cardio r/v Flashcards
(54 cards)
What does the ECG show?

- HR is 100 and regular
- vary tall R waves in V1-V3
- ST depression V1-V4
- very small R wave in V6
- R axis deviation

What’s normal range of D-dimer?
208-318 ng/ml
Possible causes of increased D-dimmer
- liver disease
- pregnancy
- trauma
- recent surgery
- advanced age
- acute MI
Treatment options for PE
- LMWH or fondaparinux →initially after a PE diagnosis
*an exception to this is for patients with a massive PE where thrombolysis is being considered. In such a situation unfractionated heparin should be used.
- a vitamin K antagonist (i.e. warfarin) should be given within 24 hours of the diagnosis
*LMWH or fondaparinux should be continued for at least 5 days or until the international normalised ratio (INR) is 2.0 or above for at least 24 hours, whichever is longer, i.e. LMWH or fondaparinux is given at the same time as warfarin until the INR is in the therapeutic range
*warfarin should be continued for at least 3 months. At 3 months, clinicians should ‘assess the risks and benefits of extending treatment’
*extending warfarin beyond 3 months for patients with unprovoked PE
*for patients with active cancer → LMWH for 6 months
- thrombolysis → first-line treatment for massive PE where there is circulatory failure (e.g. hypotension)
- IVC filters→ if repeat PEs, despite adequate anticoagulation
MoA of:
- Heparin
- Warfarin
- Rivaroxaban
- Fondaparinux

Signs of PE on ECHO

Treatment for a haemodynamically unstable patient with PE

Interpret this ECG


Biphasic P wave in V1
Normal or abnormal?
P wave in V1 is often biphasic, due to:
- early R atrial forces are directed anteriorly
- followed by L atrial forces travelling posteriorly (producing negative deflection)
*if pathological is usually more generalised
Interpret ECG

AF with a rapid ventricular rate
6 seconds rule to calculate HR

Management of AF
- Verapamil or Diltiazem → first-line
*Metoprolol or Diltiazem → if IV agent needs to be used
- Cardioversion → if symptoms continue
- CHA2DS2VASc + anticoagulation if necessary
Causes of AF
- HTN
- valvular heart disease
- HF
- IHD
- chest infection
- lung ca
- excessive alcohol intake
- hyperthyroidism
- electrolyte depletion
- infection
- diabetes
Ix in AF
- ECG
- bloods (including TFTs)
- ECHO
What else do we need to do with CHA2DS2VASc?
Calculate HAS-BLED score → risk of bleeding
How do we measure JVP?
From pulsation from internal jugular vein
How to differentiate JVP from carotid pulse?
JVP is:
- multiphasic
- non-palpable
- occludable
What does Kausmall’s sign mean?
Kussmaul’s sign describes a paradoxical rise in JVP during inspiration seen in constrictive pericarditis.
What’s cause of non-pulsatile JVP?
A non-pulsatile JVP is seen in superior vena caval obstruction
What’s ‘a’?

‘a’ wave = atrial contraction
- large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension
- absent if in atrial fibrillation
Cannon ‘a’ waves
- caused by atrial contractions against a closed tricuspid valve
- are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular pacing
What’s ‘C’?

‘c’ wave
- closure of tricuspid valve
- not normally visible
What’s ‘v’?

‘v’ wave
- due to passive filling of blood into the atrium against a closed tricuspid valve
- giant v waves in tricuspid regurgitation
What’s ‘x’ and ‘y’?

- ‘x’ descent = fall in atrial pressure during ventricular systole
- ‘y’ descent = opening of tricuspid valve
What do we use JVP for?
To measure (indirectly) pressure in R atrium and venous system































