Brainscape's Knowledge GenomeTM

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


See full index

2a RRS > cardio > Flashcards

cardio Flashcards

1
Q

what is stable angina

A

heavy tight gripping chest pain relieved by rest and worse on exertion
a symptom that occurs as a consequence of restricted coronary blood flow

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

Rfs of angina

A

diabetes mellitus
smoking
hypertension

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

when does angina occur (e.g of each)

A

when oxygen demand does not meet supply

  1. blood flow impaired (proximal arterial stenosis)
  2. increasted distal resistance (LV hypertrophy)
  3. decrease in o2 capacity of blood (anaemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

why does a small change in radius cause large change in blood flow

A

pouiselles law - r^4

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

what is an example of blood flow impairment causing angina

A

proximal arterial stenosis

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

causes of angina (stable)

A

atheroma
anaemia
cardiac abnormalities (aortic stenosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

pathophysiology behind angina mismatch on exertion

A

epicardial resistance high therefore microvasc is low to compensate (dilates to increase bf)
when excercise o2 demmand increases but cannot dilate further as already compensated so chest pain =angina

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

classifications of angina

A 
3/3 = typical angina
2/3 = atypical 
1/3 = non anginal pain
constricting heavy chest pain radiating to chest/jaw/neck/arm
occurs w exertion/stress
relieved by rest or GTN spray
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

clinical features of stable angina

A

heavy constricting chest pain radiating to chest jaw neck arm occuring on exertion/stress relieved by rest/ gtn spray
SOBOE
fatigue
N&V
sweating
xanthoma (lipid deposition in skin) = A SIGN

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

what is unstable angina

A 
deteriation of previiously stable angina with symptoms frequently occuring at rest
recent onset (<24hrs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

unstable angina buzz word clin features

A 
crescendo pattern chest pain
increasing freq and severity
breathless
new onset chest pain - pleuritic
INDIGESTION
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

difference between unstable angina and NSTEMI

A

no occludinig thrombus in unstable angina so no myocardial necrosis
= NORMAL TROPONIN or CK-MB

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

NSTEMI occlusions?

A

partial major coronary artery occlusion
complete minor coron artery occlusion
previously effected by atherosclerosis

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

NSTEMI muscle damage description

A

only partial thickness damage of heart muscle

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

what is an acute coronary syndrome an umbrella term fro

A

unstable angina nstemi and stemi

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

what is a STEMI

A

comlete occlusion of major coron artery previously affected by atherosclerosis
full thickness dameae of heard muscles so sub enthothelial myocardium - infarct zone spreads to subepicardial myocardium = transmural Q wave

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

bloods results from stemi

A

elevated troponin T and I (most sensitive)

high creatine kinase MB (CK-MB)

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

ECG of STEMI at presentation

A

pathological Q wave
ST elevation
tall T waves

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

DDx of an MI

A 
stabel and unstable angina 
pneumonia
pneuomothorax
GORD
acute gastritis
pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Signs of an MI

A 
pallor and clammy
sweating
signif hypotension
4th heart sound (forceful atria contraction overcoming stiff dysfunctional ventricle)
pansystolic murmur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

symptoms of MI

A 
sharp crushing chest pain over 20mins - radiate jaw, LEFT ARM, neck
doesnt respond to GTN spray
nausea
SOB
palpatations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Lifestyle MI modifications

A

stop smoking
healthy diet
2’ prevention - statins, warfarin, ACEi

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

ACUTE Mx of an MI

A 
MONA
Morphine
Oxygen
Nitrates
Aspirin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

STEMI Mx

A

if in 2hrs = PCI
BB (atenolol)
ACEi
Clopidogrel

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

complications of an MI

A 
cardiac arrest
unstable angina
bradycardias, heart block
tachyarrythmias
pericarditis (STEMI)
DVT/PE/systemi embolism
heart failure (ventric dysfunction post necrosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

causes of LBBB

A

ischaemic heart disease
aortic valve disease
LV hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

causes of RBBB

A

pulm embolism
ischaemic heart disease
atrial/ventric septal defects
RHV

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

Tx of BBBs

A

pacemakers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

appearance of v1 and v6 leads in RBBB

A

MaRRoW
v1 = M
v6 = W

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

appearance of v1 and v6 leads in LBBB

A

WiLLiaM
v1=W
v6=M

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

1st degree AV block findings

A 
PR prolongations (>0.22s)
constant 
every atrial signal - ventricle but w delay
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

2nd degree AV block findings (type 1 / Mobitz 1)

A

PR interval progressivley longer until dropped beat (no QRS complex) - ventricle escape beats

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

2nd degree AV block findings Mobitz 2

A

PR interval constant, QRS complexes randomly dropped

failure to conduct through purkinje system

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

3rd degree AV block

A

signal blocked completely = no electrical pulses to ventricles
A and V act INDEPENDENTLY = no assos between PR and QRS
slow ventric escape beats

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

what heart block type does an anterior MI cause

A

2nd degree/ mobitz 2

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

what type of heart block does a inferior MI cause

A

1st degree (and 2nd degree mobitz 1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

symptoms of a 1st degree AV block

A

none

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

symptoms of a 2nd degree mobitz 1 AV heart block

A

usually none but lightheaded, dizziness, syncope

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

symptoms of a 2nd degree mobitz 2 AV block

A

SOB, postural HTN, chest pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

symptoms of a 3rd degree AV block

A

fatigue, lightheadedness, blackout

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

causes of a 2nd degree mobitz 2 av block

A

anterior MI
mitral valve surgery
SLE
rheumatic fever

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

Causes of a 2nd degree mobitz 1 AV bock

A

AVN blockers so BB or CCBs or Digoxin

or inferior MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

causes of 1st degree AV block

A

inferior MI, hypokalaemia, AVN drugs (BBs, CCBs, Digoxin)

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

Tx of 2nd degree mobitz 2 block

A

pacemaker

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

tx of 3rd degree av block

A

IV atropine (slows HR) but if chronic = pacemaker

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

what can u see on BBBs ECG

A

wide QRS complex w abnormal pattern
shape depending on L or R BBB
(due to ventric contraction longer due to delay)

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

what do you see on the CXR of heart failure

A 
Alevolar oedema
B- kerley B lines
Cardiomegaly
Dilated prominaent upper lobe vessels
Effusion (pleural)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is heart failure

A

a clinical syndrome in whihc eh heart cannot provide sufficient output to meet the bodys demands

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

causes of heart failure principals

A

systolic - V cant contract normally = decreased EF
diastolic - inability to relax and fill = incomplete filling
hypertension - increased afterload = compensatory hypertrophy = less space for filling = lowers CO
increase myocardial work

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

causes of heart failure -

A 
ischaemic heart disease
MI 
Cardiomyopathy 
ventric hypertrophy - HTN
aortic stenosis
mitral/ aortic regurg
anaemia 
obesity 
hyperthyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

3 cardinal features of Heart Failure

A

SOB
fatigue
ankle oedema

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

L sided heart failure what happpens

A

blood backs up into lungs

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

R sided heart failure what happens

A

blood backs up to the body (liver etc)

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

L sided heart failure sympotoms

A

SOB, lowered exercise tolerance, frothy sputum cough (nocturnal), fatigue, paraoxysmal norturnal dypsnoea (SOB at night)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

L sided heart failure signs

A 
tachycardia
cardiomegaly (displaced apex beat)
crepitations in lung bases
cool peripheries
3rd n 4th heart sounds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

R sided heart failure symptoms

A 
peripheral oedema
ascites
fatigue
nausea
anorexia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

R sided heart failure signs

A 
peripheral oedema 
increased JVP
hepatomegaly
pitting oedema 
ascites
weight gain (fuid)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

heart failure pathophysiology

A

starts to fail so initiates compensatory changes to maintain CO and peripheral perfusion)
as heart failure progresses the mechanisms get overwhelmed and turn pathological
= DECOMPENSATION

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

role of Sympathetic stim in heart failure

A

pos inotropic effect (force of contraction)
pos chronotropic effect
incresaes heart rate
in heart failure - down regulates receptors and CO no longer increases in response

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

role of increasing preload in heart fail

A

heart muscle falure so more blood in ventricles after systole = increase in diastolic vol = stretches the myocardium = gets to point where no longing increses contraction force (STARLINGS)

61
Q

increasing afterload heart fail patho

A

resistance against which the ventricle contracts increases - increases in afterload - increase end diastolic vol and decreases stroke vol = decrease cardiac output. V dilates - fither excaberates the issue

62
Q

effect of RAAS in heart failure patho

A

decreasing cardiac output decresaes renal perfusion
this activates RAAS
increase in aldosterone - increases NA reabsorption and h2O reabsoption - ADH release = H2O retention
this increases blood volume increasing BP and venous p. therefore increase preload and the stretch and force of heart contraction
incresae of contraction req more energy and blood to cardiac myoctyes - heart fail = no increase in blood so die and force decreases along with CO === toxic effects

63
Q

what does adrenic activation do to heart in heart failure

A

increases HR/contractility hence increasing cardiac work = myocyte damage = decrease in CO
causes vasocontriction = increases afterload = increases cardiac work and thus myocyte damage thus decreasing CO

64
Q

what does a lack of renal perfusion cause in iheart fail

A

RAAS activation - Na and h2O retention = increases preload as increases vol of blood = increasing cardiac work and thus myoctye dmage
causes vasocontriction increasing afterload and cardiac work

65
Q

what is the Dx of heart failure

A

CXR, bloods (B type natriuretic peptide, increased ANP, D-dimer, U&Es, FBC)
cardiac enzymes - creatine kinase, toponin I and T
Echo - LV dysfunction and structural causes

66
Q

Mx of hert failure

A

diuretics (furosemide)
ACEi (SE-cough)
Aldosterone antagonists
Beta Blockers
Digoxin ( SE= yellow rings around lights) - inhibs Na/K
Angiotensin-II recep blockers (corsartan)

67
Q

Lifestyle mods for cardiac failure

A

obesitiy,stop smoking, diet (decrease salt), decrease alcohol

68
Q

acute heart failure management

A

100% oxygen, nitrates (dilates vessels), IV furosemide (fluid overload) IV opiates (diamorphine)

69
Q

what is found in bloods of heart falure

A

B type natriuretic peptide - secreted in response to ventricular wall stress
CK-MB
ANP - myocyte stretch - cardiomegaly
troponin I and T

70
Q

what is pericarditis

A

inflam of the peritoneum - fluid builds up and puts pressure on heart so cannot pump

71
Q

causes of pericarditis

A 
CARDIAC RIND
C- colagen vasc disease
A - aortic anneurysm
R - radiation
D- drugs - penicillin
I- infections - viral (coxsacki B, enterovirus) bacterial (TB)
A - acute renal failure - uraemic = ac of toxins
C - cardiac infarction

R- rheumatic fever/ arthritis
I- Injury
N - neoplsam
D- dresslers - post MI = autoimm secondary form of pericarditis 2-10wks after

72
Q

CFs of pericarditis

A

chest pain - relieved by sitting forward (ON A HORSE), exacerbated by lying down
pleuritic and radiates to trapezium ridge
Friction rub
Fever
Signs of pericardial effusion - dyspnoea

73
Q

Dx pericaditis BUZZ WORDS

A

SADDLE SHAPED ST ELEVATION
“not in a CAR u are on a horse SADDLE shaped ST elevation, lean forward
t waves flatten
Bloods - increased troponin
CXR - cardiomegaly and pericardial effusion

74
Q

what is cardiac tamponade

A

build up of fluid in pericarditis - constricts the heart

tamponade = p. obsstruction flow = decresed CO, HYPOTENSION, decreased tissue perfusion increased HR

75
Q

what is becks triad

A

3 Ds
Distant heart sounds
Distended jug veins
Decreased arterial p

76
Q

what is becks triad assos with

A

pericarditis

77
Q

what is a sign of cardiac tamponade

A 
pulsus paradozus (ventric independence)
heart cant fully stretch between cotnractions so doesnt filll so CO decreases
78
Q

what is contrictive pericarditis

A

caused by TB = thick and fibrous and calcified so inelastic so decerased diastolic filling

79
Q

what causes constrictive pericarditis

A

TB

80
Q

Tx for pericarditis

A

NSAID OR aspirin

colchicine if symtp still (SE = nausea)

81
Q

signs of acute periph vasc disease

A 
6 P's!
Pain
Pallor
Pulseless
Paresthesia
Paralysis
Perishingly cold
82
Q

how diagnose PVD

A

brachial ankle pulse index (0.5-0.9 =intermit claudication, <0.5 = crit limb ischaemia)

83
Q

signs of PVT

A

absent leg pulses

feet cold

84
Q

first line BP drugs for above 55 and not afro

A

ACEi or ARBs

85
Q

70yo bp first line

A

CCB (CI if have oedema or heart failure risk)

86
Q

40 year old afro bp first line

A

CCB

87
Q

2nd line BP

A

A + C (CCC)

88
Q

3rd line BP

A

A + C + D (thiazide like diuretic)

89
Q

4th line BP

A

A + C + D + further D + alpha or beta blocker

90
Q

SE of ACE-i

A

dry cough as less aldosterone so bradykinin accumulates = rash also

91
Q

SE of BB

A

fatigue and dizzy

92
Q

BB beta1 selective

A

cardio (1 = 1 heart)

93
Q

BB beta2 selective

A

lungs (2 = 2 lungs)

94
Q

CCB SE

A

ankle oedema - vasodilaters and L-type C channel blcokers

95
Q

why does hypertension cause

A

PVD
cerebrovascular disease
isch. heart disease

96
Q

how to diagnose HTN

A

24hr ambulatory bp monitoring
assess QRISK2 (for heart risk)
sphygmomanometer,

97
Q

what is classed as hypertension (figures)

A

over 140/90mmHg

135/85mmHg if 24hr ambulatory bp monitoring

98
Q

what are the 2 types of HTN

A

primary/essential - idiopathic

secondary - has a cause

99
Q

causes of secondary HTN

A 
renal disease
oral contraceptive pill
pregnancy
acromegaly
cushings
conn's
CKD
100
Q

what is malignant HTN

A

rapid rise in BP - vascular damage MED EMERGENCY

>200/120mmHg

101
Q

CFs of malignant hypertenstion

A

headaches, visual distrubances, bilateral retinal haemorrhages

102
Q

Complications of malignant HTN if not treat quick

A

aortic disection, MI, pulm oedema

103
Q

things you look for to assess HTN endstage organ damage

A

FUNDOSCOPY - eyes - papilloedema, retinal haemorrhage
CARDIAC - ECG - LV hypertrophy
KIDNEYS - urinalysis

104
Q

RFs of HTN

A

afro carrib
high BMI
lifestyle (smoking sedatory life style alchol diet)

105
Q

Atrial fib complicatios

A

increases stroke risk by 5x

106
Q

what do you give patients with AF to prevent stroke risk

A

warfarin

107
Q

what is atrial fib

A

continuous rapid activation of the atria causing uncoordinated depolarisation with not all impulses going to the ventricles = decresae in cardiac output

108
Q

what do you see on an ECG with AF

A

quivering baseline, irreg QRS complexes, 100-175bpm

109
Q

what causes AF

A 
anything that increases atrial pressure/muscle mass/inflam/fibrosis
rheumatoid heart disease
heart failure
XS alcohol
HTN
valv heart disease
110
Q

CFs of AF

A 
palpitations
fatigue
dizziness
chest pain 
IRREGULARLY IRREGULAR PULSE
111
Q

Dx of AF

A

ECG - no P waves (fine oscillations), QRS = irregular

IRREG IRREG PULSE

112
Q

DDx of AF

A

atrial flutter, supraventricular tachycardias

113
Q

how would you treat chronic AF

A 
rate control (BBs CCBs) and anticoag (DOACs, warfarin)
cardioversion - convert to sinus rhythm AND GIVE LMWH to reduce thromboemboli risk
114
Q

how would you manage acute atrial fib

A

rate control + anticoag + correct metabolite imbalance

115
Q

how to you control rate with AF

A

AV node blockers - CCB (verapamil)

BBs (bisoprolol) digoxin, amiodarone

116
Q

RF of AF

A

age, DM, obesity, XS alcohol, CVD, hyperthyroidism

117
Q

what is infective endocarditis

A

infection of heart valve or areas lined by endocardium

118
Q

how do you diagnose infective endocarditis

A

DUKES CRITERIA
major - pos blood culture, endocarium involvment, new valve regurg
minor - vasc signs, pos echo, fever over 38 degrees, preidsposition (IVDU)
IE if 2x major or 1x major + 3x minor OR all minor

119
Q

RF for Infective endocarditis

A 
IVDU
IV cannula
pacemaker
poor dental hygiene
cardiac surgery
120
Q

causes of infective endocarditis - organisms

A

Staph aureus - IVDU, surgery, diabetes
Strep virdians - dental
Staph epidermis

121
Q

Tx of staph aureus caused infection endocarditis

A

flucoxacilli

122
Q

Tx of strep virdians caused IE

A

Benzylpenicillin + Gentamycin

123
Q

Tx of IE

A

ABx - specific to blood cultures organism (4-6wks)
surgery to remove infected devices
tx complications (heart failure, arrhytmias)

124
Q

why do organisms grow in IE

A

damaged endocardium promotes platelet and fibrin depostion and organisms adhere and grow = vegitaiton

125
Q

CF pneumonic for IE

A

FROM JANE

126
Q

Cf of IE

A

Fever
Roth spots (retina)
Osler nodes (fingers n toes)
Murmor (NEW)

Janeway lesions - non tneder red fingers palms, soles
Anaemia
Nail haemorrhages - splinters, haemorrhage
Emboli (—STROKE, MI, kindey dysfunction)

also clubbing and splenomegaly

127
Q

how to Dx IE - tests done

A

Echo - transoesphageal, transthoracic
bugs grown on cultures - 3x diff sites over 24hrs
bloods - normocytic, normochromic anaemia, increased ESR, CRP, neutrophilia

128
Q

Causes of IE

A

abnormal valves (regurg or prosthetic)
surgery
bacteriaemia
malignancy/prev IE

129
Q

characteristic feature of aortic dissection

A

TEARING chest pain radiates to back

vomiting, LoC, sweating and shock

130
Q

what is aortic diessection

A

a tear inside of the aorta and blow flows in between the layers forcing them apart creating a false lumen

131
Q

causes of aortic dissection

A

atherosclerotic, marfans, trauma, cocaine

132
Q

why do you get unequal pressure in arms in aortic disection

A

as disection extends, branches seclude sequentially causing hemiplagia (L sided paralysis)

133
Q

why can you get neurological symptoms in severe aortic disection

A

spinal cord blood supply cut off

134
Q

characteristic CT scan sign for aortic disection

A

tennis ball sign

135
Q

Dx of aortic disection

A

absent peripheral pulses
CT - tennis ball sign
CXR - widened mediastinum

136
Q

Mx of aortic disection

A

BBs (metorolol), oxygen, BP ocntrol, surgical repair, morphine (analgesia)

137
Q

what is an aneurysm

A

permanent dilation of an artery cause by weaknes in vessel wall - cant withdtand pressure so diameter increases. assos w fibrosis and myocyte atrophy

138
Q

2 types of annueurysm

A

if dilation over 50% orginial diameter
true - involves all layers
false (=pseudoanneurysm) blood collects in outer layer only (adventitia)

139
Q

causes of aortic aneurysm

A 
atherosclerosis 
connective tissue (marfans)
HTN
obesity
trauma
140
Q

CFs of aortic ann

A

asymtp if unruptured - abdo back loin gorun pain. pulastile abdo swelling
ruptured - intermit or continuous abdo pain radiates to back-iliac fossa- groin
tachycardia anaemia sudden death hypotension collapse and shock

141
Q

Dx of AAA

A

abdo US - >3cm across

CT or MRI angiography scans

142
Q

DDx of AAA

A

GI bleed, isch bowel dis, appendicitus

143
Q

Tx of AAA

A

treat underlying cause
Rf modification - anti hypertensives, stop smoking
Surgery - graft onto aorta

144
Q

characteristic finding of atrial flutter

A

saw tooth flutter waves (F waves) between QRS

145
Q

4 features of tetralogy of fallot

A

pulm stenosis
r ventric hypertrophy
overriding aorta
ventric septal defect

146
Q

CXR finding of tetralogy of fallot

A

boot shaped (due to RV hypertrophy)

147
Q

why do children w tet of fallot squat alot

A

kinks femoral arteries, incresaing periph vascuarl resistance causing increasing p of systemic circulation - increase p of LV till becomes greater than RV causing shunt to REVERSE – from L to R again and blood gets oygenated - decrease cyanosis

148
Q

CFs of tet of fallot

A 
syncope
squatting
fail to thrive
clubbing
CYANOSIS
149
Q

why tet of fallot cyanosed

A

shunt from r to left so less blood to lungs to get oxygenated

2a RRS (26 decks)

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