Cardiology Flashcards
1
Q
Mortality in endocarditis according to organisms
A
- Staphylococci 30%
- Bowel organisms - 15%
- Streptococci 5%
2
Q
Poor prognostic factors of endocarditis
A
- Staphyloccocus aureus
- Prosthetic valve
- Culture negative endocarditis
- Low complement levels
3
Q
Rx of endocarditis
A
Initial blind therapy
- Native valve
- Amoxicillin
- Pen allergic
- Vancomycin** + **low-dose gentamicin
- Prosthetic valve
- Vancomycin** + **low-dose gentamicin** + **rifampicin
Native valve endocarditis caused by streptococci
-
Fully-sensitive (e.g. viridans)
- Benzylpenicillin
- If pen allergic: vancomycin** + l**ow-dose gentamicin
-
Less-sensitive
- Benzypenicillin** + **low-dose gentamicin
- If pen allergic: vancomycin** + **low-dose gentamicin
Endocarditis caused by staphylocci
-
Native valve
- Flucloxacillin
- Pen allergic or MRSA: vancomycin** + **low-dose gentamicin
-
Prosthetic valve
- Flucloxacillin** + **rifampicin** + **low-dose gentamicin
- Pen allergic: Vancomycin** + **rifampicin** + **low-dose gentamicin
4
Q
Indications for surgery in endocarditis
A
- Severe valvular incompetence
- Aortic abscess (lengthening of PRi)
- Infections resistant to antibiotics
- Cardiac failure refractory to standard medical treatment
- Recurrent emboli after ABx Rx
5
Q
Rx of ventricular tachycardia
A
1st line - Amiodarone
2nd line - Lidocaine
3rd line - Procainamide
6
Q
Mx of pulseless VT or VF
A
- Compressions with a shock of at least 150 J
- Compressions 30:2 for 2 min
- After 3rd shock (increasing voltage) - 1 mg adrenaline IV and then the same after every shock
7
Q
Cardiac catheterisation and oxygen saturation levels
A
Rules
- Deoxygenated blood returns to the R heart - SpO2 ~ 70%
- RA, RV, PA
- The lungs oxygenate blood to 98-100% - L right Z 100%
- LA, LV, Aorta
Conditions
- ASD
- Oxygenated blood in LA mixes with deoxygenated in the RA
- R heart - 85%, L heart - 100%
- Oxygenated blood in LA mixes with deoxygenated in the RA
- VSD
- Oxygenated blood in LV mixes with deoxygenated in the RV
- RA - 70%
- RV, PA - 85%
- LA, LV, Aorta - 100%
- Oxygenated blood in LV mixes with deoxygenated in the RV
- Patent Ductus Arteriosus
- PDA connects higher pressure Aorta with lower pressure PA
- RA, RV - 70%
- PA - 85%
- LA, LV, Aorta - 100%
- PDA connects higher pressure Aorta with lower pressure PA
8
Q
Management of HOCM
A
AD disorder of muscle tissue caused by defects in the genes encoding contractile proteins
- 1 in 500
Rx
- Amiodarone
- Beta-blockers or Verapamil for Sx
- Cardioverter defibrillator
- Dual chamber pacemaker
- Endocarditis prophylaxis
Drugs to avoid
- Nitrates
- ACE-inhibitors
- Inotropes
9
Q
Mx of high INR
A
Major bleeding
- Stop warfarin
- IV vitamin K 5mg
- Prothrombin complex concentrate
- If N/A then FFP
INR > 8.0, minor bleeding
- Stop warfarin
- IV vitamin K 1-3 mg
- Repeat dose of vit K if INR still too high after 24h
- Restart warfarin when INR < 5.0
INR > 8.0, no bleeding
- Stop warfarin
- Vitamin K 1-5 mg IV preparation orally
- Repeat dose of vitamin K if INR still high after 24h
- Restart warfarin when INR < 5.0
INR 5.0 - 8.0, minor bleeding
- Stop warfarin
- IV vitamin K 1-3 mg
- Restart when INR < 5.0
INR 5.0 - 8.0, no bleeding
- Withhold 1 or 2 doses of warfarin
- Reduce subsequent maintenance doses
10
Q
Treatment of PE
A
LMWH or fondaparinux initially after PE has been diagnosed
- Except for massive PE where thrombolysis is considered
LMWH/fondaparinux for at least 5 days or until INR is 2.0 or above for at least 24h (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 / DOACs for at least 3 months
Unprovoked PE - anticoagulation for at least 6 months
11
Q
Normal JVP waveform
A
The a wave
- Atrial contraction
The c wave
- Invisible flicker in the x descent due to closure of the tricuspid valve
- Just before the start of ventricular systole
The x descent
- Downward movement of the heart > atrial stretch > drop in pressure
The v wave
- Passive filling of blood into the atrium against a closed tricuspid valve
The y descent
- Opening of the tricuspid valve
- Passive movement of blood from the RA to the RV (S3 when audible)
12
Q
Causes of raised JVP (normal waveform)
A
- Heart failure
- Fluid overload
- Severe bradycardia
13
Q
Causes of raised JVP - Kussmaul’s sign
A
Normally, JVP increases upon inspiration (up), drops with expiration (down)
Kussmaul’s sign
- Opposite of what occurs in health
- = Right heart chambers cannot increase in size to accommodate increased venous return
Causes
- Pericardial disease (constriction)
- Fluid in the pericardial space
- Pericardial effusion
- Cardiac tamponade
14
Q
Raised JVP with loss of normal pulsations
A
Causes
- SVC syndrome
- Obstruction
- Mediastinal malignancy
- Bronchogenic malignancy > head, neck &/or arm swelling
- Mediastinal malignancy
- Obstruction
15
Q
a wave in diseases
A
Absent
- Atrial fibrillation - no co-ordinated contraction
Large
- Tricuspid stenosis
- Right HF
- Pulmonary HTN
Cannon
- AV dissociation - allowing the atria & ventricles to contract at the same time
- Atrial flutter & atrial tachycardias
- Third-degree (complete) heart block
- Ventricular tachycardia & ventricular ectopics
16
Q
v waves in diseases
A
Giant
- Tricuspid regurgitation
17
Q
x descent in diseases
A
- Downward movement of the heart > atrial stretch & a drop in P
Steep
- tamponade
- cardiac constriction
If steep x descent only > tamponade
18
Q
y descent in diseases
A
- Opening of tricuspid valve with passive movement of blood from RA to RV
Steep
- Cardiac constriction
Slow
- Tricuspid stenosis
19
Q
JVP waveforms in diseases
A
Atrial fibrillation
- Loss of a-wave
Tricuspid regurgitation
- Large c-V wave
R HF, Pulmonary HTN
- Raised JVP
- Prominent a-wave
Constriction
- Prominent and deep x and y descents
Tamponade
- Prominent x descent only
- y descent slow or absent
20
Q
Absent radial pulse
A
- Iatrogenic - post-catheterisation or arterial line
- Blalock-Taussig shunt for congenital heart disease (e.g. ToF)
- Aortic dissection with subclavian involvement
- Trauma
- Takayasu’s arteritis
- Peripheral arterial embolus
21
Q
Collapsing pulse
A
- Aortic regurgitation
- Arteriovenous fistula
- PDA
- Other large extracardiac shunts
22
Q
Slow rising pulse
A
- Aortic stenosis
- delayed percussion wave
23
Q
Bisferiens
A
- A double shudder due to mixed aortic valve disease with significant regurgitation
24
Q
Jerky
A
hypertrophic obstructive cardiomyopathy
25
Alternans
* Occur in **severe left ventricular dysfunction**
* Reduced EF \> elevated end-diastolic volume
* This may sufficiently stretch the myocytes (Frank-Starling physiology) to improve the EF of the next HB
* This leads to pulses that alternate **weak** and **strong**
26
Paradoxical (pulsus paradoxus)
* An excessive reduction in the pulse with inspiration
* Drop in BP \>10 mmHg
* Left ventricular compression
* Tamponade
* Constrictive pericarditis
* Severe asthma as venous return is compromised
27
Hyperkalaemia on ECG
* Tall T waves
* Prolonged PR interval
* Flattened/absent P waves
28
Very severe hyperkalaemia on ECG
* Wide QRS
* Sine wave pattern
* Ventricular tachycardia / VF / asystole
29
Hypokalaemia ECG
* Flat T waves, occasionally inverted
* Prolonged PR interval
* ST depression
* Tall U waves
30
What heart defect can present with acute ischaemic stroke?
**Patent foramen ovale**
* Present in 20% of population
* May allow embolus (e.g. from DVR) to pass from R side of the heart to the L side \> _paradoxical embolus_
31
Target INR for prosthetic valves
Aortic - 3.0
Mitral - 3.5
32
Pulmonary arterial hypertension
PAH = a resting mean pulmonary artery pressure ≥ 25 mmHg
* More common in females
* Typically 30-50 yoa
* RF
* HIV
* Cocaine
* Anorexigens (e.g. fenfluramine)
* 10% inherited - AD
* Features
* Progressive exertional dyspnoea
* Exertional syncope, exertional chest pain, peripheral oedema
* Cyanosis
* Right ventricular heave, loud P2, ^JVP with prominent 'a' waves, tricuspid regurgitation
* Management
* Anticoagulants, oxygen
* **Acute vasodilator testing** (central to deciding on the appropriate Mx strategy)
* To decide which pts show a significant _fall in pulmonary arterial P_ after administration of _vasodilators_
* E.g. IV epoprostenol, inhaled NO
* If +ve response to acute vasodilator testing (minority of pts)
* _Oral Ca channel blockers_
* If _negative_ response to acute vasodilator testing (majority)
* **Prostacyclin analogues**
* Treprostinil, iloprost
* **Endothelin receptor antagonists**
* Bosentan, ambrisentan
* **Phosphodiesterase inhibitors**
* Sildenafil
33
Describe the JVP
**'a' wave = atrial contraction**
* _large_ if atrial pressure
* tricuspid stenosis
* pulmonary stenosis
* pulmonary hypertension
* _absent_ if in AF
**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
**'c' wave**
* closure of tricuspid valve
* not normally visible
**'v' wave**
* due to passive filling of blood into the atrium against a closed tricuspid valve
* giant v waves in tricuspid regurgitation
**'x' descent** = fall in atrial pressure during ventricular systole
**'y' descent** = opening of tricuspid valve
34
Treatment of Hypertension
**Clinic reading ≥ 140/90 mmHg**
* Offer ABPM or HBPM
* **\< 135/85 mmHg**
* Not hypertensive \> monitor
* **≥ 135/85 mmHg**
* Stage **1** hypertension
* Treat if **\< 80 yrs** & any of the following
* Target organ dmg
* Established CVS disease
* Renal disease
* Diabetes
* 10-yr CVS risk ≥10%
* **≥ 150/95 mmHg**
* Stage **2** hypertension
* Treat all patients, regardless of age
35
Anteroseptal - V1-V4
Left anterior descending
36
Inferior - II, III, aVF
Right coronary
37
Anterolateral - V4-V6, aVL
Left anterior descending
Left circumflex
38
Lateral - I, aVL +/- V5-6
Left circumflex
39
Posterior - Tall R waves V1-V2
Usually left circumflex, also right coronary
40
Acute pericarditis
Features
* Chest pain - can be pleuritic
* Often relieved by sitting forwards
* Other Sx
* Non-productive cough
* Dyspnoea
* Flu-like Sx
* Pericardial rub
* Tachypnoea
* Tachycardia
Causes
* Viral infections (Coxsackie)
* Tuberculosis
* Uraemia (causes 'fibrinous' pericarditis)
* Trauma
* Post-MI \> Dressler's syndrome
* Connective tissue disease
* Hypothyroidism
* Malignancy
Ix
* ECG changes
* _Widespread ST elevation_
* _Saddle-shaped ST elevation_
* _PR depression_ - most-specific ECG marker for pericarditis
* All pts with suspected acute pericarditis should have
* _Transthoracic echocardiography_
Mx
* Treat the underlying cause
* Comb of **NSAIDs** & **colchicine**
41
Modified Duke criteria
(Modified) Duke criteria
* The Duke criteria help to diagnose infective endocarditis. To confirm the diagnosis, one of the following requirements must be met:
* Two major criteria
* One major and three minor criteria
* Five minor criteria
Major diagnostic criteria
* Two separate blood cultures positive for typical pathogens (see “Etiology” above)
* Evidence of endocardial involvement in echocardiography
* A new valvular regurgitation (worsening of a pre-existing murmur is not sufficient)
Minor diagnostic criteria
* Predisposition: underlying heart disease or IV drug abuse
* Fever ≥ 38°C (100.4F)
* Vascular abnormalities
* Immunologic disorder
Microbiology
