cardio r/v Flashcards
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
Causes of raised JVP
- HF
- cardiac tamponade
- constrictive pericarditis
- fluid overload
Cause of absent A waves
- AF →as atria contract in uncoordinated way
Causes of large A wave
A wave → R atrial contraction
Large A wave: (anything that will increase pressure in R atrium/R atrial contraction)
- R vent hypertrophy
- tricuspid stenosis
Cause of large V wave
V wave = atrial filling (venous return)
Cause of large V wave:
- tricuspid regurgitation (as more blood into R atrium due to backflow)
Meaning of all points of JVP wave
Interpret ECG
Pathologies:
- infract
- pace maker in situ
Vicious cycle of HF
Can patients with COPD/asthma be managed with CPAP (e.g. during pulmonary oedema)?
Inotropic agents used in IHD with impaired output and haemodynamic instability (e.g. low BP, urinary retention)
Name the drugs and when to initiate them in post-MI HF?
Normal ranges of cQT (corrected QT) for men and women
Channels and ion movement during cardiac cycle
How long QT can lead to arrhythmias?
What’s that?
Drugs prolonging QT
Ix (other than ECG) and Mx for long-QT
Interpret ECG + treatment options
BP is 120/80
What does ECG show?
Algorithm for NSTEMI-ACS management
If a patient presents with an NSTEMI then a risk stratification too (such as GRACE) is used to decide upon further management. If a patient is considered high-risk or is clinically unstable then coronary angiography will be performed during the admission. Lower risk patients may have a coronary angiogram at a later date.
Secondary prevention
- aspirin
- a second antiplatelet if appropriate (e.g. clopidogrel)
- a beta-blocker
- an ACE inhibitor
- a statin
Calcified aortic valve - aortic valve stenosis
- What (apart from the murmur) would you look for O/E?
- Further Ix (apart from ECHO)
Treatment options for aortic stenosis
- if asymptomatic then observe the patient is general rule
- if symptomatic then valve replacement
- if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery
- cardiovascular disease may coexist. For this reason an angiogram is often done prior to surgery so that the procedures can be combined
- balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement
Interpret the ECG
Global ST elevation in all leads apart from I and AVL
What do these images show?
Normal coronary angiogram
What’s the abnormality?
Classification of aortic dissection
Stanford classification
- type A - ascending aorta, 2/3 of cases
- type B - descending aorta, distal to left subclavian origin, 1/3 of cases
DeBakey classification
- type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
- type II - originates in and is confined to the ascending aorta
- type III - originates in descending aorta, rarely extends proximally but will extend distally
Management of aortic dissection
Type A
- surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention
Type B
- conservative management
- bed rest
- reduce blood pressure IV labetalol to prevent progression
Comment on this ECG and ECHO
Signs on auscultation of atrial septal defect (ASD)
