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Cardio Flashcards

1
Q

What is acute pericarditis?

A

Inflammation of the pericardium

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2
Q

Causes Acute Pericarditis

A

Idiopathic

OR
Secondary to :
(Common)
> VIRUSES - Coxsackie, flu, EBV, mumps, varicella, HMV
> BACTERIA - pneumoniae, rheum fever, TB, staphs, strep

(Rarer)
> FUNGI
> Myocardial infarction - Dressler’s
> Drugs - hydraline, penicillin

Also : Uraemia, Rheum Arthritis, SLE, traume, surgery, malignancy

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3
Q

Signs / Symptoms Acute Pericarditis

A

Central pain
Worse upon inspiration / when supine
Relief when sitting up
Pain is severe, sharp
Radiates to arm - trapezius ridge
Pericardial friction rub
Hiccups (phrenic involvement)
Sometimes fever

NOT crushing pain

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4
Q

Ix Acute Pericarditis

A

ECG - saddle shaped ST segment elevation - GS!!!!!!
PR depression
PeRicardiTiS
(can be normal though)

Bloods - FBC, ESR, U&E, cardiac enzymes (troponin may be ↑), Viral serology, blood cultures

CXR - will show cardiomegaly if pleural effusion

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5
Q

Tx Acute Pericarditis

A

Treat cause!

NSAIDs w/ gastric protection (PPI)
(Corticosteroids if resistant to NSAIDs)

Colchicine
Limited by nausea & diarrhoea
Reduces recurrence

Consider colchicine before steroids/immunosuppressants if relapse/continuation doesn’t occur
(bc steroids cause reoccurrence)

Rest until symptoms resolve

(Pericardiocentesis IF effusion/tamponade)

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6
Q

DDx Acute Pericarditis

A

Pneumonia
Pleurisy
Pulmonary embolus
MI
Aortic dissection
GORD

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7
Q

What is the mechanism of colchicine when used to treat acute pericarditis?

A

Inhibits migrations of neutrophils to site of inflammation to reduce risk of occurrence

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8
Q

Complications of acute pericarditis

A

Pericardial effusion
Cardiac tamponade
Chronic constrictive pericarditis

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9
Q

What is Pericardial Effusion?

A

Fluid in pericardium

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10
Q

Cause Pericardial Effusion

A

Causes of Acute pericarditis
(happens after)

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11
Q

Signs / Symptoms Pericardial Effusion

A

Effusion obscures apex beat ∴ heart sounds are soft
Dyspnoea
↑ JVP

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12
Q

Tx Pericardial effusion

A

Treat cause!
Most resolve spontaneously
If effusion recurs, excision of pericardial segment allows fluid to be absorbed through pleural and mediastinal lymphatics

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13
Q

What is constrictive pericarditis?

A

Heart is in a rigid pericardium

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14
Q

Signs / Symptoms Constrictive Pericarditis

A

RHF Sx -
o Jugular venous distension
o Oedema
o Hepatomegaly
o Ascites

↑ JVP - paradoxically w/ inspiration = Kussmaul’s sign
Diffuse apex beat
Quiet heart sounds
Diastolic pericardial knock
S3
Pulsus paradoxus
AF

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15
Q

Causes Constrictive Pericarditis

A

Often unknown
TB
After ANY type of pericarditis
Can happen after intracardial haemorrhage (during surgery)

MUST be distinguished from restrictive cardiomyopathy

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16
Q

Ix Constrictive Pericarditis

A

CXR - small/normal heart +/- pericardial calcification

CT/MRI - diagnostic !!!! shows pericardial thickening and calcification
Rules out myopathies

Echo - cardiac catheterisation

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17
Q

Tx Constrictive Pericarditis

A

Surgery - excision of pericardium

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18
Q

What is Beck’s Triad?

A
  1. ↑ JVP
  2. ↓ BP
  3. Small, quiet heart
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19
Q

What is Cardiac Tamponade?

A

MEDICAL EMERGENCY!
When pericardial fluid raises intra-cardiac pressure
∴ ↓ ventricular filling
& ↓ Cardiac filling

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20
Q

Causes Cardiac Tamponade

A

ANY pericarditis
Aortic dissection
Haemodialysis
Warfarin
Transseptal Puncture (cardiac catherisation)

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21
Q

Signs / Symptoms Cardiac Tamponade

A

↑Pulse
↓ BP
PULSUS PARADOXUS
Beck’s triad
Kussmaul’s sign
Muffled S1&2

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22
Q

Ix Cardiac Tamponade

A

CXR - big globular heart
ECG - low voltage QRS

ECHO - GS!!!!
Echo-free zone around heart (>2cm or >1cm if acute)
+/- diastolic collapse of RA + RV

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23
Q

Tx Cardiac Tamponade

A

URGENT drainage! - pericardiocentesis

Send fluid for culture

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24
Q

When should CCBs be avoided?

A

HEART FAILURE !!!!!!!!!!!! (except amlodopine)

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25
Q

What is the WHO classification of Hypertension?

A

140/90 mmHg on at least 2 separate classifications

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26
Q

Risk factors of HTN

A

Obesity
Lack of exercise
Family history
Smoking
Old age
Low birthweight
Male
Afro-Caribbean
Poor diet - high cholesterol

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27
Q

Causes of HTN

A

1°- Essential HTN (95%)

2°causes - (5%)
> Renal (MC 2°) - CKD, Glomeronephritis, PAN, polycystic kidneys, systemic sclerosis etc
> Endocrine - Phaechromocytoma, Conn’s, Cushing’s
> ALSO : Pregnancy, Coarctation of aorta, Pre-eclampsia @ 3rd trimester, Drugs (the Pill, NSAIDs, vasopressin)

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28
Q

Signs / Symptoms HTN

A

Asymptomatic
Sometimes headaches but not much more than general population

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29
Q

Ix HTN

A

If 140/90 mmHg, confirm w/ :
> 24hr ambulatory BP monitor (ABPM)
> Multiple home BP measurements (HBPM)

–
ALSO : test for end-organ damage w/ :

> Urinalysis (kidneys) - protein, creatinine:albumin ratio, haematuria
ECG/Echo (LV hypertrophy)
Fundoscopy (HTN retinopathy)
Bloods - serum creatinine, eGFR, BG (DM)
Clinical history (MI, stroke)

–
ALSO : exclude 2° causes w/ :
> U&E (e.g. ↓K+ in Conn’s, ↑ Ca2+ in Hyperparathyroidism)

–
Measure sitting AND standing BP if :
Type 2 Diabetes
> 80 years
Symptoms of postural hypotension

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30
Q

How does ABPM compare to clinical BP?

A

ABPM is always lower
Should always “add” 12/7 to “convert” to clinical if need to make decisions for Tx

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31
Q

When do you/do you not treat HTN?

A

If ≥ 160/100 mmHg, always treat
If end-organ damage, always treat
If ≥ 140/90, treat IF high risk of cardiac disease (Qrisk2 score)

–
Bear in mind, most adults over 50 will always benefit with HTN treatment no matter their BP
but idk that’s what the book says but i think its bc of money, we obvs can’t give everyone stuff
? idk

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32
Q

BP Goal for HTN treatment

A

< 140/90 (clinical)
< 135/80 (ABPM/HBPM)

Reduce slowly! Rapid reduction can be fatal !!

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33
Q

Tx HTN

A

Lifestyle changes -
Stop smoking, low fat diet & high consumption of fruit and veg, ↓Alcohol, ↓ Salt intake, ↑ Exercise, If obese - lose weight

Drugs -
Most drugs take 4-8 weeks to work properly, so be patient
Also, take multiple BP measurements before adding more

DIAGRAM !!!!!! LEARN!!!!!!!!

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34
Q

What is Malignant HTN?

A

Rapid rise in BP, causes vascular damage
Urgent care required!

Systolic > 200
Diastolic > 130

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35
Q

Risk factors Malignant HTN

A

More common in young & black people

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36
Q

Signs / Symptoms Malignant HTN

A

Headaches
Visual disturbances
Bilateral renal haemorrhages ∴ Papilloedema

Pathological hallmark = fibrinoid necrosis

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37
Q

Complications Malignant HTN

A

Hypertensive Emergencies e.g. :
AKI
HF
Encephalopathy

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38
Q

Tx Malignant HTN

A

Sodium nitroprusside

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39
Q

Why is is important not to rapidly reduce BP with Hypertension?

A

Bc cerebral auto-regulation is poor
∴ ↑ Risk of stroke

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40
Q

What is Atrial fibrillation?
Describe its pathophysiology

A

“Irregularly irregular”
Chaotic atrial rhythm
300-600 BPM
AV node responds intermittently, not all impulses are conducted to ventricles (bc AVN refractory period)
∴ Cardiac output ↓

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41
Q

Causes AF

A

Any condition that ↑Atrial pressure, e.g. :

HF
HTN
Coronary artery disease
Rheumatic heart disease
Valvular heart disease
Thyrotoxicosis
MI
PE
Pneumonia
Caffeine
Alcohol
ETC

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42
Q

RF AF

A

Elderly people
(& then obvs causes)

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43
Q

Full form - CHA2DS2VASC score
What does it measure?
When should you give medications?

A

Congestive heart failure, 1
HTN, 1
Age ≥ 75, 2
Diabetes, 1
Stroke, TIA, thromboembolism history, 2
Vascular disease, 1
Age 65-74, 1
Sex Category - FEMALE, 1

STROKE RISK
If 1, consider oral coags or aspirin
If 2+, give oral coag !! (DOACs, warfarin)

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44
Q

Full form - ORBIT score
What does it measure?

A

1 Older age (≥ 75 years),
2 Reduced haemoglobin/anaemia
2 Bleeding history - GI/intracranial bleeding, haemorrhagic stroke
1 Insufficient kidney function - eGFR < 60 mL/min/1.73 m2
1 Treatment w/ antiplatelets

BLEEDING RISK

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45
Q

Ix AF

A

ECG !!!
Irregularly irregular
Absent P waves
Rapid, irregular QRS somplexes
F waves

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46
Q

If someone has an irregular pulse, what Ix should you do?

A

ECG!! ON EVERYONE W/ IRREGULAR PULSE

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47
Q

Signs / Symptoms AF

A

USUALLY ASYMPTOMATIC
Palpitations
Fatigue, anxiety
Dyspnoea +/- chest pain
HF
Apical pulse > radical pulse
S1 variable intensity

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48
Q

Tx AF
ACUTE

A

If < 48 hours, DC cardioversion.
If haemodynamically unstable, very urgent!
Give anticoag before - must be on anticoag to have DC cardioversion!

If DC cardioversion doesn’t work, give flecaride/amiodarone

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49
Q

Tx AF
CHRONIC (most patients)

A

Assess stroke/bleeding risk with CHA2DS2VASc/ORBIT to decide what to do
–
Rate Control
1. B-blockers (bisoprolol) OR CCB (verapamil)
2. If doesn’t work, then give Digoxin and then consider Amiodarone

Rhythm control
> DC cardioversion
If DCC is chosen, first pre-treat with amiodarone OR sotalol (sotalol only if no other heart disease!!!) for AT LEAST 4 WEEKS

> If not DC C, then flecainide (if NO structural defect) /amiodarone (if structural defect, IV) instead

FOLLOWED BY :
Anti-coagulation - DOAC ! e.g. apixaban
Can do warfarin depending on patient but needs way more monitoring and both are equally affective

–
Need to decide how to balance bleeding risk and stroke risk, depends on lots of things e.g. age (falling risk) ∴Talk to them and figure a plan out

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50
Q

When treating AF, when should you not give B-blockers?

A

Don’t give with Diltiazem or verapamil without expert advice
BC risk of bradycardia

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51
Q

Main goals of Tx AF

A

Rate control
Anti-coagulation

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52
Q

Mechanism of amiodarone

A

Inhibits Na+/K+ activated myocardial adenosine
↑ Duration of ventricular + atrial muscle action
∴ Nerve impulses take longer

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53
Q

Anti-Coagulation = PREVENTION of TIA/Stroke

Rate control/Rhythm control = TREATMENT of AF

A
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54
Q

DDx AF

A

Atrial flutter

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55
Q

Complications AF

A

STROKE!!!!!!

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56
Q

What are the types of angina?

A

Stable - induced by effort and relieved by rest

Unstable (crescendo) - increases in severity, occurs at rest or recent onset (less than a month)

Variant (Pinzmetal’s) - caused by coronary artery spasm, angina w no provocation, usually at rest

Decubitus - precipitated by lying down

Nocturnal - at night, may wake patient from sleep

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57
Q

Risk factors Stable Angina
(Modifiable & non-modifiable)

A

Non-Mod :
Gender
FHx
Personal history
Age
–
Mod :
Smoking
Diabetes
Hypertension
Hypercholesterolaemia
Sedentary lifestyle
Stress

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58
Q

Precipitants of Angina

A

Reduces blood supply :
Anaemia
Hypoxaemia
Hypothermia
Hypovolaemia
Hypervolaemia
–
Increases demand :
Hypertension
Hyperthyroidism
Valvular heart disease
Tachyarrhythmia
Cold weather

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59
Q

Signs / Symptoms Angina

A

Central, crushing retrosternal chest pain - radiates to arms, jaw, neck

Chest pain comes on w/ exertion, rapidly resolved by rest and/or GTN
Exacerbated by cold weather, anger, excitement, big munch

Dyspnoea
Palpitations
Syncope
Nausea
Sweatiness
Faintness

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60
Q

How do you score angina?

A
  1. Central tight chest pain radiating to jaw, neck, arms
  2. Precipitated by exertion
  3. ## Relief by rest and GTN spray1/3 Non-anginal
    2/3 Atypical angina
    3/3 Typical angina
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61
Q

Ix Stable angina

A

ECG - normal, MAY show ST depression & T wave inversion

CT angiography - shows narrowing of coronary artery. Once seen, can open w balloon or stent

Stress ECG

Bloods - FBC, cardiac enzymes, glucose, lipid profile

CXR - heart size & pulmonary vessels

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62
Q

Tx Stable angina

A

Lifestyle - weight loss, ↑ exercise, quit smoking
Treat underlying conditions - HTN, DM
–
Drugs
PRN, FIRST FIRST LINE - Glyceryl trinitrate (GTN)
-
1. Beta blockers e.g. bisoprolol, atenolol, propranolol OR CCBs - aterodilators e.g. amlodopine
2. BB + CCB

  1. Another anti-anginal = Ivabradine
    OR long-acting nitrates
    –
    Then consider ACEi or ARBs or statins
    –
    THEN consider Surgery (PCI or CABG)
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63
Q

What is the mechanism of GTN when treating Stable angina?

A

Dilate coronary arteries which reduces preload
Nitrate is a venodilator

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64
Q

Common S/E of GTN

A

Headaches

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65
Q

What is the mechanism of Beta blockers when treating Stable angina?

A

↓HR and force of contractions
Neg chronotropic and inotropic

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66
Q

When is BB contraindicated for Stable Angina?
What alternative medications can you give instead?

A

ASTHMA !! or in patients with heart block
Use CCB instead (or Ivabradine)

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67
Q

WHEN ARE BB CONTRAINDICATED?

A

ASTHMA

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68
Q

Mechanism of CCB when used to treat Angina

A

Blocks Ca2+ influx into cell
Relaxes coronary arteries
↓ Force of LV contraction

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69
Q

Mechanism of Aspirin when used to treat heart failure

A

Inhibits platelet aggregation by inhibiting COX

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70
Q

If Aspirin is CI, what else could you use instead to treat angina?

A

Clopidogrel

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71
Q

Mechanism of statins

A

HMG-CoA reductase inhibitor
∴ Reduces cholesterol

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72
Q

To control BP in Angina, patient can be given ACEi
If condition is very severe, what other drug might you consider?

A

Angiotensin receptor blocker e.g. candesartan or losartan

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73
Q

Mechanism of Ivabradine

A

Inhibits pacemaker current in SAN
∴ ↓ HR

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74
Q

What are the risks of PCI? How could you avoid these?

A

Risk of restenosis or thrombosis
Drug-eluting stents reduces this risk

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75
Q

Advantages & disadvantages of CABG

A

Good prognosis
Longer recovery

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76
Q

Mechanism of PCI

A

Balloon dilation of stenotic vessels

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77
Q

DDx Angina

A

Pericarditis
PE
Chest infection
GORD

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78
Q

What does Acute coronary syndrome include?

A

STEMI
NSTEMI
Unstable angina

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79
Q

Describe unstable angina

A

New onset of angina or deterioration of previously stable angina
Chest pain occurs at rest, not relieved by GTN
Crescendo chest pain
More frequent, lasts longer

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80
Q

State the differences between a STEMI, NSTEMI & Unstable angina

A

ECGs & cardiac markers

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81
Q

Difference in STEMI and NSTEMI pathology

like artery shit

A

STEMI - complete occlusion of major coronary artery
Full thickness cardiac muscle damage

NSTEMI - partial occlusion of major or complete occlusion of minor artery
Partial thickness cardiac muscle damage
Infarction distally + ischaemia proximally
Usually diagnosed retrospectively w troponin and ECG results
–
-> Artery previously affected by atherosclerosis

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82
Q

Pathology of ACS

A

Rupture/erosion of fibrous cap of coronary artery atheromatous plaque
∴ formation of platelet-rich cloth, inflammation & vasoconstriction !
-> from platelet release of serotonin and thromboxane A2

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83
Q

ECG changes in ACS

A

Unstable angina - Normal/T wave depression

STEMI - ST elevation, tall T waves OR sometimes new LBBB (in larger MIs)
After hours/days - Q waves

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84
Q

In which leads would you see ST elevation in an anterior MI?
Which Coronary artery is occluded?

A

V1-V6
LAD

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85
Q

In which leads would you see ST elevation in an Septal MI?
Which Coronary artery is occluded?

A

V1-V4
No septum Q in V5+6 (???)
LAD-septal branches

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86
Q

In which leads would you see ST elevation in an Lateral MI?
Which Coronary artery is occluded?

A

I, avL, V5, V6
Circumflex branch of left coronary artery or MO

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87
Q

In which leads would you see ST elevation in an Inferior MI?
Which Coronary artery is occluded?

A

II, III, avF
RCA or RCX

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88
Q

In which leads would you see ST elevation in an Posterior MI?
Which Coronary artery is occluded?

A

ST DEPRESSION in V1-V4 (bc view of heart is inverted on ECG)
ST elevation in V7-V9

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89
Q

In which leads would you see ST elevation in an Right ventricle MI?
Which Coronary artery is occluded?

A

V1, V4
RCA

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90
Q

In which leads would you see ST elevation in an Atrial MI?
Which Coronary artery is occluded?

A

PTa in I, V5, V6
RCA

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91
Q

What is the PTa segment?

A

Segment between P and Q wave

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92
Q

Causes of ACS

A

Less common:
Coronary vasospasm (without plaque rupture)
Drug abuse (cocaine etc)
Dissection of coronary artery
Thoracic aortic dissection

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93
Q

Ix ACS

A

Bloods - FBC, U&E, Glucose, Lipids
–
Cardiac enzymes :
> Troponin T & I - vvv sensitive and specific but not diagnostic
Rise within 3-12 hours
Peak at 24-48 hours
<14ng/L = normal, >30ng/L = definite MI (in between is possible but not definite)

> Creatinine Kinase - CK-MB! vvv specific and sensitive
Will peak earlier if reperfusion occurs
Rise within 3-12 hours of pain
Can be used to determine reinfarction -> levels drop to normal after 36-72 hours

> Myoglobin
1-4 hours after pain
↑ sensitive but not specific
–
CT angiography

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94
Q

Types of Creatinine Kinase

A

CK-MM, skeletal muscle
CK-BB, brain
CK-MB, heart!

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95
Q

State some cardiac causes of increased troponin

A

CHF
ACS or Chronic coronary artery disease
Myocarditis, Endocarditis, Pericarditis
Tachy/Bradyarrhythmia’s
Heart block

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96
Q

State some non-cardiac causes of increased troponin

A

PE
Gram neg sepsis
Severe pulmonary HTN
Renal failure
COPD
Diabetes
Drugs
Acute neurological events

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97
Q

Why is it very important to treat unstable angina?

A

Bc 50% of Px will get an infarction within 30 days if left untreated

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98
Q

If a patient presents with unstable angina but their QRISK2 score is low, what could you do?

A

Elective stress test

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99
Q

Tx Unstable Angina

A

> ## RF modification !!! i.e. stop smoking, lose weight, healthy diet, exercisePCI & CABG - if risk assessment score is medium/high
–
Antiplatelet therapy
ASPIRIN - 300mg initially, then 75mg daily !!
Dual therapy with P2Y12 receptor inhibitors e.g. Clopidogrel

> ## Platelet glycoprotein IIb/IIIa receptor inhibitors - high risk PxsAnti-Coagulants
LMWH
Fondaparinux
–
Nitrates - GTN spray, IV
Beta blockers - bisoprolol
Statins - simvastatin
ACEi - ramipril
CCBs - amlodopine (If BB CI)

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100
Q

Describe the prescription - dual therapy of Aspirin with P2Y12 receptor inhibitors

A

Clopidogrel - 300mg initially, then 75mg for 12 months
OR
Ticagrelor - 180mg initially then 90mg bd
OR
Prasugrel

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101
Q

Mechanism of dual therapy
(Aspirin w/ P2Y12 receptor inhibitors)

A

Inhibits ADP-dependent activation of IIb/IIIa glycoproteins
∴ prevents amplification of platelet aggregation

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102
Q

Aspirin mechanism

A

Irreversibly inhibits COX-1
∴ ↓ production of thromboxane A2
∴ less platelet aggregation

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103
Q

Give an example of a Platelet glycoprotein IIb/IIIa receptor inhibitors

A

Abciximab

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104
Q

Common Signs / Symptoms MI

A

Crushing central chest pain - “Elephant sitting on chest’
Levine’s sign
Pain may radiate to left arm, neck or jaw

Sweating
SOB/Dyspnoea
Fatigue
Nausea
Pallor
Palpitations
4th heart sound
> 20 mins
Not relieved by GTN spray
Pulse/BP may ↑ or ↓
Pansystolic murmur

THERE ARE ALSO ATYPICAL PRESENTATIONS

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105
Q

When does a silent infarction occur?

A

In elderly patients, diabetics or those with HTN

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106
Q

How does a silent infarction present?

A

Hypotension
Arrhythmias
Pulmonary oedema

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107
Q

Initial management of MI

A

HOSPITAL &
MONAC :
Morphine
Oxygen (sats <94%)
Nitrates
Aspirin - 300mg chewed!
Clopidogrel
–
Beta blocker IV
Refer for PCI, thrombolysis (IV alteplase) or CABG ASAP

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108
Q

When is IV betablockers CI when treating MI?

A

Hypotension
HF
Bradycardia
Asthma

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109
Q

Secondary management MI
(prevention)

A

ACAAB
Aspirin - 75mg od
Clopidogrel/Tricagralor
Atovorstatin - or any statin
ACE-i - to maintain BP
BBs - ↓HR to prevent shearing of arteries

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110
Q

Ix MI

A

ECG
STEMI - ST elevation, tall T waves
Might present as a new LBBB
Pathological Q waves

Cardiac enzymes - troponin T, creatinine kinase, myoglobin

CT angiography
CXR
FBC
U&E
Blood glucose and lipids

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110
Q

Comps MI

A

DARTH VADER

Death
Arrhythmia
Rupture
Tamponade
Heart failure

Valve disease
Aneurysm
Dressler syndrome
Embolism
Recurrence regurg

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111
Q

What advice do you give to a patient who’s just had an MI?

A

Return to work after 2 months - NOT ALL e.g. not airline pilots, divers, air traffic controllers

No air travel for 2 months

No sex for 1 month

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112
Q

Quick!
Breathlessness, fluid retention, fatigue - What is the disease?

A

Heart failure
(Anything with ↓CO)

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113
Q

Describe the NYHA classes

A

I No limitation of physical activity, so so calm

II Comfy at rest but slight breathless, palpitations etc during ordinary exercise

III Still comfy at rest, marked limitation of physical activity, symptoms at less than ordinary exercise

IV Symptoms even at rest! Getting dressed in the morning etc is uncomfortable.

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114
Q

RF heart failure

A

Age (65+)
Obesity
Male
If previous history of MI
African

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115
Q

Two types of Heart Failure

A

Systolic
Diastolic

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116
Q

Ejection fraction of systolic heart failure

A

Ejection fraction < 40% (Stroke vol/End diastolic vol)

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117
Q

Ejection fraction of diastolic heart failure

A

Ejection fraction > 50% (Stroke vol/End diastolic vol)

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118
Q

Why is there reduced preload in diastolic heart failure?

A

Bc abnormal filling of LV

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119
Q

Systolic heart failure Causes

A

Ischaemic heart disease!!
MI
HTN
Cardiomyopathy

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120
Q

Diastolic heart failure causes

A

Constrictive pericarditis
Cardiac tamponade
HTN

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121
Q

Name some compensatory changes for Heart Failure

A

Sympathetic stimulation
RAAS
Cardiac changes (ventricular dilation, myocyte hypertrophy)

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122
Q

Describe how sympathetic stimulation makes compensatory changes against heart failure

A

When SNS is activated - it improves ventricular function (by ↑HR and myocardial contractibility)

Also,

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123
Q

Describe how RAAS makes compensatory changes against heart failure

A

↓CO and ↑Sympathetic tone means ↓Renal perfusin
∴ RAAS IS ACTIVATED
∴ ↑Na+ and H2O retention

Further increases venous pressure and maintains stroke vol (Starling mechanism)

& then, as salt and water retention increases, periph and pulmonary congestions cause OEDEMA
∴ dyspnoea

ALSO : Angiotensin II also causes arteriolar constriction which increases afterload

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124
Q

Describe what cardiac changes are made to compensate against heart failure

A
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125
Q

If changes are made to compensate for heart failure, why do patients become symptomatic?

A

Bc compensatory changes become overwhelmed
∴ becomes pathological

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126
Q

3 cardinal symptoms of HF

A

SOB
Fatigue
Ankle swelling (fluid retention)

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127
Q

What is Left-sided heart failure?

A

When heart is unable to transport blood around the body

USUALLY SYSTOLIC FAILURE
aka unable to pump properly
but can be diastolic (unable to fill properly)

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128
Q

Causes LHF

A

IHD
HTN
Cardiomyopathy
Aortic stenosis - aortic valve narrows

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129
Q

Signs / Symptoms LHF

A

Cardiomegaly - displaced apex beat
Pulmonary oedema
S3 + S4
Pleural effusion
Crepitations in lung bases
Tachycardia
↓BP
Cool peripheries
Heart murmur
Exertional dyspnoea
Weight loss
Paroxysmal nocturnal dyspnoea
Nocturnal cough - pink, frothy sputum
Orthopnoea

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130
Q

Explain the pathophysiology of HTN as a cause for left-sided heart failure

A

↑Arterial pressure
∴ harder for LV to pump blood out
∴ LV hypertrophy
∴ greater demand for oxygen

Coronaries are squeezed by the extra muscle
∴ ↓Blood delivered to tissues

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131
Q

Describe the pathophysiology of Cardiomyopathy as a cause for Left-sided HF

A

DCM - heart chamber dilates so ventricles can fill w more blood (↑ preload)
∴ muscle wall gets tinner and wear
∴ systolic HF

RCM - heart becomes stiff ∴ less compliant ∴ can’t stretch
∴ diastolic HF

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132
Q

Causes RHF

A

Left ventricular failure
HTN
Pulmonary stenosis
Lung disease (COR PULMONALE)
Atrial/Ventricular shunt

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133
Q

Signs / Symptoms RHF

A

Ascites
Nausea
Anorexia
↑JVP
Hepatomegaly/Splenomegaly
Pitting oedema
Weight gain (fluid)

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134
Q

Ix Heart Failure

A

CXR - ABDCDE
Alveolar oedema (Bat’s wing)
Kerley B lines (interstitial oedema(
Cardiomegaly
Dilated upper lobe vessels of lung
Effusion (pleural)
–
ECG - can show underlying causes (e.g. arrhythmias, IHD, LV hypertrophy etc)

Bloods - Brain Natriuretic Peptide
Not spec (can be raised in acute PE)
FBC
LFTs
U&Es
TFTs

Cardiac enzymes - Creatinine kinase, troponin I, troponin T, Myoglobulin

Echocardiogram (TTE) GS!!!!
Do if ECG and BNP abnormal

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135
Q

When might Brain Natriuretic Peptide be raised?

A

In acute PE
Secreted by ventricles in response to myocardial wall stress
↑HF patients

Levels correlate with ventricular wall stress and severity of HF

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136
Q

Acute Tx HF

A

100% oxygen
Nitrates - GTN spray (dilates vessels to allow adequate perfusion of heart)
IV opiates
IV furosemide - to reduce fluid overload

Consider inotropic drugs to ↑contractibility of dilated vessels

137
Q

Chronic Tx HF

A

ABAL

ACE-inhibitors (e.g. ramipril or ARB)
Beta-blocker
Aldosterone antagonists - spironolactone
Loop diuretics (e.g. furosemide)
–
Also : Calcium glycoside (digoxin)
Ventricular assist device
HEART TRANSPLANT

138
Q

When can ACE-i NOT be used to treat HF?

A

If patient has bilateral renal artery stenosis

139
Q

S/E ACE-i

A

Cough - accumulation of bradykinin
Hypotension
Hyperkalaemia
Renal dysfunction

140
Q

What can you give instead of ACE-i?
i.e. in HF if cough is too bad

A

Angiotensin-II-receptor blocker

141
Q

When are BBs CI?

A

ASTHMA
3RD DEGREE HEART BLOCK

142
Q

What must you remember when giving BB for a HF patient?
(idk if it’s in general or just for HF patients)

A

Must give a low dose
Slow up titration

143
Q

What lifestyle advice would you give a HF patient?

A

Education
Obesity control
Diet
Stop smoking
Cardiac rehab

144
Q

How do ACE-i work?

A

Dilate blood vessels

145
Q

How does calcium glycoside (Digoxin) help to treat HF?

A

Inhibits Na/K pump
∴ slows HR

146
Q

What is an Acute Medical failure?

A

Medical emergency!!!!!!!
LHF or RHF developing over mins/hours
Ix and causes are similar to chronic HF

147
Q

Clinical features of Acute Heart Failure

A

Cardiogenic shock - Hypotension, tachycardia, oliguria, cold extremities

Hypertensive HF - ↑BP, preserved LV function, pulmonary oedema on CXR

High output HF – septic shock, warm peripheries, pulmonary congestion, BP may be low

Right HF – low CO, elevated jugular venous pressure, hepatomegaly, hypotension

Acute pulmonary oedema – acutely breathless, tachycardia, profuse sweating (SNS overactivity), wheezes and crackles throughout chest, hypoxia, pulmonary oedema on CXR

148
Q

Comps Acute HF

A

Arrhythmias

149
Q

Describe the pathophysiology of IHD as a cause for LHF

A

IHD caused by atherosclerosis
(↓blood to heart ∴ ↓O2 ∴ myocardium damaged)

∴ dead myocytes
∴ scar tissue (which doesn’t contract)
∴ ↓ contract force
∴ systolic heart failure

150
Q

Describe in which scenarios LFH can sometimes be diastolic

A

Chronic HTN AND aortic stenosis
Both cause LV hypertrophy
∴ ↑contract force
∴ concentric hypertrophy
∴ ↓ LV col
∴ ↓ Room for filling
∴ diastolic heart failure

HCM - causes LV hypertrophy
∴ ↓ room for filling
∴ diastolic HF

RCM (described already)

151
Q

Describe why HF presents with pulmonary oedema

A

↓ Blood pumping into body
∴ Blood backs up into lungs
∴ ↑ pressure and ∴ ↑ fluid moving from blood vessels into interstitial sace

∴ Pulmonary Oedema

152
Q

Describe why HF presents with dyspnoea

A

Extra fluid in pulmonary veins/capillary beds = bad
bc ↓ O2 <–> CO2 exchange
BC more fluid in alveoli ∴ more time for gases to diffuse through

∴ Dyspnoea

153
Q

MI Treatment Guidlines

A

idk i need to learn this

154
Q

What does S1 describe?

A

Closing of mitral and tricuspid valve

155
Q

What does S2 describe?

A

Closing of aortic and pulmonary valve

156
Q

What does S3 describe?

A

When blood strikes a compliant LV during passive LV filling

157
Q

What does S4 describe?

A

When blood strikes the LV during atrial contraction if LV is non-compliant

158
Q

When do symptoms occur in aortic stenosis?

A

When valve area = 1/4 of normal
Normal = 3-4 cm2

159
Q

What are the types of aortic stenosis?

A

Supravalvular - above valve
Valvular - MC
Subvalvular - below valve

160
Q

Causes Aortic Stenosis

A

Calcification of congenital bicuspid aortic valve (BAV) - MC, presents in middle age

Degen and calcification of a normal valve - elderly

Rheum heart disease

161
Q

How does GTN spray help relieve Angina symptoms?

A

GTN spray = nitrates
Nitrates cause release of nitric oxide in smooth muscles
∴ activates guanylate cyclase

Guanlycate cyclase then converts GTP to cGMP
∴ smooth muscle relaxation
∴ vasodilation

162
Q

RF Aortic Stenosis

A

Congenital BAV

163
Q

Quick!
Elderly person is SAD
Exertional Syncope, Angina, Dyspnoea
What is the disease?

A

Aortic stenosis

164
Q

Signs / Symptoms Aortic Stenosis

A

CLASSIC TRIAD : Exertional syncope, Angina, Dyspnoea

Heart failure
Slow rising carotid pulse (pulsus tardus)
Weak carotid pulse (pulsus parvus)

Heart sounds - Soft/absent S2
Prominent S4 - bc LV hypertrophy

EJECTION SYSTOLIC MURMUR
Crescendo-decrescendo character

165
Q

Pathophysiology Aortic Stenosis

A

Narrowing of aortic valve
∴ ↓LV emptying
∴ pressure gradient develops between LV and aorta
∴ LV HYPERTROPHY

∴ ↑ Myocardial O2 demand
∴ supply does not meet demand
∴ ischaemia of some myocardium
∴ eventually LV failure

166
Q

Ix Aortic Syncope

A

GS!!! Echocardiography

CXR - normal heart size, LV hypertrophy
Ascending aorta prominent, post-stenotic dilation
Maybe valvular calcification

ECG - ST depression and T inversion in aVL, V5 and V6
LV hypertrophy if severe

To exclude coronary artery disease, cardiac catherisation

167
Q

Tx Aortic Stenosis

A

SURGERY
Aortic valve replacement - in Sx patients

If not medically fit for surgery, then Transcatheter Aortic Valve Implantation (TAVI) w/ balloon stent

ALSO :
Dental hygiene is important!! Risk of IE

168
Q

Describe the mortality of someone who has symptomatic aortic stenosis

A

75% mortality at 3 years once symptomatic

169
Q

Causes Mitral Stenosis

A

Rheumatic heart disease !
Infective endocarditis
Mitral annular calcification
Congenital

170
Q

RF Mitral Stenosis

A

History of rheumatic fever
Untreated strep infections

171
Q

Pathophysiology Mitral Stenosis

A

Thickening of valve = obstruction from LA to LV
∴ ↑ LV pressure + R heart dysfunction + pulmonary HTN

AF is common bc ↑ LA pressure
ALSO, thrombus risk↑ bc of dilated L atrium - can become systemic emboli! stroke risk!!

If LA pressure is chronically increased, then ↑pulmonary pressure
∴ pulmonary oedema

172
Q

Signs / Symptoms Mitral Stenosis

A

Progressive exertional dyspnoea
Cough w/ blood-tinged sputum
Haemoptysis (bc rupture of bronchial vessels bc ↑pulmonary pressure)

RHF Sx !
Palpitations
Chest pain
Malar flush !
Low vol pulse
Tapping, non-displaced apex beat
AF signs (not necessarily)
Loud S1 at apex

Since LA might get larger bc LVH, can compress n therefore lead to DYSPHAGIA

Diastolic murmur - best heard when patient is lying on left side w expiration

173
Q

What does loudness signify when listening to a murmur?

A

NOTHING
DOES NOT INDICATE ANYTHING ABOUT SEVERITY

174
Q

Ix Mitral Stenosis

A

Echo !!!! (GS)

CXR - LA enlargement, pulmonary HTN, sometimes calcified mitral valve, double heart border?? (passmed said)

ECG - AF, LA enlargement

175
Q

Tx Mitral Stenosis

A

Rate control - if AF, prevent clots and embolisation e.g. digoxin, betablockers

Anti-coags - AF Pxs, prevents clots and embolisation e.g. warfarin

Diuretics - HF e.g. furosemide

Percutaneous mitral balloon valvotomy!

176
Q

Causes Mitral Regurg

A

Myxomatous degeneration - mitral valve prolapse
Rheum heart disease
IE
Ischaemic mitral valve
DCM

177
Q

RF Mitral Regurg

A

F
↓BMI
Age
Renal dysfunction
Previous MI

178
Q

Pathophysiology Mitral Regurg

A

Leakage from LV into LA
∴ LA dilation

Includes compensatory mechanisms :
↑LA enlargement
↑LVH - bc LV same effort for less blood
↑Contractility
Progressive LA dilation and RV dysfunction
Progressive LV vol overload
∴ progressive HF !

179
Q

Signs / Symptoms Mitral Regurg

A

Exertional dyspnoea
Fatigue/Lethargy
Palpitations
R HF -> can lead to congestive HF

Hyperdynamic, displaced apex beat
Soft S1
Pansystolic murmur at apex (radiates to axilla)
Diastolic blowing murmur at L sternal border
Systolic ejection murmur
Austin flint mumur at apex

180
Q

What is a Austin flint murmur caused by?

A

FLuttering of mitral valve cusps bc of regurg

181
Q

What is a pansystolic murmur?

A

Uniform intensity
May be accompanied by soft S1
Merges w S2

182
Q

When is a diastolic blowing murmur heard?

A

When blood flows retrograde into LV
Heard best at Left lower sternal border

183
Q

Ix Mitral Regurg

A

CXR - shows enlarged LA and LV
The more dilated, the more severe

Echo - (TOE) estimation of LA, LV, size & function

ECG - NOT diagnostic

184
Q

Tx Mitral Regurg

A

IE prophylaxis !

Vasodilators - ACEi and hydralazine
Rate control for AF - BBs, CCBs, digoxin
Anti-coag for AF and flutter
Diuretics e.g. furosemide

Valve replacement IF patient has any Sx at rest
OR if new onset AF OR if ejection fraction < 60%

185
Q

What is Aortic Regurg?

A

Blood leaks into LV during diastole
bc aortic cusps are leakyyy

186
Q

Causes Aortic Regurg

A

Congenital bicuspid aortic valve
Rheumatic heart disease
Infective endocarditis

187
Q

Signs / Symptoms Aortic Regurg

A

Collapsing waterhammer pulse
Wide pressure pulse
Quincke’s sign
De Musset’s sign
Muller’s sign

Heart sounds - displaced hyperdynamic apex beat
Early diastolic murmur at left sternal edge at 4th IC space (accentuated if Px sits forward w breath held in exp!)
Systolic ejection murmur

188
Q

Ix Aortic Regurg

A

Echo

ECG - shows evidence of LVH

CXR - cardiomegaly, sometimes also dilation of ascending aorta

189
Q

Tx Aortic Regurg

A

IE prophylaxis

Vasodilators - ACEi
ONLY if Sx or HTN

SURGERY - replace valve asap before LV dysfunction

190
Q

What can decrease the intensity of an ejection-systolic murmur with Aortic Stenosis?

A

Valsava manouvre

191
Q

What can increase the intensity of an ejection-systolic murmur with Aortic Stenosis?

A

Amyl Nitrate
Raising legs
Squatting
Expiration

Bc increases blood flow through valve

192
Q

Pathophysiology Pulmonary Stenosis

A

Narrowing of outflow of right ventricle

193
Q

Signs / Symptoms Pulmonary Stenosis

A

MILD/MOD :
Well tolerated
RVH

**SEVERE : **
RV failure as a neonate
Collapse
Poor pulmonary blood flow
RVH
Tricuspid regurg

194
Q

Tx Pulmonary Stenosis

A

Balloon valvuloplasty
Open valvotomy
Open trans-annular patch
Shunt (to bypass blockage)

195
Q

What is Infective Endocarditis?

A

Infection of heart valves/other structures WITHIN the heart
e.g. pacemakers, surgical patches etc

196
Q

RF IE

A

Elderly
IVDU
Congenital heart disease
Prosthetic heart valves or pacemakers
Poor dental hygiene
Male

197
Q

Causes IE

A

Staphylococcus Aureus MC !!
IVDU, diabetes, surgery
Infects damaged and healthy valves
Can destroy valve

Streptococcus viridans - dental problems
Attacks previously damaged valves
Doesn’t destroy valve
LOW virulence

Staphylococcus epidermis
Infects prosthetic material

Psuedomonas aeruginosa

198
Q

Signs / Symptoms IE

A

FROM JANE

Fever!
Roth spots
Osler’s nodes
Murmur (arrhythmias)

Janeway lesions
Anaemia
Nail bed splinter haemorrhages
Emboli - stroke, MI etc

–
+ Headache, fever, malaise, confusion, night sweats, clubbing

199
Q

What is the diagnostic criteria for IE?

A

Duke’s Criteria
2 Major Criteria*
1. 2 +ve blood cultures
2. Echo TOE shows vegetations on valve

5 Minor Criteria
1. Predisposing factors
2. Fever
3. Vascular phenomena
4. Immune phenomena
5. Equivocal blood cultures
–
Diagnostic IF :
2 majors
or 1 major + 3 minors
or 5 minors

Possible IE IF :
1 major
or 1 major + 3 minors
or 5 minors

200
Q

Ix IE

A

Transoesophageal Echo (TOE) - GS!!!

Transthoracic Echo (TTE)

Cardiac Muscle Biopsy - will give definite diagnosis but v risky. Only use if will change treatment plan

ECG
CXR - cardiomegaly

Blood cultures - 3 sets from DIFFERENT sites over 24 hours !!
MUST be taken before ABx
But don’t delay meds if patient v unwell (e.g. sepsis)

201
Q

Tx IE

A

Antimicrobials - IV for 6 weeks
Depends on culture

If staph - use vancomycin and rifampicin
If not - use penicillin (benzylpenicillin, gentamycin)

Treat Comps - arrhythmias, HF, heart block, stroke etc

Surgery

202
Q

What is a Cardiomyopathy?

A

Disease of myocardium that affects mechanical or electrical function of heart

203
Q

Types of Cardiomyopathys

A

Hypertrophic Cardiomyopathy
Dilated Cardiomyopathy
Restrictive Cardiomyopathy

204
Q

What is the most common cause of sudden death in young and adults?

205
Q

Causes HCM

A

Autosomal dominant mutation

206
Q

Signs / Symptoms HCM

A

Can be asymptomatic

Angina
Dyspnoea
Palpitations
Dizzy spells
Syncope
Crescendo-decrescendo murmur (Aortic stenosis) !!
S4

207
Q

Ix HCM

A

ECG - usually always abnormal
Deep T wave inversion

Echocardiogram

Microscopically - Myocyte disarray
On a ultrastructural level - myofibrils are in disarray
When stained = blue
Fibrosis
Hypertrophy in coronary arteries

208
Q

Tx HCM

A

Amiodarone - anti arrhythmic
CCB e.g. amlodopine, diltiazem
BB - atenolol

Surgery

DIGOXIN IS CONTRAINDICATED

209
Q

Pathophysiology HCM

A

Diastole is main problem, NOT systole bc hearts are stiff and don’t relax properly

LV becomes hypertrophied and hypertrophy is asymmetrical
∴ LV outflow tract is blocked during systole

210
Q

Which is the most common cardiomyopathy?

A

Dilated cardiomyopathy

211
Q

Pathophysiology DCM

A

Walls either normal or thin
∴ weak contraction
∴ less pumped out
∴ biventricular congestive HF

212
Q

Causes DCM

A

Idiopathic !! - MC
Infection - coxsackie B
Ischaemia
Alcohol
Thyroid
Genetic

213
Q

Signs / Symptoms DCM

A

HF Sx usually
SOB
Arrhythmias
↑JVP

214
Q

Ix DCM

A

CXR - large heart
ECG - non-spec T wave changes
Echo

215
Q

Tx DCM

A

HF and AF treated like usual

L ventricular assist device
Heart transplant

216
Q

Pathophysiology RCM

A

Poor dilation of heart = ↓ability to take on blood and pass to rest of body

aka
Ventricles stiffer
∴ Less compliant
∴ ↓cardiac output
∴ HF

217
Q

Causes RCM

A

Amyloidosis
Sarcoidosis
Idiopathic
Endocardial fibroelastosis
Löffler endocarditis - eosinophils in the heart
Haemochromatosis

218
Q

Signs / Symptoms RCM

A

Similar to constructive pericarditis

Dyspnoea
↑ JVP
Hepatomegaly
Ascites
S3 + S4

219
Q

Ix RCM

A

CXR
ECG - low amplitude, smaller QRS
Echo
Cardiac catherterisation

220
Q

Tx RCM

A

Treat underlying cause
Heart transplant

221
Q

Name some congenital heart defects
From MC to LC

A

Bicuspid aortic valve
Atrial septal defect
Ventricular septal defect
Coarctation of aorta
Pulmonary stenosis

222
Q

Pathophysiology Bicuspid Aortic Valve defect

A

Normally, aortic valve = 3 cusps
but in BAV = 2

Leads to aortic stenosis +/- aortic regurg

Valve degens quicker than normal
ALSO, predisposes to IE, aortic dilation and aortic dissection

223
Q

Ix BAV

A

Echo - intense exercise makes comps appear faster

224
Q

Tx BAV

A

Surgical valve replacement

225
Q

Which side murmurs are emphasised with expiration?

A

Left sided murmurs
Meanwhile, R sided are louder with inspiration bc ↑ venous return to heart

226
Q

Describe the 4 stages of chronic limb ischaemia

A

Stage 1 - asymptomatic
Stage 2 - intermittent claudication
Stage 3 - Rest pain/Nocturnal pain
Stage 4 - Necrosis/Gangrene

227
Q

RF Peripheral Vascular Disease

A

Same as atherosclerosis!
e.g.
Smoking
Diabetes
Dyslipidaemia
HTN

228
Q

Causes PVD

A

Atherosclerosis

229
Q

PVD : Hip/Buttock pain
Which artery?

A

Aortic or iliac arteries

230
Q

PVD : Thigh pain
Which artery?

A

Common femoral artery

231
Q

PVD : Upper 2/3rd calf pain
Which artery?

A

Superior femoral artery

232
Q

PVD : Lower 2/3rd calf pain
Which artery?

A

Popliteal artery

233
Q

PVD : Foot pain
Which artery?

A

Tibial or Peroneal artery

234
Q

Define Intermittent Claudication

A

Nerve pain caused by release of adenosine in response to muscle ischaemia

235
Q

6 Ps of Limb Ischaemia

A

Pain
Pallor
Pulseless
Perishing cold
Paraesthesia
Paralysis

236
Q

Signs / Symptoms
Compare PAD and PVD

A

PAD : 6 Ps
PVD : Red, swollen, warm

237
Q

Ix
Compare PAD and PVD

A

PAD : ABPI
PVD : D-dimer and dopper US

238
Q

Tx
Compare PAD and PVD

A

PAD : Anti-coags
PVD : Anti-coags, DOACs, warfarin, heparin

239
Q

Comps
Compare PAD and PVD

A

PAD : Acute limb ischaemia, loss of limb
PVD : PE

240
Q

Describe Beurger’s test

A

Patient supine, lift both legs to 45 deg
Hold for 2 mins
Observe feet colour

Then Px sits up, hangs legs over bed at 90 deg
Skin will be blue, then red

241
Q

Why does skin first become blue then red in a positive Beurger’s test?

A

As legs hang over bed at 90 deg (after supine and 45 deg), blood is deoxygenated in passage through ischaemic tissue
Then red, bc reactive hyperaemia from post-hypoxic vasodilation

242
Q

Ix PAD/PVD

A

APBI - Ankle Brachial Pressure Index
Normal is 1-1.2
PAD = 0.5 - 0.9

Colour Duplex USS
Shows vessels and blood flow within

MT/CRI angiography - identify stenosis and quality of vessels

Bloods - ↑CK-MM, shows muscle damage

Auscultation - bruit

–
Venous US imaging
CT scan
^idk about these 2

243
Q

What does Starling’s Law generally state?

A

That stroke volume in the heart responds to end-diastolic vol (preload)

244
Q

Tx DVT

A

Lifestyle - RF modifications
To relieve symptoms and ↓MI risk

Medications - anti-coag
Apixaban = 1st line !!!

245
Q

Causes Critical Leg Ischaemia

A

Thrombosis (vasculopaths)
Emboli
Graft occlusion
Trauma

246
Q

Signs / Symptoms Critical Leg Ischaemia

A

Pain in thighs, calves, feet, buttocks
Ulcers - more likely on limb w/ poor blood supply (healing takes longer bc ↓perfusion)

6 Ps
Foot pain at night, relieved by hanging foot over bed at night

247
Q

Quick!
Deep duskiness of limb + Sudden deterioration = ?

A

ARTERIAL OCCLUSION
NOT Gout or cellulitis

248
Q

Tx Critical Limb Ischaemia

A

Surgical embolectomy
Local thrombolysis with tissue type plasminogen activator (t-Pa)

249
Q

Comps of treatment for Critical limb ischaemia

A

Risk of reperfusion injury and compartment syndrome post-surgery

250
Q

How would you assess the probability of a DVT?

A

Wells score

251
Q

Other than AF and atrial flutter, where else can sinus tachycardia occur in?

A

Anaemia
Fever
HF
Thyrotoxicosis
Acute PE
Hypovolaemia
Atropine

252
Q

Causes Atrial Fibrillation

A

Any conditions that causes ↑atrial pressure - atrial fibrosis, inflammation etc

HF
HTN
Coronary artery disease
Rheumatic heart disease
Valvular heart disease
Thyrotoxicosis
Cardiac surgery
Cardiomyopathy (RARE)

253
Q

Pathophysiology AF

A

Atria = 300-600/min

Only some of these impulses are conducted to the ventricles - due to the refractory period of AVN

HR = 120-180 BPM

254
Q

Clinical classes of AF

A

Acute - onset within prev 48 hours
Paroxysmal - stops spontaneously within 7 days
Recurrent - 2 or more episodes
Persistent - continuous for 7 days or more and not self-terminating
Permanent

255
Q

Signs / Symptoms AF

A

Palpitations
Irregularly irregular pulse
Dyspnoea
Hypotension
Chest pain & discomfort
Fatigue
Anxiety
S1 heart sound variable in intensity

256
Q

Ix AF

A

ECG - irregularly irregular
F waves
No clear P waves
Rapid and irregular QRS complex

257
Q

Tx AF

A

If unstable (i.e. syncope, shock, chest pain, HF) = DC synchronised cardioversion (Control Rhythm) by defib

If stable/long term =
> BBs or CCBs (Controls Rate)
> Digoxin - more in sedentary patients
> Amiodarone

Anticoag w warfarin - prevents thromboemboli

258
Q

Give an example of a CCB

259
Q

Describe the CHADS2VASC

A

Congestive heart failure (1)
HTN (1)
Age > 75 (2)
Age 65 - 74 (1)
DM (1)
Stroke or TIA (2)
Vascular disease (1)
Sex = female (1)

260
Q

What does the CHADS2VASC score measure?

A

Stroke risk in AF

261
Q

What do you do with the results of the CHADS2VASC score?

A

0 = lowe it
1 = consider oral anticoag or aspirin
2 = oral anticoag (warfarin, rivaroxaban)

262
Q

What is atrial flutter?

A

Regular heart rhythm but faster than normal
Atrial HR = 300BPM while ventricular rate = 150BPM

263
Q

In atrial flutter, why is the ventricular rate half the atrial rate?

A

Bc AV node conducts every second “flutter beat”

264
Q

Causes Atrial Flutter

A

Idiopathic
Coronary artery disease
HTN
Pericarditis
Obesity

265
Q

Signs / Symptoms Atrial flutter

A

Palpitations
Chest pain
Syncope
Fatigue

266
Q

Ix Atrial flutter

A

ECG - sawtooth flutter waves (F waves)
Often 2:1 block (2 p waves for every QRS)

267
Q

Tx Atrial flutter

A

If unstable - DC synchronised cardioversion

IV amiodarone - restore rhythm
Beta blocker (or CCB) - rate

Radiofrequency catheter ablation of re-entry circuit

Oral anticoag - prevent thromboemboli

268
Q

What does the HASBLED score assess?

A

Risk of major bleeds in AF patients on anticoagulation
Should do regularly

269
Q

Comps AF

A

HF
Ischaemic stroke
Mesenteric ischaemia

270
Q

Compare AF to atrial flutter
(severity, rarity)

A

AF is more common and more severe

271
Q

What is Wolff-Parkinson-White Syndrome?

A

It is a type of :
Atrioventricular Re-entrant Tachycardia (AVRT)

When there is an extra accessory pathway bypassing AVN

272
Q

Pathophysiology AVRT

A

Accessory pathway bypassing AVN
∴ Normally AVN causes a delay but the pathway (Bundle of Kent) reaches slightly earlier - PRE-EXCITATION
(∴ narrow QRS + short PR)

Impulses can travel normally along the Bundle of HIS but then meet the Bundle of Kent and RE-ENTER ATRIA !

273
Q

Signs / Symptoms AVRT

A

Palpitations
Dizziness
Dyspnoea
Central chest pain
Syncope

274
Q

Ix AVRT

A
  1. Short PR interval
  2. “Slurred” start to QRS (DELTA waves)
  3. Narrowed QRS

Also Px are prone to AF and MAYBE ventricular fibrillation

275
Q

What does AVNRT stand for?

A

AV node re-entry tachycardia

276
Q

What does AVRT stand for?

A

Atrioventricular re-entrant tachycardia

277
Q

RF AVNRT

A

2x as common in women than men!

278
Q

Pathophysiology AVNRT

A

2 pathways within AV node - one with a shorter refractory period, slow conduction and longer refractory period, fast conduction

Creates a “ring” of conducting pathways
∴ allows re-entry circuit
∴ produces tachycardia in atria

aka impulse can go round the slow path then bam quickly sneak up the fast path back to the atria!

279
Q

Signs / Symptoms AVNRT

A

Rapid, regular palpitations - abrupt onset and sudden termination!

Neck pulsation - JVP pulsation
Polyuria
Chest pain
SOB

280
Q

Why does AVNRT sometimes present with polyuria?

A

AVNRT can cause tachycardia
∴ ↑ atrial pressure
∴ ANP release
which causes polyuria

281
Q

Ix AVNRT

A

ECG - P waves not visible, seen immediately before or after QRS complex
QRS - normal shape

282
Q

Tx AVRT & AVNRT

A

If stable - vagal manouvres
e.g. breath holding, carotid massage, valsalva manoeuvre

If manoeuvres unsuccessful, IV adenosine

Consider surgical radiofrequency ablation of Bundle of Kent

283
Q

How does IV adenosine work to fix AVRT and AVNRT and atrial flutter etc ?

A

Causes a complete heart block for a fraction of a second
∴ Should warn a patient, will feel like they are dying for a second ! jeeeez

284
Q

Causes Sinus Bradycardia

A

INTRINSIC
Acute ischaemia
SAN infarction
Sick sinus syndrome

EXTRINSIC
Drug therapy - BB, digoxin
Hypothyroidism
Hypothermia
↑Intracranial pressure

285
Q

Tx Intrinsic Sinus Bradycardia

A

Atropine
Permanent pacemaker
Temporary pacing in acute cases

ATROPINE IS CONTRAINDICATED IN MYASTHENIA GRAVIS AND PARALYTIC ILEUS

286
Q

Tx Extrinsic Sinus Bradycardia

A

Treat underlying cause

287
Q

Describe 1st degree heart block

A

Delayed AV conduction
Still reaches the ventricles

Prolonged PR interval > 0.22s on ECG

288
Q

Causes 1st degree heart block

A

LEV’s disease
IHD - scar tissue blocks conduction pathway
Myocarditis
Hypokalaemia

289
Q

Tx 1st degree heart block

A

Asymptomatic
∴ no treatment required

290
Q

What is 2nd degree heart block?

A

When atrial impulses fail to reach ventricles

291
Q

Describe Mobitz type 1 pathophysiology

A

AV node block

Progressive PR interval prolongation until P wave fails to conduct
Then, QRS is absent after first P wave

Eventually, ventricle pacemaker cells kick in
∴ PR interval returns to normal
CYCLE REPEATS

DIAGRAM

292
Q

Signs / Symptoms Mobitz Type 1

A

Light headedness
Dizziness
Syncope

293
Q

Pathophysiology Mobitz Type 2

A

Block at intra-nodal level
∴ QRS is widened

QRS complexes are dropped without PR prolongation !!
Randomly dropped beats

294
Q

Signs / Symptoms Mobitz Type 2

A

Chest pain
SOB
Syncope
Postural hypotension

295
Q

Tx 2nd degree heart block

A

If severe, permanent pacemaker insertion

296
Q

Pathophysiology 3rd degree heart block

A

Complete disassociation between atrial + ventricular activity
P waves + QRS complex occur independently

297
Q

Causes 3rd degree heart block

A

CHD
Infection
HTN

298
Q

Signs / Symptoms 3rd degree heart block

A

Syncope
Dyspnoea
Chest pain
Confusion

299
Q

Ix 3rd degree heart block

A

ECG - P waves and QRS occur independent

300
Q

Tx 3rd degree heart block

A

IV atropine (acute)
Permanent pacemaker insertion

301
Q

Causes Bundle Branch Block

A

Acute - Ischaemia, MI, Myocarditis
Chronic - HTN, Cardiomyopathies

302
Q

Which side is more common to have an accessory pathway and ∴ pre-excitation in AVRT ?

303
Q

Ix Bundle Branch Block

A

ECG - wide QRS complex
0.08 - 0.12 seconds (incomplete BBB)
> 0.12 (complete BBB)

RBBB - Deep S wave in leads 1 & V6
Tall late R wave in V1

LBBB - Deep S wave in lead V1
Tall late R wave in leads 1 & V6

304
Q

When does RBBB occur?

A

PE
RVH
Isolated diastolic HTN
Congenital heart disease e.g. atrial/ventricular septal defects, Tetralogy of Fallot

305
Q

When does LBBB occur?

A

IHD
Aortic stenosis
HTN
Aortic valve stenosis

306
Q

Tx Bundle Branch Block

A

Cardiac pacemaker

307
Q

Pathophysiology Bundle Branch Block

A

Bundle branches become blocked (fibrosis etc)
∴ Impulse is blocked on one side of heart
∴ ventricles don’t get impulses at the same time
Instead, spread from left to right or vice versa

308
Q

Signs / Symptoms Bundle Branch Block

A

Usually asymptomatic

309
Q

Describe WiLLiaM MaRRoW

A

W - QRS looks like W in V1 & V2
i
LL - LEFT bundle
ia
M - QRS looks like M in V4-V6
–
M - QRS looks like M in V1
a
RR - RIGHT bundle
o
W - QRS looks like W in V5 & V6

310
Q

Why does LBBB also produce abnormal Q waves?

A

Because Left bundle branch conduction is responsible for initial ventricular activation

311
Q

What can be heard on auscultation in LBBB?

A

Reverse splitting of S2

312
Q

What can be heard on ausculation in RBBB?

A

Wide physiological S2 splitting

313
Q

Types of Aortic Aneurysm

A

True - degeneration affecting all 3 layers (intimal, media and adventitia)

False - collection of blood under adventitia only

314
Q

What arteries are commonly involved in a true aortic aneurysm?

A

Abdominal aortia - MC!
Iliac
Popliteal
Femoral
Thoracic

315
Q

What shapes are formed in a true aortic aneurysm?

A

Saccular - one side
Fusiform - both sides

316
Q

When can a false aneurysm form?

A

After trauma

317
Q

RF Abdo Aortic Aneurysm

A

Smoking
FHx
Age
Male
HTN
Trauma
COPD
Hypercholesterolaemia

318
Q

Signs / Symptoms AAA

A

If unruptured, asymptomatic
Once ruptured, SUDDEN epigastric pain radiating to flank!

Abdo, loin, groin pain - pressure effects
Pulsatile abdo swelling - if diameter > 5.5cm, suggests it’s unruptured

Expansile aorta - suggests rupture
Presents w: Epigastric pain radiating to back
Hypovolaemic shock

Hypotension
Collapse

319
Q

Ix AAA

A

Abdo US - cheap, easy, sens, spec
CT +/- MRI angiography

320
Q

Tx AAA

A

Small aneurysm monitoring
Manage RF (↓smoking etc)
Treat underlying cause

Surgery - EVAR (Endovascular repair)
Stent inserted through femoral/iliac artery
OR open surgery - fewer comps but more invasive
–
IF RUPTURED - EMERGENCY!
ABCDE, fluids, surgery!
AAA graft surgery = replace weakened walls w graft

321
Q

Causes Thoracic aortic aneurysm

A

Cystic medial necrosis
Atherosclerosis
Connective tissue disorders - Marfan’s, Ehlers-Danlos

322
Q

Signs / Symptoms Thoracic Aortic aneurysm

A

Asymptomatic mostly

Pressure effects - Back/neck/chest pain, dysphagia, cough
Aortic regurg - if aortic root involved
Collapse
Cardiac tamponade
Haemoptysis

323
Q

DDx AAA

A

Acute pancreatitis - but this is non-pulsatile and more assoc with Cullen’s & Grey-Turner’s sign
GI bleed
Perforated GI ulver
Appendicits
Pyelonephritis

324
Q

DDx Thoracic aortic aneurysm

A

MI
Thoracic back pain

325
Q

Ix Thoracic aortic aneurysm

A

Screen men between 65 - 74 with aortic US
CT angiography
MRI

326
Q

Tx Thoracic Aortic Aneurysm

A

Surgical replacemet
BP control - BB

327
Q

What is AAA?

A

Abdo aortic aneurysm
Permanent aortic dilation exceeding 50%
Diameter > 3cm

328
Q

In whom is Inflammatory AAA found?

A

Found in younger patients who smoke + atherosclerotic arteryies
Some Px present with pyrexia

329
Q

A patient can be perfectly healthy with a BBB. Which side?

330
Q

What is aortic dissection?

A

Surgical emergency!!
Tear in aortic intima, causing blood to dissect through the media - separating the layers

331
Q

Common patient for Aortic Dissection

A

Man 50 - 70 years old

332
Q

RF Aortic Dissection

A

HTN - can be caused by stress, pregnancy, coarctation
Connective tissue - Marfan’s, ED
FHx
AAA
Trauma
Smoking

333
Q

Types of Aortic Dissection

A

Type A - involves ascending aorta MC!!!
Type B - not involving ascending aorta

334
Q

MC locations Aortic dissection

A
  1. Sinotubular junction - where aortic root becomes “tubular”, within 2-3cm of aortic valve MC!
  2. Just distal to L subclavian artery (in descending thoracic aorta)
335
Q

Signs / Symptoms Aortic Dissection

A

Sudden onset of severe, central tearing chest pain - radiates to back and down arms !
Similar to MI but MI pain gets more intense with time but aortic dissection, the pain is worst at the beginning

Absent peripheral pulses
Unequal BP in arms
Neuro Sx / Shock
Hypotension
Aortic regurg (new murmur)
Cardiac tamponade
Compression of other arteries (renal, subclavian) - ∴ AKI, limb ischaemia

336
Q

Ix Aortic dissection

A

CT/MRI angiogram OR TOE - GS!
CT/MRI CI if renal disease

CXR - widened mediastinum
> 8cm - sus!

337
Q

DDx Aortic dissection

338
Q

Causes Aortic dissection

A

Chronic HTN - pregnancy!
Connective tissue disorder - M/ED
Aneurysms
Infection
Atherosclerosis
Trauma

339
Q

Tx Aortic dissection

A

SURGERY
Type A - open repair
Type B - EVAR (endovascular aneurysm repair)

Prevention/Additionally -
1. BB - esmolol or labetolol
2. Vasodilator sodium nitroprusside

If hypotensive, also consider : IV fluids, blood transfusions, adrenaline

340
Q

Comps Aortic dissection

A

Cardiac tamponade
Aortic insufficiency (regurg)
Pre-renal AKI
Stroke - ischaemic

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