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Phase 2a med mine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the S1 heart sound due to?

A

Mitral and tricuspid valve closing

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2
Q

What is the S2 heart sound due to?

A

Aortic and pulmonary valve closing

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3
Q

What does the S3 heart sound show?

A

Shows rapid ventricular filling in early diastole
-Normal in young/pregnant patients
-Can be pathological: mitral regurgitation+ heart failure

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4
Q

What is the S4 heart sound due to and in which conditions can it be heard?

A

Pathological ‘gallop’
Due to blood being forced into stiff hypertrophic ventricle
Seen in: LVH and aortic stenosis

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5
Q

How long should the PR interval be?

A

0.12-0.2s

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6
Q

How long should the QRS interval be?

A

0.08-0.1s

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7
Q

What does the P wave show?

A

Atrial depolarisation

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8
Q

What does the PR interval show?

A

AVN conduction delay

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9
Q

What does the QRS complex show?

A

Ventricular depolarisation and atrial repolarisation

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10
Q

What does the ST segment show?

A

Isovolemic ventricular relaxation

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11
Q

What does the T wave show?

A

Ventricular repolarisation

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12
Q

Which conditions can ECGs help diagnose?

A

MI(STEMI/NSTEMI)
Arrhythmias
Electrolyte disturbances
Pericarditis
Chamber hypertrophy
Drug toxicity, like digoxin

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13
Q

What values does 1 small square of ECG paper stand for?

A

0.04s(horizontal)
0.1mV(vertical)

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14
Q

What values does 1 big square of ECG paper stand for?

A

0.2s(horizontal-time)
0.5mV(vertical-amplitude)

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15
Q

Which ECG leads corresponds to the RCA and which part of the heart does it show the function of?

A

aVF, 2, 3
Inferior

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16
Q

Which ECG leads corresponds to the LAD and which part of the heart does it show the function of?

A

V1-V4
Anterior and septal

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17
Q

Which ECG leads corresponds to the left circumflex artery and which part of the heart does it show the function of?

A

V5,V6,aVL,1
Lateral

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18
Q

Which 2 conditions can ischaemic heart disease cause?

A

Angina
MI

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19
Q

How does myocardial ischaemia cause anginal pain?

A

Decreased coronary artery flow

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20
Q

Describe the features of stable angina

A

-Central crushing chest pain, radiating to neck/jaw
-Brought on with exertion
-Relieved with 5 mins rest/GTN spray

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21
Q

What is the Levine sign?

A

‘Fist over chest’
Crushing chest pain: angina

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22
Q

What is the QRISK score?

A

Predicts risk of CV in next 10 years
Takes into account:
-Age
-BP
-BMI
-Socioeconomic status
-Ethnicity

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23
Q

What is the Grace score?

A

Predictor of mortality from MI in next 6months-3 years in ACS patients

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24
Q

Which conditions make up ACS’s?

A

Unstable angina->NSTEMI->STEMI

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25
Q

Describe the features and cause of unstable angina

A

Pain at rest
Not relieved with inactivity/GTN spray
Severe ischaemia

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26
Q

What kind of infarction is an NSTEMI?

A

Partial infarction

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27
Q

What kind of infarction is a STEMI?

A

Transmural infarct

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28
Q

What causes Prinzmetal’s angina?

A

Due to coronary vasospasm (NOT CV atherogenesis)

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29
Q

When is Prinzmetals angina commonly seen?

A

Cocaine users

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30
Q

What does the ECG of Prinzmetal’s angina show?

A

ST elevation

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31
Q

What is decubitis angina?

A

Induced lying flat

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32
Q

Name some risk factors for angina

A

Obesity
T2DM
HTN
Smoking
Old age
Male
FHx
Cocaine use

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33
Q

What causes atherogenesis?

A

Endothelial injury induces cells to site via chemokines IL1, IL6, IFN gamma

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34
Q

What are the 3 stages of atherogenesis that lead to angina?

A

-Fatty streak
-Intermediate lesion
-Fibrous plaques

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35
Q

In which part of the vessel do fatty streaks form?

A

Intima

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36
Q

What are the components of a fatty streak?

A

T cells
Foam cells

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37
Q

What happens during intermediate lesion formation?

A

Platelets aggregate and adhere to site inside the vessel lumen

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38
Q

What are the components of intermediate lesions?

A

Foam cells
T cells
Smooth muscle cells
Platelets

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39
Q

What happens during formation of fibrous plaques?

A

Fibrous cap develops over large lesion

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40
Q

Describe the components of a fibrous plaque

A

Leisons: foam cells, T cells, smooth muscle cells, fibroblasts, lipids with necrotic core

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41
Q

What is the fibrous cap like in a patient with stable angina?

A

Fibrous cap is strong and less rupture prone

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42
Q

What hppens if the fibrous cap is prone to rupture?

A

->Prothrombotic state->platelet adhesion and accumulation->progressive luminal narrowing

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43
Q

Name some symptoms of ACS’s

A

Central crushing chest pain radiating to jaw/neck, crescendo pattern
Hypotension
Tachycardia
‘Impending sense of doom’
Palpitations
Nausea
Sweating
Fatigue
Dyspnoeic we lbreathing

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44
Q

What investigations are carried out to diagnose stable angina?

A

ECG: Should be normal at rest-exercise induced ischaemia-changes
CT angiography: looks for stenosed atherosclerotic arteries

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45
Q

Describe the treatment for stable angina

A

Symptomatic: GTN spray
Lifestyle modifications
Pharmacological:
1)CCB(CI: heart failure) or BB(CI: asthma)
2)CCB+BB
3)CCB+BB+antianginal like ivabradine/nitrates

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46
Q

Which extra drugs should be considered in patients with anigna?

A

ACEi
Aspiring
Statins
HTN treatment

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47
Q

What kind of CCB should be used to treat stable angina?

A

Non rate limiting-can cause excessive bradycardia
Amlodipine
NOT verapamil/diltiazem

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48
Q

What treatments cane be used for angina if pharmacological treatments aren’t successful?

A

PCI: balloon stent of coronary artery
CABG: bypass graft

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49
Q

Name a disadvantage and advantage of using a PCI

A

Advantage: Less invasive
Disadvantage: risk of restenosis

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50
Q

Name a disadvantage and advantage od using a CABG

A

Advantage: Better prognosis
Disadvantage: More invasive

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51
Q

Describe the ECG changes seen after an MI

A

Hyperacute T waves
Pathologically deep alpha waves
LBBB

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52
Q

Describe the extent of occlusion in unstable angina, NSTEMI and STEMI

A

Unstable: partial occlusion of minor coronary artery
NSTEMI: Major occlusion of minor CA or minor occlusion of major CA
STEMI: Total occlusion of major CA

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53
Q

Describe the infarction seen in unstable angina, SNTEMI and STEMI

A

Infarction: none-ischamia only
NSTEMI: Sub endothelial infarction(area away from CA dies)
STEMI: transmural infarction

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54
Q

Describe the ECG changes seen in a patient with unstable angina

A

Often normal
May have ST depression/T wave inversion

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55
Q

Describe the ECG changes seen in a patient with an NSTEMI

A

ST depression
T wave inversion
No Q waves

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56
Q

Describe the ECG changes seen in a patient with a STEMI

A

ST elevation in local leads
Q waves

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57
Q

Why is creatine kinase a useful marker of myocardial damage?

A

Troponin has a shorter half like than CK
CK is a better marker after a few days

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58
Q

What are the 2 main markers for myocardial damage?

A

Troponin
Creatine kinase

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59
Q

What would you expect troponin and creatine kinase to be in an unstable angina patient?

A

Normal

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60
Q

What would you expect troponin and creatine kinase to be in an NSTEMI patient?

A

Elevated

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61
Q

What investigations are carried out to diagnose ACS?

A

ECG
Biomarkers
CT ANGIOGRAPHY to show extent of occlusion

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62
Q

Describe the acute treatment of ACS’s

A

MONAC:
Morphine
O2: is sats<94%
Nitrates: GTN
Aspiring: 300mg
Clopidogrel: 75mg

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63
Q

What is the short term treatment for NSTEMI/unstable angina?

A

Use Grace score:
Low risk: monitor
High risk: Immediate angiogram and consider PCI

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64
Q

What is the short term treatment for a STEMI?

A

PCI: if within 12hr onset/2hrs of first medical intervention
Thrombolysis with alteplase if >12 hours, then PCI if this fails

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65
Q

What is the purpose of thrombolysis with alteplase?

A

clot buster: acts as tPa to activate plasmin: eats fibrin

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66
Q

Describe the long term prevention of ACS’s

A

Beta blockers
Aspirin: Initially 300mg, life 75mg + clopidogrel (75mg)
Atorvastatin: 80mg (cholesterol)
ACE-i

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67
Q

Name some acute complications that can arise from ACS’s

A

Heart failure due to ventricular fibrillation
Mitral incompetence
Left ventricular free wall rupture
Cardiogenic shock

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68
Q

Name some potential long term complications of ACS’s

A

Dressler syndrome (AI pericarditis)
Heart failure
LV aneurysm

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69
Q

Define heart failure

A

Inability for the heart to deliver oxygenated blood to the tissues at a satisfactory rate for the tissue’s metabolic requirements

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70
Q

Is heart failure a diagnosis or a syndrome?

A

Syndrome

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71
Q

What is the most common cause of heart failure?

A

IHD

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72
Q

Name some causes of heart failure

A

IHD
Cardiomyopathy
Valvular disease
Anything that increases cardiac work: pregnancy hyperthyroidism, obesity, htn, arrhythmias

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73
Q

Name some risk factors for developing heart failure

A

Age: >65
Smoking
Obesity
Previous MI
Male

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74
Q

What is cor pulmonale?

A

RH failure due to disease of lungs and pulmonary vessels

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75
Q

Describe the pathophysiology of heart failure

A

Frank-Starling law: High preload=high afterload-high CO
In failing heart: Dysfunctional Frank Starling law in failing hearts: low CO

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76
Q

Describe the compensatory mechanisms for heart failure

A

1)RAAS and SNS activation initially works to maintain cardiac output:
Increases aldosterone and ADH
increases Adr/NAd

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77
Q

What happens when heart failure compensatory mechanisms stop working

A

Heart undergoes cardia remodelling(lowers CO( in repsonse to compensation
Heart is less adapted to function and RAAS and SNS activations exacerbates fluid overload-> congestive heart failure

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78
Q

What is congestive heart failure?

A

Heart failure affecting both left and right circuits

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79
Q

How can heart failure be classified?

A

Acute or chronic
By ejection fraction

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80
Q

What is a normal ejection fraction?

A

50-70%

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81
Q

Describe hear failure with a preserved ejeciton fraction

A

> 50%
Diastolic failure: pump function preserved, filling issues
E.g. hypertrophic cardiomyopathy, LVH, aortic stenosis

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82
Q

Describe heart failure with a reduced ejection fraction

A

<40%
Systolic failure: low CO due to pump issues
E.g IHD

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83
Q

What kind of oedema does LHS failure result in and why?

A

Pulmonary oedema: pulmonary vessel backlog

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84
Q

What kind of oedema does RHS failure result in and why?

A

Peripheral oedema: Systemic venous backlog

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85
Q

Describe the symptoms of heart failure

A

3 cardinal non-specific: SOBASFAT
SOB, ankle swelling, fatigue
Also:
Orthopnoea
Oedema
S1+S2+S3+S4
Increased JVP
Bibasal crackles (pulmonary oedema)
Hypotension
Tachycardia

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86
Q

Describe the NY heart association classification of heart failure severity

A

1)No limit on physical activity
2)Slight limit on moderate activity
3)Marked limit on moderate and gentle activity
4)Symptoms even at rest

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87
Q

How is heart faiure diagnosed?

A

Bloods: BNP>400
ECG: abnormal, e.g. LVH evidence
CXR: ABCDE (alveolar bat wing oedema, kerley bluyes, cardiomegaly, dilated upper lobe vessels, pleural effusion)
Echo: assess heart chamber dimension

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88
Q

What abnormalities can be used to detect heart failure on a chest x-ray?

A

ABCDE
Alveolar bat wing oedema
Kerley B lines(horizontal lines in lower lung fields)
Cardiomegaly
Dilated upper lobe vessels
Pleural effusion

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89
Q

Describe the treatment for heart failure

A

Conservative: lifestyle changes: lose weight, exercise, smoking + alcohol cessation)
Pharmacological: ABAL
ACEi+BB
Spironolactone and furosemide
Consider cardiac resynchronization therapy
Surgery:
Revascularisation
Valve surgery
Heart transplant

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90
Q

What is an abdominal aortic aneurysm?

A

Permanent aortic dilation exceeding 50% where diameter >3cm

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91
Q

Where are aortic aneurysms commonly found?

A

Below renal arteries

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92
Q

What is the biggest risk factor for AAA’s?

A

Smoking

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93
Q

Name some risk factors for developing AAA’s

A

Connective tissue disorders: EDS, Marfans
Smoking
Obesity
HTN
Trauma(atherosclerosis)
fHx
Ageing

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94
Q

Describe the pathophysiology of AAA’s

A

Smooth muscle, elastic and structural degeneration in all 3 layers of vascular tunic (intima, media, adventitia) with leukocyte infiltrate

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95
Q

What is the difference between a true aneurysm and a pseudo aneurysm?

A

All 3 layers: true aneurysm
Not all 3: pseudo aneurysm

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96
Q

At what size does an aortic aneurysm have an increased rupture risk?

A

> 5.5cm

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97
Q

Describe the symptoms of an AAA

A

Asymptomatic until ruptured
Sudden epigastric pain radiating to flank
Pulsatile mass in abdomen
Hypotension
Tachycardia

98
Q

What is a differential diagnosis for a ruptured AAA?

A

Acute pancreatitis
Typically non-pulsatile and more associated with Grey Turner and Cullen signs

99
Q

How are AAA’s diagnosed?

A

Abdominal US to assess aorta

100
Q

Describe the treatment of a non ruptured AAA

A

Conservative: manage RF’s: smoking cessation, weight loss, statins, BP treatment
aSx and <5.5cm: Monitor
>5.5cm or growing rapidly: surgery

101
Q

What surgical procedures can be used for non ruptured AAA’s?

A

EVAR: endovascular repair: stent inserted through femoral/iliac artery-less invasive but more post-op complications
Open surgery: more invasive but fewer complications

102
Q

Describe the treatment for a ruptured AAA

A

Stabilise: ABCDE, fluids, transfusion then surgery
AAA graft surgery to replace weakened walls with graft

103
Q

What are the main causes of thoracic aortic aneurysms? How are they treated?

A

Marfans/EDS
Atherogenesis
Monitor with CT/MRI
If symptoms: immediate surgery

104
Q

What is an aortic dissection?

A

Tear in intima leading to blood dissecting through media and separating the layers apart
Due to mechanical wall stress

105
Q

What is the main risk factor for an aortic dissection?

A

Hypertension

106
Q

Name some risk factors for aortic dissections

A

Connective tissue disorders: Marfans, EDS
fhX of AAA/AD
Trauma
Smoking

107
Q

Where are the most common locations for an aortic dissection?

A

1)Sinotubular junction-where aortic root becomes tubular, near aortic valve
2) Just distal to left subclavian artery in descending thoracic aorta

108
Q

Descirbe the Stanford classification for AD’s

A

A: proximal to left subclavian artery (ascending arch)
B: distal to left subclavian artery (descending thoracic)

109
Q

In which location are aortic dissections more commonly found?

A

Stanford classification A: proximal to left subclavian artery (2./)

110
Q

Describe the pathophysiology of an aortic dissection

A

Blood dissects media and intima and pools in false lumen->decreased perfusion to end organs->organ failure and shock

111
Q

Describe the symptoms of an aortic dissection

A

Sudden onset ripping/tearing chest pain
Shock, hypotension
New aortic insufficiency murmur
Neurological deficit (syncope etc due to affected carotid perfusion)
Decreased left arm peripheral pulse, decreased radial if left subclavian involved) or radio-radial differences
Cardiac tamponade

112
Q

How are aortic dissections diagnosed?

A

CXR: widened mediastinum: >8cm-suspicious
TOE: transoesophageal echo: more invasive than TTE but very sensitive-shows intimal flap/false lumen
CT angiogram: intimal flap, false lumen, rupture/leak

113
Q

When is a CT angiogram used over TOE to diagnose aortic dissections?

A

CT angiogram more used if patient is hemodynamically stable

114
Q

Describe the surgical treatment of an aortic dissection

A

Open repair for type A
EVAR more for B (stent)
If hypotensive: IV fluids, blood transfusions, adrenaline etc

115
Q

Describe the medical preventative treatment for an aortic dissection

A

Special BB: esmolol or labetalol: bb and partial ab-prevents reflex tachycardia to keep BP low
Vasodilator: sodium nitroprusside

116
Q

What are the aims of medical preventative treatment for aortic dissections?

A

SBP: 100-120
HR:60

117
Q

Name some complications of aortic dissections

A

Cardiac tamponade
Aortic insufficiency(regurgitation)
Pre-renal AKI
Ischaemic stroke

118
Q

What baseline values count as hypertension?

A

In clinic:
>140/90mmHg
At home:
>135/85mmHg

119
Q

Describe the causes of hypertension

A

Primary: idiopathic:95%
Secondary: Underlying cause-5%

120
Q

Name some secondary causes of hypertension

A

CKD-often from diabetic nephropathy
Iatrogenic
Pregnancy
Endocrine: Conn’s, Cushing’s, phaeochromocytoma

121
Q

Describe the risk factors for developing hypertension

A

Increasing age
Black ethnicity
Overweight
Lack of exercise
Smoking
Diabetes
Stress
High salt intake
fHx

122
Q

Describe the staging of hypertension

A

Stage 1:
140/90 in hospital or 135/85 at home
Stage 2:
160/100 in hospital or 150/95 at home
Stage 3:
180 and/or 110: start immediate treatment

123
Q

Describe the pathophysiology of hypertension

A

All mechanisms will increase RAAS and SNS activity(so also CO) and increase TPR
BP=TPR x CO so BP will increase

124
Q

Describe the symptoms of hypertension

A

Mostly asymptomatic
Might have pulsatile headaches
Consider signs of secondary causes (pheochromocytoma sx etc)

125
Q

What is malignant hypertension?

A

Markedly raised diastolic (180/12)
Black males: 30-40

126
Q

Describe the signs/symptoms of malignant hypertension

A

LVH/heart failure
Blurred vision(papilloedema, retinal haemorrhage)
Haematuria and renal failure(glomerulonephritis)
Headaches: risk of cerebral haemorrhage

127
Q

What investigations are done to diagnose patients with hypertension?

A

BP reading in hospital >140/90mmHg
ABPM for 24 hrs to confirm diagnosis >135/85
Assess end organ damage
Fundoscopy: papilloedema
Urinalysis, eGFR, serum creatinine, glucose-renal function and diabetes risk
Echo/ECG: LVH risk

128
Q

What is the 1st line treatment for a patient<55 with hypertension?

A

ACE inhibitor

129
Q

What is the 1st line treatment for a patient with T2DM and hypertension?

A

ACEi

130
Q

What is the 1st line treatment for a patient >55 with hypertension?

A

CCB

131
Q

What is the 1st line treatment for a black African patient with hypertension?

A

CCB

132
Q

Describe the treatment for hypertension

A

Either ACEi or CCB
2)ACEi+CCB
3)ACEi+CCB+thiazide like diuretic: bendorflumethiazide
4)ACEi+CCB+TLD+4th drug(a/b blocker or sipronolactone depending on potassium levels)

133
Q

Name some complications of hypertension

A

Heart failure
Increased IHD risk
CKD
Increased cerebrovascular risk

134
Q

What is a DVT?

A

Thrombus in deep leg vein
Less concerning: below calf(most common): minor veins, anterior and posterior tibial)
More concerning: above calf(less common but life-threatening): occlusion can impede distal flow

135
Q

What is Virchow’s triad?

A

Risk factors for developing a blood clot
Hypercoagulability
Venous stasis
Endothelial injury

136
Q

Give some examples of things that cause hypercoagulability

A

Pregnancy
COCP
Obesity
APS
Sepsis
DIC
Malignancy

137
Q

Give some examples of things that cause endothelial injury and explain how

A

Smoking
Trauma/surgery
Endothelial cells normally secrete anticoagulant, chemicals damage endothelial cells so they can’t secrete it

138
Q

What causes venous stasis?

A

Usually laminar flow->aggregation of clotting factors
Immobility-long flights, post op

139
Q

How does a PE cause cor pulmonale?

A

Increases peripheral vascular resistance->increased RV straining to overcome this->RVH->RV fails secondary to increased pulmonary pressure

140
Q

Name 3 conditions that commonly present with pleuritic chest pain and how can you tell the difference between them

A

PE-normal CXR
Pneumothorax
Pneumonia

141
Q

Describe the symptoms of a PE

A

Sudden onset pleuritic chest pain
Dyspnoea (+/-haemoptysis)
Evidence of DVT
Tachycardia, hypotension, increased JVP, ankle oedema

142
Q

What scoring system is used to assess DVT/PE

A

Well’s score

143
Q

How would you diagnose a PE?

A

D-dimer, CTPA
ECG-sinus tachycardia, S1Q3T3(cor pulmonale), T wave inversion of anterior and inferior leads, new RBBB
CXR-normal

144
Q

What test is diagnostic for PE?

A

CTPA

145
Q

What is a D-dimer test?

A

Measure of clot burden-protein released into blood when blood clot fibrinolysed
Sensitive but not specific

146
Q

Which would you do first: a D-dimer or a CTPA?

A

D-dimer

147
Q

Describe the treatment for a PE

A

If massive: Thrombolytics->alteplase (clot buster)
Non-massive: DOAC:
1st line apixaban/rivaroxaban
CI: renal impairment: LMWH

148
Q

Describe the symptoms of a DVT

A

Unilateral swollen calf with engorged leg veins: typically warm
If complete occlusion of a large vein@ severe ischaemia-leg turns blue

149
Q

What score indicates the presence of a DVT?

A

Wells score>1
e.g. calf swelling >3cm, pitting oedema etc

150
Q

How are DVT’s diagnosed?

A

D-dimer first-if raised:
Duplex ultrasound-diagnostic

151
Q

Describe the treatment for a DVT

A

DOAC anticoagulation
Apixaban/rivaroxaban
LMWH if CI(renal impairment)
Mobilisaton, compression stockings

152
Q

Name a differential diagnosis for DVT and how can you tell between them?

A

Cellulitis(usually Staph.aureus/strep.pyogenes): will show leukocytosis on FBC, DVT should be normal
D-dimer and DUSS can confirm DVT

153
Q

What is peripheral vascular disease?

A

IHD of lower limb arteries

154
Q

Name some risk factors for developing peripheral vascular disease

A

Smoking
htn
ageing
obesity
CKD
T2DM

155
Q

What are the different types of peripheral vascular disease?

A

Intermittent claudication(least severe)->atherosclerotic, partial lumen occlusion, pain on exertion
Critical limb ischemia (more severe)->large occlusion, blood supply struggles to meet metabolic demand. Pain at rest and risk of gangrene/infection

156
Q

What is acute limb ischaemia?

A

Total occlusion of vessel due to embolic/thrombotic formation at site of critical limb ischaemia lesion

157
Q

What are the 6P’s: PVD

A

Pulselessness
Pallor
Pain
Persistingly cold
Paralysis
Parasthesia

158
Q

When are the 6P’s present and what is their significance?

A

Acute limb ischaemia
Also in chronic limb ischaemia
The more you have the more limb-threatening
All6: emergency

159
Q

What are the 3 consequences of BV supplying region occlusion?

A

1)Irreversible nerve damage(<6hrs)
2)Irreversible muscle damage(6-10hrs)
Skin changes last to appear: sign of gangrene

160
Q

Describe the symptoms of PVD

A

Ankle brachial pressure index <0.9 or lack of lower leg pulse
Skin changes on leg: colour, ulcerations, warmth
Bruits
Positive Buerger test
Some of 6P’s: most characteristic

161
Q

What are bruits?

A

Pulsatile regions due to turbulent blood flow

162
Q

What is the Buerger test?

A

Elevate leg for 1 minute: pallor then reactive hyperaemia

163
Q

What classification is used for PVD?

A

Fontaine classification 1-4

164
Q

Describe the 4 stages of the fontaine classification

A

1)asymptomatic
2)intermittent claudication
3)chronic limb ischaemia: pain at rest
4)ischaemic ulcers->gangrene

165
Q

Describe the diagnosis of PVD

A

ABPI-compare blood in posterior and anterior tibial artery to brachial artery with doppler US
0.5-0.9: intermittent claudication
<0.5: critical chronic limb ischaemia
Colour duplex US: assess degree of stenosis
CT angiography if surgery considered(GS but too invasive)

166
Q

Describe the treatment for intermittent claudication

A

RF management:
smoking cessation
lower BMI
BP control: ACEi
Statins
Antiplatelts: clopidogrel, aspirin
T2DM drugs

167
Q

Describe the treatment for chronic limb ischaemia

A

Revascularisation surgery: PCI if small, bypass if big
Amputation if severe

168
Q

Describe the treatment for acute limb-threatening ischaemia

A

Surgical emergency: revascularisation within 4-6hrs or high amputation risk

169
Q

Name some complications that can arise from PVD

A

Amputation
Permanent limb weakness
Rhabdomydysia
Increased risk of cerebrovascular events and CVD

170
Q

What is pericarditis?

A

Inflammation of the pericardium with/without effusion

171
Q

Is pericarditis without effusion dry or wet?

A

Dry

172
Q

Is pericarditis acute or chronic?

A

Typically acute, can be chronic

173
Q

What are the 2 types of pericarditis?

A

Dry: fibrous: wihtout effusion
Wet: with effusion

174
Q

What are the 2 types of wet pericarditis?

A

Exudative
Haemorrhagic: bleeding

175
Q

What kind of things cause exudative pericarditis?

A

Malignancy
Infection

176
Q

Name the causes of pericarditis

A

Idiopathic
Viral: Coxsackie virus
Bacterial: TB
Fungal: histoplasmosis in immunocompromised patients
Autoimmune: SLE, RA, Sjorgens
Dressler’ syndrome (post MI)
Neoplastic (lung, breast)

177
Q

What is the most common cause of pericarditis?

A

Viral: Coxsackie
AI also very common

178
Q

Describe the pathophysiology of pericarditis

A

Inflammation causes narrowing of the pericardial space so the inflamed pericardial layers rub against each other leading to further inflammation

179
Q

Describe the signs and symptoms of pericarditis

A

Severe sharp pleuritic chest pain with referral to left shoulder (phrenic), relieved when sitting forward and worse laying flat or on inspiration
Pericardial friction rub on auscultation
May have signs of RHS failure: SOB, peripheral tachycardia, tachycardia

180
Q

What does a pericardial friction rub sound like and when can it be heard?

A

Heard when patient leans forward, squeaky leather to and for sound

181
Q

What is constrictive pericarditis?

A

Granulation tissue formation in the pericardium results in impaired diastolic filling: sign of poor heart prognosis

182
Q

What is a differential diagnosis for pericarditis?

A

MI-central crushing chest pain not related to lying down, no pericardial rub

183
Q

How is pericarditis diagnosed?

A

ECG diagnostic: widespread saddle-shaped ST elevation and PR depression
CXR: cardiomegaly, pneumonia seen in bacterial pericarditis
ESR:high in autoimmune
WCC: high in infection

184
Q

What ECG changes can be seen in pericarditis?

A

Widespread saddle-shaped ST elevation
PR depression

185
Q

Describe the treatment for idiopathic, viral and bacterial pericarditis

A

NSAID’s like aspirin for 2 weeks
Colchicine (antiinflammatory) for 3 weeks
Antibiotics if bacterial

186
Q

Name some complications of pericarditis

A

Pericardial effusion->cardiac tamponade
Myocarditis
Constrictive pericarditis

187
Q

What is pericardial effusion?

A

Accumulation of fluid in the pericardial space

188
Q

How does pericarditis lead to cardiac tamponade?

A

Pericardial effusion->if large volumes of fluid that are enough to impair ventricular filling->cardiac tamponade

189
Q

Describe the cause and risk factors of cardiac tamponade

A

Cause: pericarditis
RF: pericarditis related: viral, IA etc

190
Q

Describe the signs and sympotms specific to cardiac tamponade

A

Beck’s triad: hypotension, increased JVP, muffled S1+S2 heart sounds
Pulsus paradoxicus: fall of systolic BP of >10mmHg on inspiration

191
Q

What is Beck’s triad?

A

Seen in cardiac tamponade
Hypotension, increased JVP, muffled S1+S2 heart sounds

192
Q

How is pulsus paradoxicus different to Kussmaul’s sign?

A

Pulsus paradoxicus: fall in systolic BP >10mmHg on inspiration
Kussmaul’s sign: Paradoxical increase in JVP with inspiration

193
Q

How can cardiac tamponade be diagnosed?

A

ECG: electrical altermans: carying QRS amplitudes due to heart bouncing back and forth in extra pericardial fluid
CXR: big globular heart
Echo: diagnostic

194
Q

What ECG changes can be seen in cardiac tamponade?

A

Electrical altermans
Varying QRS complexes due to heart bouncing in extra pericardial fluid

195
Q

What is the treatment for pericardial effusion?

A

Treat underlying cause e.g. NSAID’s and colcichine

196
Q

What is the treatment for cardiac tamponade?

A

Urgent pericardiocentesis

197
Q

What is infective endocarditis?

A

Infection of endocardium due to causative bacteria colonising abnormal endothelium and causing vegetation

198
Q

Describe the causes of infective endocarditis

A

Bacteria:
S.aureus(mc in IVDU, T2DM, surgery)
S.Viridans (poor dental hygiene)
S. bovis(colon cancer), p.aeruginosa
HACEK organisms

199
Q

Which bacteria tends to cause acute infective endocarditis?

A

S.aureus: sx onset days-weeks

200
Q

Which bacteria tends to cause subacute infective endocarditis?

A

S. viridans: sx onset weeks-months

201
Q

Which 2 clinical findings mean IE should be considered as a diagnosis?

A

Fever and new murmur

202
Q

Name some risk factors for developing infective endocarditis

A

Male, elderly with prosthetic valves
Young IVDU
Young with congenital heart defect
Rheumatic heart disease

203
Q

Which valve does IE typically affect and how is this different in IVDU?

A

Typically: Mitral valve(left side)
IVDU: Tricuspid(right side)

204
Q

Describe the pathophysiology of infective endocarditis

A

Abnormal/damaged endocardium have higher platelet deposition which bacteria can adhere to and cause vegetation
Typically around valves
Can cause regurgitation (aortic and mitral insufficiency-> increased risk of heart failure

205
Q

Describe the signs and symptoms of IE

A

Non specific: fever, non-specific new valve regurgitation, sepsis/emboli of unknown origin, petechiae
Specific:
Osler nodes(finger nodules)
Janeway lesions (painful marks on hands)
Splinter hemorrhages
Roth spots (retinal haemorrhage)

206
Q

Which criteria are used to diagnose infective endocarditis?

A

Duke criteria

207
Q

Describe the Duke criteria

A

Used to diagnose IE
2 major or 1 major+2 minor
Major:
>2 positive blood cultures
TOE echo shows vegetation
Minor:
Immunological signs
IVDU
Septic emboli
1 positive blood culture
Pyrexia

208
Q

Describe the diagnosis of IE

A

ECG: prolonged PR-aortic root abscess
High ESR, CRP, neutrophilia
TOE echo: GS
Blood cultures: 3 sites over 24 hours

209
Q

Describe the treatment of IE

A

S aureus: vancomycin and rifampicin (+gentamicin if prosthetic valve)
S viridans: Benzylpenicillin and gentamicin
For 4-6 weeks
Surgery to replace valve is incompetent

210
Q

Name some potential complications of infective endocarditis

A

Heart failure
Aortic root abscess
Septic emboli->sepsis

211
Q

What is regurgitation and what does it lead to?

A

Defective, floppy valve: leaks through
Causes insufficiency and proximal chamber dilation-loss of structural chamber integrity and strength

212
Q

What is stenosis and what does it lead to?

A

Narrowed valve/lumen->increased upstream pressure
Causes proximal chamber hypertrophy and dilation
Heart becomes rigid: poorly compliant

213
Q

Which main valve disorders cause murmurs?

A

Aortic regurgitation and stenosis
Mitral regurgitation and stenosis

214
Q

How are murmurs best heard?

A

RILE
Right side defects(pulmonary/tricuspid valves)-insipration
Left side defects(aortic/mitral valves)-expiration

215
Q

After which heart sounds do systolic and diastolic murmurs occur?

A

Systolic: after S1
Diastolic: after S2

216
Q

Are most murmurs systolic or diastolic?

A

Systolic

217
Q

In which valvular conditions can you hear systolic murmurs?

A

ASMR:
Aortic stenosis
Mitral regurgitation
Also:
Mitral valve prolapse
Tricuspid regurgitation

218
Q

In which valvular conditions can you hear diastolic murmurs?

A

ARMS:
Aortic regurgitation
Mitral stenosis

219
Q

Where is the aortic valve found?

A

Between the left ventricle and aorta

220
Q

What is aortic stenosis?

A

Narrowing of the aortic valve resulting in obstruction to the left ventricular stroke volume

221
Q

What is the normal area of the aortic valve?

A

3-4cm2

222
Q

At what lumen size would you begin to experience symptoms with aortic stenosis?

A

1/4 of lumen size so 0.75-1cm2

223
Q

What is the most common valve disorder?

A

Aortic stenosis

224
Q

What changes to he heart does aortic stenosis result in?

A

LV dilation and hypertrophy

225
Q

Name 2 conditions that can cause S4

A

Aortic stenosis
Hypertrophic cardiomyopathy-associated with sudden death in young men

226
Q

Describe the causes of aortic stenosis

A

Calcificied aortic heart disease
Congenital bicuspid aortic valve(normally tricuspid)
Rheumatic heart disease

227
Q

Describe the pathophysiology of aortic stenosis

A

Narrowing of aortic valve->decreased stroke volume->increased afterload->increased LV pressure->compensatory LVH->increased oxygen demand->ischaemia

228
Q

Describe the signs/symptoms of aortic stenosis

A

Syncope
Angina
Dyspnoea
Ejection systolic crescendo-decrescendo murmur

229
Q

How can aortic stenosis be diagnosed?

A

ECG
CXR: LVH, calcified aortic valve
Echo: LV size and function, doppler derived gradient and valve area

230
Q

Describe the murmur associated with aortic stenosis

A

Ejection systolic crescendo-decrescendo
Radiating to carotids
Right sternal border
2nd IC space
Prominent S4:LVH
Narrow pulse pressure + slow rising pulse

231
Q

Describe the treatment for aortic stenosis

A

Surgical aortic valve replacement
TAVI(transcutaneous Aortic Valve Implantation)-more at risk patients, stents valve open

232
Q

What is mitral stenosis?

A

Stenosis of the mitral valve->prevents proper LV filling

233
Q

What is the normal lumen size of the mitral valve and at what size would you expect mitral stenosis symptoms?

A

4-6cm2
Sx when <2cm2

234
Q

Name some risk factors for developing mitral stenosis

A

Men
Hx of rheumatic fever
Ageing

235
Q

Name some causes of mitral stenosis

A

Rheumatic heart disease-most common, post strep pyogenes infection
Valve calcification-older patients
Infective endocarditis

236
Q

Describe the pathophysiology of mitral stenosis

A

RHD disease causes mitral reactive inflammation-exacerbated over years with calcification->obstruction of blood flow from left atrium to left ventricle->LA pressure increases causing hypertrophy and dilation

237
Q

Describe the symptoms of mitral stenosis

A

Malar cheek flush
Dyspnoea
Dyspnoea
Haemoptysis
Oedema
Low pitched mid diastolic murmur

238
Q

Describe the murmur and heart sounds associated with mitral stenosis

A

Low pitched mid diastolic murmur
Loudest at apex
Best heard on expiration with patient lying on LHS

239
Q

Describe the investigations carried out to diagnose mitral stenosis

A

Echo: assess valve area, gradient, mobility
ECG: AF and left atrial enlargement
CXR: Pulmonary oedema, LA enlarged

240
Q

Describe the surgical treatment of mitral stenosis

A

Mitral valve replacement
Percutaneous mitral balloon valvotomy

241
Q

Which heart condition is associated with mitral stenosis and why?

A

AF
Causes left atrium hypertrophy->more chances of embolisation as blood is actively pumped from LA harder->Afib

Phase 2a med mine (11 decks)

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