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Phase 2a Revision > Cardio > Flashcards

Cardio Flashcards

1
Q

Describe the two processes of atherosclerosis

A
  • fatty deposits in the artery walls

- the process of hardening or stiffening of the blood vessel walls

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2
Q

what are the non-modifiable risk factors of CVD (3)

A
  • age
  • FHx
  • male
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3
Q

What are the modifiable risk factors of CVD (7)

A
  • smoking
  • alcohol consumption
  • poor diet
  • low exercise
  • obesity
  • poor sleep
  • stress
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4
Q

What medical co-morbidities are associated with CVD

A
  • DM
  • HTN
  • CKD
  • Inflammatory conditions (RA)
  • atypical antipsychotic medication
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5
Q

What are the typical complications of CVD

A
  • angina
  • MI
  • TIA/Stroke
  • PVD
  • chronic mesenteric ischaemia
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6
Q

What is chronic mesenteric ischaemia

A

when plaque builds up in the major arteries that supply blood to the small intestine or small bowel

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7
Q

define primary prevention

A

intervening before health effects occur

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8
Q

define secondary prevention

A

detecting and treating disease or injury as soon as possible to halt or slow the process of disease

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9
Q

What does the QRISK score do

A

calculate the pts risk of having a stroke or MI in the next 10 yrs

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10
Q

what percentage on the QRISK indicates treatment? and what treatment?

A

> 10% means the pt should be started on statins

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11
Q

what is the secondary prevention of CVD

A

4 As

  • aspirin (plus 2nd antiplatlet, clopidogrel for 12mths)
  • atorvastatin 80mg
  • atenolol (or other B-blockers)
  • ACEi (ramipril)
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12
Q

What are the notable side effects of statins (3)

A
  • myopathy
  • T2DM
  • haemorrhagic strokes (RARE)
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13
Q

what is myopathy

A

any disease that affects the muscles that control voluntary movement in the body resulting in muscle weakness

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14
Q

what is angina

A

it is a symptom - ‘attacks’ of chest pain

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15
Q

what defines stable angina

A

when the symptoms are always relieved by GTN (glyceryl trinitrate)

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16
Q

what defines unstable angina

A

when the symptoms come on random at rest and aren’t relieved by GTN

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17
Q

what drug class does GTN spray belong to

A

nitrates

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18
Q

how does GTN work

A

relax the muscle walls of the blood vessels and reduce the workload of the heart

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19
Q

what is the gold standard Ix for angina

A

CT coronary angiography

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20
Q

what other baseline Ix are commonly done for angina

A
  • physical exam (?heart sounds, HF, BMI)
  • ECG
  • FBC (?anaemia)
  • U&E (prior to starting ACEi)
  • LFTs (prior to starting statins)
  • lipid profile
  • TFT (?hypo/hyperthyroid)
  • HbA1C & fasting glucose (?DM)
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21
Q

Why are U&Es performed prior to commencing ACEi?

A

ACEi reduce GFR and raise serum potassium

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22
Q

Why are LFTs performed prior to commencing statins?

A

statins elevate liver enzymes

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23
Q

What is the immediate symptomatic management of angina?

A

GTN spray

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24
Q

What is the long term symptomatic management of angina

A

B-blocker (bisoprolol 5mg OD)

Ca channel Blocker (amlodipine 5mg OD)

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25
Q

what surgical interventions can be used for angina?

A

Percutaneous Coronary Intervention (PCI)

Coronary Artery Bypass Graft (CABG)

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26
Q

define thrombus

A

a blood clot formed in situ within the vascular system, impeding blood flow

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27
Q

what are thrombus from fast flowing arteries mainly made of

A

platlets

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28
Q

what are the different types of acute coronary syndrome (ACS)?

A
  • unstable angina
  • STEMI
  • NSTEMI
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29
Q

how is a STEMI classified

A
  • ST segment elevation

- New LBBB

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30
Q

how is NSTEMI classified

A
  • ST segment depression
  • deep T wave inversion
  • prolonged Q wave
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31
Q

how is unstable angina classified

A
  • chest pain when at rest
  • no ECG changes
  • no rise in troponin
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32
Q

what is a differential for unstable angina

A

musculoskeletal chest pain

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33
Q

what can cause raised troponins

A
  • MI
  • chronic renal failure
  • sepsis
  • myocarditis
  • aortic dissection
  • PE
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34
Q

what symptoms suggest ACS

A
  • central crushing chest pain
  • pain may radiate to L arm and jaw
  • N+V
  • SOB
  • sweaty/clammy
  • palpitations
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35
Q

how can DM pts experience an ACS

A

a silent MI

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36
Q

Ix for ACS

A
    • physical exam (?heart sounds, HF, BMI)
  • ECG
  • FBC (?anaemia)
  • U&E (prior to starting ACEi)
  • LFTs (prior to starting statins)
  • lipid profile
  • TFT (?hypo/hyperthyroid)
  • HbA1C & fasting glucose (?DM)
  • CT coronary angiogram
  • CXR
  • ECHO (after event to look at function damage)
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37
Q

Tx for STEMI

A

<2hrs - Primary PCI

> 2hrs - Thrombolysis

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38
Q

Name two drugs that are used in thrombolysis

A

alteplase

streptokinase

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39
Q

define thrombolysis

A

the dissolution of a blood clot

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40
Q

Tx for NSTEMI

A

BATMAN!!!

  • B (b-blocker)
  • A (aspirin 300mg stat)
  • T (ticragrelor 180mg stat/clopidogrel 300mg stat)
  • M (morphine)
  • A (anticoags, LMWH eg. enoxaparin)
  • N (nitrates eg. GTN)
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41
Q

what risk score is used for NSTEMI

A

GRACE score

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42
Q

What does the GRACE score evalute

A

a pts risk of death in the next 6mths of an NSTEMI

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43
Q

what are the different GRACE scores

A

<5% - LOW risk
5-10% - MEDIUM risk
>10% - HIGH risk

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44
Q

When does the GRACE score suggest treatment

A

> 5% (pt is a medium to high risk of mortality) means it is indicated that the pt be considered to early PCI tx (within 4days of admission

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45
Q

what are the complications of an MI

A

DREAD

D - death
R - rupture of the cardiac septum or papillary muscles
E - oEdema (heart failure)
A - arrhythmia/aneurysm
D - Dressler's syndrome
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46
Q

What is Dressler’s Syndrome

A

Pericarditis 2-3wks after an MI

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47
Q

What causes Dressler’s syndrome

A

localised immune response

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48
Q

How does Dressler’s syndrome present

A
  • pleuritic chest pain
  • low grade fever
  • pericardial rub on auscultation
  • PMHx of MI
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49
Q

What Ix is used to diagnose Dressler’s syndrome & what does it show

A

ECG

  • global ST elevation
  • T wave inversion
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50
Q

Tx of Dressler’s syndrome

A

NSAIDs (1st)
Steroids

Pericardiocentesis - in severe cases

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51
Q

Secondary Prevention for ACS

A

the 6A’s!

  • Aspirin 75mg OD
  • Another antiplatlet (clopidogrel/ticagrelor) for 12mths
  • Atorvastatin 80mg OD
  • ACEi (ramipril max 10mg OD)
  • Atenolol
  • Aldosterone antagonist for pts with clinical HF (eplerenone 50mg OD)
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52
Q

what secondary prevention lifestyle advice is given for ACS

A
  • smoking cessation
  • reduce alcohol consumption
  • healthy diet (Mediterranean)
  • cardiac rehabilitation
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53
Q

what is Hypertension

A

high blood pressure >140/90

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54
Q

what are the types of HTN

A
  • primary/essential HTN (no underlying cause)

- secondary

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55
Q

What are the causes of secondary HTN

A

ROPE

  • Renal (MOST COMMON)
  • Obesity
  • Pregnancy induced HTN/pre-eclampsia
  • Endocrine (mainly hyperaldosteronism)
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56
Q

What are the complications of HTN

A
  • ischaemic heart disease
  • CVA
  • hypertensive retinopathy
  • hypertensive nephropathy
  • HF
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57
Q

how is HTN classified

A
  • stage 1 >140/90

- stage 2 > 160/100

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58
Q

what is the medical management for HTN for pts under 55yrs and non-black

A

step 1 : A
step 2: A+C
step 3: A+C+D
step 4: A+C+D+D

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59
Q

what is the medical management for HTN for pts over 55yrs and black

A

step 1 : C
step 2: C + ARB
step 3: C+ARB+D
step 4: C+ARB+D+D

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60
Q

What metabolite needs to be considered when administering diuretcis

A

serum potassium

>4.5mmol/L = higher dose thiazide-like diuretic
<4.6mmol/L = potassium sparing diuretic
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61
Q

name a higher dose thiazide-like diuretic

A

indapamide

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62
Q

name a potassium sparing diuretic

A

spironolactone

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63
Q

how do potassium sparing diuretics work

A

blocking the action of aldosterone in the kidneys resulting in Na excretion and K retention

= aldosterone antagonist

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64
Q

what is monitored when taking ACEi or diuretics

A

regular U+Es for hyperkalaemia

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65
Q

which patients would you prescribe a CCB over an ACEi for HTN

A

pregnant women

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66
Q

define heart failure

A

a clinical syndrome resulting in a reduced cardiac output and/or elevated intracardiac pressures at rest or during stress

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67
Q

what are the two types of heart failure (HF)

A

Acute & Chronic

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68
Q

How does NICE define acute HF

A

New onset HF in a pt with no known cardiac dysfunction

Acute decompensation of Chronic HF

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69
Q

Define Left Ventricular Ejection Fracture (LVEF)

A

the percentage of the blood in the left ventricle which is pumped out with each heartbeat

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70
Q

What are the triggers for Acute HF

A
  • Iatrogenic (aggressive IV tx)
  • SEPSIS
  • MI
  • Arrhythmia
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71
Q

Symptoms of Acute HF

A
  • rapid onset breathlessness
  • SOB
  • cough with ‘frothy white/pink sputum’
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72
Q

Signs of Acute HF

A
  • raised RR
  • reduced Sp02
  • tachycardia
  • 3rd heart sound
  • bilateral basal crackles
  • hypotension
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73
Q

What type of respiratory failure will acute HF present with

A

T1RF

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74
Q

What causes the 3rd heart sound in Acute HF

A

early-diastolic rapid distention of the L ventricle + rapid ventricular filling +abrupt deceleration of the atrioventricular blood flow

  • the force of the blood filling the L ventricle due to the high pressure of the overloaded vasculature system -
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75
Q

What are the signs of R-sided HF

A
  • raised JVP

- peripheral oedema (ankles/legs/scrotum)

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76
Q

Ix for Acute HF

A
  • ECG
  • ABG
  • CXR
  • BNP
  • ECHO
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77
Q

CXR findings of HF

A 
A - alveolar oedema
B - Kerley B lines (interstitial oedema)
C - cardiomegaly 
D - dilated prominent upper lobe vessels
E - pleural effusion
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78
Q

in Acute HF what takes priority Ix or Tx

A

Tx - pts can deteriorate rapidly

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79
Q

What does BNP stand for

A

B-type natriuretic Peptide

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80
Q

What is BNP

A

a hormone released from the ventricles when the myocardium is stretched beyond the normal range

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81
Q

What does BNP do

A
  • relaxes the smooth muscle reducing the systemic vascular resistance
  • acts as a diuretic on the kidneys promoting more excretion of H20
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82
Q

What are the other causes of a raised BNP

A
  • tachycardia
  • sepsis
  • PE
  • renal impairment
  • COPD
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83
Q

Mx for Acute HF

A

Pour SOD

  • Pour away IV fluids (stop IV fluids)
  • Sit up
  • O2
  • Diuretics (furosemide 40mg stat)
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84
Q

what is monitored in Acute HF

A
  • fluid intake
  • UO
  • U&Es
  • daily body weight
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85
Q

What are the two types of Chronic HF

A
  • systolic heart failure (impaired contraction)

- diastolic heart failure (impaired relaxation)

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86
Q

Symptoms of Chronic HF

A
  • SOB (worse on exertion)
  • cough with frothy white/pink sputum
  • orthopnoea
  • paroxysmal nocturnal dyspnoea
  • peripheral oedema
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87
Q

what is Orthopneoa

A

the sensation of SOB when lying flat - how many pillows do pts have to use to sleep

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88
Q

what is paroxysmal nocturnal dyspnoea

A

sudden waking during the night with a severe attack of SOB and cough

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89
Q

what is the first line Ix for HF

A

BNP blood test

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90
Q

what is the diagnostic Ix for HF

A

ECHO

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91
Q

What are the causes of Chronic HF

A
  • Ischaemic Heart disease
  • HTN
  • Valvular disease (AS)
  • Arrhythmias (AF)
92
Q

What lifestyle advice is given for chronic HF

A
  • smoking cessation
  • yearly flu and pneumococcal vaccine
  • exercise as tolerated
  • optimise tx of co-morbidities
93
Q

what is the first line management for Chronic HF

A

ACEi (ramipril 10mg OD max)
B-blocker (bisoprolol 10mg OD max)

if not controlled

Aldosterone antagonists (eplerenone/spironolactone)
Loop diuretics (furosemide 40mg OD)
94
Q

What does ARB stand for

A

angiotensin receptor blocker

95
Q

Name an ARB

A

candesartan

96
Q

What classification is used to assess the severity of HF

A

The New York Heart Association’s (NYHA) Classification of Heart Failure

97
Q

How does the NYHA define the different levels of HF

A

Class I: no symptoms on ordinary physical activity.

Class II: slight limitation of physical activity by symptoms.

Class III: less than ordinary activity leads to symptoms.

Class IV: inability to carry out any activity without symptoms.

98
Q

What are the common SE of ACEi

A
  • dry cough
  • hyperkalaemia
  • hypotension
99
Q

how do ACEi work

A

inhibits angiotensin-converting enzyme from converting angiotensin 1 to angiotensin 2 stimulating the dilation of blood vessels

  • increased Na + Urine excretion
  • reduced resistance in kidney blood vessels
  • increased venous capacity
  • decreased CO + SV
100
Q

contraindications for ACEi

A
  • hyperkalemia (>5.5mmol/L)
  • renal artery stenosis
  • pregnant
  • previous bad reaction
101
Q

how do Beta Blockers work

A

block the hormone ephinephrine

102
Q

common SE of Beta Blockers

A
  • bradycardia (fatigue/dizzy/lightheaded)
  • cold figners/toes
  • difficulties sleeping
  • nausea
103
Q

contraindications for Beta blockers

A
  • asthma
  • uncontrolled HF
  • bradycardia
  • hypotension
  • certain cardiac rhythm issues
104
Q

How do Calcium Channel Blockers work?

A

Block Ca2+ from entering the myocardium and smooth muscle of the arteries. Preventing contraction = reduced BP

105
Q

what is R sided heart failure called

A

Cor Pulmonale

106
Q

what causes Cor Pulmonale

A

respiratory disease

107
Q

what is the pathophysiology of Cor Pulmonale

A

raised pressure and resistance in the pulmonary arteries causes pulmonary HTN, resulting in back pressure throughout the systemic venous system

108
Q

what are the respiratory causes of Cor Pulmonale

A
  • COPD
  • PE
  • Interstitial lung disease
  • CF
  • Primary pulmonary hypertension
109
Q

how do pts with Cor Pulmonale usually present

A

SOB

  • peripheral oedema
  • increased breathlessness on exertion
  • syncope
  • chest pain
110
Q

what are the signs of Cor Pulmonale

A
  • hypoxia
  • cyanosis
  • raised JVP
  • peripheral oedema
  • 3rd heart sound
  • murmurs (pan-systolic/tricuspid regurgitation)
  • hepatomegaly
111
Q

Mx of Cor Pulmonale

A
  • tx underlying symptoms

- long term oxygen therapy

112
Q

what causes the first heart sound

A

closing of the atrioventricular valve

113
Q

what causes the second heart sound

A

closing of the semilunar valves

114
Q

what can cause a third heart sound

A

rapid ventricular filing causing the chordae tendineae to pull to their full length and twang like a guitar string

115
Q

what can cause a fourth heart sound

A

indicates a stiff or hypertrophic ventricle and therefore caused by turbulent bloodflow

116
Q

when is the fourth heart sound heard

A

heard directly before S1

117
Q

what does a large square on the ECG represent

A

0.2secs (5mm)

118
Q

what does a small square on the ECG represent

A

0.04sec (1mm)

119
Q

what is the normal width of a QRS complex

A

2-3 small squares (0.08/0.12sec)

120
Q

what does a narrow QRS complex typically suggest

A

an arrhythmia arising in the atria or junctional region

121
Q

what does a broad QRS complex typically suggest

A

an arrhythmia arising from below the AV node (eg. ventricules) OR a co-existing bundle branch block

122
Q

what are the common types of atrial arrhythmia

A
  • sinus tachycardia
  • atrial flutter
  • AF
123
Q

what is the main cause of irregular QRS complexes

A

AF

124
Q

what are the different types of Ventricular Tachycardia (VT)

A
  • monomorphic VT
  • fascicular VT
  • polymorphic VT
  • torsades de pointes tachycardia
125
Q

what is monomorphic VT

A
  • broad QRS (>0.12s)

- regular rhythm

126
Q

what is fascicular VT

A
  • narrow QRS (0.11-0.14)
127
Q

what is polymorphic VT

A
  • repeated progressive changes in the QRS axis.
128
Q

what is torsades de pointes

A

subgroup of polymorphic

  • prolongation of QT interval
129
Q

what is AF

A

when the contraction of the atria is uncoordinated, rapid and irregular

130
Q

what causes AF

A

disorganised electrical activity of the SA node

131
Q

Presenting symptoms in AF

A
  • palpitations
  • SOB
  • syncope
  • symptoms of associated conditions (eg.stroke, sepsis, thyrotoxicosis)
132
Q

what are the two causes of irregularly irregular pulse

A
  • AF

- ventricular ectopic

133
Q

what ECG changes are seen with AF

A
  • absent P waves
  • narrow QRS complex tachycardia
  • irregularly irregular ventricle rhythm
134
Q

what is valvular AF

A

AF in pts with mitral stenosis or a mechanical heart valve

135
Q

what are the most common causes of AF

A

mrs SMITH

Sepsis
Mitral valve pathology (stenosis/regurg)
Ischaemic heart disease
Thyrotoxicosis
Hypertension
136
Q

what are the two main principles of treating AF

A
  • rate & rhythm control

- anticoagulation

137
Q

what should be the first line Mx for AF pts

A

rate control

138
Q

which different medications can be used for rate control

A
  • beta blocker (eg.atenolol) = FIRST LINE
  • CCB (eg. diltiazem)
  • digoxin
139
Q

what is the purpose of rate control

A

reduce HR to extend the time during diastole when the ventricles can be filled with blood

140
Q

what is the alternative to rate control

A

rhythm control

141
Q

when can rhythm control be used

A
  • reversible causes of AF
  • new onset AF
  • AF thats causing heart failure
  • remain symptomatic despite effective rate control
142
Q

what is the purpose of rhythm control

A

return the pt to normal sinus rhythm

143
Q

how is rhythm control done

A

cardioversion

144
Q

what is cardioversion

A

puts the pt back into sinus rhythm

145
Q

what are the two types of cardioversion

A
  • pharmacological

- electrical

146
Q

which medication are first line for cardioversion

A
  • flecanide

- amiodarone

147
Q

what medication can be used for long term medical rhythm control

A
  • beta blockers
  • dronedarone
  • amiodarone
148
Q

what is paroxysmal AF

A

when AF comes and goes

149
Q

what score is used to assess a pts risk of a stroke with AF

A

CHADSVASc

150
Q

what score is used to assess a pts risk of bleeding whilst on anticoags

A

HAS-BLED

151
Q

what is warfarin

A

vitamin K antagonist

152
Q

what does NOACs stand for

A

novel anticoagulants

153
Q

what does DOACs stand for

A

Direct acting Oral Anticoagulants

154
Q

what is the target INR for AF

A

2-3

155
Q

give examples of a NOAC/DOACs

A
  • apixaban
  • dabigatran
  • rivaroxaban
156
Q

how are CHADVASc scores used

A 
0 = no anticoag
1 = consider anticoag
2 = offer anticoag
157
Q

what does CHA2DS2-VASc stand for

A 
Congestive heart failure
Hypertension
Age>75 (scores 2)
Diabetes
Stroke/TIA (scores2)
Vascular disease
Age (65-74)
Sex (female)
158
Q

what does HAS-BLED stand for

A 
Hypertension
Abnormal liver/renal function
Stroke
Bleeding
Labile INR
Elderly
Drugs/alcohol
159
Q

what is an arrhythmia

A

abnormal heart rhythm

160
Q

how many cardiac arrest rhythms are there

A

4

161
Q

what are the 4 cardiac arrest rhythms

A
  • Ventricular tachycardia
  • ventricular fibrillation
  • pulseless electrical activity (all normal activity including sinus rhythm without a pulse)
  • asystole
162
Q

what are the two shockable rhythms in a cardiac arrest

A
  • VT

- VF

163
Q

what are the tx options in unstable tachycardia

A
  • consider up to 3 synchronised shocks

- amiodarone infusion

164
Q

what are the 3 types of narrow complex tachycardia

A
  • AF
  • atrial flutter
  • SVT
165
Q

what are the 3 types of broad complex tachycardia

A
  • VT
  • SVT with bundle branch block
  • ?variation of AF if irregular
166
Q

what is the cause of atrial flutter

A

re-entrant rhythm in the atria where the electircal signal recirculates in a self-perpetuating loop due to an extra electrical pathway

167
Q

what conditions are associated with atrial flutter

A
  • HTN
  • IHD
  • cardiomyopathy
  • thyrotoxicosis
168
Q

tx for atrial flutter

A
  • rate/rhythm control with beta blockers/cardioversion
  • tx underlying condition
  • radiofrequency ablation
  • anticoagulaiton
169
Q

what is the cause of SVT

A

electrical signal re-entering the atria

170
Q

what is paroxysmal SVT

A

where SVT reoccurs and remits

171
Q

what are the 3 types of SVT

A
  • atrioventricular nodal re-entrant tachycardia
  • atrioventricular re-entrant tachycardia (WOLF-PARKINSON-WHITE syndrome)
  • atrial tachycardia
172
Q

what is atrioventricular nodal re-entrant tachycardia

A

when the re-entry point is back through the AV node

173
Q

what is atrioventricular re-entrant tachycardia

A

re-entry point is an accessory pathway

174
Q

what is atrial tachycardia

A

where the electrical signal originates somewhere other than the SA node

175
Q

acute Mx of stable SVT

A
  • continuous ECG monitoring
  • valsalva manoeurve
  • carotid sinus massage
  • adenosine
  • verapamil
  • direct current cardioversion
176
Q

how does adenosine work

A

slowing cardiac conversion primarily through the AV node

177
Q

what conditions mean that adenosine should be avoided

A
  • asthma
  • COPD
  • HF
  • heart block
  • severe HTN
178
Q

long-term mx of paroxysmal SVT

A
  • beta blockers
  • CCB
  • amiodarone
  • radiofrequency ablation
179
Q

what causes Wolff-Parkinson-White syndrome

A

an extra electrical pathway connecting the atria and ventricles

180
Q

what is the extra pathway in Wolff-Parkinson-White syndrome called

A

bundle of kent

181
Q

what is the definitive tx in Wolff-Parkinson-White syndrome

A

radio-frequency ablation of the accessory pathway

182
Q

what ECG changes are seen in Wolff-Parkinson-White syndrome

A
  • short PR interval
  • wide QRS complex
  • “delta wave” - slurred upstroke on the QRS complex
183
Q

what is Torsades de Pointes

A

a type of polymorphic VT - translates as twisting of the tips

184
Q

how does look Torsades de Pointes

A

height of the QRS complexes progressively get smaller, then larger then smaller and so on

185
Q

what are the two possible outcomes of Torsades de Pointes

A
  • spontaneously revert back to normal sinus rhythm

- progress to VT

186
Q

what are the ECG changes of Torsades de Pointes

A
  • prolonged QT interval
187
Q

what are the causes of prolonged QT

A
  • inherited (Long QT syndrome)
  • medication
  • electrolyte disturbance
188
Q

what medications can cause prolonged QT

A
  • antipsychotics
  • citalopram
  • flecainide
  • sotalol
  • amiodarone
  • macrolide abx
189
Q

what electrolyte disturbances can cause a prolonged QT

A
  • hypokalaemia
  • hypomagnesaemia
  • hypocalcaemia
190
Q

acute Mx of Torsades de Pointes

A
  • correct cause
  • Mg infusion
  • defibrillation if VT occurs
191
Q

long term Mx of Torsades de Pointes

A
  • avoid certain medication
  • correct electrolyte disturbance
  • beta blockers (not sotalol)
  • pacemaker/implantable defib
192
Q

what are ventricular ectopics

A

premature ventricular beats

193
Q

what is bigeminy

A

when a ventricular ectopic occurs after every sinus beat

194
Q

what is first degree heart block

A

delayed atrioventricular conduction through the AV node

195
Q

how does first degree heart block present on an ECG

A

prolonged PR interval > 0.20s (1 big square)

196
Q

what is second degree heart block

A

when some of the atrial impulses do not make it through the AV node

197
Q

how many types of second degree heart block are there

A

3

198
Q

what are the different types of second degree heart block

A
  • Mobitz Type 1
  • Mobitz Type 2
  • 2:1 Block
199
Q

what is Mobitz type 1

A

where the atrial imputes gradually become weaker until they do not pass through the AV node, then the cycle restarts

200
Q

how does Mobitz type 1 present on an ECG

A

an increasing PR interval until there is an absent QRS then the cycle repeats

201
Q

what is Mobitz type 2

A

intermitted failure or interruption of AV conduction

202
Q

how does Mobitz type 2 present

A

missing QRS complexes

203
Q

what is 2:1 Block

A

where every other atrial impulse is not strong enough to pass through the AV node

204
Q

how does 2:1 Block present on an ECG

A

2 p waves for every QRS omplex

205
Q

what is third degree heart block

A

complete heart block

206
Q

how does third degree heart block present on an ECG

A

no relationship between p waves and QRS complexes

207
Q

what are pts with thrid degree heart block at significant risk of

A

asystole

208
Q

what is the mx for stable AV node blocks

A

observation

209
Q

what is the first line mx for unstable AV node blocks

A

Atropine 500mcg UV

210
Q

what is the second line mx for unstable AV node blocks

A
  • Atropine 500mcg IV (repeated up to 6 doses - max 3mg)
  • other inotropes (eg. noradrenaline)
  • transcutaneous cardiac pacing
211
Q

how does atropine work

A

inhibiting the parasympathetic nervous system

212
Q

what is atropine

A

antimuscarinic

213
Q

what are alpha blockers used for

A
  • BPH

- add-on tx in resistant HTN

214
Q

example of an alpha blocker

A
  • doxazosin
  • tamsulosin
  • alfuzosin
215
Q

how do alpha blockers work

A
  • selective to the a1-adrenoceptor

- causes smooth muscle relaxation = vasodilation = BP fall and reduced resistance to bladder outflow

216
Q

adverse affects of alpha blockers

A
  • postural hypotension
  • dizziness
  • syncope
217
Q

Which alpha blocker is licenced for both HTN and BPH

A

Doxazosin

218
Q

Which alpha blocker is only licenced for BPH

A

Tamsulosin

219
Q

what is adenosine

A

a first-line diagnostic and therapeutic agent in SVT

220
Q

how does adenosine work

A

agonist of adenosine receptors which when activated in the heart

  • reduce the frequency of spontaneous depolarisations
  • increasing resistance to depolarisation
221
Q

how long does adenosine last

A

plasma half life < 10seconds

222
Q

Adverse effects of adenosine

A

bradycardia

asystole

223
Q

which pts should not be given adenosine

A
  • hypotension
  • coronary ischaemia
  • decompensated heart failure
  • asthma (can cause bronchospasm)
  • COPD
224
Q

how is adenosine given

A

6mg IV

225
Q

when is adrenaline used

A
  • cardiac arrest
  • anaphylaxis
  • surgical setting (local vasoconstriction)
226
Q

what is adrenaline

A

potent agonist of the a1-, a2-, b1- and b2- adrenoceptors

227
Q

how does adrenaline work

A

agonist of adrenoceptors = sympathetic (fight/flight) response

  • vasoconstriction
  • increased HR
  • increase force of contraction and myocardial excitability
  • vasodilation of vessels supplying heart and muscle
  • bronchodilation
  • suppression of inflammatory mediator release from mast cells

Phase 2a Revision (13 decks)

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