CVS Signs Flashcards
Radiofemoral delay
Coarctation of aorta (congenital narrowing usually distal to L SCA)
Radio radial delay
Aortic arch aneurysm. Coarctation aorta Aortic dissection External tourniquet Severe atherosclerosis Compartment syndrome
PP changes
Narrow in- Aortic stenosis Hypovolaemia Wide in- Aortic regurg Septic shock
Malar flush
Mitral stenosis
Low CO
Carotid pulse character
Irregularly irregular in AF
Regularly irregular in 2nd degree HB
Character and volume-
-Bounding in CO2 retention, liver failure, sepsis.
-Small volume in aortic stenosis, shock, pericardial effusion.
-Collapsing water hammer (early peak then rapid descent, exaggerated by lift arm, associated with wide PP)-aortic incompetence, AV malformations, PDA.
-Ancrotic slow rising (gradual upstroke, reduced late peak)-aortic stenosis.
-Bisferiens (double systolic peak with dip in btw)-combined aortic stenosis and regurg.
-Pulsus alternans (strong to weak, normal rhythm)-LVF, cardiomyopathy, aortic stenosis.
-Pulsus paradoxus (systolic pressure falls in inspiration more than normal-over 10mmHg) in severe asthma, cardiac tamponade.
Bruits- atherosclerosis, vasculitis in young.
JVP
Raised with normal wave- fluid overload, RHF. Acute PE, COPD.
Fixed raised with absent pulsation- SVC obstruction.
A wave due to RA contraction.
Large a wave- pulmonary HTN and TV stenosis.
Cannon a wave- T3 HB, ventricular arrhythmia.
Absent a wave- AF.
V wave due to atrial filling during systole when tricuspid closed.
Large v wave- tricuspid regurg.
C wave rare- due to tricuspid closure.
High plateau- pericarditis
Kussmauls sign- paradoxical rise of JVP on inspiration in tamponade, RVF, restrictive cardiomyopathy.
Absent JVP when flat- reduced circulatory volume.
Abdominojugular test- press over liver= raise venous return to RH=raise JVP temporarily.
Normally falls with inspiration due to reduced IT pressure.
Prevent wave by occluding vein at base of ECG with finger.
Palpation
-apex beat-
Heaving (pressure loaded undisplaced)- aortic stenosis, systemic HTN.
Thrusting (pressure loaded, displaced)- AR/MR
Tapping (pressure loaded undisplaced)- MS tapping, palpable S1.
Diffuse- LVF, cardiomyopathy.
Absent DOPES- death, obesity, pericarditis, emphysema, dextrocrdia.
Deviation- mediastinal shift, cardiomegaly, scoliosis, pectus excavatum, dextrocardia.
-Left parasternal heave- RVH eg pulmonary stenosis, cor pulmonale.
-Thrills- murmurs.
Basal creps and pleural effusion
HF
Xanthomata, xanthelasma, corneal arcus
Hyperlipidaemia.
Corneal arcus common in over 60 normally.
Heart sounds
S3- loud in dilated cardiomyopathy and MV regurg. High pitch in pericarditis.
CAN BE NORMAL.
S4- NEVER normal. In stiff ventricle eg aortic stenosis, HTN.
murmurs
Ejection systolic- aortic stenosis. Quiet S2 with advancing murmur. Due tocalcified AV, bicuspid valve, rheumatic fever.
Pansystolic- MV or TV regurg, VSD. Radiates to axilla.
Early diastolic- aortic and pulmonary regurg. (High pitch easily missed).
Mid diastolic- mitral stenosis, aortic regurg, rheumatic fever. (Low and rumbling).
Aortic stenosis radiates to carotid.
Mitral regurg radites to axilla.
Expiration- increases blood to L heart so accentuates LH murmurs.
Inspiration- accentuates RH murmurs. (RILE).
Lean forward for aortic regurg L sternal edge.
Left lateral for mitral stenosis (LSITEN WITH BELL), Exercise accentuates.
Continuous murmurs- PDA, AV fistula, ruptured sinus of Valsalva.
Superficial pericardial friction rub- pericarditis.
Radial pulse
Irregularly irregular- AF
Regularly regular- 2nd degree HB, ventricular trigeminy
Collapsing- aortic regurg
Scars
Median sternotomy
PPM
Sub mammary throacotomy
Chest pain
CARDIAC-
Myocardial ischaemia- central diffuse tightening.
Pericarditis- sharp.
Aortic dissection- severe tearing pain start mid chest to back and down spine.
RESP-
Pneumonia, PE, pneumothorax- lateral pleuritic pain, worse no inspiration and cough.
GI-
Reflux oesophagitis- chest and epigastric burning
Gastric/GB/pancreatic pain.
MSK-
Trauma- injury in hx or excessive use.
Muscle pain- often localised and worse on movement.
Bone mets
Marfans
Reduced EC microfibres formation and poor elastic fibre formation due to mutated fibrillin gene.
Valve and vessel wall disease.
Aortic dissection.
Postural hypotension
Hypovolaemia
Drugs eg nitrates, diuretics, antiHTN, antiP.
Addisons
Hypopituitary
Signs of aortic regurg
Head nodding with pulse Systolic pulsation of uvula Visible carotid pulse Capillary nailbed pulsation Pistol shot femorals To and fro diastolic murmur when compress femorals
Route of electrical activity
SAN, IN tracts, AVN, bundle of his, LBB, RBB, PK
Depolarisation endo to epicardium
Repolarisation after 280ms, epi to endocardium
Leads
Limb leads coronal bipolar Chest leads horizontal unipolar Augmented leads coronal unipolar Towards positive sensing electrode -LII, III, aVF- inferior MI, RCA. -LI, aVL, V5+6- anterolateral LV, L circumflex -aVR- atrial and ventricular cavities. -V1+2- anterospetal, LAD. -V3+4- anteroapical, distal LAD. -LI, aVL, V2-6- extensive anterior, proximal LCA. -tall R in V1- true posterior, RCA.
Section of the trace
P= atrial depolarisation. isol electric A to V Q=septum to ventricle L to R R=ventricular depolarisation S=end ventricular depolarisation T= ventricular repolarisation epi to endo
Timings
5LS= 1 second
1SS= 0.04 seconds
Rate= 300/ LS of RR interval
PR= start P to start Q, should be 0.12-0.2 sec
QRS= start Q to end S, should be under 0.12 sec
QT= start Q to end T, should be 0.45 sec
Narrow QRS= atrial/AVN origin. Wide= ventricular origin or BBB.
Abnormal ECG
AF= irregularly irregular, no P, narrow QRS
1st degree HB= long PR
2nd degree mobitz 1= progressively longer PR, drop QRS
2nd degree mobile 2= normal PR, drop QRS
2rd degree= normal PR, not all cause QRS. Slow ventricular escape, wide QRS.
Ventricular ectopic= wide QRS
VT= 3+ ectopics in row
VF= fast, irregular shape QRS. NO CO or pulse.
Subendocardial ischaemia= STD
Fully evolved MI= STE, wide Q, T inversion. Pathological Q=over 1SS wise, over 2mm deep, in full thickness MI, remains after.
Axis (direction of spread of ventricular depolarisation)
Normal -30 to 90
R axis deviation= over 90 eg RVH
L axis deviation= under -30 eg LVH, conduction block anterior LBB
WiLLiaM MaRRoW
LBBB eg aortic stenosis, dilated cardiomyopathy, MI, CAD
RBBB eg ASD, PE, MI
-in LBBB- QRS looks like a W in V1 and an M in V6
-in RBBB- QRS looks like M in V1 and W in V6
Coronary BF
Epi to endocardium to subendocardial muscle vulnerable.
Increase HR= decrease disatole more
Cardiac enzymes
Mb peaks first 6-12 hours.
Trop I and T peak 18-36 hours. Start to rise after 4 hours. Slow fall.
CK-MB peak 24 hours. Falls slower.
MI ECG over time
- immediate- STE
- hours- start of pathological Q, decrease R
- days- T inversion, deeper Q
- more days- ST normal, T inversion
- weeks- ST and T normal, Q persists
VF (most common CA)
Causes-
MI
K imbalance
Arrhythmia eg long QT, torsades de pointes
HyperK ECG
With increasing concentration
- normal
- high T
- increase PR, STD, high T
- very wide QRS, no P
- VF
HypoK ECG
With decreasing concentration
- normal
- low T
- low T, high U
- low T, high U, low ST
Haemodynamic shock (poor perfusion) Due to low CO or low TPR
Low CO:
-cardiogenic pump fails to empty- MI, arrhythmia, acute HF.
= low maBP, low coronary A flow, oliguria.
-mechanical shock fail to fill due to obstruction- tamponade, PE.
=high VP, low maBP
-hypovolaemic reduced venous return- haemorrhage over 30%, burn, diarrhoea and vomiting very severe, Na loss.
=low VP and low AP. SNS compensation by increase TPR for while.
Low TPR:
-distributive- toxic shock sepsis, anaphylaxis.
=low TPR. SNS compensation.
Urinalysis for kidney hypoperfusion
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Causes of regurg
CT disease eg marfans, ehlers danlos. Rheumatic HD Cardiomegaly. Chordae tendinae damage eg MI. Infective endocarditis.
Causes of stenosis
Senile calcification
Atherosclerosis
Vegitations due to infection
Rheumatic HD scarring
