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Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

SAN is made of_____ cells with automaticity so they depolarise regularly causing localised activation and contraction __ ___ ____.

A
  • pacemaker cells

- of the atria

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2
Q

SAN sits -
In sinus ryhthm, the p wave should be:
+ in lead __ and - in lead ___

A
  • superior in the RA near the junction with the superior vena cave
  • positive in lead II, negative in lead aVR
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3
Q
  • SAN pulse goes through atria to AVN which lies in the

- what is the name of the tissue that separates both the atria and ventricles from eachother

A
  • intra atrial septum

- the annulus fibrosis

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4
Q

What are the 2 reasons the annulus fibrosis is important

A
  • prevents direct conduction from atria to ventricles so the atrial kick can supply filling (20%) to ventricles, esp important in tachycardias
  • in v rapid intrinsic atrial rates e.g AF (~250bpm) its good AVN delays conduction down to ventricles so prevents VT/VF dangerous tachycardias.
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5
Q

Where is the ANV nodal delay seen on the ECG?

A

PR-interval indicates electrical stimulation starting at SAN, travelling through atria and AVN and about to travel down bundle of his

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6
Q

What may a prolonged or a short PR interval on ECG suggest?

A
  • prolonged: delay/conduction disease at level of AVN

- short: accessory pathway allowing rapid conduction from atria to ventricles that bypasses the AVN

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7
Q

What artery supplied the SAN and ANV therefore which MI can affect these? May present clinically with _____ or ___

A
  • the right coronory artery
  • inferior MIs
  • sinus bradycardias or heartblocks
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8
Q

From AVN where does the excitation pass? (detail)

A
  • through annulus fibrosis
  • through bundle of His
  • divides into left (LV) and right bundle branches (RV)
  • left bundle branch divides into left anterior and left posterior fasicles
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9
Q

The Q wave on an ecg identifies the wave of electicity passing through the ___

  • in normal physiology this goes in the direction ___
  • so in the lateral leads the q wave will be small ___ because
A
  • interventricular septum
  • from left to right
  • small negative deflection as wave travels L -> R /away from those leads through the IV septrum
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10
Q

QRS should be less than:

1 reason qrs may be broad is ___

A

<0.12 seconds

Bundle branch block

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11
Q

Any of the conducting tissues of the heart can initiate heart rate e.g. __can be pacemaker cells but the further down the conduction system the heart rate is initiated by, the:

  • ____ heart rate and the
  • ___QRS will be
A
  • e.g.(AVN-50bpm max, bundle of His, purkinje, myocardium-max 35bpm for example)
  • slower the heart rate
  • broader the QRS will be (myocyte to myocyte conduction is much slower)
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12
Q

Cardiac arrhythmia is __ occurs either when there is _ or _

A
  • failure of sinus rhythm which can occur either when there is abnormal impulse formation
  • abnormal impulse conduction
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13
Q 
7step approach to rhythm analysis
1-how is pt clinically
2-is there any \_\_\_ activity present
3-what is the \_\_ rate
4-is the \_\_\_ rhythm regular or irregular
5-is the \_\_ \_\_ or \_\_\_
6-is there any\_\_ activity present
7-how is the \_\_ and \_\_\_ activity \_\_\_
A

2-is there any ventricular _ activity present
3-what is the ventricular rate
4-is the ventricular rhythm regular or irregular
5-is the QRS Broad or Narrow__
6-is there any_Atrial activity present
7-how is the _Atrial _ and _ventricular__ activity __related

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14
Q

7step approach to rhythm analysis
1-how is pt clinically
What adverse signs should you be looking for?

A
  • ABCDE
  • ischaemia? - on ecg, or chest pain
  • syncope? or reduced GCS
  • shock? or low BP
  • heart failure? or pulmonary oedema or high O2 requirement
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15
Q

7step approach to rhythm analysis

2-is there any ventricular activity present.
If no, why not and what can you do?

A
  • asystole , check pts pulse, if no pulse, start CPR

- if flat-lining, check the ECG leads incase misplaced

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16
Q

7step approach to rhythm analysis

  1. Is the ventricular rate regular or irregular?
    If bradycardia and irregularly irregular with no p waves, how could AF have caused this
A

-SLOW AF: irregular atrial depolarisation occurs at rapid rates, but whether ventricles are activated depends on AVN conduction, if there is conduction disease at this level, the ventricular activity will always be irregularly irregular

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17
Q

7step approach to rhythm analysis

  1. Is the ventricular rate regular or irregular?
    If its regular, and bradycardia, and broad QRS and no p waves, what could have happened
A
  • AF and complete heart block as there is a complete dissociation between the atria and ventricles
  • if in AF and was conducting, the ventricular activity would be irregularly irregular so the fact the ventricular activity is regular, shows pt is in complete heart block.
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18
Q
  1. is the QRS Broad_ or _Narrow? Helps identify if the impulse is __ or __ in origin
A

-ventricular or supraventricular

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19
Q

If the QRS is narrow, we know, although it has a supraventricular origin, it is using what?

A

the normal conduction fibres of heart to produce its narrow complex.

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20
Q

If there is the presence of a ventricular rhythm it means the rhythm is arising away from the ____ or below the level of the ____
and it causes a broad QRS as there is ____

A
  • away from the conducting system of the heart or
  • below level of the bundle of his
  • broad complex as there is slower myocyte to myocyte contraction through the ventricles
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21
Q

If you have a supraventricular rhythm like AF but you also have a heart block (e.g. BBB) what rhythm and QRS may result?

A

a Broad complex tachycardia

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22
Q
  1. Is there atrial activity present? What is it like? Options could be:
A
  • are they p waves (sinus tachycardia)
  • fibrillation waves (AF)
  • flutter waves (atrial flutter)
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23
Q

Disease at SAN can cause sinus bradycardia, name 5 pathological causes

A
  • IHD, MI
  • hypothyroidism
  • hypothermia
  • electrolyte..e.g high K+, high Ca2+
  • raised ICP
  • sick sinus syndrome
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24
Q

What is sick sinus syndrome? Mostly caused by idiopathic fibrosis of SAN (also drugs, MI, amyloidosis…)

A

Dysfunction at the level of the SAN resulting in impaired generation and conduction of impulses

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25
Q

Sino Atrial Exit Block can occur in sick sinus syndrome, on ECG you will see:

A

will be a completely missed PQRST segment, then next p wave arises exactly as you’d expect

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26
Q

In sick sinus syndrome we can have complete sinus arrest where we have no p wave activity. If this continues what can we have as ultimate pacemakers of the heart begin to take over? How can we recognise these?

A
  • junctional escapes
  • absence of p waves and narrow qrs so coming from close to the AVN/bundle of his (NB: if was broad qrs it would be coming lower down the conduction of the heart)
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27
Q

If you have sino atrial exit block/sinus arrest coexisting with paroxysmal atrial tachycardia’s, what syndrome can result? If symptomatic/need rate control what may be needed?

A
  • “tachy-brady syndrome”

- pacemaker implantation (PPM)

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28
Q

Conduction disease at AVN. what is 1st degree AV block findings?

A
  • slowed conduction but no dropped qrs
  • PR interval will be >0.20s
  • pts are asymptomatic, no rx needed
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29
Q

Causes of 1st degree AV block?

e.g. increased vagal tone in sleep or athletes

A
  • IHD,
  • High or low K+
  • lymes disease
  • rheumatic myocarditis
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30
Q

What are the findings of 2nd Degree AV block? Describe the 3 subgroups of this:

  • Mobitz I
  • Mobitz II
  • 2:1 AVB
A
  • intermittent failure of AVN, so there will be dropped QRS complexes
  • Mobitz I : PR interval gradually lengthens with each beat until 1 p wave fails to conduct
  • Mobitz II : PR interval is fixed but occasionally a p wave fails to produce a QRS
  • 2:1 AVB: if alternate p waves are not followed by a QRS
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31
Q

Is a pacemaker needed for Mobitz I 2nd degree AV block?

A
  • No it’s benign

- PPM not needed unless the frequency of dropped beats causes a symptomatic bradycardia

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32
Q

Is mobitz II concerning ? Why?

A
  • more likely to progress to a 3rd degree AV block

- may need a PPM

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33
Q

Does 2:1 AV block need a pacemaker? why?

A

Yes, PPM may be indicated as it has a high chance of converting into a 3rd degree complete AV block

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34
Q

What is 3rd degree AV block?

A
  • presence of independent activity of atria and ventricles
  • QRS complexes typically arise as escape rhythms which may be junctional (narrow) or ventricular (broad)
  • NB: can occur in the presence of any atrial rhythm
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35
Q

Conduction disease at left bundle branch means the left ventricle is stimulated via the RBB which gives a ___ QRS due to __. What is the delay in LV activation called?

A
  • broad QRS due to slower myocyte to myocyte conduction

- called interventricular dyssynchrony (has bad impact on LV)

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36
Q

Name 4 causes of LBB?

A
  • cardiomyopathy
  • IHD
  • LVH
  • Hypertension
  • aortic stenosis
  • fibrosis of the conduction system
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37
Q

Name 4 causes of LBB?

A
  • cardiomyopathy
  • IHD
  • LVH
  • Hypertension
  • aortic stenosis
  • fibrosis of the conduction system
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38
Q

For LBB, what leads do we look at any why? Explain the WILLIAM

A

v1-looks at right of heart
v6-looks at left of heart
in ventricular activation of LV, v1 will show a negative qrs and positive qrs in v6.
-in LBB, we have activation across the interventricular septum from the RBB to the left, so we get a positive deflection in V6 (M) and negative deflection in lead 1 (W).
-QRS is broad >0.12s

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39
Q

RBB means the RV is stimulated via the LBB which gives a __ QRS due to __
the delay in RV activation is called ___
Causes of RBB include, normal variant in some people >60, also:

A
  • broad QRS due to slower myocyte to myocyte contraction
  • interventricular dyssynchrony
  • other causes: IHD, cardiomyopathy, atrial septal defects, PEs
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40
Q

Supraventricular tachycardias will have a ___ QRS and arise _____. Symptoms include: and is associated with longer term risk of __ due to ___

A
  • narrow QRS, arise above bundles of his
  • chest pain, palpitations, SOB, syncope, fatigue
  • risk of HF due to tachycardiomyopathy
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41
Q

Sinus tachycardia causes:

A
  • excercise, fear, pain
  • anaemia, hypovolaemia, PE, MI, drugs
  • heart failure
  • hyperthyroidism
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42
Q

AF affects ~2%, and increased risk of stroke and HF, incidence increases with age. on ECG findings:

A
  • absence of distinct repeating p waves
  • irregular atrial activations
  • irregularrly irregular RR intervals
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43
Q 
Atrial flutter(M>F) is caused by a \_\_
ECGs show an atrial tachycardia of \_\_
A
  • macro re-entry circuit within the right atrium
  • 240-300bpm without an isoelectric baseline (sawtooth pattern) represents the impulse travelling towards the lead then away
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44
Q

Atrial Flutter incidence is >Men and increases with:

A
  • age
  • HF
  • COPD and HT
  • previous cardiac surgery
  • atrial septal defects
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45
Q

Atrial flutter ECG.. RA circuit takes ~0.2s for an impulse to travel around the circuit = 5 circuits per second which gives us an atrial rate of ~300bpm, why is the ventricular rate slower? What do we call the resultant blocks?

A
  • AVN delays conduction (doesnt want ventricles to keep up with this rapid rate) so the AV block occurs resulting in slower ventricular rates depending on the degree of AV block.
  • 2:1 is when 2 p waves -> 1 qrs so V rate is 150bpm
  • 3:1 block 3 p waves –> 1 qrs
  • 4:1 block 4 paves –> 1 qrs = 75pbm V rate
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46
Q

A sinus tachy persisting at 150bpm could also be ___, to work out what it is, we can give IV ___ this can allow us to see the __

A
  • can be atrial flutter with a 2: 1 block
  • adenosine (AV node blocker)
  • allows us to see the atrial activity and makes it more obvious if there are flutter waves present
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47
Q

Atrial flutter rx:

A
  • re-estabish sinus rhythm, cardiovert with shocking heart back into sinus
  • control ventricular rate: BB, verapamil, digoxin
  • ablate the abnormal pathway
  • anti-coagulate before cardioverting (risk of stroke!)
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48
Q

What is AV re-entry tachycardia? What does it require?

A
  • needs an accessory pathway between the atria and ventricles - occurs as a congenital abnormality
  • the presence of this accessory pathway along the presence of normal conduction via the AVN allows AVRT to occur through a continuous re-entry circuit.
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49
Q

AVRT: on ECG look for pre-excitiation changes that occur due SAN activation activating both atria and then the waves reaches both the ANV and also the accessory pathway, what happens next and how does this appear on ECG?

A
  • the wave that is at the AVN is held/slowed, but the wave at accessory pathway doesn’t slow down, it travels directly to ventricles
  • on ECG: short PR interval (no pause at AVN) and presence of a delta wave (slow myocyte to myocyte contraction occurs from site of accessory pathway depolarising the ventricles)
  • rest of QRS is narrow as after AVN delay, the normal conduction fibres transmit the wave quickly down bundle of his
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50
Q

AV re-entry tachycardia doesn’t cause a tachycarida always but it predisposes to pt having a AVRT because the impulse can:

A

-there can be a circuit that travels through the AVN and up through the accessory pathway and round

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51
Q

Wolf parkinson white ECG changes are seen in (0.2% population) and most asymptomatic, but in some it pre-disposes them to having an ___ when this happens its called ____

A

-AVRT, Wolf Parkinson White syndrome

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52
Q

Most pts with WPW syndrome have orthodromic AVRT, what does this mean?

A
  • the impulse travels down the AVN and travels retrogradely through the accessory pathway back to the atria
  • this is caused by an atrial ectopic which arrives at the AVN there is normal conduction (narrow QRS) then the wave travels up the accessory pathway back into atria and back down into the AVN,
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53
Q

What does antidromic AVRT mean?

A

Ventriculae have been activated by the accessory pathway

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54
Q

In Most pts with WPW syndrome have orthodromic AVRT, why does the ECG change in this tachycardia?

A

-narrow QRS and no delta wava as the pathway uses the natural heart conduction down AVN and fast fibres.

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55
Q

tachycardias treatment:

  • if pts stable: breaking the re-entry circuit by inhibiting the AVN by ______
  • cardioversion should be attempted if there are adverse features of:
  • treatment of choice ideally is: ___
A
  • inhibit AVN: valsalva manouvre, carotid sinus massage, flecanide
  • cardiovert if: shock, ischeamia, synchope, HF
  • rx of choice: ablation
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56
Q

AV Nodal Re-entry tachycaridas are micro circuits, more common in females and are the most common paroxysmal SVT, most common type is “slow-fast”, explain this..
-an atrial ectopic beat arrives at ___ when the fast pathway is _____ but the slow pathway can ____…

NB: the p waves can be burried in the QRS complexes or occur after the QRS complexes

A
  • ectopic arrives at AVN, fast-repolarising, slow-can conduct
  • so impulse must travel down the slow pathway, it reaches bundle of his and stimulates ventricles naturally (therefore narrow QRS tachy)
  • by the time the slow pathway reaches B of His, the fast pathway has repolarised and is able to conduct an impulse
  • so impulse can travel down slow pathway and retrogradely up the fast pathway, forming this re-entry circuit, stimulating the ventricles with a tachycardia.
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57
Q

AVNRT Treatment:

  • cardiovert if nay adverse features of:
  • otherwise inhibit the AVN by:
  • if reccurrent, rx of choice is:
A
  • fts of shock, ischaemia, syncope, HF
  • inhibit AVN: Valsalva manoeuvre, carotid sinus massage, adenosine-blocks the slow AVN pathway
  • recurrent: ablation is rx of choice
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58
Q

What is VT? From where does it commonly occur? What is the typical rate?
NB: symptoms vary from mild palpitations to cardiac arrest, can be pulseless or VT with a pulse

A
  • A broad complex tachycardia, defined as 3+ successive ventricular beats >100bpm
  • can arise from a re-entry circuit around an area of myocardial scarring in ventricle
  • HR 150-200bpm
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59
Q

Common causes of VT:

A
  • MI, -myocarditis
  • dilated cardiomyopathy
  • hypertrophic cardiomyopathy
  • Brugada syndrome
  • electrolyte disturbance
  • pro-arrythmic drugs
  • long QT syndrome
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60
Q

What is VF? (!)

A

A rapidly fatal arrhythmia, always in a cardiac arrest scenario, requires prompt rx
-irregular ventricular actvity on ecg

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61
Q

VF treatment pathway:

  • check airway-are they breathing
  • check for pulse
    then. .
  • if shockable/non-shockable?
A
  • call resus team
  • perform CPR while waiting for defibrillator to be attached
  • assess rhythm, if VF or pulseless VT we can shock (1 shock, resume 2mins of CPR, repeat)
  • if asystole or PEA they are non-shockable so require drugs and resume CPR)
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62
Q

What is an acute coronary syndrome? 2 of the following 3:

A
  • cardiac symptoms eg. chest pain, acute SOB
  • ECG changes
  • troponin elevation
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63
Q

Coronary artery normal diameter (3-4mm) breach of what lining can lead to clot formation?
In atherosclerosis what happens in terms of diameter?

A
  • of endothelial lining

- the arteries thicken

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64
Q

What area of the atherosclerotic plaque is vulnerable? What stress occurs here?

A

The “shoulder” where there is increased sheer stress

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65
Q

Compare and contrast NSTEMI and STEMI plaques, the material and what they affect

A

NSTEMI: plaque erosion, platelet rich thrombus, microembolisation, vasoconstriction/ intermittent occlusion

STEMI: plaque rupture, fibrin rich thrombus formation, vessel occlusion

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66
Q

Explain how the ion channel changes in MI link with an ST elevation MI

A

When myocytes die from coronary ischaemia, there will be fall in ATP from the infarcted cells, so less energy to keep the K+ channel closed so the cells leak K+ so they depolarise relatively faster than non-ischemic close by tissue, so current flows in these quicker depolarised areas. Ie. the baseline is shifted downwards becasuse of the faster depolarisation so the ST segment appears elevated

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67
Q

Explain how the ion channel changes in MI link with an non-ST elevation MI

A

-this is ischeamia not infarction, usually this is not full thickness, it’s just the sub-endocardium (most vulnerable) ions move from the ischamic area towards the normal (from endo to epicardium) leads to a positive deflection in the ECG (so whole baseline is shifted upwards) so baseline appears depressed

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68
Q

to diagnose a STEMI you need how many mm of elevation in what leads:

A
  • 1mm of ST elevation in the limb leads
  • or 2mm ST elevation in the chest leads
  • must be in 2 contiguous leads
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69
Q

What are other causes in which troponin may be raised (1 in 20people will have raised if tested)
i.e. causes of Type 2 MI = raised troponin but not caused by a primary problem within the coronary arteries

A
  • the test is so so sensitive
  • -tachyarrhythmias, HF
  • critical illness (shock, sepsis, burns..)
  • myocarditis, -valvular disease e.g. AS
  • aortic dissection, PE, pulmonary hypertension
  • renal dysfunction and associated cardiac disease
  • extreme endurance, rhabdomyolysis, stroke..
70
Q

What are other causes in which troponin may be raised (1 in 20people will have raised if tested)
i.e. causes of Type 2 MI = raised troponin but not caused by a primary problem within the coronary arteries

A
  • the test is so so sensitive
  • -tachyarrhythmias, HF
  • critical illness (shock, sepsis, burns..)
  • myocarditis, -valvular disease e.g. AS
  • aortic dissection, PE, pulmonary hypertension
  • renal dysfunction and associated cardiac disease
  • extreme endurance, rhabdomyolysis, stroke..
71
Q

What leads look at the anteroseptal area of heart? Changes seen in this area may be related to which artery?

A
  • V1-V4

- left coronary artery

72
Q

What leads look at the inferior area of heart? Changes seen in this area may be related to which artery?

A
  • leads II, III and aVF

- right coronary artery

73
Q

What leads look at the posterior area of heart? Changes seen in this area may be related to which artery? How can you see ST elevation in a posterior MI?

A
  • leads V7-V9
  • no ST elevation because infarct is at back of heart (so paradoxically you will see deep ST depression in the leads looking at this area)
  • if you put the leads on the patients back you can see ST elevation
74
Q

What is the best treatment for pts with STEMI?

A
  • Primary PCI (achieves TIMI 3 flow in >90% pts)

- better than thrombolysis

75
Q

What is tombstone ST elevation an indicator of?

A

-occlusion of one of the main coronary arteries

76
Q

If when chest pain is worse there are dynamic changes on the ECG such as initally T wave inversion on anterior leads, with severe pain ECG shows NSTEMI in ant. leads and when pain free, back to T wave inversion..what does this suggest

A

ACS

77
Q

What is the following risk factors more common in:

-older, more co-morbities, multi-vessel disease, smaller infarct size and more ischaemia?

A

-Non STEMI

78
Q

What affects younger pts with less co-morbidites and is often a larger infarct and less ischamia?

A

STEMI

79
Q

NSTEMI management:

A
  • Dual anti-platelet therapy w aspirin/ticagrelor
  • LMWH/Fondaparinaux
  • Coronary revascularisation
  • B blockade, ACEi, Intensive statin
80
Q

Which NSTEMI pts are v high risk

-these will need to go asap to the ___ __ for ___

A

haemodynamic compromise
ongoing chest pain with ST depression
lifetheatening arrythmias
-cath lab for early angiography

81
Q

Definition of HF: a clinical syndrome characterised by typical symptoms (e.g.__________) that may be accompanied by signs (eg. _________) caused by a structural and/or functional cardiac abnormality resulting in a reduced ___ ___ and/or _____ intra-cardiac ____ at rest or during exercise.

A

e. g. SOB, ankle swelling, fatigue
e. g. elevated JVP, pulmonary crackles, p/ oedema
- reduced CO
- elevated intra-cardiac pressures

82
Q

Heart failure with reduced ejection fraction.. how is ejection fraction calculated?

A

=( EDV - ESV ) / EDV

83
Q

What is heart failure with preserved ejection fraction associated with? What type of patient does it commonly occur in?

A
  • reduced relaxation of the heart ( a stiff heart)
  • pts often older, female and hypertensive for years (thicker ventricle cannot relax to accommodate the blood well anymore)
84
Q

HF wit reduced EF is EF __%

A

HF wit reduced EF is EF <40%
HF with midrange EF is ~40-49%
HF with preserved EF is EF >50%

85
Q

Name 2 compensatory mechanisms in HF:
-decreased CO causes hypoperfusion of kidneys so RAAS system activates, ACE II causes vasoconsriction increases afterload, aldosterone causes more fluid retention, increases preload

A
  • these further damage the heart muscle causing further dilatation of heart decreasing CO further
  • adrenergic system activated, more vasoconstriction occurs that increases afterload, the tachycardia means the diastolic time is shorter so congestion all round is worse further increasing the cardiac work
  • these loops lead to further and further adverse remodelling with thickening of muscle fibres.
86
Q

Medical Therapy for HF: think ABBA

A

ACE inhibitor (ramipril, lisinopril)
ARB (losartan)
BB (bisoprolol)
MRA (spironolactone, eplerenone)

These target the RAAS system

87
Q

explain class I to IV of the NY heart assosciation functional classificatiion of HF:

A

Class I: no limitation of physical activity
Class II: slight limitation of physical activity
Class III: marked limitation of physical activity
Class IV: unable to carry on any physical activity without discomfort, symptoms can be present at rest

88
Q

What is BNP when is it released?

A

BNP is a molecule produced by the ventricular wall under stress from volume overload
Its function is to cause natiuresis -loss of water from the body
The value varies with age, interpret with clinical history

89
Q

Name some blood tests to carry out in a pt with recently diagnoses HF to look for treatable causes/morbities inferfering with HF?
Along with CXR for pulmonary congestion

A
  • Hb and WCC(anaemia can worsen)
  • Na/K/urea/creatinine and eGFR (kidney hypoperfusion)
  • LFTs (liver congestion could cause derangements)
  • glucose, HbA1c (DM is risk factor for IHD)
  • lipid profile, TSH (RF for IHD)
  • ferritin, TIBC
  • natriuretic peptides
90
Q

Do diuretics affect prognosis?

A

No

they improve haemodynamics and symptoms but dont need to be continued once pt is dry.

91
Q

HF pts on diuretics need what monitoring?

A
  • daily weights (weight loss indicates diuresis, aim for >1kg weight loss/day)
  • U&Es esp K+ (risk of arrhythmias)
  • Fluid balance (restrict)
92
Q

How does Ivabradine work in severe tachycardic HF pts that cannot tolerate BBs?

A

-works on the If (funny channels) in the SAN to cause bradycardia without any negative effect on the blood pressure

93
Q

STEMI management… give ___mg loading dose ___ ASAP and continue indefinitely unless contraindicated. Assess eligibility for _____ therapy, if eligible offer ASAP otherwise offer ____ management.

A
  • 300mg aspirin
  • reperfusion therapy
  • medical management
94
Q

What is the medical management for a STEMI.

If there is a high bleeding risk consider what?

A
  • ticagrelor with aspirin

- if high bleeding risk: clopidogrel with aspirin or aspirin alone

95
Q

If a STEMI is managed with reperfusion, what are the options? (3)

A
  • angiography with follow on primary PCI
  • Drug therapy for primary PCI
  • Fibrinolysis
96
Q

When can angiography with follow on primary PCI be offered for a STEMI by what time limitation?

A
  • offer if presenting within 12hrs symptoms onset
  • PCI can be delivered within 120mins
  • or presenting >12hrs after symptoms but continuing myocardial ischaemia or cardiogenic shock
97
Q

What is drug therapy for primary PCI treatment for a STEMI, what drugs are considered?

A
  • prasugrel + aspirin if not already on oral anticoagulant
  • clopidogrel + aspirin if taking an oral anticoagulant
  • UFH with bailout GPI for radial access
  • Bivalirudin with bailout GPI is femoral access needed
98
Q

When can fibrinolysis be offered to treat a STEMI, what is the process? What agent should be given at the same time?

A

-offer if presenting in 12hrs symptoms and PCI not poss in 120mins
-give an antithrombin at same time
-do ECG 60-90mins after fibrinolysis
(do not repeat this, if ECG indicates, offer immediate angio with follow on PCI)

99
Q

Symptoms of HF: name 5

A
  • SOB
  • PND
  • reduced excercise tolerance
  • fatigue
  • ankle sweling
100
Q

Signs of HF, name 3

A
  • elevated JVP
  • hepatojugular reflux
  • third heart sound (gallop rhythm)
  • laterally displaced apex beat
101
Q

The NYHA class classifies HF from stage I to IV, what do each mean with regards to ____ of ____

A 
I : no limitation
II: normal activity
III: minimal activity
IV: reset
With regards to limitation of physical activity
102
Q

NYHA functional class should be monitored when?

A

-at baseline
-at initial diagnosis
-through the continuum of care
(helps prognostically)

103
Q

HF with reduced EF is when the LVEF is

A

< 40%

-treatment that works well

104
Q

Main cause of HF? What investigations would be recommended in these pts to confirm dx?

A
  • CAD e.g. MI, angina, arrythmias

- IX: angio, echo, nuclear, CMR

105
Q

If HT is the suspected cause of HF, what Ix can be done?

A

-24hr ambulatory BP
-Plasma metanephries
-renal artery imaging
-renin and aldosterone
(looks into underlying causes of HT)

106
Q

IF valvular heart disease is suspected as cause of HF, this can be primary e.g AS or secondary to what?
Ix: for valvular disease?

A

e. g. functional regurgitation (arises as a result of dilated atria//ventricles)
- Ix with Echo

107
Q

Arrythmias (atrial/ventricles) can –> tachycardia induced myopathy, e.g. frequent ventricular ectopy can lead to ventricular impairment, investigate with?

A
  • ambulatory ECG recording
  • Electrophysiology study

NB: can do cardioversion, or ablation and heart can recover good function

108
Q

Cardiomyopathies are heart muscle disorders, name 4

A
  • dilated
  • hypertrophic
  • restrictive
  • peripartum
  • takotsubo syndrome
  • toxins: alcohol, cocaine, iron, copper
109
Q

If Cardiomyopathy is expected as cause of HF, what 2 investigations can be useful?

A
  • CMR
  • genetic testing

(angio/trace elements/toxicology/LFTs, GGT)

110
Q

Name 3 infective causes of HF and the investigations that would be useful:

A
  • viral myocarditis
  • chagas disease
  • HIV
  • Lyme disease
  • do CMR, EMB (endomyocardial biopsy), serology
111
Q

What is the favourable effects of diuretics in treating HF?

A
  • increased UO
  • reduced total body volume
  • this relieves dyspnoea symptoms and oedema in most pts
112
Q

Name 3 adverse effects of diuretic therapy for treating HF:

A
  • activation of neurohormonal vasoconstrictor systems (RAAS, SNS)
  • electrolyte abnormalities
  • worsening renal function
  • diuretic resistance
113
Q

In pts with acute decompensated HF that are fluid overloaded, suggest 3 things we can do?

A

-fluid restriction (<1.5/2 L per day)
-low sodium diet
-loop diuretics e.g. furosemide
-daily weights, fluid balance
escalation..:
..increase loop diuretics…continuous infusion…add 2nd…add 3rd diuretic e.g. metolazone/spironolactone

114
Q

What new treatment is the first to show excellent results in treating HFpEF in the PRESERVE trial?

A

empagliflozin (SGLT2 inhibitor)

115
Q

HFrEF best treatments (think ABBA)

A
  • ACEi/ARB
  • BB
  • MRA e,g. spiro
116
Q

HFrEF: new rx Entresto is an ARNI, what is this combo?

A

ARB and necrolysin inhibitor e.g sucubitral valsartan

117
Q

50% of pts with HF are ___ deficient, so if you replace it, it reduces hospitalisation and mortality to a degree

A

-iron deficient

118
Q

Ivabradine does what?

A

-slows HR

119
Q

For pulmonary oedema in heart failure, what NIV may need to be administered

A

CPAP

120
Q

CPAP increases ___ ___, which reduces ____ by decreasing venous return.
CPAP reduces _____by increasing the pressure gradient between the left ventricle and the extrathoracic arteries, which may contribute to the associated increase in ___ ___

A
  • intrathoracic pressure
  • reduces preload
  • reduces afterload
  • stroke volume
121
Q

MRA e.g. spironolactone or ___

A

eplerenone

122
Q

2 causes of cardiac syncope

why are they dangerous?

A
  • arrhythmias
  • structural
  • no prodrome (!)
123
Q

pathogenesis of transient LOC with cardiac syncope:

A

-HR increases to an extent that CO drops therefore mean arterial pressure plummets as does cerebral perfusion pressure (O2 and glucose to supply to brain interrupted)

124
Q

Describe cardiac syncope in terms of cause, onset, duration, and recovery:

A
  • caused by v fast or v. slow HR unable to maintain CO or structural defects
  • sudden onset, no warning/prodrome
  • last only 1-2mins
  • complete recovery in seconds
125
Q

Suggest some structural defects that could cause a cardiac syncope:

A
  • inflow obstruction: cardiac tamponade, MI-dyskinesia, pericardial effusion
  • outflow obstruction: pulmonary HT, massive PE, AS, hypertrophic cardiomyopathy –> syncope OE (cannot meet CO needs), aortic dissection
126
Q

What condition can cause a pericardial effusion which rarely compromises ventricular function:

A

-Hypothyroidism

127
Q

What is a cardiac tamponade?

A
  • medical emergency
  • large amount of pericardial fluid, accumulating in sac, restricts diastolic ventricular filling and causes a marked reduction in CO
128
Q

Name 4 clinical features of a cardiac tamponade:

what is Kaussmaul’s sign and pulsus paradoxus?

A
  • effusion obscures the apex beat
  • HS are soft
  • Hypotension
  • Tachycardia
  • Elevated JVP-which paradoxically rises with inspiration - Kussmaul’s sign
  • pulsus paradoxus: fall in BP >10mmHg on inspiration (result of increased venous return to the right side of heart during inspiration, the increased RV volume thus occupies more space within the rigid pericardium and impairs LV filling).
129
Q

Cardiac tamponade investigations:

invasive ix only needed in certain situations like..

A
  • CXR: large globular heart
  • ECG: low voltage complexes with sinus tachycardia (+/- pulsus alterans - 1 big, 1small QRS)
  • Echo: diagnostic: echo-free space around heart

-Pericardiocentesis (under echo guidance) + pericardial biopsy for culture/cytology/histology/PCR give more diagnostic info if needed e.g. TB, persistent effusion, purulent or malignant effusion suspected/secondary to underlying illness..

130
Q

Cardiac tamponade management:

-if effusion recurs… excision of … allows….

A

-emergency pericardiocentesis (drain pericardial fluid percutaneously by needle in pericardial sac)
-If effusion recurs, despite rx of underlying cause, excision of a pericardial segment
allows fluid to be absorbed through the pleural and mediastinal lymphatics

130
Q

Constrictive pericarditis = heart encased in a rigid fibrotic pericardial sac which prevents adequate diastolic filling of the ventricles, clinical fts resemble those of __ HF with:

A
  • resemble right-sided HF
  • jugular venous distention
  • dependent oedema
  • hepatomegaly
  • ascites
  • Kussmaul’s sign: JVP rises paradoxically with inspiration
  • +/- pulsus paradoxus, AF, pericardial knock on auscultation caused by rapid ventricular filling
131
Q

Ix and

Rx for constrictive pericarditis:

A
  • CXR: normal heart size and pericardial calcification on lateral film
  • CT/MRI for diagnosis: pericardial thickening and calcification seen
  • Rx: surgical excision of the pericardium
132
Q

The normal pericardium is a ___ ___ sac containing a thin layer of fluid (__ml) that surrounds the heart and the roots of the great vessels:

A
  • fibroelastic sac

- 50ml

133
Q

Acute inflamm of pericardium in UK is most commonly secondary to: ___ infections e.g….. or secondary to an ___

A

-viral infections: Coxsackie B, echovirus, HIV or
- MI
(NB rare causes: uraemia, autoimmune rheumatic diseases, trauma, infection, TB, fungal, and malignancy-breast/lung/blood)

134
Q

Acute pericarditis clinical fts:

A
  • sharp retrosternal chest pain, characteristically relieved on leaning forward
  • pain may be worse on inspiration and radiate to neck and shoulders
  • pericardial friction rub
135
Q

Acute pericarditis diagnosis:

A

ECG: concave upwards ST elevation (saddle-shaped) across all leads. Return to baseline as inflamm. subsides

136
Q

Acute pericarditis management:

A
  • treat underlying disorder + NSAIDs
  • if resistant, give systemic corticosteroids

NB: NSAIDs shouldn’t be used in days post-MI as are associated with increased risk of myocardial rupture

137
Q

Give 2 complications that can arise from acute pericarditis:

A
  • pericardial effusion

- chronic pericarditis (>6months)

138
Q

How are most pericardial effusions treated?

A
  • supportive

- as most resolve spontaneously

139
Q

Myocarditis (inflamm. of myocardium) most common cause in UK is ___, other causes include…

A
  • viral: esp. Coxsackie infection

- Diptheria, rheumatic fever, radiation injury, some drugs, HIV

140
Q

Clinical fts of myocarditis:

  • acute illness with ___ and varying degrees of ______ ____
  • what can also occur?
A
  • acute illness with fever and varying degrees of bi-ventricular failure
  • cardiac arrhythmias and pericarditis may also occur
141
Q 
Investigations/findings for myocarditis include:
CXR:
ECG:
Increase in serum \_\_\_ \_\_\_
Elevated cardiac \_\_\_\_
A

CXR: cardiac enlargement
ECG: non-specific T-wave and ST changes and arrhythmias
Increase in serum viral titres
Elevated cardiac enzymes

142
Q

Management of Myocarditis

A
  • bed rest and treatment of heart failure

- good prognosis

143
Q

Hypertrophic cardiomyopathy is characterised by marked ____ and __ ___hypertrophy in the absence if abnormal loading conditions e.g. ___, ___ ____. The hypertrophied non-compliant ventricles impair ____ filling so __ is reduced.
Most cases are familial, __ pattern of inheritance, caused by mutations in the genes encoding ____ proteins e.g. Troponin T and myosin.
It is the most common cause of what?

A
  • ventricular and IV septum hyperttophy
  • e.g. HT, valvular disease
  • impair diastolic filling so SV is reduced
  • AD pattern of inheritance
  • genes encoding sarcomeric proteins
  • most common cause of sudden cardiac death in young people
144
Q

Clinical features of HCOM: (can be asymptomatic)

e.g symptoms…carotid pulse appearance…murmurs..

A
  • SOB, angina, syncope
  • jerky carotid pulse because of rapid ejection and sudden obstruction to the ventricular outflow in systole
  • ejection systolic murmur because of LV outflow obstruction (+/ipan-systolic murmur of functional mitral regurg.)
145
Q

-Complications of HCOM:

A
  • sudden death
  • atrial and ventricular arrhythmias
  • thromboembolism
  • infective endocarditis
  • heart failure
146
Q

Investigations for HCOM:

A
  • ECG: LV hypertrophy with no discernible cause is diagnostic
  • Echo/CMR imaging: shows ventricular hypertrophy and fibrosis
  • Genetic analysis can confirm dx/provide prognostic info
147
Q

Management of HCOM:
____ reduces risk or arrhythmias and sudden death
-high risk individuals are fitted with an __
-Chest pain/SOB treated with __ and ___ (a CCB)
-rarely how may outflow tract gradients be reduced?

A
  • amiodarone
  • ICD
  • B-blockers and Verapamil
  • reduced by: surgical resection, alcohol ablation of the septum or dual-chamber pacing
148
Q

In the management of HCOM what medication class should be avoided and why?

A
  • vasodilators

- they can aggravate LV outflow obstruction / cause refractory hypotension

149
Q

Dilated cardiomyopathy is characterised by a dilated __ which contracts poorly.
Inheritance is __
Presenting complaint:
Subsequent –> progressive __ with symptoms and signs of _-___ ___

A
  • dilated LV
  • AD
  • PC: SOB, less often can present with embolism (from mural thrombus) or arrhythmia
  • Progressive HF, signs of bi-ventricular failure
150
Q

Investigation findings for Dilated cardiomyopathy:
CXR:
ECG:
Cardiac imaging:

A

CXR: +/- cardiac enlargement
ECG: abnormal non-specific changes e.g. T wave flattening, arrhythmias
Echo/CMR: dilated ventricles with global hypokinesis

(NB: angio, viral, autoimmune screen, endomycocardial biopsy…may be needed to rule out other diseases)

151
Q

Management of Dilated cardiomyopathy:

A
  • treat the HF and any AF as usual
  • cardiac resynchronisation therapy and ICDs used with NYHA III/IV grading
  • heart transplant last line
152
Q

Primary rigid cardiomyopathy resembles fts of constrictive pericarditis, the rigid ___ restricts ____ ____ filling. Most common cause in the UK is _____. CXR/ECG/Echo findings are usually ____ but ____. Diagnosis is by cardiac ____ - shows characteristic _____ changes. An ______ biopsy may be taken during - provides a histological dx. Treatment/prognosis? Rarely what surgery may be performed?

A
  • rigid myocardium restricts diastolic ventricular filling
  • Amyloidosis
  • usually abnormal but non-specific
  • dx by cardiac catheterisation, characteristic pressure changes
  • endomyocardial biopsy
  • no specific rx, prognosis poor (most pts die <1yr post-dx)
  • Rarely heart transplant is done
153
Q

Arrhythmogenic right ventricular cardiomyopathy is a condition when there is progressive ____-____ replacement of the ___ of the __. The typical presentation is __ or ____ ___ in a young man :(

A
  • progressive fibro-adipose replacement of the wall of the RV
  • presentation: VT or sudden death
154
Q

Infective endocarditis is an infection of the ____ or vascular ____ of the heart. It may occur as a ____ or acute infection, but more commonly runs an ____ course and is known as SBE (“___ bacterial endocarditis)

A
  • endocardium or vascular endothelium
  • fulmination
  • insidious course
  • subacute
155
Q

In what situations/valves does infective endocarditis usually effect?

  • valves that have …
  • in association with a ___ or ___
  • on right side more in ____
  • on normal valves w virulent organisms e.g. __ __ or __ __
  • on ____ valves, can be early (
A
  • valves that have a congenital or acquired defect
  • association with a VSD or patent ductus arteriosus
  • right sided more in IVDU addicts
  • virulent organisms e.g. strep pneumo or staph aureus
  • prosthetic valves (early <60days post op)
156
Q

Name 2 organisms that can cause IE
How reliable are blood cultures in diagnosis?
Which organisms are esp hard to isolate in culture (“atypical”)

A
  • strep viridans, staph aureus, enterococci
  • in 5-10% pts, blood cultures will remain negative
  • difficult to isolate: Coxiella burnetti, chlamydia spp., Bartonella spp., Legionella..
157
Q

Pathology of Infective Endocarditis

  • a mass of ___, ____ and ____ _____ forms ____ along the edge of the valve
  • virulent organisms ____ the valve, producing _______ and worsening ___
A
  • A mass of fibrin, platelets and infectious organisms form vegetations
  • Virulent organisms destroy the valve, producing regurgitation and worsening HF
158
Q

Name a few major criteria in Duke’s criteria for dx of infective endocarditis? NB: they relate to blood culture results and endocardial involvement…

A
  • typical microorganism for IE on 2 separate blood cultures in absence of a primary focus
  • persistently + blood cultures (drawn more than 12hrs apart)
  • single + blood culture for Coxiella Burnetti or antiphase IgG antibody titre >1:800
  • TTE showing oscillating intracardiac mass on a valve/supporting structure in the path of regurgitant jet or on implanted material, in absence of an alternative anatomic explanation
  • abscess
  • new partial dehiscence of a prosthetic valve
  • new valvular regurgitation
159
Q

name 2 of the minor criteria in Duke’s for IE:

A
  • predisposition e.g. prosthetic valve, IVDU
  • fever
  • vascular phenomena e.g. major arterial emboli, septic pulmonary infarcts
  • immunological phenomena e.g. Osler’s nodes, glomerulonephritis
  • Echo/microbiological cultures positive findings but not meeting major criteria
160
Q

Clinical signs and explanations of Infective Endocarditis:

A
  • systemic: fever, malaise, night sweats, weight loss, anaemia, splenomegaly
  • valve destruction –> HF and new or changing heart murmurs
  • vascular phenomena due to embolisation of vegetations and metastatic abscess formation in the brain, spleen and kidney (emboli from right sided IE -> pulmonary infarcts and pneumonia)
  • immune complex deposition in blood vessels -> vasculitis and petechial haemorrhages in skin, under nails and in retina
  • in joints –> arthralgia and gout
  • in kidney –> acute glomerulonephritis, + microscopic haematuria
161
Q

Name the following 3 rare clinical signs of infective endocarditis: immune complex deposition in blood vessels -> vasculitis and

  • under nails
  • in retina
  • painless erythematous macules on the palms
  • tender subcut nodules in fingers
A
  • splinter haemorrhages
  • Roth spots
  • Janeway lesions
  • Osler’s nodes
162
Q

Name 5 Investigations of Infective endocarditis

A
  • blood cultures (3 sets over 24hours)
  • TTE/TOE to see vegetations/valve dysfunction
  • serological testing e.g. for atypical bacteria
  • CXR: may see HF or septic emboli evidence
  • ECG: may show MI or conduction defects
  • FBC: normocytic normochromic anaemia with raised ESR +/- high WCC
  • urine dip: haematuria (70% cases)
  • serum Igs: raised
  • complement levels: low (as result of immune complex formation)
163
Q

Infective endocarditis definitive diagnosis requires direct evidence by histology/culture of organism or…

  • __ major criteria
  • ___major and ___ minor criteria
  • ____ minor criteria
A
  • 2 major
  • 1 major and 3 minor
  • 5 minor
164
Q

Management of endocarditis

  • drug therapy:
  • surgery: considered when..

while awaiting blood culture results, combo of what abx is given?

A

drug: 2 weeks of IV bactericidal abx then 2-4 further weeks by oral
- while awaiting culture, combo of benzylpenicillin and gentamicin is given
- surgery: replace valve is there is severe HF, early infection of prosthetic material, worsening renal failure or extensive valve damage

165
Q

How do varicose veins develop?

A
  • gravity pull on blood causes the walls of the leg veins to stretch apart over time, valves fail to close properly
  • blood can leak backwards and pool in the veins
  • subsequent veins stretch out and fail
  • from the additional blood they become tortuous
  • affects superficial veins of leg, as have high pressures when standing
166
Q

Varicose veins in scrotum is what and develops how? Esp on what side and why?

A
  • varicoele
  • left testicular vein joins left renal vein at a 90degree angle - tricky
  • so blood backs up around testicle, so L testicular vein enlarges and gets tortuous
  • so scrotum looks like a bag of worms
  • larger when standing (less when lying)
167
Q

How does the stagnant blood in a varicocele affect fertility?

A
  • the venous warm blood lies stagnant in the testicles
  • the temperature is warm
  • this causes testicular atrophy
  • poor quality sperm and infertility
168
Q

How can a varicocele be treated?

A
  • embolization or surgery

- then testicles drain through smaller collateral veins

169
Q

What can bad varicose veins in the legs progress to? What are signs of this?

A
  • Chronic venous insufficiency (CVI)
  • stagnant blood –> inflammatory reaction in deep veins
  • leads to fibrosis and venous stasis ulcers
  • hyperpigmentation
  • pruritis and pain
  • oedema (fluid leaks out veins into ankle tissue)
170
Q

RFs of varicose veins:

A
  • women
  • prolonged standing
  • crossing knees
  • obesity
171
Q

Treatment of varicose veins:

A
  • manual compression (helps blood flow)
  • compression stockings
  • legs elevated above heart frequently
  • surgery: vein transplant/repair/removal

Medicine (10 decks)

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