CARDIOLOGY Flashcards
what technique can be used acutely to halt paroxsysmal supraventroicular tachycardia?
carotid massage
cold water immersion
valsalva
nitrates cause vasodilation in arteries and veins < = > ?
veins > arteries
(decrease preload)
Hydralazine causes vasodilation veins, arterioles < = >
Arterioles > veins
(decreased afterload)
nitroprussides cause vasodilation veins, arteries < = >
veins = arteries
(cyanide toxicity)
what’s the pentad (5) of Kawasaki disease
C – Conjunctivitis (bilateral, non-purulent)
R – Rash (polymorphous)
A – Adenopathy (LN cervical, usually unilateral)
S – Strawberry tongue (oral mucosal changes, mucolitis)
**H **- Hands and feet changes (edema, erythema, desquamation).
**“Burn” **– Fever lasting ≥5 days
coronary artery aneurysms
symptoms of measles
coryza
cough
conjunctivitis
koplik spots
erythematous rash
whats a complication of mononucleosus
splenic rupture
(avoid sport)
list derivates of aortic arches 1-6
What condition are these seen in (cardiac muscle)
ashcoff bodies - acute rheumatic fever
what is the genetic inheritence of hypertrophic cardiomyopathy
autosomal dominant
What feature does this ECG show
WPW
‘delta’ wave
What arrythmia does this describe:
short PR <120
slurred broad upstroke QRS
QRS widening
+/- ST / T wave changes
WPW
what is a common origin trigger of A fib
pulmonary veins
plasma volume rises OR falls at altitude
falls
decreased renal bicarbonate & water reabsorption compensating for respiratory alkalosis,
fluid shift from the intravascular to ICS, IS spaces
triad of aortic stenosis
SAD
syncope
angina
dyspnoea
healthy pregnant person, what’s the cause of systolic ejection murmur
dilated cardiomyopathy
increased SV
what murmur is heard with ToF (tetralogy of fallot)
holosystolic
(underlying VSD)
R-L shunt (cyanosis) in infancy
squatting helps
pulmonary infundibular stenosis
overriding aorta
ventral septal defect
right ventricular hypertophy
what murmur is heard in ASD
fixed wide split S2
low grade ejection murmur
delays closure pulmonic valve
A2——P2
volume overload R atrium/ventricle
might see
failure to thrive
systolic murmur
increased pulmonic flow - fixed wide split S2
hypertrophy right atrum, ventricle, pulmonary arteries (R overload, R-L shunt)
use of ACEi and accumulation of bradykinin can cause
AE
angioedema
nonproductive cough - bradykinin
effect of ACE on bradykinin
ACE degreades bradykinin
ACEi prevents this degradation –> bradykinin levels increase
contributes to vasodilation –> lowers BP
bradykinin can cause persistant non-productive cough
AV fistula is a connection between
artery and vein
bypasses capillary bed
increased venous return
increased HR, CO
increased myocardial O2 demand
thrill
bruit
AV fistula
(high out put heart failure)
congenital or aquired (i.e. put in for dialysis
increased VR to heart
increased HR, CO (High output)
increases myocardial O2 demand
decompensates –> HF
increased JVP
peripheral oedema
congestive hepatopathy or ascites
RHF
constrictive pericarditis
RHF
impaired diastolic filling
4 chambers equal pressures
dont confuse with cirrhosis - less likely JVP
hypervolemia
peripheral oedema
pulmonary oedema
pleural effusions
ascites
RHF
cirrhosis
dont confuse with constictive pericarditis (increased JVP)
JVP rarely in cirrhosis
localised hypokinesis on echocardiogram can indicate
flow limiting stenosis of a coronary artery
RCA gives rise to:
PDA
R marginal branch
AV & SA node
sinoatrial nodal artery
LCA gives rise to:
LAD
L circumflex
L Marginal
L Diagnonal
LV apex dysfunction
apical ballooning
reduced LVEF
Takotubo cardiomyopathy
(broken heart syndrome)
disruption to SNS nerves of LV (increased SNS stim)
‘stress induced cardiomyopathy’
octopus trap
can mimic MI s/s
dyspnoea
orthopnoea
fatigue
are common symptoms of
heart failure
signs: S3 sound, rales, jvp, pitting oedema
list 3 occurences of LHF
pulmonary oedema
orthopnoea
paroxysmal noctoural dypnoea
hemosiderin laden macrophages (HF cells)
RAAS activation (poor anterograde flow)
list 3 occurences of RHF
JVP increased
cardiac cirrhosis
LL pitting oedema
nutmeg liver - central vein congestion
cor pulmonale (isolated RHF - from lung disease)
cause of cor pulmonale
isolated RHF
(pulmonary cause)
lung disease –> hypoxia -> vessel constriction -> RH can’t pump against pressure
increased EDV
decreased contractility
2’ to ischaemia/MI/dilated cardio
systolic dysfunction
reduced ejection fraction HF
normal EDV
decreased compliance
(increased EDP)
2’ to myocardial hypertrophy
diastolic dysfunction
preserved ejection fraction HF
Dyspnoea
Cough
Tachypnoea
Chest tightness
Fatigue or reduced exercise tolerance
heart condition
cardiogenic pulmonary oedema
(HF)
Bilateral perihilar shadowing (batwing)
Kerley B lines (interstitial oedema)
Cardiomegaly (chronic heart failure)
Upper lobe venous diversion
Pleural effusions
Increased vascular markings
Alveolar oedema (fluffy, ill-defined opacities)
ST segment depression in angina caused by ischaemia to what location
subendocardial ischaemia
stable and unstable angina
ST segment elevation in angina caused by ischaemia to what location
transmural ischaemia
prinzmetal angina
list causes of MI (4)
rupture atherosclerotic plaque (thrombosis)
coronary artery vasospasm
emboli
vasculitis (Kawasaki disease)
kawasaki -> coronary aneurysm -> turbulent flow -> thrombosis
heart failure can cause transudate or exudate pleural effusion - characterised by ___ protein and ___ LDH
transudative
low
low
heart failure, cirrhosis, nephrotic syndrome are examples of ___ effusions
transudative effusion
lights criteria not met
pneumonia, malignancy, TB, rheumatologic diease are examples of ___ effusions
exudative effusion
lights criteria met
what peptides inhibit RAAS, promote peripheral vasodilation
BNP, ANP
neprilysin is a ___
metalloprotease inhibitor
neprilysin breaks down ANP, BNP
metalloprotinase: break down proteins, particularly those found in the extracellular matrix (ECM)
neprilysin inhibitors given as a treatment in ___ to enhance ___ function
heart failure
ANP, BNP
activate GMP
diuresis
vasodilation
i.e. sacubitril
ANP and BNP are released from
cardiomyocytes
in response to stretching
BNP (left vetrincle)
ANP (atria)
what factors increase peripheral oedema
increased capillary HSP
decreased plasma oncotic pressure
impaired lymphatic drainage
i.e. copd –> increased pulmonary vasoconstriction –>increased PAP –> RHF (cor pulmonale)
ectatic aorta
enlarged/dilated aorta
(aneurysm like)
commonly occurs below renal vein (near SMA, IMA)
Beck triad is a finding of
cardiac tamponade
(hypotension, distended neck veins, distant heart sounds),
male
abdo pain
HTN
family history - similar s/s or sudden collapse
smoker
hypercholesterolemia, atherosclerotic disease
pulsatile abdominal mass
AAA
often infrarenal AA
hepatomegaly - can present similarly: but no pulsatile mass and hepatitis, liver failure, portal THn or cirrhosis
rupture: back pain, tachycardia, hypotension
name 2 causes of congenital long QT syndrome
romano-ward (AD) - no deafness
jervell and lange-neilsen (AR) - deafness
risk of: arrythmias, syncope, sudden cardiac death
Romano-Ward syndrome—autosomal dominant, pure cardiac phenotype (no deafness).
Jervell and Lange-Nielsen syndrome—autosomal recessive, sensorineural deafness.
long QT syndrome is a disorder of
prolonged ventricular depolarisation and repolarisation
i.e. methadone known to cause this
congenital:
romano-ward (AD)
jervell and lange-neilsen (AR) - deafness
m/c cause of aortic stenosis in <65yo
bicuspid aortic valve
or
chronic rheumatic heart disease
calcification m/c older patients
bicuspid and rheuatic HD cause early onset aortic stenosis
m/c cause aortic stenosis in patients >65yo
calcification aortic valve
younger patients m/c bicuspid valve or rheumatic heart disease = cause of early aortic stenosis
hypotension
cool / pale extremities
jugular venous distension
pulmonary oedema
type of shock
cardiogenic shock
AMI, valvular disease, HF, heart block, arrythmia
decreased CO
increased PCWP
SVR increased
*Hypotension (BP 70/40 mmHg) and Tachycardia (HR 128/min) → Suggests shock.
Cool, pale extremities and faint peripheral pulses → Indicates poor perfusion due to low cardiac output.
Jugular venous distention (JVD) → Suggests elevated central venous pressure (CVP), which is seen in cardiogenic and obstructive shock.
Bibasilar crackles in the lungs → Indicates pulmonary congestion/edema, suggesting left ventricular failure.
No murmurs → Likely excludes acute valvular dysfunction.**
