption of circulation to part of the Brian due to embolism or thrombus in brain arteries
‘mini stroke’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

how long is the recovery in a TIA

A

24 hours

usually know by 3-4 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what are the common symptoms of a haemorrhage stroke

A

loss vision in one eye
weakness/numbness in a limb/part of a limb
unable to speak properly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

is time of onset of a stroke important and why

A

yes- allows us to distinguish between diff types of stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

why might a person be at risk of having a stroke? why might these factors place someone at risk?

A
  • high BP = promotes atherosclerosis so changing vessel wall and blood flow
  • atrial fibrillation = alters blood flow in L atrium, promoting thrombosis and embolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what kind of drug is someone with atrial fibrillation usually on?

A

digoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

hat route would a blood clot take?

A 
left atrium 
left ventricle 
aorta 
brachiocephalic artery 
R common carotid artery 
R internal artery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what type of scan allows us to differentiate between a ischemic and haemorrhage stroke? how?

A

CT scan
Haemorrhage - bleeding = white area with surrounding oedema = black
infarction = dark

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

why is it important to differentiate between cerebral ischemia and haemorrhage?

A

symptoms of both very similar

however one is a clot, one is a bleed and so treatment for the 2 will largely differ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

where is the common sight of build up for atherosclerosis

A

carotid arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

how does a atherosclerotic plaque rupture lead to clot formation?

A

due to the atherosclerotic plaque ending up int he carotid arteries there is turbulent blood flow in this area. once the plaque ruptures a blood clot can form on top, occulting the artery or embolising to the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what scans/investigations take place to confirm a stroke ?

A

CT scan
echocardiography/ECHO
MRI - look at brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

in what type of stroke is an ECHO usually used and what does it show?

A

undergone in those with ischemic stroke

shows how well heart is beating- any decrease of circulation of blood through chambers due to clotting

63
Q

what is the drug digoxin and what does it do?

A

cardiac glycoside

increases refractory period in AV bundle and so decreases ventricular rate in AF = slows everything down

64
Q

why is time a crucial factor in strokes?

A

if patient diagnosed within the first 4.5 hrs potential life saving thrombolysis/ thrombectomy treatment given
the longer the symptoms are left the increase in the likelihood of irreversible damage to brain (brain starved of O2)

65
Q

what drugs can we use for rate control in strokes?

A

digoxin
B-blocker
calcium channel blocker

66
Q

what’s the initial treatment strategies for strokes?

A

antiplatlet drugs:

  • patients treated with aspirin for 2 weeks (given to all patents having a stroke)
  • ongoing treatment with clopiclogerl after 14 days
anticoagulant drugs (give if high risk of stroke)
- if AF present anticoagulation to start 2 weeks after stroke
67
Q

what’s Lisinopril and why is it used

A

ACE inhibitor

potent drug in lowering BP and reducing risk of stroke

68
Q

what are the different ways we can prevent strokes

A
  • modify existing risk factors: BP control, smoking cessation
  • screen for AF - anticoagulants if necessary
  • statin = 2nd prevention
  • antiplatlet therapy
  • diet/exercise/ lifestyle measures
69
Q

how might myocarditis cause heart failure?

A

may cause dysrhythmia or acute heart failure –> chronic heart failure or sudden cardiac death

70
Q

what is myocarditis?

A

inflammation of the heart following an infection, immune disorders or drugs or toxins

71
Q

what might cause systolic heart failure?

A

alcohol, thyroid disease, congenital heart disease, hypertensions, CORONARY HEART DISEASE, genetic conditions, valvular heart disease

72
Q

what is hepatomegaly?

A

enlargement of the liver

73
Q

what is ascites?

A

fluid in the abdomen

74
Q

what are some signs and symptoms of systolic heart failure?

A 
low mood
elevated jugular 
breathlessness on exertion
orthopnoea
paroxysmal nocturnal dyspnoea
pulmonary and peripheral oedema
bloating
hepatomegaly
ascites
fatigue
75
Q

what is orthopnoea?

A

breathlessness when lying down due to fluid pooling in chest

76
Q

what is paroxysmal nocturnal dyspnoea?

A

waking up from sleep breathless

77
Q

why does heart failure cause its symptoms?

A

cardiac output is severly decreased
blood still comes into the heart via the venous system
pressure builds up behind ventricle

78
Q

what is N-T pro BNP?

A

n terminal pro-brain natiuretic peptide - released in response to stretching of heart muscle during hypervolemia

79
Q

what are ionotropic drugs?

A

increase force of contraction of heart

dobutamine mimics sympathetic nervous system - heart beat faster and stronger)

80
Q

give two diuretics

A

loop - furosemide
thiazide - bendrofulmethianide
promote increased urine production

81
Q

what long term drugs are there for systolic heart failure?

A

RAAS system - ACE inhibitors and aldosterone antagonists

overactive sympathetic nervous system - beta blockers

82
Q

what is an LVAD?

A

left ventricular assist device

- bridge to transplantation

83
Q

Why would someone lose consciousness? highlight the steps from the source to effect

A
  • no coordinated electrical activity
  • no coordinated ventricular contraction
  • no CO
  • no cerebral perfusion
  • loss of consciousness
84
Q

why would someone’s pulse be absent? highlight the steps from source to effect

A
  • no coordinated electrical activity
  • no coordinated ventricular contraction
  • no CO
  • No pulse
85
Q

why does a defibrillator do and when do we use it?

A

shocks heart back into rhythm - heart rhythm reset back to sinus rhythm
- use immediately in cardiac arrest

86
Q

why would a defribrilator work on a collapsed person with ventricular fibrilation?

A

shocks the heart into normal rhythm

87
Q

why is it important to take a family history in the case of ventricular fibrilation?

A

vital to discover underlying cause

17% of sudden cardiac death is due to cardiomyopathies and inherited arrythmias

88
Q

when would you perform basic life support? highlight the steps in order

A

when someone is unresponsive or breathing abnormally
1- call 999
2- 30 chest compressions
3- 2 rescue breathes
4- continue CPR 30:2
5- As soon as defibrillator arrives switch on and follow

89
Q

what abnormality would an ECG of a person suffering from ventricular fibrillation show?

A

QT period (repressing ventricular depolarisation to depolarisation) is prolonged

90
Q

what causes long QT syndrome

A
  • disorder or 1+ ion channels (sodium, calcium or potassium) in myocytes so depolarisation takes longer than normal
  • due to a gentic defect in ion channel structure or function
91
Q

why do we get prolonged depolarisation in long QT syndrome?

A

due to prolonged refectory period

therefore when a new electrical impulse in generated there heart is still in refractory period

92
Q

what is the consequence of long QT syndrome?

A

dangerous uncoordinated heart rhythms (eg. VF or types of ventricular tachycardia)

93
Q

what is the R to T phenomena on ECG

A
  • extra heart beat (an ectopic) in the refractory/QT interval leading to a dangerous heart rhythm
94
Q

what is Torsades de Pointes? what does it cause and lead to?

A

Polymorphic Ventricular Tachycardia
uncoordinated heart rhythms
leads to cardiac arrest

95
Q

what are the long term treatment we use for VF

A
  • arrhythmia modifying drugs - eg. B blockers, amiodarone

- if drugs fail- implanted cardioverter defibrilator-ICD- pacemaker

96
Q

how does a ICD work and where is it implanted

A

implanted under skin

- delivers electric shock directly to heart and terminated dysthymia to restore sinus rhythm

97
Q

why might ventricular fibrillation lead to loss of consciousness?

A

no co-ordinated electrical activity = no co-ordinated ventricular contraction
no cardiac output
no cerebral perfusion
loss of consciousness

98
Q

why might ventricular fibrilation lead to stopped breathing?

A

no cerebral perfusion = anoxia of brain stem = hypoxia, hypercapnoea, acidosis

99
Q

why would there be absent pulse after a collapse of a person with ventricular fibrilation?

A

no cardiac output as no co-ordinated electrical activity and ventricular contraction

100
Q

why would a defribrilator work on a collapsed person with ventricualr fibrilation?

A

shocks the heart into normal rhythm

101
Q

why is it important to take a family history in the case of ventricular fibrilation?

A

vital to discover underlying cause

17% of sudden cardiac death is due to cardiomyopathies and inherited arrythmias

102
Q

what are the 4 steps of basic life support and why is it important?

A

buys time to maintain adequate perfusion until definitive form of resus is found (an AED)

  1. call 999
  2. 30 chest compressions
  3. 2 breaths
  4. continue until AED arrives
103
Q

how might ventricular fibrillation be expressed on an ECG?

A

prolonged QT interval

104
Q

what is long QT syndrome?

A

disorder of ion channels (potassium, calcium and sodium)

leads to abnormal depolarisation

105
Q

what is Torsades de Pointes?

A

if something causes an extra impulse (ie ectopic heart beat), the heart is not properly repolarised due to long QT and can cause a dangerous arrythmia = polymorphic ventricular tachycardia

106
Q

what would be a long term prevention for ventricular fibrilation?

A

arrhythmia modifying drugs (beta blockers)

107
Q

what would be long term treatment for ventricular fibrilation?

A

an implanted cardioveter defribilator (ICD) - safety net that delivers electric shock when it senses an arrhythmia

108
Q

what does congenital mean?

A

present at birth

DOES NOT MEAN GENTIC

109
Q

what state if the heart and closure of which valves are the heart sounds ‘Lub’ and ‘Dub’ associated with?

A 
- 'Lub':
diastole-S1 
closure of tricuspid and mitral valves 
- 'Dub':
diastole- S2
closure of aortic and pulmonary valves
110
Q

why do we get heart murmurs

A

caused by turbulent flow through the heart

111
Q

what are the causes of heart murmurs

A
  • narrow valve- stenosis
  • leaky valve- regurgitation
  • hole in heart (ventricular septal or arterial septal defect)
112
Q

why is a ventricular septal defect dangerous?

A

allows oxygenated blood to mix with deoxygenated blood

113
Q

what route does the blood travel through in a heart with a VSD?

A
  • through normal anatomical route, but through the ventricular defect itself
  • pass from L to R side through hole
114
Q

what do we call it when blood travels through L to R side in VSD

A

L to R shunt

115
Q

what are the consequences of a L to R shunt in VSD?

A
  • usually blood flow down pressure gradient from L systemic to R pulmonary
  • but amount of blood coming from R ventricle to pulmonary circuit increases due to L to R shunt
  • blood flows down the pressure gradient from L to R
  • increases pressure in pulmonary circuit over time
116
Q

why is it dangerous if the the VSD is large or not closed over time? what syndrome will this lead to

A
  • can cause permanent damage to arteries as the increase in pressure can cause pulmonary hypertension - increases BP in lungs
  • pulmonary pressure may increase systemic pressure and cause a R to L shunt = eisenmenger’s syndrome
117
Q

what is the treatment for VSD?

A

open heart surgery:

  • patch a bit of tissue on top
  • in children keyhole surgery performed instead
118
Q

is surgery always necessary in VSD?

A

in those with small VSD’s this treatment may not be needed- it may close on its own

119
Q

why is it dangerous if the VSD is close to aortic valve?

A

can develop a leak and cause blood which is pumped from LV to aorta to leak back into LV and lead to endocarditis if not treated

120
Q

what 4 abnormalities are involved in Fallot’s tetralogy?

A
  • pulmonary stenosis
  • VSD
  • overriding aorta
  • Ventricular hypertrophy
121
Q

what is pulmonary stenosis

A

narrowing of pulmonary valve - may be above or below the valve
can be due to excess smooth muscle

122
Q

what is an overriding aorta

A

aortic valve is enlarged and the opening of the aorta lies over the LV and VSD

123
Q

what are the consequences of an overriding aorta?

A

easier for poorly O2 blood to enter circulation

124
Q

how does ventricular hypertrophy develop ?

A

over time due to obstruction of the heart

RV has to work harder to pump blood through narrower ventricular heart flow tract

125
Q

what is cyanosis and why does it occur?

A

blue/purple colouration of skin

due to poor O2 saturation in tissues from mixing of oxygenated and deoxygenated blood

126
Q

what is a hypercyanotic attack? how serious is it?

A
  • acute episode of hypoxia

- secretion cases may lead to hypoxia brain injury and death

127
Q

what are the symptoms of a hypercyantoic attack?

A
  • shortness of breath
  • cyanosis
  • agitation
  • light- headed
  • loss of consciousness
128
Q

why does a hypercyantoic attack occur?

A
  • reduced vascular resistance in systemic circuit
  • any increase in parasympathetic tone (crying, bowel movement) promotes R to L shunt
    = hypercanosis
129
Q

how can the symptoms of a hypercyantic attack be relieved? why?

A

squatting:
increases systemic resistance
induces temporart shunt
promotes blood through pulmonary circuit

130
Q

what are the signs of tetralogy of fallot in children/babies?

A
  • difficulty feeding
  • failure to Gian weight
  • delayed growth and physical development
131
Q

what test can we sue to diagnose ToF

A

ECHO

132
Q

how can we treat ToF? what age? what does this repair

A

open heart surgery :
- enlarge pulmonary artery
- close VSD (swing patch of material)
- excess heart muscle under valve removed
about 6 months
repair R ventricular outflow tract and pulmonary stenosis and VSD

133
Q

what are the risks of an untreated ToF?

A

progressive R ventricular hypertrophy leading to heart failure

134
Q

what is a consequence of ToF surgery?

A

pulmonary regurgitation

pulmonary valve may be damaged causing a leak and so blood from RV to pulmonary artery returns to RV

135
Q

What is the cause of aortic stenosis at birth? (congenital)

A

The valve may have two cusps (bicuspid) instead of three (tricuspid)

136
Q

What is the cause of atrial stenosis that develops over time?

A

The valve becomes calcified (causing stiffening) and narrowed (stenosed)

137
Q

What effect does aortic stenosis have on the left ventricle?

A

The left venticle becomes hypertrophied as it has to generate a greater force to push blood through the narrowed valve

138
Q

What patients most frequently suffer from aortic stenosis?

A

Males over 65 yr

139
Q

What are the symptoms of aortic stenosis?

A
  • angina type chest pain (worse with exercise and improved during rest)
  • breathlessness with exercise
  • syncope with exercise
  • some patients have no symptoms for many years
140
Q

What are the clinical signs of aortic stenosis?

A
  • harsh and loud “ejection systolic” murmur heart loudest in the right aortic area
  • reduced pulse pressure
  • forceful apex beat
141
Q

What is pulse pressure?

A

The difference between diastolic and systolic blood pressure

142
Q

Where is the apex beat felt?

A

The left side of the chest in the mid-clavicular line at the 5th intercostal space

143
Q

What tests can be carried out for aortic stenosis? What would these show?

A
  • ECG: evidence more muscular left ventricle, QRS is increased
  • Echocardiogram: narrowed aortic valve and hypertrophied left ventricle
144
Q

What medical/surgical intervention is considered for aortic stenosis?

A
  • if pressure difference is 60 mmHg, patient is kept under observation
  • if left ventricle stats to dilate or symptoms are present, surgery is considered
  • valve replacement surgery
    • open heart/percutateous
    • metal or plastic valve (prothetic)/ tissue (biprosthetic)
145
Q

What is required after insertion of a replacement valve?

A
  • prosthetic means patient has to be on lifelong anticoagulant treatment with warfarin
  • patients with tissue valves do not require warfarin
146
Q

What is the physiology behind atrial fibrillation?

A
  • pacemaker activity of the heart
  • conduction of electrical depolarisation through the atrium
  • stimulation of electrical activity in ventricles
147
Q

What structural abnormalities are associated with atrial fibrillation?

A

There must be a structural substrate present such as dilated atria or fibrosis of the atrial muscle

148
Q

What physiological abnormalities are associated with atrial fibrillation?

A
  • arrythmogenic environment eg due to an electrolyte imbalance or sepsis
  • ectopic activity from around the pulmonary veins
149
Q

What are the prior events to atrial fibrillation?

A
  • hypertension
  • coronary artery disease
  • excessive alcohol consumption
  • hyperthyroidism
  • heart failure
150
Q

What are the experienced symptoms of atrial fibrillation?

A
  • palpitations (awareness of the heart rate as fast, irregular or both)
  • fatigue and/or breathlessness with exercise
  • chest tightness (angina) or ankle swelling (oedema)
151
Q

What are the clinical signs of atrial fibrillation?

A
  • pulse is irregularly irregular
  • signs of underlying cause eg high blood pressure, valve murmur heard through stethoscope, weight loss with overactive thyroid
152
Q

What are the medical interventions for atrial fibrillation?

A
  • RATE CONTROL - beta blockers, calcium channel blockers, digoxin
  • RYTHM CONTROL - using drugs such as amiodarone or DC cardioversion
  • SURGERY - catheter ablation where pulmonary veins are electrically isolated from leg atrium
153
Q

What are the primary and secondary interventions for atrial fibrillation?

A
  • early and effective treatment of diseases that cause atrial fibrillation
  • avoidance of excessive alcohol and stimulants such as nicotine, caffeine
  • prevention of blood clot formation in the atrium through treatment with warfarin or oral anticoagulant

year 1 flash cards (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions