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Week 14: Palpitations > palpitation case > Flashcards

palpitation case Flashcards

1
Q

50% of Down syndrome patients have cardiac defects. What is the most likely reason for this?

A

Gene dosage. trisomy 21 results in extra genetic material, but not necessarily entire extra chromosome - can have rearrangements of it

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2
Q

22q11.2 deletion syndrome (DiGeorge syndrome) is an example of which of the following?

a) locus heterogeneity
b) compound heterozygote
c) pleiotropic effect
d) allelic heterogeneity

A

c) pleiotropic effect

one gene influences multiple seemingly unrelated phenotypic traits (remember CATCH-22: cardiac abnormalities, abnormal facies, thymic aplasia, cleft palate, hypothyroidism)

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3
Q

what is the most common cardiac cause of death in the under 35’s, associated with exercise?

A

hypertrophic cardiomyopathy

autosomal dominant inheritance

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4
Q

name an autosomal dominant cardiac condition that is associated with a delay in repolarisation

A

Long QT

may lead to sudden death, not associated with exercise

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5
Q

what is Xanthoma a sign of?

A

hypercholesterolemia (LDL >4mM; total >7.5mM). Risk of atherosclerosis (e.g. coronary heart disease)

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6
Q

what major vessel is at risk during tracheostomy?

A

left brachiocephalic

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7
Q

which structures are at risk in thoracic outlet syndrome?

A

subclavian artery and inferior brachial plexus (C8+T1)

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8
Q

posterior and anterior intercostal arteries anastomose and may form collateral circulation in what condition?

A

coarctation of the aorta

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9
Q

which structure in the thorax is an important site for porto-systemic anastomosis?

A

oesophagus

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10
Q

at what thoracic level can the diaphragm rise up to? what prevents it descending too far?

A

4th intercostal space

attachment to the pericardium

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11
Q

give an example of a moderate blockage Na+ channel blocker and its uses in arrhythmias

A

disopyramide. used to treat ventricular dysrhythmias (ventricular tachycardia and ventricular fibrillation) prevention of recurrent atrial fibrillation triggered by vagal overactivity

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12
Q

what subclass of Na+ channel blocker has no affect on the refractory period of an AP?

A

1C e.g. flecainide

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13
Q

what drug would be fatal if given to treat a supraventricular arrhythmia in a patient with Wolff-Parkinson-White syndrome?

A

Class 4 - calcium channel blockers e.g. verapamil

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14
Q

what drugs can be used to treat the following arrhythmias?

  1. SVTs
  2. VTs
  3. SV and V dysrhythmias
A
  1. adenosine, BB, CCB, digoxin
  2. NaCB, KCB
  3. KCB, BB, NaCB
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15
Q

which of the following is not represented on an ECG?

a) ventricle depolarisation
b) atrial depolarisation
c) ventricle repolarisation
d) atrial repolarisation

A

d) atrial repolarisation

masked by the QRS complex

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16
Q

what 3 criteria must be met to classify sinus rhythm on ECG?

A
  1. presence of P waves (no taller than 2.5 boxes)
  2. QRS complex (no wider than 3 boxes)
  3. 3 consecutive R-intervals
17
Q

compare ECG findings of atrial fibrillation and atrial flutter

A

AF:

  • absence of p-waves
  • wont see regular QRS complex (probably narrow)
  • irregular R-intervals

A.flutter:

  • sawtooth p-waves
  • normal QRS complex
  • regular R-intervals

(NB: use same criteria for classifying rhythm)

18
Q

what finding in ECG would suggest left ventricular hypertrophy?

A

R wave in V5 >25mm (measure from isometric line to tip). also axis may be deviated to left and if so - negative QRS deflections in leads II and III

19
Q

what should a normal Q wave look like and when might you expect it to differ?

A

no longer than 1 box or deeper than 2. it is deeper if patient has had previous MI (remains for life)

20
Q

define syncope and give 3 distinguishing features. compare these with 3 distinguishing features of a seizure

A

Transient loss of consciousness due to cerebral hypoperfusion, characterized by a rapid onset, short duration and spontaneous complete recovery.

seizure: tongue biting, post-event delirium and convulsions

21
Q

what investigation would you request when investigating possible cardiovascular syncope (e.g. associated with palpitations, exercise or have significant FHx)?

A 
ECG
24 hour tape (Holter)
Echocardiogram 
ETT
Cardiac MRI
CT coronary artery scan
22
Q

what is the primary cause of cardiac syncope?

A

arrhythmias

23
Q

list some red flags of a syncopal event?

A
  • new onset chest discomfort
  • dyspnoea
  • abdominal pain
  • syncope during exertion or supine
  • sudden onset of palpitations after syncope
  • family history of sudden death
24
Q

what are the two types of cardiac resynchronisation therapy?

A
  1. pacemaker (CRT-P): delivers small electric impulses to the L and R ventricles to help them contract at the same time
  2. Defibrillator (CRT-D): used in heart failure patients with high risk of sudden cardiac arrest. functions as a normal pacemaker, it can perform anti-tachycardia pacing and shocking
25
Q

what are the short-term mechanisms of regulating blood pressure?

A
  • changes to CO
  • neural input from sympathetic (HR +SV) and parasympathetic (HR)
  • myogenic reflex response to an increase in MABP
  • circulatory hormonal influence of adrenaline
26
Q

what factors affect venous pressure?

A

blood volume
skeletal muscle pumps
sympathetic innervation
respiratory pump

27
Q

what is the long-term mechanisms of regulating blood pressure?

A

changes in blood volume influenced by the kidneys - renal-body fluid feedback system

28
Q

in what situations would you get an increase in ADH?

A
  • increase in osmotic pressure (blood more concentrated) detected by the hypothalamic osmoreceptors
  • severe hypovolemia (not compensated by vasoconstriction mechanism. detected by atrial baroreceptors)
  • hypotension (suggested by atrial baroreceptor decreased firing rate - usually inhibit ADH)
29
Q

what is the role of ADH?

A

increase blood volume by increasing water permeability in the renal collecting ducts. in severe hypovolemia the release of ADH is so great that it has influence on TPR by causing vasoconstriction

30
Q

what triggers Renin release in the RAAS pathway?

A
  • sympathetic nerve activation
  • renal artery hypotension
  • decreased sodium in kidney distal tubules
31
Q

where does angiotensin II have effect?

A
  • on resistant vessels increasing TPR
  • directly on the kidneys constricting renal aa., therefore, decrease BF via kidneys
  • causes release of aldosterone from adrenal gland influencing sodium and water reabsorption
  • stimulates the release of ADH
32
Q

what is the role of atrial-natriuretic hormone?

A

released by the walls of the atria in response to stretch. help oppose the RAAS to prevent overfilling of the system

33
Q

fill in the blanks:

A greater volume of fluid creates higher _______ pressure and a greater concentration of proteins creates a greater ______ pressure

A

A greater volume of fluid creates higher hydrostatic pressure and a greater concentration of proteins creates a greater oncotic pressure

Week 14: Palpitations (1 decks)

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