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Physiology - Hayley > Cardio > Flashcards

Cardio Flashcards

1
Q

Which of these leads are bipolar and unipolar

A

I, II, III = biopolar
aVR, aVL, aVF - unipolar

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2
Q

When does a U wave appear on an ECG

A

After the T wave - typically smaller then the T wave

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3
Q

What polarity (positive of negative) is on each corner of Einthoven’s triangle and what is the resulting direction of the deflection of a wave travelling towards that corner

A

LA - has negative and positive charge
RA - negative
LL - positive

Depolarisation towards positive = positive deflection
Depolarisations towards negative = negative deflection

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4
Q

What degrees does the heart need to be at to be in left axis deviation

A

When the QRS axis falls between -30 and -90 degrees

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5
Q

What direction to each of the limb leads travel in

A

Negative to positive

I : RA > LA
II : RA > LL
III : LA > LL

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6
Q

What is the primary cause of coronary artery disease

A

Athlerosclerosis

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7
Q

What are three common approaches to treatment of coronary artery disease

A

1) Lifestyle modifications
2) Medication - antiplatelet agents, statins, beta blockers
3) Revascularisation - stents, bypass grafting

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8
Q

What is the definition of heart failure

A

Impairment in the hearts ability to pump blood and is insufficient to meet the needs of the body

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9
Q

What are the two primary blood markers in heart failure and what do they each indicate

A

Troponin - usually found inside the cardiomyocytes, if this is present in the blood we know there is cardiac damage

BPN - this is created when the heart is working hard, so increases during cardiac stress. (>100ph/ml is considered positive and indicative of HF)

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10
Q

What is the difference in mechanism between heart failure with preserved ejection fraction and heart failure with reduced ejection fraction

A

HF with preserved EF - the heart is contracting normally but the volume of blood is very small. Because the proportion of the blood in and out is the same, the EF is preserved

HF with reduced EF - due to cardiomyocytes death so the heart isn’t contracting properly

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11
Q

What are the different treatment options for people with HF with preserved EF and those with HF with reduced EF

A

HF preserved EF - no treatment

HF reduced EF - medication, lifestyle changes or pacemakers

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12
Q

What is cardiac resynchronisation therapy

A

A 3 lead pacemaker is put into the RA, RV and LV to detect irregularities and provide shock if need be

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13
Q

What is restrictive cardiomyopathy and what pathological remodelling is usually associated with it

A

When the ventricle stiffen and cant fill with blood

Atrial enlargement is common

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14
Q

Infiltration of amyloids, sarcoidosis, too much iron, fibrosis and inherited metabolic disorders are all causes of what disease

A

Restrictive cardiomyopathy

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15
Q

What 3 blood markers will be present in a patient with restrictive cardiomyopathy

A

eosinophils, hemochromatosis, BNP

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16
Q

What is Left ventricular non-compaction and what other 2 pathologies can it cause

A

This occurs when the muscles in the LV don’t compact during development, leaving the muscle of the LV soft and spongy

Atrial enlargement
LBBB

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17
Q

What is Takotsubo Cardiomyopathy and what changes does it cause to the heart

A

Heart condition developed in response to an intense emotional or physical experience.

Ventricles change shape affecting it’s ability to pump blood

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18
Q

What is Desmoplakin Cardiomyopathy and what causes

A

This is a rare genetic disorder that is caused by dysfunctional desmosome complex.

Can result in repeated myocardial injury or infiltration of immune cells causing fibrosis

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19
Q

What are the mechanisms of bradycardia and tachycardia in channelopathies

A

Bradycardia - failure of impulse formation or conduction

Tachycardia - re-entry and mechanism of abnormal automaticity

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20
Q

What does Long QT syndrome effect, what are common symptoms and what is the primary treatment

A

K+ efflux

fainting, seizures

Medication (usually Na+ channel blockers or beta blockers)

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21
Q

What is the cause of Brugada syndrome

A

Mutation in voltage gated Na+ channel gene

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22
Q

What causes Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) and what are common treatments for this. What is a common pathological feature associated with CPVT

A

Inherited mutation of cardiac Ca2+ channels (RyR)

Treatment: beta blockers, antiarrhythmics

Arrythmias are common

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23
Q

What causes Arrhythmogenic cardiomyopathy and what cardiac pathologiy is commonly caused by this disease

A

Mutation of desmosome proteins

Can lead to HF - lack of desmosomes causes infiltration of fibroses leading to weakening of the heart muscle

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24
Q

1st degree AV block

A

Delay in the conduction of electrical signal from the atria to the ventricles.

Every impulse from the atria are conducted to the ventricle but at a slower speed

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25
Q

2nd degree AV block

A

type I - progressive delay in AV conduction until an impulse is blocked

type II - some atrial impulses are blocked without prior delay

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26
Q

3rd degree AV block

A

No conduction between the atria and ventricle

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27
Q

What are the different modes of treatment for AV block

A

type I - no treatment
type 2:1 - is symptomatic, medication
type 2:2/3 - pacemaker

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28
Q

What 5 things is acute inflammation characterised by

A

Redness - vasodilation increasing blood flow
Swelling
Increased permeability of capillaries
Migration of granulocytes and monocytes into the tissue
Activation of macrophages

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29
Q

BNP, tumour necrosis factor-alpha, transforming growth factor beta, growth differentiation factor 15 are all types of what

A

Cardiokines (heart immune molecules)

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30
Q

What is myocarditis and what are some non-infectious causes of this

A

Inflammation of the myocardium

idiopathic (no cause), rheumatic fever, cardiotoxic substances, systemic disease

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31
Q

What is pericarditis and what are some non-infectious causes of this

A

Inflammation of the pericardium

post MI pericarditis, radiation exposure

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32
Q

What is endocarditis

A

Inflammation of the lining of the heart and heart valves

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33
Q

What blood markers would you expect during general inflammation

A

Elevated WBC
Elevated RCB sedimentation rate
Elevated C-reactive protein (CRP)

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34
Q

What blood markers would you expect indicating damage to the heart, brain or muscle

A

Creatine phosphokinase (CPK)

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35
Q

Endothelial dysfunction is a hallmark of what

A

Several immune mediated pathologies (myocarditis, vasculitis, thyroiditis)

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36
Q

What type of cholesterol creates fatty streaks in atherosclerosis

A

LDL cholesterol

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37
Q

What are pericytes important for

A

Vascular formation, remodeling and function

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38
Q

What are cardiac tissue macrophages and what do they do and what do they secrete

A

Resident leukocytes activated by DAMPS

Release cytokines that initiate inflammatory cascades

Secrete proteolytic and inflammatory agents

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39
Q

What can activate pro-inflammatory responses

A

cellular injury and death

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40
Q

What is associated with arterial thrombotic conditions such as myocardial infarction and stroke

A

Hyperactive platelets

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41
Q

What are some extrinsic causes of bradycardia

A

hypothermia, hypothyroidism, antiarythmic drugs

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42
Q

What are some intrinsic causes to bradycardia

A

acute ischemia
infarction of the sinus note
ischemic heart disease
cardiomyopathy
myocarditis

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43
Q

In RBBB and LBBB what changes are their in the path of conduction

A

The conduction is travelling through the slow ventricular myocytes rather then the fast purkunjie fibres

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44
Q

What two divisions can LBBB be broken into

A

left anterior fascicular block (LAFB)
left posterior fascicular block (LPFB)

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45
Q

What conditions are commonly associated with RBBB

A

congenital cardiac disorders, pulmonary embolism, pulmonary hypertension

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46
Q

What conditions are commonly associated with LBBB

A

left ventricular disease, aortic stenosis, hypertension

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47
Q

What are the symptoms of CVD in men and woman

A

Men - burning chest pain, pressure in chest, pain in neck, jaw, shoulders
Woman - stabbing pain in chest, stomach pain

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48
Q

How does alcohol effect heart health

A

Increases blood pressure
Modifies NO generating system
Increases ROS

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49
Q

How does smoking effect cardiovascular health

A

Increases heart rate and blood pressure
Chemicals increase atherosclerotic changes

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50
Q

What are normal blood pressure ranges

A

120-129/80-84

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51
Q

What blood pressure range would be considered hypertension

A

140/90

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52
Q

What happens to our blood pressure during sleep

A

Systolic blood pressure drops 10% during sleep

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53
Q

During an exercise stress test what is happening in the heart that is causing symptoms to occur

A

Ischemia is causing symptoms like chest pain and breathlessnes

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54
Q

What is the Bruce Protocol preparation used for and what is it

A

It is used for patients before exercise stress testing
- no eating 4 hours before
- no caffeine or smoking 4 hours before
- must bring all medication to test
- no lotions, self tan, oils, ect on test area

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55
Q

During an exercise stress test, ST segment depression is usually driven by what

A

Hypoxic conditions lead to diminished ATP, decreasing the activating of ATP dependant processes. This includes the Na+/K+ATPase, in injured cells this isn’t working so there is no current during depolerisation.

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56
Q

What changes in ST interval would you need to see to stop an exercise stress test

A

ST depression up to 4mm
ST elevation up to 3mm

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57
Q

What is the effect of stenosis valves

A

stiffening of the valves restrict blood flow, increasing the workload on the chamber ejecting the blood

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58
Q

What is the value of the following on an ECG
1 small square
1 large square
5 large squares

A

1 small square = 1mm = 40ms
1 large square = 5mm = 200ms
5 large squares = 1second

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59
Q

What is the normal, bradycardic and tachycardic rate on an ECG

A

Normal: 600-100blm (3-5 large boxes)
Bradycardic: <60bpm (>5 large boxes)
Tachycardic: >100bpm (<3 large boxes)

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60
Q

Normal PR interval duration

A

120-200ms (3-5 small squares)

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61
Q

What is happening in the heart during the PR interval

A

Conduction through the AV node

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62
Q
A
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63
Q

Normal QRS complex duration

A

80-110 ms (<3 small boxes) measured in the lead where it is the biggest

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64
Q

Normal QT interval in men and woman

A

Men < 440ms
Woman < 460ms

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65
Q

What sort of pathologies are usually associated with QT changes

A

Channelopathies

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66
Q

Normal duration and amplitude of T waves

A

Duration: 120-200ms (3-5 small boxes)
Amplitude: <5mm in limb leads, <10mm in precordial leads

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67
Q

What are common causes of right ventricular hypertrophy

A

pulmonary hypertension, tricuspid stenosis, pulmonary embolism, chronic lung disease

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68
Q

What is the SA nodes intrinsic discharge rate

A

100bpm

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69
Q

What nervous system controls the SA node

A

Autonomic

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70
Q

What changes in normal sinus rhythm are seen in children and why

A

Their normal sinus rhythm is faster than adults due to having a smaller heart, decreased stroke volume, and decreased blood volume

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71
Q

What is happening during 2nd degree type 1 heart block

A

Malfunctioning AV node cells tend to progressively fatigue until they failue to conduct an impulse

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72
Q

What is happening to the conduction system during 2nd degree type 2 AV block

A

usually due to a failure of conduction at the level of the his-purkinjie system

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73
Q

What is causing the rhythm seen in 3rd degree heart block

A

Junctional or ventricular escape rhythms

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74
Q

What is happening during RBBB

A

LV is depolarised normally but the right ventricles only depolarise ones the left ventricular conduction crosses the septum so the right ventricles are delayed in depolarising

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75
Q

What is the conduction pathway in LAFB

A

Impulses are conducted to the LV via the posterior fascicle which inserts into the inferoseptal wall of the LV along its endocardial surface

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76
Q

How are junctional escape rhythms made

A

Pacemaker cells are found at various sites throughout the conducting system, with each site capable of independently sustaining the heart rhythm.

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77
Q

When do accelerated junctional rhythms occur

A

Accelerated junctional rhythm (AJR) occurs when the rate of an AV junctional pacemaker exceeds that of the sinus node. This situation arises when there is increased automaticity in the AV node coupled with decreased automaticity in the sinus node.

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77
Q

When do accelerated idioventricular rhythms occur

A

when the rate of an ectopic ventricular pacemaker exceeds that of the sinus node

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78
Q

What is atria flutter and what causes it

A

Atrial flutter is a rapid regular atrial rhythm due to small reentry circuit around the RA

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79
Q

What is atrial fibrillation

A

Completely disorganised atrial firing around 350-500bpm

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80
Q

What is the effect of atrial fibrillation on cardiac function

A

The loss of atrial systole means the 20% contribution the atria have to filling the ventricles is lost. So the ventricles aren’t filling fully, reduced cardiac output

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81
Q

What are the three main areas for treatment of atrial fibrillation

A

Rate control, anticoagulation and rhythm control

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82
Q

What drug is used in atrial fibrillation patients when treating rate control

A

Beta blockers

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83
Q

What are the clinical requirements a patient must meet before beginning anticoagulation therapy

A

CHA2S2-VASc must be >2
HAS-BLED > 3

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84
Q

If a patient is not suitable for anticoagulation therapy to treat atrial fibrillation, what is the alternative anticoagulation therapy technique that can be used

A

Left atrial appendage closure could be considered as this is the most likely site of clot formation

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85
Q

Where do focal atrial tachycardias originate from

A

Single ectopic focus within the atria but outside of the sinus node

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86
Q

What is happening in the heart to cause atrioventricular reentrant tachycardia

A

Additional connection between the atria and ventricles creates an assesory pathway. Impulses can conduct through this cause tachycardia.

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87
Q

What changes have occurred to the heart in Wolff-Parkinson-White syndrome

A

Congenital accessory pathway has formed. Because the accessory pathway lacks the intrinsic slowness of the AV node, ventricular depolarisation through the his-purkunjie system creates premature beats

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88
Q

How does atrioventricular re-entrant tachycardia differ from AV nodal re-entrant tachycardia

A

AVRT is due to a accessory pathway and reentry throughout the whole atria, whereas AVNRT is due to re-entry within the AV node only

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89
Q

How long does a ventricular tachycardia need to be going on for for it to be considered sustained

A

> 30 seconds

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90
Q

What are the typical treatments for recurrent ventricular tachycardia

A

Antiarrythmics, ICD, alblation

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91
Q

When does myocardial ischemia occur

A

When myocardial perfusion is disrupted and there is insufficient blood flow to the myocardium

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92
Q

What is Prinzmetal angina

A

angina due to spasms of the coronary arteries

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93
Q

Acute coronary syndrome

A

Describes a range of conditions related to sudden blood flow to the heart caused by acute rupture of a thrombus

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94
Q

What differentiates a STEMI and NSTEMI based on thrombus location

A

STEMI - if the thrombus is occluding a large artery
NSTEMI - if thrombus is occluding a small branch OR occlude and spontaneously repursues a large branch

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95
Q

Type 1 MI

A

Spontaneous MI related to ischemia due to primary coronary events such as plaque erosion and/or rupture

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96
Q

Type 2 MI

A

Secondary MI to ischemia due to either increased oxygen demand or decreased supply

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97
Q

Type 3 MI

A

sudden unexpected cardiac death often with symptoms suggestive of MI

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98
Q

Type 4 MI

A

MI associated with percutaneous coronary intervention (4a) or stent thrombosis (4b)

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99
Q

Type 5 MI

A

MI associated with surgery

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100
Q

What is MINOCA

A

acute myocardial infarction with angiographically no obstructive coronary artery disease or stenosis that is <50%

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101
Q

If a patient has elevated troponin levels and ischemic ECG changes what is their likely pathology

A

NSTEMI

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102
Q

What is the Sgarbossa Criteria used for

A

In patients with LBBB or ventricular paced rhythm MI diagnosis based on the ECG can be difficult so this criteria allows physiologists to differentiate the disorders

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103
Q

What is myocarditis

A

inflammation of the myocardium

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104
Q

What is pericarditis

A

Inflammation of the pericardium

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105
Q

What is a cardiac tamponade

A

medical emergency that takes place when abnormal amounts of fluid accumulate in the pericardial sac compressing the heart and leading to a decrease in cardiac output and shock

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106
Q

Normal concentration of K+ in the blood for the heart

A

3.5-5 mmol/L

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107
Q

What is Dextrocarida

A

rare congenital disorder where the heart is on the right side of the chest cavity

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108
Q

How do you calculate velocity of a ultrasound wave from frequency and wavelength

A

V=fλ

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109
Q

How many piezoelectric crystals are requires for continuous wave doppler ultrasound

A

2 - one transmission, one reception.

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110
Q

What type of ultrasound is used to measure velocity of blood flow

A

Continous wave doppler

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111
Q

In continuous doppler ultrasound, what is the effect on the trace if the fluid in the vessel is moving towards the probe

A

There is a positive shift

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112
Q

is continuous doppler able to have depth perception

A

No

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113
Q

How does continuous wave and pulsed wave doppler ultrasound differ

A

Both measure velocity of fluid, however pulsed wave doppler is able to measure blood flow at specific locations or depth

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114
Q

How many piezoelectric crystals are used in a pulsed doppler probe

A

1

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115
Q

What is pulse repetition frequency

A

number of pulses transmitted in one second

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116
Q

In pulsed wave doppler, what determines the interval between the transmission and reception of the ultrasound

A

The depth of the region of interest

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117
Q

Does continuous wave or pulsed wave doppler involve aliasing

A

Pulsed wave

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118
Q

Based on Nyquist Theorem, what does the sampling rate need to be to ensure no signal is lost in ultrasound

A

The sampling rate needs to be at least twice the highest frequency present in the signal

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119
Q

What are is one advantage and one disadvantage of continuous wave doppler

A

Accurately measures high velocity rates

Lack range resolution

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120
Q

What are is one advantage and one disadvantage of pulsed wave doppler

A

Ability to measure velocities at a specific location

Aliasing of velocities above Nyquist limit (so if there are frequencies returning to the probe that are higher then the Nyquist limit then these wont be recorded)

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121
Q

What is the parasternal long axis good at looking at

A

Shows intraventricular septum and inferior wall

Good for looking at mitral valve, aortic valves and thickness of LV

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122
Q

What is the parasternal short axis window good for seeing

A

Shows anatomy of aortic valve and its 3 leaflets
Can also see the pulmonary artery where pulsed doppler can be used to measure velocity through this

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123
Q

What is the apical 4 chamber view axis good for seeing

A

Shows 4 chambers of the heart

Can perform doppler on both tricuspid and mitral valve

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124
Q

What is the apical 5 chamber window good for seeing

A

This is apical 4 chamber view but with the apical valve in view.

Continuous wave doppler used to look at velocity of blood through aortic valve and LVOT

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125
Q

What can be seen on the apical 2 chamber axis

A

Left atrium and the inferior and anterior walls of the LV

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126
Q

What can be seen in the apical long axis window

A

Used to look at the left side of the heart

Can see the LA, LV and aortic valve

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127
Q

What can we see in the subcostal echo window

A

Good for seeing the pericardium

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128
Q

What can we see in the suprasternal notch view on echo

A

Aortic arch

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129
Q

what are the most common sized catheters used in the cath lab

A

JR4 and JR34

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130
Q

What are the 5 ideal parts of a catheter used in a cathlab

A

A short as possible
As rigid as possible
Long enough to reach the heart
Flexible
Narrow

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131
Q

If we were measuring aortic pressure in the cath lab and the pressure damped what does this indicate

A

The catheter has occluded the arteries, impeding perfusion

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132
Q

What is normal peak systolic pressure in LV

A

90-140mmHg

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133
Q

What normal end diastolic pressure of the LV

A

5-12mmHg

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134
Q

What does a left ventriculogram allow us to see

A

Provides assess to systolic function, degree of mitral valve motion abnormality and ventricular wall defects

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135
Q

In a healthy patient, what would be the pressure differences between the aorta and the LV during systole

A

There should no pressure gradient between the LV and aorta because the valve opens fully, allowing free flow of blood

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136
Q

What is normal systolic and diastolic aortic pressure

A

Systolic - 120mmHg
Diastolic - 70mmHg

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137
Q

What sort of catheter is used to calculate cardiac output

A

Swan-Ganz catheter

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138
Q

what is the normal cardiac output

A

4-8L/min

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139
Q

What is the normal cardiac index

A

2.4-4.2L/min/m^2

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140
Q

What is the equation for calculating the amount of oxygen consumed by the body

A

VO2 = 125 x body surface area

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141
Q

What is the cardiac output equation when using Ficks principle

A

CO = Oxygen consumption (Vo2) / Arteriovenous Oxygen Different

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142
Q

What is more accurate at measuring cardiac output, thermodilution or ficks method

A

Ficks method because it is based off actual blood concentrations of oxygen

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143
Q

What pathology would you not be able to perform an accurate thermodilution test of cardiac output

A

Patients with severe tricuspid regurgitation

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144
Q

What are intracardiac shunts

A

abnormal pathways for blood flow in the heart that form in additions to or in place of normal pathways

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145
Q

Ventricular septal defects, overriding aortic root, pulmonary stenosis, and right ventricular hypertrophy are all symptoms of what congenital heart disorder

A

Tetralogy of Fallot

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146
Q

When is it particularly important that the transducer is zeroed in the cathlab

A

When doing right heart pressure measurements because we are dealing with much smaller numbers

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147
Q

What can be the effect of catheter whip when measuring pressure in cathlab

A

The large waveforms caused by movement of the catheter can cause the measured pressure value to be inaccurate (underestimated or overestimated)

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148
Q

What is systemic vascular resistance

A

Resistance to blood flow by all the systemic vasculature, excusing the pulmonary vasculature

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149
Q

What is the effect of the RV when the pulmonary vascular resititance is high

A

An increase in vascular resistance means the RV needs to pump harder to move blood through the pulmonary valve. This can cause dilation of the RV

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150
Q

Normal RA pressure

A

2-6mmHg

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151
Q

Normal systolic and diastolic RV pressure

A

systolic - 15-25mmHg
diastolic - 0-8mmHg

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152
Q

Pulmonary artery pressure in systole and diastole

A

systolic - 15-30mmHg
diastolic - 8-15mmHg

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153
Q

Normal pulmonary wedge pressure

A

6-12mmHg

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154
Q

What pressure does the pulmonary artery need to be for someone to be considered to have pulmnoary hypertension

A

> 25mmHg

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155
Q

What pressure can you get through right heart catheratization that can estimate the LA pressure

A

By measuring the pressure in the pulmonary wedge you can use this to estimate the LA pressure

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156
Q

What parts of the heart does the right coronary sinus supply blood too

A

RA, RV and SA node

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157
Q

What areas of the heart does the Lcx and LAD supply blood too

A

Lcx - lateral wall of the left ventricle

LAD - left ventricle (diagonal branch purfuses the anterior wall, septal branch supplies the anterior septum)

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158
Q

What type of wire is used in cathlab

A

J wire

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159
Q

What percentage does a coronary artery need to be blocked to be considered flow limiting and requiring PCI

A

lesion that is >70% of the vessel diameter

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160
Q

What is FFR

A

This is a type of coronary flow study - the ratio of blood flow in a coronary artery in the presence of stenosis is compared with the flow in the same vessel in the theoretical absence of stenosis

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161
Q

What FFR values indicate a vessel is and isnt responsible for ischemia

A

FFR > 0.8 unlikely vessel is responsible for ischemia

FFR < 0.75 vessel is likely inducing ischemia

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162
Q

Patients with ischemia and no obstructive artery disease may have what pathology

A

Microvasculature dysfunction

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163
Q

What is intravascular ultrasound

A

A method of ultrasound where you are able to see cross sectional images of inside the arteries

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164
Q

What does OCT use to image the arteries

A

Infrared light

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165
Q

What coronary imaging method is able to differentiate between tissue characteristics

A

Optical coherence tomography (OCT)

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166
Q

If someone had a SYNTAX score of <23, would they be recommended for PCI or CABG

A

PCI

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167
Q

What is the principle goal of duel antiplatelet therapy following a PCI

A

prevention of stent thrombosis

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168
Q

What is defined as chronic total occlusion

A

100% occlusion of the coronary artery for a duration of greater than or equal to 3 months

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169
Q

What is a thrombectomy

A

It is a procedure used to remove a clot that has developed at the site of acute plaque rupture in MI

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170
Q

What is pericardiocentesis

A

Procedure to remove fluid from the pericardial sac

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171
Q

What are the three types of hypertension

A
  1. White coat hypertension - due to stress
  2. secondary hypertension - increase BP secondary to a known pathology
  3. Essential (primary) hypertension - more common and unknown cause
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172
Q

How do diuretics decrease hypertension and what is an example of one

A

Decrease Na+ absorption = increase water excretion = decrease blood volume

Thiazide

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173
Q

How do sympathetic blockers help hypertension

A

These bind to B1 receptors in the heart and bock vasocontriction.

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174
Q

How do ACE inhibitors work to reduce hypertention

A

These block the conversion of angiotensin 1 to angiotensin 2 so the renin-aldosterone system is suppressed and BP reduced

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175
Q

How does angiotensin II receptor antagonists work to reduce hypertension

A

Angiotensin 2 causes vasocontraction. By blocking this you are reducing constriction

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176
Q

How do Ca2+ channel blockers lower hypertension

A

Inhibit contraction of vascular smooth muscle to reduce peripheral resistance

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177
Q

How are Na+ channel blockers antiarrhythmic drugs

A

These block the sympathetic nervous system effect on the heart, slowing down the heart rate and reducing the atomicity of the heart muscle.

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178
Q

What is the effect on the refractory period of the myocardial action potential if strong and weak Na+ channel blockers are used, respectfully

A

Weak blockers - slightly reduce refractory period
Strong blockers - significantly decrease the time to depolarise but doesn’t change the refractory period

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179
Q

How do K+ channel blocker work as an antiarrhythmic

A

These make repolarisation last longer so contractions are prolongated

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180
Q

What is the class of drug used to treat heart failure and what is it’s mechanism of action

A

cardiac glycosides

stops the Na+/K+ pump pumping Na+ ut of the cell = increases contractility, slows heart rate and slow conduction velocity

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181
Q

What are the three types of drugs used to treat angina

A

Nitrates, b-blockers and Ca2+ channel blockers

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182
Q

What is the function of thrombolytics

A

Break down existing clots by breaking down fibrin

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183
Q

What do anticoagulants do

A

Inhibit formation and enlargement of existing blood clots but doesn’t dissolve existing clots

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184
Q

What is the mode of action of antiplatelets

A

Inhibit the step of platelet aggregation so no clot forms

185
Q

When taking measurements in echo, should you measure from the inner and outer walls?

A

Inner

186
Q

In what phase of the cardiac cycle must all measurements be taken from in echo

A

End of diastole

187
Q

What phase of the cardiac cycle is the heart in when the mitral valve just opens and the aortic valve just closes

A

End systole

188
Q

What is the position of the mitral valve at end diastole

A

Closed

189
Q

What is a normal ejection fraction % and severe ejection fraction %

A

> 55%
Severe <35%

190
Q

When you zoom into the aortic valve on parasternal long axis what three measurements would you take

A

SOV
STJ
PAA

191
Q

Where in the aortic arch is the SOV located

A

The widest point above the aortic valve

192
Q

When using M mode in parasternal long axis, what are you measuring

A

Measure the internal diameter of the LV

193
Q

What are the names of the three aortic valve flaps

A

R - Right coronary cusp
N (bottom) - non coronary cusp
L - Left coronary cusp

194
Q

What does TAPSE allow you to measure

A

Using M mode you can assess how well the RV is pumping

195
Q

When using TAPSE, where does the M mode cursor need to cross through

A

The bottom of the RV and the angelus of the tricuspid valve

196
Q

How do you interpret the results from TASPE

A

You can measure how much the RV is pumping by measuring the amplitude of the M mode waves in TAPSE

197
Q

What is the normal TASPE measurement

A

> 1.7cm

198
Q

What type of doppler is used to measure the velocity of the aortic valve in apical 5 chamber

A

Continous wave doppler

199
Q

What type of doppler would you use to measure the velocity of the LVOT in apical 5 chamber

A

Pulsed wave doppler

200
Q

What is the most commonly used technique for quantitative estimation of the LV systolic function

A

Transthoracic echocardiology (TTE)

201
Q

What is stroke volume and its normal value

A

Volume of blood pumped from the ventricle per beat

70mls

202
Q

What is cardiac output and its normal value and its equation

A

Amount of blood pumped out by the ventricle each minute

4900mls/5L

SVxHR = CO

203
Q

What is the end diastolic volume and its normal value

A

volume of blood in the ‘full’ ventricle

120mls

204
Q

What is end systolic volume and its normal value

A

volume of blood in the emptied ventricle

40mls

205
Q

What is the equation for ejection fraction

A

(SV/EDV) x 100

SV = EDV-ESV

206
Q

What is the Simpson method of Disc

A

To measure the volume of total left ventricle, it is sliced into discs apex down to mitral valve annulus into a series of discs
The diameter and thickness of each slice is then used to calculate the total LV volume.

207
Q

How can accuracy be improved in the Simpsons method of disc

A

using diameters in 2 perpendicular planes (apical 4 and apical 2) so that the disc area is more defined.

208
Q

What is a intra-aortic balloon pump and what does it do

A

Mechanical device that increases myocardial oxygen perfusion and indirectly increases cardiac output.

Inflates throughout diastole which pushes blood back towards the aortic root and increasing blood flow to the coronary arteries

209
Q

What part of the aorta is a intra-aortic balloon pump located in

A

Descending aorta

210
Q

What part of the ECG triggers the inflation of the intra-aortic balloon pump and which part of it triggers the deflation of the balloon

A

Inflation - midpoint of T wave
Deflation - dichrotic notch (peak of R wave).

211
Q

What is the Impala and what does it do

A

This is a device inserted across the aortic valve that draws block from the LV and expels it directly into the ascending aorta, effectively offloading the hearts work

212
Q

What is temporary pacing and when is it used

A

Electric shocks delivered to the ventricle to treat bradycardia or heart block.

Used in emergency situations before a more permanent solution can be done

213
Q

During TAVI, is the old valve removed?

A

No it stays in the heart

214
Q

What is TAVI

A

Transcatheter Aortic Valve Replacement/Insertion.

A new aortic valve is inserted in those who have severe aortic stenosis

215
Q

What is Balloon Aortic Valvuloplasty and what does it do

A

This is a temporary treatment for people with aortic stenosis.

A balloon is inserted into the aortic valve and inflated multiple times to expand the opening and improve blood flow.

216
Q

What three situations is ballon aortic valvuloplasty used

A
  1. bridge the gap for those wating for surgery
  2. Patients who are severely symptomatic but their AS is not urgent cardiac surgery
  3. In congenital disorders in children and younger adults as first line treatment
217
Q

How long goes balloon aortic valvuloplasty tend to alleviate symptoms for

A

3-12 months

218
Q

What is a mitral clip and what does it do

A

This is a small clip placed on the mitral valve that helps the mitral valve leaflets close better, reducing mitral regurgitation.

219
Q

What is foramen ovule

A

This is a gap between the right and left atrium that is normal in fetal development and should close at birth

220
Q

Explain the difference between these 4 types of atrial septum defects: secundum, primum, sinus venous and coronary sinus

A

Secundum - most common type. Occurs in middle of the septum

Primum - affects lower part of the septum

Sinus venous - affects upper part of the septum

Coronary sinus - rare, where the wall between the coronary singular and the left upper heart chamber is missing

221
Q

What is the role of the left atrial appendage during atrial fibirllation

A

During atrial fibrillation, blood can pool in the left atrial appendage, increasing the risk of clot formation, leading to strokes.

222
Q

A notched p wave usually is a result of pathology in what part of the heart? And what can contribute to this.

A

Due to left atrial enlargement.

The enlargement of the atria tends to be due to increased pressure in the LA. This can be causes my deformities in the Mitral valve

223
Q

A hyperacute/peaked p wave usually is a result of pathology in what part of the heart? And what can contribute to this.

A

Enlargement of right atrium

Due from an increased in right atrial pressure. Can be due too tricuspid valve deformities or pulmonary hypertension

224
Q

Why are the AV node cells unable to conduct, cause Mobitz Type 2 AV block

A

They are in their absolute refractory period

225
Q

What is the normal beats per minute of the SA node, AV node and bundle of his

A

SA node 60-100bpm
AV node 40-60bpm
Bundle of His 20-40bpm

226
Q

What are some indications for pacing treatment

A

Symptomatic sinus bradycardia
Sinus node dysfunction
Sinus arrest/sinoatrial block
AV block

227
Q

What is the battery status at the input time of the pacemaker and what does this decline to when the pacemaker needs replacing

A

Input = 3.2V
End of service = 2.8V

228
Q

What 4 things is pacemaker battery longevity affected by

A

Pulse amplitude
Pulse width
Battery capacity
Pacing percentage

229
Q

How does a pacemaker battery decline over time

A

For the first few years there is very little decline in battery, however there is a sudden decrease towards the end of service

230
Q

When will a pacemaker deliver a pace

A

If the interval is timed out (there is no intrinsic beat within a set time frame) then the pacemaker will send a beat

231
Q

What factors make up the output of the pacemaker

A

Pacing impulse - made up of pulse amplitude and pulse width

232
Q

What is the safety margin for a lacemaker lead in relation to pulse amplitude

A

Safety margin of a lead is twice the threshold pulse amplitude

(if threshold is 1mV at 0.4s, output should be 2mV at 0.4s)

233
Q

What is threshold in regards to pacemakers

A

minimum energy required to consistently elicit a myocardial depolarization

234
Q

What 4 factors will affect the threshold of a pacemaker

A

Antiarrhythmics
Myocardial infarction
Hyperkalemia
Severe acidosis or alkalosis

235
Q

What is the current of injury in pacemakers

A

When a pacemaker lead is screwed into the myocardium this causes injury to this part of the muscle.
This is seen as S-T elevation on the ECG

236
Q

What do pacemaker leads contain to reduce current of injury

A

Steroid dexamethasone is at the top of the leads to reduce the inflammation at the site of injury

237
Q

What is slew rate of a pacemaker and what is the normal slew rate for atria and ventricles, respectfully

A

Slew rate is the change in electrical potential (voltage) overtime

Atria = >0.5V/s
Ventrical = >0.75V/s

238
Q

What does the strength duration curve for a pacemaker tell us

A

This tells us the quantity of charge/voltage required from the pacemaker to cause a myocardial contraction in the heart

239
Q

What is rheobase in regards to the strength duration curve of a pacemaker and after what duration should this be reached usually

A

The minimum intensity required to stimulate a muscle at infinite duration

Rheobase should be reaches 1-2ms after the pulse

240
Q

What value can you use to estimate the most efficient pacemaker pulse duration

A

Chronaxie Time - this is double the rheobase number

241
Q

How do pacemakers sense cardiac depolarisation

A

Measuring changes in electrical potential of myocardial cells between the anode and cathode

242
Q

In pacemaker lead sensitivity, what parts of the ECG do you want to ensure the pacemaker is sensing in both atrial sensing and ventricle sensing, respectfully

A

When sensing atria - want it to only detect P waves
When sensing ventricles - want it to only detect the R wave

Sensitivity should be half the value of the wave you want to see

243
Q

To make a pacemaker less sensitive, what must you do to the sensitivity value and what is the effect of this

A

Must increase the sensitivity value (make the fence taller)

This will mean the pacemaker will see less activity, and will pace more then necessary

244
Q

To make a pacemaker more sensitive, what must you do to the sensitivity value and what is the effect of this

A

Must lower the sensitivity value (make fence shorter)

This could cause the pacemaker to double count the waves, thinking it is an arrythmias

245
Q

What faults to the pacemaker leads will cause an decrease and increase in impedance, respectfully

A

Insulation break = low impedance (<300 ohms)
Lead fracture - high impedance (1200 ohms)

246
Q

What three things is sensing accuracy affected by in a pacemaker

A

Pacemaker circuit (lead integrity)
Electrode placement in the heart
Lead polarity

247
Q

What is the Ab marker channel on a pacemaker

A

Atrial Blanked Event - a period of time in which the pacemaker sense amplifiers are off and the pacemaker does not sense anything

248
Q

What does AR marker on a pacemaker mean

A

Atrial Refractory Event = a period of time in which sensed events are seen but ignored due to timing purposes

249
Q

What does VR marker on pacemaker mean

A

Ventricular Refractory Event

250
Q

What sort of filter and what bandwidth quantities are used in a pacemaker

A

Band pass filter used - 20-40Hz are sensed

251
Q

What is the timing circuitry made of in a pacemaker

A

Crystal oscillator

252
Q

What is a bipolar lead configuration of a pacemaker

A

The lead has both the anode and cathode at the tip of the lead

253
Q

In bipolar pacemakers, what electrode is doing the pacing

A

Cathode

254
Q

In a unipolar pacemaker where are the anode and cathode loacted

A

Anode in pacemaker box
Cathode at tip of lead

255
Q

Which type of pacemaker is less susceptible to oversensing of non-cardiac signals

A

Bipolar

256
Q

What type of pacemaker has a smaller lead diameter

A

Unipolar

257
Q

What are the two ways pacemaker leads can be implanted

A

Intracardially - within the heart
Epicardial - sutured to the outside of the heart

258
Q

What is the difference between an active and passive transvenous pacemaker lead

A

Active - helix is screwed into the endocardial tissue
Passive - lodged into the trabeculae of the apex

259
Q

What is the most commonly used transvenous pacemaker lead and where can this be positioned in the heart

A

Active fixation lead - these can be screwed into anywhere of the heart

260
Q

VVI Pacemaker Mode
- What chambers are paced
- What chamber are sensed
- When is pacing inhibited
- What patients is this used in

A

Pace ventricles
Sense ventricle

When intrinsic QRS is sensed, pacing inhibited

Used in patients with chronic AF or those whose ventricular rate is very slow (heart block)

261
Q

AAI Pacemaker Mode
- What chambers are paced
- What chamber are sensed
- When is pacing inhibited
- What patients is this used in

A

Pace atrium
Sense atrium

When intrinsic P wave is sensed, pacing inhibited

Sick sinus node syndrome patients. But normally apart of duel pacing.

262
Q

DDD Pacemaker Mode
- What chambers are paced
- What chamber are sensed
- What patients is this used in

A

Pace both A and V
Sense both A and V

Used to maintain AV synchrony between A and V. Most commonly used in high grade AV block

263
Q

How do you calculate the rate of pacemaker when knowing the interval

A

60,000 / interval = rate (bpm)

264
Q

How do you calculate the interval of pacemaker when knowing the rate

A

60,000 / rate = interval (ms)

265
Q

What is the lower rate interval in pacemakers

A

Lowest rate the pacemaker will pace at if no intrinsic event is sensed

266
Q

When is the lower rate interval of a pacemaker reset

A

If an intrinsic event is sensed, it resets the lower rate interval and if no intrinsic events are sensed, the pacemaker will pace

267
Q

What is a pacemakers response to exercise

A

A pacemaker will increase its rate of pacing to exercise if the patient does not increase their intrinsic rate

268
Q

What is VOO and AOO pacing

A

VOO is permanently pacing the ventricle

AOO is permanelty pacing the atrium

269
Q

What is loss of capture in pacemakers

A

When the pacemaker paces but there is no response from the myocardium

270
Q

What are three possible reasons for loss of capture in a pacemaker

A

Increased pacing output (has the threshold increased)

Lead dislodged and not in contact with myocardium

Lead fracture

271
Q

What occurs if the pacemaker is under sensing

A

This will result in the pacemaker not sensing the intrinsic beats of the heart, so it will pace at the lower rate of the device. This is overpaced.

272
Q

What occurs is the pacemaker is oversensing

A

This will result in under pacing - the pacemaker is sensing too much and resetting the timed interval, potentially leading to it not pacing when it needs to

273
Q

What setting do you change to help reverse undersensing

A

Want to make the pacemaker more sensitive by decreasing the sensitivity value

274
Q

What settings do you change if the pacemaker is oversensing

A

Make pacemaker less sensitive by increasing the sensitvity value

275
Q

What is the main indication for duel pacemaker

A

AV block

276
Q

In a duel pacemaker, what events mark the beginning and end of the lower rate interval

A

Lower rate interval begins with AS/AP. This then is reset if there is another AS/AP

277
Q

In duel chamber pacemakers, when does a pace AV delay occur and when does a sensed AV delay occur

A

Paced AV delay - occurs after an AP event

Sensed AV delay - occurs after an AS event

278
Q

What two pacemaker markers usually make up a AV delay in duel chamber pacemaker

A

usually a AV delay will consist of a AB (atrial blanking period) then a AV (atrial refractory period) before the QRS

279
Q

What is the difference in time between a paced AV delay and a sensed AV delay in duel chamber pacemakers

A

PAV delay is usually programmed 30ms longer then the SAV delay to allow conduction of the paced atrial beat to reach the left atrium

280
Q

In what phase of the ECG is the atrial refractory in duel chamber pacemakers

A

From the beginning of the P wave to the beginning of the QRS

281
Q

In duel chamber pacemakers, what is the post ventricular atrial blanking (PVAB) and when does it occur

A

Time period too prevent sensing of the ventricular signal on the atrial channel

Occurs for the QRS and T wave

282
Q

In duel chamber pacemakers, what is the post ventricular atrial refractory period (PVARP) and when does it occur

A

Time period to prevent oversensing of retrograde P waves

Occurs from beginning of QRS to halfway through T wave

283
Q
A
284
Q

In duel chamber pacemakers, what is the total atrial refractory period (TARP) and when does it occur

A

This is the total refractory period of the atrial channel

TARP is made up of the sensed AV delay (P wave - QRS) and the PVARP (QRS - end of T wave)

In total TARP covers from the beginning of the P wave to the end of the T wave

285
Q

In duel chamber pacemakers, what is the post atrial ventricular blanking (PAVB) and when does it occur

A

Timing interval to prevent ventricular oversensing to a paced atrial beat

This occurs after the P wave

286
Q

In duel chamber pacemakers, what is the ventricular blanking period (VB) and when does it occur

A

Prevents the ventricle from oversensing the ventricular paved signal or the already depolarising ventricle

Occurs during the QRS

287
Q

In duel chamber pacemakers, what is the ventricular refractory period (VRP) and when does it occur

A

Period where sensed events are ignored after the ventricular depolerisation

Occurs from beginning of QRS to end of T wave

288
Q

If a ventricular channel was oversensing T waves, what setting could you change

A

Extend the ventricular refractory period (VRP)

289
Q

What is the upper rate interval in a pacemaker

A

The maximum rate the ventricle can be paced in response to sensed atrial activity

290
Q

Why is the upper rate interval in duel pacemakers

A

The ventricle will increase in pacing if the atria have increased in intrinsic activity. However, we don’t want the ventricle continue to increase infinitely with the atria. The upper rate interval allows there to be a maximum rate at which is will increase the ventricle pacing.

291
Q

What happens to AV syncrony once the upper rate interval is met in duel pacemaker

A

AV synchrony wont be maintained

292
Q

What is the upper sensor rate in duel pacemaker

A

This sensor rate can drive up atrial rate is the SA node isnt working/is lazy

293
Q

In a duel pacemaker what happens is the atrial rate goes over the upper tracking rate

A

The venticle is still limited to the upper tracking rate and will not continue to rise with the atria

294
Q

When the atria are beating faster then the upper tracking rate, what is the first behaviour the ventricles will exhibit

A

Wenckebach Behaviour

295
Q

Explain how Wenckebach behaviour occurs in duel chamber pacemakers

A

When the atrial are beating faster then the upper tracking rate, Wenckebach behaviour is the first to occur in the ventricle

The AV delay progressively gets longer until a P wave falls into the PVARP. This means the P wave isn’t sensed so the ventricle wont beat. There is a skipped ventricular pace.

296
Q

When does 2:1 behaviour occur in duel pacemakers and why

A

Occurs when the atria is beating above the upper tracking rate

Every second P wave falls into the PVAVRP. These refractory P waves are no sensed by the ventricle so no VP is delivered.

297
Q

How do you calculate the rate at which 2:1 behaviour will occur in duel pacemakers

A

rate at which 2:1 will occur = 60,000 / TARP

298
Q

How would you increase 2:1 block rate

A

You would shorten TARP

Do this but either shortening PVARP or SAV delay

299
Q

Why do yo want a relatively high 2:1 block rate

A

You don’t want 2:1 behaviour to occur immediately as the atria exceed the upper tracking rate. You want there to be wenckebach first

300
Q

When is it desirable to decrease the RV pacing

A

In patients with intact AV node or 1 degree AVB or high grade AVB

301
Q

What is the pacing algorithm used for reduced RV pacing in Medtronic devices

A

AAI-DDD

302
Q

What is occurring in the pacemaker in AAI-DDD algorithm

A

The pacemaker is constantly pacing the atrium, but it is able to sense if there is loss of AV conduction and then switch into DD mode and pace the ventricle

303
Q

What changes in the Av delay are seen in pacemakers reducing RV pacing

A

They extend the AV delay to allow AV conduction to be seen if there is any.

If there isnt any sensed then it will switch to DDD and pace the ventricle

304
Q

In what patients is rate response used in duel pacemakers

A

Patients that are chronotropic incompetence (their heart cant increase in rate with metabolic demand)

Patients with sinus node dysfunction and chronic AF

305
Q

What is the mode switch rate for pacemakers

A

171 bpm

306
Q

When would the mode of a DDD pacemaker switch

A

If the atrial rate exceeded the mode switch rate - this usually occurs during AF and atrial flutter

307
Q

Once the atrial rate exceeds the mode switch rate, what mode does the pacemaker switch into.
What rate is the ventricle paced at in this new mode

A

Switched from DDDR to DDIR (non-tracking mode)
Ventricle is paces at the lower rate or the sensor rate (which ever is highest)

308
Q

Why is mode switching important for patient symptoms

A

If the pacemaker didn’t switch modes when atrial rate increased, it would continue to increase ventricular rate. Fast ventricular pacing can make a patient very symptomatic

309
Q

When does pacemaker mediated tachycardia occur

A

When there is loss of AV conductions and triggers retrograde conduction (V-A) and causes rapid ventricular pacing

310
Q

How do we terminate pacemaker mediated tachycardia

A

We want the retrograde P wave to fall under a refractory period (PVARP). The pacemkaer can extend the PVARP period for one beat to break the cycle

311
Q

What do we have to be careful of if we are increasing the PVARP permanently to avoid pacemaker tachycardia

A

By increasing PVARP you are increasing TARP which can increase in a decrease in rate of 2:1 behaviour

312
Q

What is pacemaker syndrome

A

An assortment of symptoms related to the adverse hemodynamic impacts from the loss of the AV syncrony

313
Q

What usuallly causes pacemaker syndrome

A

Atria contracting against closed AV valves

314
Q

What are two symptoms of pacemaker syndrome

A

Neck palpitation and dizziness

315
Q

What is the approach to managing pacemaker syndromes

A

to restore AV synchrony using a duel chamber pacemaker instead of a single chamber

316
Q

How are the pacemaker leads usually implanted

A

Via the subclavian, cehalial or axillary vein which advances to the SVC and down the RA/RV

317
Q

What changes could be expected to see in the oxygen saturation and blood pressure upon insertion of a pacemaker leads in EP lab

A

Blood pressure can drop and oxygen saturations can drop

318
Q

What are the 7 elements that are checked in a pacemaker follow up

A

PBL-STOP

Presenting rythum/rate
Battery status
Lead status
Sensing
Threshold
Observation
Programming

319
Q

What should the sensing quantities be for the P and R wave respectfully

A

P wave > 1.5mV
R wave > 5mV

320
Q

Where is an ICD implanted

A

Prepectoral Pocket

321
Q

What patients are ICDs implanted in

A

Patients with high risk of sudden cardiac death, usually via ventricular arrythmias

322
Q

What heart chambers are ICD leads in

A

Single lead CIS - in right venticle
Duel lead CID - in RV and SVC

323
Q

What is the voltage of the shock delivered by an ICD

A

40J, 80V

324
Q

How long will the capacitor hold the charge for a shock for in an ICD before it needs to be recharged

A

15 seconds

325
Q

How are ICD leads different to pacemaker leads

A

ICD leads, unlike pacemaker leads, are delivering a shock

326
Q

Can you defib someone with an ICD

A

Yes, the pads just cant be over the ICD

327
Q

What configuration of leads are used in pacemaking and ICD

A

IS-1

328
Q

What is the difference between DF1 and DF3 ICD leads and which one is used most commonly

A

DF1 - multiple leads come out of the main lead
DF4 - all components are in one lead (mostly used)

329
Q

What shock configuration is used in ICD these days

A

Single coil ICD leads with RV coil to can

330
Q

In relation to heart rhythm, when is a VT shock always delivered by an ICD

A

VT shock is always synced up with the R wave to ensure the heart return to synchronous rhythm

331
Q

What is the difference between VT and VF sensing in ICD

A

VT tends to be monomorphic and regular so the ICD can detect this is it exceeds the maximum rate intervals

VF tends to be polymorphic and irregular, so it is likely to be under sensed on intervals alone. The ICD instead uses intervals (NID) and rate to detect VF

332
Q

What is auto adjusting sensitivity in regards to a ICD

A

The ICD resets its sensitivity threshold at each R wave based off the preceding R wave

333
Q

Why cant ICDs ever be configured in unipolar

A

They would be too sensitive to noise and innaproporately shock

334
Q

What two configurations can an ICD be put in

A

True bipolar - tip to ring (used commonly)

Integrated bipolar - tip to RV coil (larger sensing circuit that can cause oversensing)

335
Q

What are the 4 channels on a ICD display

A

Leadless ECG - coil to can
Far field channel (shock channel) - Can to RV
Near field channel (sensing channel) - Top to ring
Marker channel - shows how the device is working

336
Q

Following a ICD shock for VF, what will the ICD continue to monitor for a short time afterwards

A

The device will continue to count the intervals between R waves and monitor the rate to ensure another VF episode is detected immediately is there is another one

337
Q

What is atrial tachycardia pacing (ATP)

A

Sequence of pacing pulses faster then the arrythmia occurring to excite the excitable gap in the VT circuit

338
Q

How quick is the pacing in atrial tachycatia pacing in ICD

A

20-30ms

339
Q

What is burst atrial tachycardia pacing (ATP)

A

Sequence of pacing pulses with fixed coupling intervals

340
Q

What is ramp atrial tachycardia pacing (ATP)

A

Sequence of pacing pulses with auto-decremental values so the coupling interval get progressively shortened

341
Q

What is a risk associated with ramp ATP in ICDs

A

It can accelerate the VT into a VF

342
Q

What is the timeline of ATP therapy to treat VT in an ICD

A

First therapy is burst ATP
Second therapy is ramp ATP
Third - Sixth is a shock

343
Q

What will the SVT and VT morphologies look like in compared to normal sinus rhythm

A

SVT will match normal sinus rhythm morphology as it originates from the atrium

VT will look different as VT originates from the ventricle

344
Q

How much do SVT and VT morphologies have to match sinus rhythm to be considered normal VT

A

Morphologies have to match by 70% or more

345
Q

What channel in the ICD is responsible for collecting morphology template and comparing it to the VT rhythm

A

Far field channel (RV coil to can)

346
Q

How does onset help differentiate between VT and sinus tachycardia in an ICD

A

VT routinely starts with a sudden onset whereas sinus tachycardia would be more gradual

347
Q

How can stability be used in ICD

A

Stability can be used to differentiate between atrial fibrillation and VT on the basis that the AF is irregular and monomorphic VT is stable

348
Q

How is stability set on an ICD

A

There can be a set value of variation between the R-R interval that can be allowed. Once this is exceeded, the ICD will class the rhythm as AF

349
Q

What percentage of shocks from ICDs are inapproproate

A

30%

350
Q

What conditions do we want to try minimise VT shocks occuring in to minimise the amount of inapproporate shocks in an ICD

A

We want to minimise shocks in non-sustained VT that will self terminate or that could terminate with ATP

351
Q

What are some reasons inapproporaite shocks can occur in ICD

A

Atrial Fibrillation
Atrial Tachycardia
SVT
Sinus Tachycardia
Lead Failure

352
Q

How can AF cause an ICD to sense it as a VT/VF

A

AF that is rapidly conducted to the ventricles can be extreamly fast and enter the VT/VF zone which may cause an inapproporate shock

353
Q

What patients are at risk for T wave oversensing

A

Those with brugada syndrome or long QT syndrome

354
Q

What two things can we adjust to avoid T wave oversensing

A

Increase ventricular sensitivity or turn on auto-adjusting sensitivity

355
Q

What is the Frank Starling compensatory in heart failure

A

In normal conditions - stroke volume increases and the end diastolic volume increases, causing strain on the cardiac wall forcing the muscles to contract more forcefully

In HF - the contractility is unable to increase with this demand and the left ventricle will become dilated

356
Q

What is the neurohormonal alteration compensatory mechanisms in HF

A

Increase in SNS nervous system leads to an increase in HR, contractility and vasoconstriction.
Renin-aldosterone system overactive and causes fluid retention

357
Q

What is the role of BNP in blood

A

Helps blood circulate around the body

358
Q

What are some lifestyle modifications to treat HF

A

Na+ restriction, appropriate fluid intake, exercise, smoking cessation, weight loss

359
Q

What is ventricular dyssynchrony

A

When there is late activation of the lateral region of the LV in respect to the activation of the septum

360
Q

What are the mechanical, structural and electrical causes of ventricular desynchrony

A

Mechanical - regional wall abnormalities

Structural - disruption of the myocardial collagen matrix

Electrical - conduction delay

361
Q

What is the best predictor for optimal CRT response in an ECG

A

QRS width > 130ms

362
Q

What is the aim of CRT

A

Cardiac device that attempts to normalise the timing of the activation of the left and right ventricle or lateral wall and septum to improve desynchrony seen in LBBB

363
Q

How does LBBB occur as a result to HF

A

In HF the left ventricle dilates, this can cause LBBB where the RV contracts before the LV

364
Q

Where are the leads placed in the heart in CRT

A

1 lead in RA, one lead in RV, one lead in LV implanted through the coronary sinus

365
Q

What is the coronary sinus

A

A branch that is accessed from the bottom of the RA

366
Q

Why does the left ventricular lead in CRT aim for the lateral wall of the LV

A

The lateral wall is the latest point of activation of the LV so by activating this we can cover the whole LV with stimulus to reduce the dysynchrony

367
Q

What are some positive outcomes of CRT

A

LV and RV are synchronised - narrowing QRS

LV septal and free wall synchronised, improving LV contraction

Improves EF

Improves HF symptoms

368
Q

What is the main configuration of LV lead in CRT and what is the benifit of this

A

IS4 - quadripolar

Having a large range of vectors helps capture the whole LV when it is pacing

369
Q

What is the ideal impedance for pacing devices

A

500-1000 ohms

370
Q

What configuration of the LV lead in CRT has been used hisotrically and when would it be used in patients today

A

IS-1 - bipolar

Used when patients vessels are very small

371
Q

What is Optivol in CRT

A

Feature on Medtronic devices that measures transthoracic impendence - as fluid increases in the lungs, Optivol increases and transthoracic impedance decreases

372
Q

Besides from the LV, where are two other locations that pacing can occur in CRT

A

His Bundle and Left Bundle

373
Q

Where are the leads implanted in Left Bundle Pacing CRT

A

Lead is implanted slightly distal to the His Bundle and is screwed deep into the LV septum, ideally to capture the left bundle branch

374
Q

Where is a leadless pacemaker implanted

A

Directly into the RV from the femoral vein

375
Q

When are leadless pacemakers used

A

In patients with occluded veins as they are prone to pocket infections

376
Q

What is a subcutaneous ICD

A

Where the leads are implanted under the muscle and the leads run from the can to the left side of the atrium

377
Q

What shocks is a subcutaneou ICD able to deliver and not able to deliver

A

It can give shocks for VT/VF but cant deliver ATP or bradycardia support pacing

378
Q

What is the effect of holding a magnet over an ICD

A

This will temporality suspend tachycardia detection so no shocks will be delivered

379
Q

What are indications for EP study

A

Patients with palpitations, dizziness and syncope

380
Q

What is the aim of a EP study

A

See what the cause of the arrythmia is or to induce an arrythmia

381
Q

What is the bachman bundle

A

The conduction path between the SA node and LA

382
Q

What phase of the action potential is accelerating to cause abnormal automaticity

A

Phase 4 (resting phase)

383
Q

Atrial tachycardia, reperfusion VT, ischemic VT and fascicular VT are die to what tope of arrythmia mechanisms

A

Abnormal Automaticity

384
Q

Atrial tachycardia, AVNRT, atrial fultter, VT scar mediated and idopathic VT are due to what mechanism of arrythmia

A

Re-entry

385
Q

What is the most common mechanims of tacyarrythmia

A

Re-entry

386
Q

Atrial tachycardia, RVOT and LOT are caused by what mechanism of arrythmia

A

Triggered activity

387
Q

What is occuring on the ionic level in absnormal automicity arrythmias

A

Leakage of positive ions into the cardiac cell leading to late phase 3 or early phase 4 of the AP

388
Q

What is the arrythmia mechanism of torte de poides

A

Triggered activity

389
Q

How is the heart accsess in EP study via the femoral vein

A

Femoral vein > RA > coronary sinus > RV

390
Q

How many catheters are used in EP study

A

4

391
Q

What type of catheter is used during EP study in the high right atrium and where should the tip be located

A

Quadripolar catheter
Tip should be on the lateral wall

392
Q

What type of catheter is used during EP study in the right ventricular apex and where should the tip be located

A

Quadripolar catheter
Tip as close as possible to the RV apex

393
Q

What type of catheter is used during EP study in the coronary sinus and where should the tip be located

A

Octapolar catheter
Located along mitral valve annulus

394
Q

What type of catheter is used during EP study in the His bundle and where should the tip be located

A

Hexapolar Catheter
Top is straddling the tricuspid annulus

395
Q

What is the normal sweep speed in EP study

A

100ms

396
Q

What is the IEGMS showing in an EP study

A

This represents the local electrical activity of the groups of cells in contact with the catheter giving infoamtion on the local electricla acticity

397
Q

What is the PA interval on IEGMS and what is a normal duration for this

A

PA interval measure’s from the onset of P wave to the rapid defelction of the A wave on the his-bundle catheter

25-50ms

398
Q

What is the AH interval on IEGMS and what is a normal duration for this

A

Measures the his bundle catheter from A signal to onset of H signal

50-125ms

399
Q

What is the HV interval on IEGMS and what is a normal duration for this

A

measures the onset of the Hi deflection to the earliest ventricular activation on any channel

35-55ms

400
Q

What pacing algorithyms are used in the atrium and ventricles, respectfully, in EP study

A

VOO in vetricle
AOO in atrium

401
Q

What is pacing drive train in EP study

A

series of -10 fixed stimuli at a constant rate, refered to as S1

402
Q

What is pacing drive train with premature extra stimuli in EP study

A

Consists of introducing one or more premature stimuli (S2) for a short train impulses (S1)

403
Q

What is the funtional refractory period

A

The period of time when an action potential cannot be initated by a normal pacing stimulus

404
Q

What is the effective refractory period

A

The longest coupling interval that faults to capture the tissue (S1-S2)

405
Q

What is the wencheback interval in EP study

A

The longest cycle length that does not result in 1:1 conduction during constant pacing

406
Q

What is decremental atrial pacing in EP studies, how it is performed and what does it reveal

A

This assesses the function of the AV node

Method: pace at a cycle length shorter then the sinus cycle then gradually decrease the cycle length.

The cycle lenght at which a beat is skipped is the wenchback cycle legnth

407
Q

What is the purpose of atrial extra stimulus pacing in EP study

A

induce arrhythmias and out the AV nodal refractory period

408
Q

In atrial extrastimulus pacing in Ep study, what happens to the interval lengths as the conducting intervals decreased

A

As the conducting intervals decrease, the conduction velcoity through the AV node progressively decreases and the AH interval progressively lengthens

409
Q

How is atrial extrastimulus pacing performed in EP study

A

Giving a drive train at fiixing intervals progressively decreasing until AV refractory period occurs

410
Q

What does decremental ventricular pacing reveal in EP study

A

How the atria and ventricles are electriclaly connected as well as AV nodal regractory period

411
Q

What would how up during pacing manoeuvres in an EP study if AVNRT was present

A

AH jump and slow pathways

412
Q

What is sinus node recovery time

A

The interval between the last paced atrial depolarisation and the first spontaneous atrial depolarisation resulting from the SA node

413
Q

What is the normal sinus node recovery time

A

<1500ms

414
Q

What is an abnormal CSNRT in EP study

A

> 525ms

415
Q

What is corrected sinus node recovery time and how is it calculated in EP study

A

CSNRT is the difference between the baseline cycle legnth of the SA node and the SNRT when the atria is pacing in overdrive

CSNRT = SNRT - SA node baseline

416
Q

How is SNRT measured in EP study

A

This is the time taken for the sinus rhythm to resume after 30 seconds of overdrive atrial pacing at several cycle lengths

417
Q

If there is AV block above the His bundle what changes would be observed in an EP study

A

Prolongation of AH interval

418
Q

If there was a AV block below the His bundle what changes would be seen in an EP study

A

HV interval block

419
Q

What length of HV block needs to be seen in an EP study to indicate pacemaker implantation

A

> 100ms would suggest a permentnt pacemaker

420
Q

What is the normal impedance of a RF ablation catheter

A

100-150 ohms

421
Q

If the impedance of a RF ablation catheter in an EP lab goes down to 0 what does this mean

A

The cathather is in contact with the tissue

422
Q

What does it mean if the impedance of a RF apblation catheter increases too high

A

This could mean you are burning tissue that doesnt need to be burnt

423
Q

What are the two possible pathways of AVNRT

A

Beta - fast pathway with long refractory period

Alpha - slow pathway with short refractory period

424
Q

What pathways, fast or slow, does a conduction usually travel down in sinus ryhtum

A

Fast pathwya

425
Q

When a PAC arrives at the atria, what conduction pathway, fast or slow, does it travel down to reach the his bundle

A

Slow pathway - this is because the fast pathway is still in its long refractory period but because of the short refractory period of the slow pathway it will be able to travel down there

426
Q

In regards to the refractory periods of the AV conductio pathways, under what situation would a PAC travel down the fast pathway

A

If the fast pathway recovers in time the PAC that is travelleing down the short pathway could conduct retrogradly up the fast pathway

427
Q

How does AVNRT look on the EP study screen

A

The atrial and ventricle electrical signals will line up as they are being activated at the same time

428
Q

What is the treatment of AVNRT in EP study

A

RF ablation of the short pathway

429
Q

A sudden abrupt prolongation of the AH interal signal in the EP study tells you what

A

The signal has moved from the fast pathway to the slow pathway

430
Q

What length of prolongation of the AH interval in the EP study is indicative of the conduction pathway now going down the short pathway and not the fast pathway

A

> 50ms

431
Q

What type of accessory pathway has developed in AVRY

A

A accessory pathway in the form of muscle connection between the atrium and ventricle which means this can bypass the AV node and cause preexcitation of the ventricles

432
Q

Orthodromic AVRT

A

Anterograde conduction through AV node

433
Q

Antidromic AVRT

A

Retroradde conduiton through AV node

434
Q

What is the most common form of accessory pathway in AVRT and i what direction do signals travel through this

A

Concealed ventricular preexcitation

Can only conduct retrogradely

435
Q

How do they know where they will ablate to treat AVRT

A

The earliest electrical signal seen on the EP screen is where they abalte

436
Q

What temperature is AVRT ablation done at

A

60 degrees

437
Q

Where specifically in the RA does atrial flutter usually originate from

A

Cavotricusptid isthmus (CTI) - located between the inferior vena cava ostium and the tricuspid valve

438
Q

What direction is CTI dependant flutter (typical flutter) moving in

A

Couterclockwise

439
Q

What temperature is used in atrial flutter ablation

A

80 degrees

440
Q

Following atrial flutter ablation, what signals would be indicative of unsucsessful ablation

A

Signals from the Halo catheter should be the last to activate - if this is not the case then the signal is breaking through the CTI still

441
Q

Once you have ablated a clockwise atrial flutter what should you do

A

pace from distal halo catheter 102 and measure the proximal CS7-8

442
Q

If the CTI is fully blocked by atrial flutter ablation what should the Distal Halo 1-2 and CS7-8 be in relation to each other

A

They should be the exact same if the CTI is fully blocked

443
Q

Where is atrial fibrillation commonly located

A

Pulmonary veins

444
Q

What is the treatment for atria fibrillation in EP study

A

Pulmonary Vein Isolate (PVI)

445
Q

What is pulmonary vein isolate (PVI)

A

Pulmonary veins are electrically isolated from the body of the LA using ablation

446
Q

What method is most commonly used for PVI

A

WACA

447
Q

How do you test if atrial fibrillation ablation was sucsessful

A

Pace from the ablation catheter in the pulmonary veins - there is no capture on the heart signal then it is sufficnetly blocked

448
Q

When is fast anatomical mapping (FAM) used in the EP study

A

Used to map the LA and 4 pulmonary veins in preapration for a PVI

449
Q

On a FAM, what colour indicates scar tissue/ablated tissue and what colour represents healthy tissue

A

Ablated tissue - red
Health tissue - purple

450
Q

What is the last resort ablation for atrial fibirllation

A

AV node ablation

451
Q

Why is AV node ablation the last resort for treatment of atrial fibirlation

A

Ablating the AV node will give the patient complete heart block, making them pacemkaer dependant

452
Q

When do you choose to ablate when someone has a PVC

A

Most people have isolated PVCs but they are infrequent so dont require ablation

20,000 PVC’s a day would indicate a ablation

453
Q

What types of ventricular tachycardia is the only type that can be treated with ablation

A

Monomorphic

454
Q

What is the most common form of monomorphic VT

A

Re-entry VT

455
Q

What is activation mapping used for in EP lab

A

used to record the electrical signal sequence during the VT - showing where to alblate

456
Q

What is entrainment mapping used for in EP study

A

Used to prove the location of the catheter is close to the VT circuit

457
Q

How do you perform a post pacing interval (PPI) following a VT ablation

A

Measured from the last pacing stimuli to the next electrical acitivty seen on the ablation catheter tip

458
Q

What do you want the PPI to be following successful VT ablation

A

PPI should be equal to or with (less than 10-30ms) of the tachy cycle length

459
Q
A
460
Q
A

Physiology - Hayley (9 decks)

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