Randoms Flashcards
Recent chest pain which resolved followed by this ECG is? What does it mean
Wellens syndrome
biphasic or deeply inverted T waves in V2-3, plus a history of recent chest pain now resolved.
Specific for critical stenosis of the LAD artery
What is goldenhar syndrome
Abnormal development of eye, ear and spine.
Usually UNILATERAL
[oculo-auriculo-vertebral spectrumor OAV]
Which vessles do these correspond to
Beta blocker overdose. Bb od management ?
Monitoring
High dose insulin + dextrose
Insulin bolus:
Bolus with regular insulin 1 unit/kg IV
If blood glucose is <11, give 25 g of dextrose IV
Insulin continuous infusion (1 unit/mL concentration)
Initial dose: regular insulin 0.5 to 1 unit/kg/hr IV drip (for adults this is usually 35 to 100 units/hour)
Titration:
If no significant response is achieved in 30 minutes, increase the drip 0.5 units/kg/hr every 10-15 minutes to a maximum dose of 4 units/kg/hr (though success is reported with doses in the 10-14 U/kg/hr range) or until improvement hemodynamics improve
Dextrose:
IV dextrose should be administered to maintain blood glucose (BG) levels between 6-11mmol
Start infusion at 0.5 mg/kg/hr as either D5, D10, or D25 (D10 being the most commonly used concentration)
Initial dextrose requirement may vary based on initial BG and underlying diabetes
D5W has high free water content, and serum sodium should be monitored closely
D25 and D50 infusions require central venous administration due to local tissue irritant effects of concentrated dextrose
Check BG every 10-15 minutes and titrate dextrose accordingly
MONITORING
Blood glucose should be monitored every 15-30 minutes and corrected with IV dextrose
Once BG have consistently been 6-11 for 4 hours, can decrease frequency of checks to hourly
Potassium and acid-base status should be monitored every 15 to 30 minutes and corrected with IV potassium or bicarbonate
Assess cardiac function and blood pressure every 15 to 30 minutes
Benefits of TAVI over AVR
Puncture of vessel
Does not require cardiac bypass for surgery
Which has better outcomes TAVI vs AVR? main benefits of each
The risk of mortality is similar
Stroke risk is the same 1-2%
TAVI - less risk for dialysis/blood transfusion / respiratory failure
-Faster recovery
AVR - less risk for pacemaker 5% [in TAVI 15%]
AVR lasts much longer
Main populations for TAVI vs AVR
TAVI in older >80
- less invasive
- Unknown how long the valve will last for (probably around 10-15 years)
AVR known to last longer
- used in young people <60
-Also if multiple valves / CABG needed
TAVI vs AVR effect on MR/TV regurg?
TAVI - 25% worse, 25% better 50% the same
AVR - Usually makes MVRegurg/TVRegurg better
Procainamide dosing in AVNRT ? Oral option?
Loading - IV procainamide is 10 to 17 mg/kg and administered at a rate of 20 to 50 mg/min.
[Alternatively, this may be dosed at 100 mg every 5 minutes in adult patients. ]
The maintenance dose is from 1 to 4 mg/minute;
Administration of oral procainamide dosing for supraventricular arrhythmia is at 50 mg/kg/24 hours divided into doses every 6 hours.
What causes a junctional rhythm? What is a accelerated junctional rhythm?
junctional tachy?
junctional brady?
SA node failure -> AV node take over
All just based on rate
Junctional - 40-60bpm
Accelerated junctional rhythm = 60-100bpm
junctional tachy- >100bpm
junctional brady <40bpm
NYHA heart failure classes
Class I No limitations. Ordinary physical activity does not cause undue fatigue,
dyspnoea or palpitations (asymptomatic LV dysfunction).
>7
Class II Slight limitation of physical activity. Ordinary physical activity results in
fatigue, palpitation, dyspnoea or angina pectoris (mild CHF).
5
Class III Marked limitation of physical activity. Less than ordinary physical
activity leads to symptoms (moderate CHF).
2–3
Class IV Unable to carry on any physical activity without discomfort. Symptoms of CHF present at rest (severe CHF).
1.6
What is Eplerenone?
selective mineralocorticoid receptor antagonist
[so it lacks the anti-androgenic side effects of spironolactone.]
Eplerenone is associated with lower rates of impotence, gynecomastia or breast pain in comparison to spironolactone.
Entresto doses
24 mg/26 mg,
49 mg/51 mg,
and 97 mg/103 mg
[of sacubitril/valsartan]
When do you presribe entresto
Symptomatic heart failure
(NYHA Class II-IV).
[Used in place of ACEi or ARB]
When treat cholesterol
Cholesterol >6.2
HDL 1
LDL > 1.9
Recurrent VT on b blocker and amiodarone with ICD - not suitable for VT ablation what could you add in?
Mexiletine 150mg TDS
How do the type 1 antiarrythmics work
Na channel blockers
- Primary prevent conduction in SA node
If going for VT ablation what do you need to do? Eg patient is on amiodarone, Mexiletine and bisoprolol
Change to short acting
Amio -> stop
Mexiletine -> Change to IV lidocaine so can stop pre op
Bisop -> change to short acting Eg Metoprolol tartate
How long does prothrombinex take to work and for how long? Dose?
More or less straight away
(Can check an INR after 45 mins if needed)
Lasts 6-12 hours
50units/kg
What happens in BMPR2 gene induced pulmonary hypertension?
Proliferation of smooth muscles in pulm vessles
How does scleroderma cause pulmonary hypertension
Damages endothelial layer of pulm vessles
-> Release endothelin 1, thromboxane, serotonin
-> Smooth muscle hypertrophy
Classes of pulmonary hypertension
1 - From pulm arteries
- Idiopathic
- HIV, Portal HTN, Schisto, drugs
2 - Left heart disease
3 - Hypoxic lung disease
4 - CTEPH (Chronic ThromboEmbolism Pulmonary Hypertension)
5 - Others
Why is dopamine used over other initropes in CCU for patients with fluid overload and hypotension
At low dose (0.5-2mcg/kg/min) the primary effects are on D1 receptors
-> Includes renal vasodilation, augmenting diuresis
[Selective vasodilation in renal, coronary, mesenteric and cerebral vessles[]
Dose dependent effects of Dopamine
0.5-2mcg/kg/min. D1 / D2 receptors
- Vasodilation of visceral receptors including renal
2-10mcg/kg/hr Beta 2 receptors
- Increased myocardial contractility -> Increases CO (by increasing SV)
> 10mcg/kg/hr Beta 1, beta 2, alpha - 1
- Vasocontriction and increased BP
Most common type of SVT
AVNRT
in comparison to AVRT, which involves an anatomical re-entry circuit (Bundle of Kent), in AVNRT there is a functional re-entry circuit within the AV node.
re-entry-tachycardias
Alrternate re-entry loops: Functional circuit in AVNRT (left), anatomical circuit in AVRT (right)
What is the most common type of AVNRT?
ECG features?
Slow-fast
[Associated with slow AV nodal pathway for anterograde conduction and fast AV nodal pathway for retrograde conduction]
P waves are often hidden – being embedded in the QRS complexes
Pseudo R’ wave may be seen in V1 or V2
Pseudo S waves may be seen in leads II, III or aVF
In most cases this results in a ‘typical’ SVT appearance with absent P waves and tachycardia
Top strip: Normal sinus rhythm. Absence of pseudo-R waves
Bottom strip: Paroxysmal SVT. The P wave is seen as a pseudo-R wave (circled) in lead V1 during tachycardia. This very short ventriculo-atrial time is frequently seen in typical Slow-Fast AVNRT
Which SVT is this
Slow-Fast (Typical) AVNRT:
Narrow complex tachycardia at ~ 150 bpm
No visible P waves
There are pseudo R’ waves in V1-2
Which SVT is this
Fast-Slow (Uncommon) AVNRT:
Narrow complex tachycardia ~ 120 bpm.
Retrograde P waves are visible after each QRS complex — most evident in V2-3.
