Flashcards in Finals Medicine Surgery Deck (496)
Hyperkalemia on ECG
Tall tented T wave
QRS a complex broaden
P wave flattened
Managing hyper kalmia
10ml 10% calcium chloride/gluconate over 5-10 min
Identify and manage underlying cause
Wolf Parkinson white syndrome
Delta wave (characteristic slurred up slope)
(Pre-excited AF sometimes)
(Accessory pathway: bundle of Kent)
ECG changes of ACS (chronological)
Peaked T wave
ST segment elevation
Q wave formation and loss of R wave (anterior chest leads)
T wave inversion
4 criteria for STEMI/Emergency re perfusion
2 mm ST elevation in 2 or more contiguous chest leads
1 mm ST elevation in 2 or more limb leads of same territory
New LBBB or LBBB in clinical MI
True posterior MI
RV hypertrophy on ECG
R axis deviation
Dominant R wave in lead V1
Inverted T waves spreading from right side of the heart
Look at I and avF
If away from each other then L axis deviation
If towards each other then R axis deviation if both positive then normal
The HACEK organisms are a group of fastidious Gram-negative bacteria that are an unusual cause infective endocarditis (IE), which is an inflammation of the heart due to bacterial infection. HACEK is an abbreviation of the initials of the genera of this group of bacteria: Haemophilus, Aggregatibacter (previously Actinobacillus), Cardiobacterium, Eikenella corrodens, Kingella. The HACEK organisms are a normal part of the human flora, living in the oral-pharyngeal region.
Causes of dominant R wave in V1/V2
DUchenne muscular dystrophy
Why is it important to diagnose posterior MI?
Posterior MI can cause back pressure and raise JVP.
Usually when we see JVP elevation, we tend to give diuretics because we think it's R heart failure. However diuretics can be fatal for posterior MI as we're decreasing the preload, ie stretching... (Sterling law)
Mesenteric ischemia (classic triad)
Underlying cardiac disease
How to differentiate a jugular venous pulse from the carotid pulse
Obliterated by pressure.
Characterised by a double waveform.
Variable with respiration - it decreases with inspiration.
Enhanced by the hepatojugular reflux
Waveforms of JVP
a - presystolic; produced by right atrial contraction.
c - bulging of the tricuspid valve into the right atrium during ventricular systole (isovolumic phase).
v - occurs in late systole; increased blood in the right atrium from venous return.
x - a combination of atrial relaxation, downward movement of the tricuspid valve and ventricular systole.
y - the tricuspid valve opens and blood flows into the right ventricle.
The a and v waves can be identified by timing the double waveform with the opposite carotid pulse. The a wave will occur just before the pulse and the v wave occurs towards the end of the pulse. Distinguishing the c wave, x and y descents is an almost impossible task.
Causes of raised jugular venous pressure
Constrictive pericarditis (JVP increases on inspiration - called Kussmaul's sign).
Fluid overload, eg renal disease.
Superior vena cava obstruction (no pulsation).
Abnormalities of jugular venous pressure
Abnormalities of the a wave: disappears in atrial fibrillation.
Large a waves occur in any cause of right ventricular hypertrophy (pulmonary hypertension and pulmonary stenosis) and tricuspid stenosis.
Extra large a waves (called cannon waves) in complete heart block and ventricular tachycardia.
Prominent v waves
Tricuspid regurgitation - called cv or v waves and occurring at the same time as systole (a combination of v wave and loss of x descent); there may be earlobe movement.
Slow y descent
Right atrial myxoma.
Steep y descent
Right ventricular failure.
(The last two conditions have a rapid rise and fall of the JVP - called Friedreich's sign.)
soft mid-diastolic rumble heard at the apical area. It appears when regurgitant jet from the severe aortic insufficiency renders partial closure of the anterior mitral leaflet.(in similar way to MS)
large-volume, 'collapsing' pulse also known as: Watson's water hammer pulse
Corrigan's pulse (rapid upstroke and collapse of the carotid artery pulse)
low diastolic and increased pulse pressure
de Musset's sign (head nodding in time with the heart beat)
Quincke's sign (pulsation of the capillary bed in the nail; named for Heinrich Quincke)
Traube's sign (a 'pistol shot' systolic sound heard over the femoral artery; named for Ludwig Traube)
Duroziez's sign (systolic and diastolic murmurs heard over the femoral artery when it is gradually compressed with the stethoscope)
Drugs not to be used in severe AS
Nitrates (risk of syncope)
Transcatheter aortic valve implantation
Uncoordinated and disordered contraction of atria at fast rate which leads to initiation of ventricular contraction through the AV node at varying intervals... Thus leading to an irregularly irregular pulse
NY Heart Association classification of HF
I Cardiac disease, but no symptoms and no limitation in ordinary physical activity, e.g. shortness of breath when walking, climbing stairs etc.
II Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activity.
III Marked limitation in activity due to symptoms, even during less-than-ordinary activity, e.g. walking short distances (20–100 m).
Comfortable only at rest.
IV Severe limitations. Experiences symptoms even while at rest. Mostly bedbound patients.
What sign is pathognomic of HF?
3rd heart sound
Most common causes of HF in UK
Lifestyle modifications in HF?
Limit fluid intake (<2L)
TTT of HF
Diuretics for fluid overload but don't impact prognosis
Other ttt for HF
Revascularisation if CAD
Bi ventricular pacemaker /defibrillator if dysynchrony
Symptoms of IE
New heart failure
Embolic phenomena (stroke)
IE on examination
Embolic phenomena (splinter hges, osler's nodes, janeway lesions, petechiae
Evidence of aetiology: IVDA, infected cannula, recent surgery