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2A content- Sameera > 6. CARDIOVASCULAR > Flashcards

6. CARDIOVASCULAR Flashcards

1
Q

what value is defined to be hypertension

A

140/90 or above

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2
Q

what value defines malignant hypertension

A

180/110

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3
Q

what is malignant hypertension (3)

A

very high blood pressure that develops quickly and causes organ damage

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4
Q

what are the categories of hypertension and how many cases are in each category and describe the difference between the two

A

primary 90%
secondary 10%
primary has no known cause and secondary has known causes

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5
Q

what is the most common cause of secondary hypertension

A

renal disease

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6
Q

what are the causes of secondary hypertension (6)
3 Cs, 2Ps, 1R

A

renal disease
pregnancy
phaechromocytoma
cushings
conns
coarctation of the aorta (congenital narrowing of the aorta)

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7
Q

why is primary hypertension not usually presented

A

its usually asymptomatic

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8
Q

what are the 4 main areas that malignant hypertension has symptoms in

A

brain, eye, heart and kidneys

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9
Q

how can end organ damage be assessed for hypertension (3)

A

fundoscopy= for papilloedema
urinalysis= for renal function
Echo/ECG= assesses left ventricular hypertrophy

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10
Q

what can malignant hypertension cause in the brain (3)

A

cerebral oedema and haemorrhage and stroke

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11
Q

what can malignant hypertension cause in the eye (2)

A

cotton wool spots
papilloedema

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12
Q

what can malignant hypertension cause in the heart (2)

A

acute heart failure
aortic dissection

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13
Q

what can malignant hypertension cause in the kidneys and what are the symptoms of this (1, 2)

A

acute kidney injury
proteinuria, haematuria

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14
Q

what is the method that hypertension can be diagnosed with 1

A

ambulatory blood pressure
(home blood pressure monitoring)

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15
Q

how is hypertension staged and what are the actions for each stage (3)

A

stage 1: 135/85 (assess risks- including assessing organ damage)
stage 2: 150/95 (medications)
stage 3: 180/110 (malignant- medications)

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16
Q

what is the treatment approach for stage 1 hypertension 1

A

BP monitored every 5 years

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17
Q

if the bp is measured at GP and is 140/90 then what is the next step

A

check ambulatory blood pressure at home

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18
Q

what is always the first line of management for stage 2 hypertension 2

A

lifestyle changes and medication combined

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19
Q

what is the treatment for a patient with malignant hypertension and signs of renal/ eye damage (2)

A

same day admission
start antihypertensive drug immediately

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20
Q

what two things are offered to a person who has been diagnosed with hypertension

A

assessment of Cv risk
investigation for secondary hypertension

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21
Q

what is the treatment for under 55s and not of African/ Caribbean origin (2)

A

ace inhibitor or angiotensin receptor blocker

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22
Q

what is the treatment for over 55s and of African/ Caribbean origin (1)

A

calcium channel blocker

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23
Q

what is the 2nd step if one drug is not controlling hypertension for the two categories of people to treat

A

<55 not A/C origin= CCB or thiazide like diuretic eg indapamide can be added
>55 of A/C origin= ACEi or ARB or thiazide like diuretic eg indapamide can be added

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24
Q

if a patient is on ACEi and BB already but still symptomatic what should be given to them 1

A

spironolactone

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25
Q

give an example of an ARB, ACEI, beta blocker, calcium channel blocker

A

losartan, ramipril, bisoprolol, amlodipine

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26
Q

what is ACEi contradicted in 3

A

asthma and pregnancy and renal stenosis

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27
Q

what is a side effect of ACEi and what can be given instead

A

dry long term cough
ARB- losartan

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28
Q

side effect of beta blockers 1 and what can this cause 1

A

postural hypotension which cause cause loss of consciousness

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29
Q

what is the first line medication for diabetics with hypertension

A

ACEi

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30
Q

what happens when hypertension persists even when multiple medications are prescribed (2)

A
  1. talk about adherence
  2. add a beta blocker or spironolactone
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31
Q

what happens in ischaemic heart disease and what is the effect on cardiac myocytes

A

cardiac myocytes r damaged due to insufficient oxygenated blood supply

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32
Q

what are the two causes of ischaemic disease (2)

A

coronary artery occlusion caused by atherosclerosis
insufficient blood supply caused by valvular disease or anaemia

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33
Q

rate the severity of ischaemic heart disease (4)

A

stable angina-> unstable angina-> NSTEMI-> STEM

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34
Q

what are the investigations of ischaemic heart disease 3 (2, 3, 3)

A
  1. resting ECG/ exercise ECG to induce ischaemia
  2. blood tests: HBA1C, FBC, cholesterol profile
  3. biological markers: troponin, creatine kinase and myoglobin
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35
Q

what is the treatment for unstable angina and NSTEMI (4)

A

BMOAN; beta blocker, morphine, oxygen, aspirin, nitrate
bmoaN for Nstemi and uNstable angina

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36
Q

what is the treatment for acute and for chronic ischaemic heart disease and what type of drug is it (1,1)

A

acute: clopidogrel (anti-platelet)
chronic: beta blocker eg atenolol

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37
Q

what is the treatment for acute STEMI (2)

A

PCI if available, otherwise fibrinolysis (alteplase/ streptokinase)

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38
Q

whata re the surgical interventions for ischaemic heart disease 2 and what does each stand for

A

PCI- percutaneous coronary intervention
or CABG- coronoary artery bypass graft

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39
Q

for what patients is CABG prefered over PCI 2

A

patents with diabetes over 65 years

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40
Q

what is acute coronary syndrome and what does it include

A

umbrella term including unstable angina, STEMI and NSTEMI

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41
Q

how is the diagnosis done for acute coronary syndromes

A

ECG to see if there is ST elevation
if there is ST elevation= STEMI
if no ST elevation, then a troponin test is done
if high troponin then its is a NSTEMI, if normal then it is unstable angina

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42
Q

what are the ECG changes shown for unstable angina, NSTEMI and STEMI (2, 2, 2)

A

unstable: normal/ ST depression and T wave inversion
NSTEMI: ST depresion and T wave inversion
STEMI: ST elevation in leads 2-3, pathological Q waves

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43
Q

what is the most common cause of reduced blood flow to the heart

A

coronary artery disease

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44
Q

what is angina

A

blood supply is less than the demand in the heart

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45
Q

what is stable angina induced by (3)

A

physical exertion, emotional stress or the cold

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46
Q

when does angina cause symptoms

A

when vessel is 70-80% occluded

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47
Q

how can stable angina be relieved (2)

A

rest or sublingual Glyceryl trinitrate spray

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48
Q

symptoms of stable angina (4)

A

central chest tightness/ discomfort
pain radiating to arms, neck or jaw
dyspnoae
sweating

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49
Q

what is the main investigation for stable angina and results (2)

A

ECG- ST interval can be normal or depressed and no T wave inversion

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50
Q

treatment for stable angina in order (4)

A

modify risk factors: stop smoking, exercise etc
GTN spray for relief
beta blocker
revascularisation (PCI/CABG)

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51
Q

how does a GTN spray work

A

PDE-5 inhibitor- causes coronary artery vasodilation

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52
Q

what is the first medicine treatment for stable angina 1 and what is after this 2 and names

A

GTN spray
beta blockers/ CCB
eg verapamil/ diltiazem

VERAPAMIL
DILTIAZEM

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53
Q

differentials for stable angina (chest pain during exertion) 4- 3 r non heart related

A

pericarditis
Pulmonary E
mbolism
chest infection
Gastro Oesophageal Reflux Disease

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54
Q

what is unstable angina (2)

A

chest pain that occurs at rest, not relieved by GTN spray

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55
Q

compare unstable and stable angina chest pain in terms of duration and frequency

A

unstable lasts for longer and occurs more frequently

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56
Q

what is the first thing to do with unstable angina

A

immediate admission to hospital

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57
Q

what causes a STEMI vs NSTEMI

A

STEMI= complete occlusions of a major coronary artery
NSTEMI=partial occlusion of a major coronary artery or complete occlusion of a minor coronary artery

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58
Q

compare the heart damage in STEMI vs NSTEMI

A

STEMI=causes full thickness damage of heart muscle
NSTEMI=causes partial thickness damage of heart

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59
Q

after which results are STEMIs vs NSTEMIs diagnosed

A

STEMI= ecg results
NSTEMI= on troponin results (high)

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60
Q

what are the biological markers of STEMI and NSTEMI (3)

A

both have an increase in troponin, myoglobin and CK levels

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61
Q

what is prinzmetal’s angina caused by and when does it happen

A

caused by coronary vasospasm
occur at rest/ night

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62
Q

what does the ECG show for prinzmental’s angina and what are the characteristic of patients that have this

A

ST elevation
seen in cocaine users

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63
Q

compare an MI and angina in terms of occlusion level and permanent damage (2)

A

angina is usually due to narrowed coronary arteries but MI is due to blocked
angina has no permanent heart damage but MI has permanent heart damage

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64
Q

what are the 2 types of MI and their respected causes

A

type 1= due to ischaemic heart disease
type 2= due to increased demand or coronary artery vasospasm

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65
Q

risk factors for MI (4 non modifiable, 2 modifiable)

A

older age, male sex, family history of ischaemic heart disease, ethnicity (blacks and hispanics), smoking, sedendary lifestyle

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66
Q

symptoms of MI (6)

A

central pain, sweating, dyspnoea, palpitations, pallor, nausea

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67
Q

what is significant about diabetics that get MIs and what is the complication of this

A

MIs can be silent because no cardiac pain is felt from diabetic neuropathy
these patients can die form sudden collapse

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68
Q

what can STEMI show on an ECG a few days after the MI (3)

A

pathological Q waves, hyperacute T waves, LBBB

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69
Q

what is the treatment for MI 2

A

300mg loading dose of aspirin then maintenance dose of 75mg

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70
Q

differentials for MI (5)

A

pericarditis
myocarditis
pulmonary embolism
gastro oesophageal reflex disease
aortic dissection

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71
Q

complications of MI (10)- acronym

A

DARTHVADER
death
arrhythmia
rupture
tamponade
heart failure
valve disease
aneurysm
dressler syndrome (pericarditis due to injury to heart)
embolism
recurrence/ regurgitation

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72
Q

compare systolic and diastolic heart failure

A

systolic heart failure= inability of ventricle to contract properly
diastolic heart failure= inability of the ventricle to relax and fill

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73
Q

what are the ejection fraction values for diastolic and systolic heart failure

A

diastolic: EF > 40%
systolic: EF <40%

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74
Q

what r common causes of systolic failure 2

A

MI
poorly controlled HPT

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75
Q

what is cardiac failure

A

heart unable to pump enough blood to supply metabolising tissues in the body

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76
Q

compare left sided and right sided heart failure causes (3,3)

A

left causes: hypertension, coronary artery disease, valvular disease (divided into diastolic and systolic)
right
right causes: left ventricular failure, right MI or pulmonary hypertension

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77
Q

symptoms of left sided failure (8)

A

respiratory crackles
pink-tinged sputum
tachycardia
fatigue
CYANOSIS
EXERTION DYSPNOEA
cough
PULMONARY oedema due to vessel backflow

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78
Q

symptoms of right sided failure (5)

A

ASCITES
hepatosplenomegaly
WEIGHT GAIN
palpable JVP
PERIPHERAL OEDEMA due to systemic venous backflow

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79
Q

why is there increased jugular venous pulse? 1 and what condition is this indicative 1

A

due to increased pressure in right atrium
venous hypertension

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80
Q

what is myopathic heart failure

A

disease of the heart muscle that affects its size/ shape/ thickness and makes it harder for the heart to pump sufficient blood to the rest of the body

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81
Q

what is hypertensive heart failure

A

long term heart failure that develops over a long period of time in people who have hypertension

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82
Q

what is cor pulmonale heart failure and what does this lead to

A

enlargement of right ventricle which causes right side heart failure

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83
Q

what can cor pulmonale cause 3

A

venous overload, peripheral oedema and hepatic congestion

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84
Q

what can disease of lung/ pulmonary vessels cause 2 and what does this lead to 1, give an example of such a disease

A

pulmonary hypertension and right ventricular hypertrophy
leads to right side heart failure
COPD

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85
Q

what is congestive heart failure

A

failure on both sides of heart

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86
Q

what are the two methods the body uses to compensate for heart failure (2) and why is this only effective short term?

A

RAAS system activation (increased salt and water reabsorption to increase bp)
sympathetic system activation (increases inotrophy and chronotrophy)
short term as high RAAS and SNS activation exacerbates fluid overload

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87
Q

compare inotrophy and chronotrophy

A

inotrophy- force of heart contraction
chronotrophy- rate of heart contraction

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88
Q

what is the most common cause of heart failure

A

coronary artery occlusion

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89
Q

causes of cardiac failure (7- 4 heart and 3 non heart)

A

ischaemic heart disease, cardiomyopathy, valvular heart disease, arrythmias, anaemia, excess alcohol,
hyperthyroidism

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90
Q

risk factors for cardiac failure (5)

A

65+, african athnicity, male, obesity, history of MI

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91
Q

clinical signs of cardiac failure (7)- remember mneumonic

A

cyanosis, murmers, COUGH, oedema, displaced apex beat, orthopnoea, resp crackles

(many cardiac organs can omit deaths rhythm)

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92
Q

compare acute and chronic cardiac failure in terms of duration and emergency

A

chronic= occurs over time
acute= occurs suddenly, more of an emergency

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93
Q

acute cardiac failure treatment (4)
remember mneumonic

A

oxygen, morphine, furosemide, GTN spray
OMFG

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94
Q

explain chronic cardiac failure treatment- only lifestyle (3)

A

lifestyle: stop smoking, watch diet, avoid NSAIDs

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95
Q

explain chronic cardiac failure treatment- meds only (remember mneumonic) 4 lines

A

1st line- ACEi and Beta blocker
2nd- ARB and nitrate
3rd- cardiac resynchronisation or digoxin
4th-diuretics eg furosemide for symptoms relief

ABANCDD

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96
Q

how do diuretics work when treating heart failure

A

reduces blood volume which decrease blood pressure and reduces how hard the hear has to work

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97
Q

what four drugs can deal with reduced ejection fraction but what is a risk of these drugs

A

ACEi/ ARB/ beta blocker/CCB
increases likelihood of falls

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98
Q

what is the first line of treatment for oedema

A

diuretics

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99
Q

what is the marker for chronic heart failure but what is it not?

A

BNP
not diagnostic

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100
Q

what are the 2 types of murmurs and which is more common

A

systolic or diastolic
systolic is more common

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101
Q

what are the two types of systolic murmurs (remember mneumonic)

A

aortic stenosis
mitral regurgitation
ASMR

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102
Q

what are the two types of diastolic murmurs (remember mneumonic)

A

aortic regurgitation
mitral stenosis
ARMS

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103
Q

what is valve regurgitation and what does this lead to 2 and how does this affect the heart

A

floppy valve
= proximal chamber dilation and hypertrophy
which leads to heart becomes huge and rigid and poorly compliant

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104
Q

what is valve stenosis and what does this lead to 2 and how does this affect the heart

A

narrowed valve opening
=proximal chamber dilation and hypertrophy
which leads to heart becomes huge and rigid and poorly compliant

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105
Q

what are the three investigations done for valve disorders and what does each show

A

Echo- heart and valve function whilst beating
ECG- hypertrophy
CXR- calcifications/ masses of valves and aortic root

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106
Q

what is the GS diagnostic investigation for ALL valvular diseases and what does this look at

A

echocardiograms- looks at valve function during the cardiac cycle

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107
Q

what is the most common valve disorder

A

aortic stenosis

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108
Q

2 risk factors for aortic stenosis

A

calcified aortic value disease
congenital bicuspid aortic valve

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109
Q

pathophysiology of aortic stenosis- how does it cause ischaemia of heart 3

A
  1. narrowed aortic valve opening causes reduced blood flow out of the left ventricle
  2. the heart compensates to pump out more blood by undergoing left ventricular hypertrophy
  3. this increases cardiac oxygen demand, leading to ischaemia
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110
Q

symptoms of aortic stenosis (2)

A

syncope on exertion
dyspnoea

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111
Q

what is the murmur for aortic stenosis 3

A

ejection systolic crescendo-decrescendo murmur at right sternal border 2nd ICS which radiates to carotids

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112
Q

what is the heart sound for aortic stenosis 1

A

prominant S4

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113
Q

investigations for aortic stenosis (3) and what would each show

A

GS: echocardiogram
ECG: ventricular hypertrophy
chest x-ray: calcified aortic valve

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114
Q

what is the treatment for aortic stenosis (2) and which is less invasive

A

surgical aortic valve replacement
or TAVI (transcutaneous aortic valve implantation) which is less invasive

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115
Q

differential for aortic stenosis

A

mitral regurgitation

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116
Q

causes of mitral regurgitation (4)

A

infective endocarditis
Post MI= papillary muscle dysfunction or ischaemic mitral valve
connective tissue disorders

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117
Q

what is the pathophysiology for mitral regurgitation and how it causes right ventricular dysfunction

A
  1. leaky mitral valve= blood regurgitates into the left atrium
  2. = left atrial enlargement
  3. left ventricular hypertrophy as smaller volume of blood that can be pumped out
  4. = pulmonary hypertension
  5. = right ventricular dysfunction
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118
Q

symptoms of mitral regurgitation (2) and explain both

A

exertion dyspnoea- due to pulmonary hypertension
symptoms of heart failure- due to right side dysfunction

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119
Q

what is the mitral regurgitation murmur 3

A

pan systolic blowing murmur at apex radiating to axilla

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120
Q

what r the heart sounds for mitral regurgitation 2

A

soft S1, prominent S3 in heart failure

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121
Q

investigations for mitral regurgitation (2)

A

GS- echo
CXR and ECG

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122
Q

treatment for mitral regurgitation (3) and what r the 2 conditions for this surgery (mentioned in no. 3)

A

vasodialtors eg ACEi
rate control eg beta blockers
mitral valve surgery if ejection fraction is less than 60% or new onset atrial fib

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123
Q

causes of mitral stenosis (4) and what is the main cause

A

rheumatic heart disease
untreated streptococcal infections- MC
mitral valve calcification
infective endocarditis

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124
Q

pathophysiology of mitral stenosis- how does it cause right ventricular hypertrophy

A

more blood remains in left atrium so higher pressure in atria causes atrial hypertrophy
this causes pulmonary hypertension
this causes right ventricular hypertrophy

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125
Q

2 signs and 1 symptom of mitral stenosis and what is the characteristic of the symptom presentation

A

atrial fibrillation
malar cheek flush
dyspnoea
symptoms can appear years later

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126
Q

what is the murmur for mitral stenosis and how can this be heard best and how can u position the patient to hear this murmur

A

low pitched mid diastolic murmur, loudest at apex
best hear on expiration when patient lying on left

3Ls (Low pitched, Loudest at apex, Left side inspiration for patient)

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127
Q

investigations for mitral stenosis (3)

A

echocardiogram
ECG
CXR

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128
Q

treatment for mitral stenosis (4)

A

rate control- beta blockers
diuretics- furosemide
surgical mitral valve replacement or percutaneous balloon mitral valvotomy (less invasive)

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129
Q

what is aortic regurgitation

A

aortic valve doesnt close tightly (leaky aortic valves), allowing blood to leak into left ventricle from aorta during diastole

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130
Q

acute and chronic causes of aortic regurgitation (2,3)

A

acute:
aortic dissection
infective endocarditis
chronic:
congenital bicuspid aortic valve
rheumatic heart disease
connective tissue disorders (M/ED)

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131
Q

explain the pathophysiology of aortic regurgitation and how does this cause ischaemia of the heart

A

back flow is compensated for with left ventricular hypertrophy
this causes left ventricular hypertrophy and causes increased cardiac oxygen demand which causes ischaemia

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132
Q

1 symptom and 2 signs of aortic regurgitation

A

exertional dyspnoea
collapsing carrigon pulse with wide pulse pressure

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133
Q

what is the aortic regurgitation murmur

A

early diastolic blowing decrescendo murmur at right sternal border 2nd ICS

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134
Q

what is significant about the mitral stenosis murmur

A

longer the murmur means it is more severe

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135
Q

investigations for aortic regurgitation (3)

A

echocardiogram
ECG
CXR

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136
Q

treatment for aortic regurgitation 3

A

IE prophylaxis
vasodilators ie ACEi
monitor progression and do aortic valve replacement if symptoms r getting worse

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137
Q

what is a differential for aortic regurgitation

A

IE

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138
Q

what is infective endocarditis an infection of

A

infection of endocardium (inner lining of the heart) and valves

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139
Q

what are the two causes of IE

A
  1. causative bacteria
  2. colonising abnormal endothelium (vegetations)
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140
Q

what valve is affected in IE and what is the exception

A

mitral valve typically
tricuspid in IV drug users

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141
Q

risk factors for IE (6)

A

poor dental hygeine
prosthetic valve
intravenous drug use
rheumatic heart disease
male
elderly
2 lifestyle, 2 to do with heart, 2 non-modifiable risk factors

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142
Q

3 bacterial causes of IE, where from and which are the most common

A

most common= staphylococcus aureus (from intravenous drug use)
strep viridian’s due to mouth surgery/ dentists (common in developing countries)
staph epidermis due to prosthetic valve surgery

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143
Q

pathophysiology of IE vegetation formation

A

damaged endocardium has increased platelet deposition and bacteria adheres to this, causing vegetation to be formed

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144
Q

signs of IE 4

A

splinter haemorrhages
Janesway lesions
Osler nodes
Roth spots

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145
Q

symptoms of IE (4

A

fever
confusion
night sweats
finger clubbing

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146
Q

what are the specific signs of IE caused by

A

vasculitis (inflammation of small blood vessels)

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147
Q

when should you suspect IE

A

if someone comes in with a fever and a new murmur, suspect IE

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148
Q

investigations for IE (3 plus diagnostic)

A
  1. blood cultures (3 separate from different sites over 24 hours, before antibiotics)
  2. TOE for diagnosis
  3. FBC- high CRP, ESR and neutrophillia
  4. ECG if long PR interval= aortic root abscess
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149
Q

how is IE diagnosed (criteria)

A

duke’s criteria= either of these:
1. 2 separate blood cultures are positive with typical pathogens that cause IE
2. new valvular regurgitation OR echocardiogram positive for IE (shows vegetations)

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150
Q

what is the advantage of TOE over TTE and what they stand for

A

trans-oesophageal echocardiogram
Transthoracic echocardiogram
TOE is more sensitive and diagnostic

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151
Q

treatment for IE 3

A

prolonged course of antibiotics (6 weeks)
2 weeks IV then switch to oral
if valve is incompetent, replace valve with a different prosthetic

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152
Q

what antibiotics should be prescribed for IE (Staph, non staph, MRSA, prosthetic valve, unknown)

A

staph= flucloxacillin and rifampicin (replace flucloxacillin with vancomycin if MRSA)
strep= benzylpenicillin and gentamicin
MRSA= vancomycin and rifampicin
gentamicin for prosthetic valve
1st line when the organism is unknown= ampicillin and gentamicin

153
Q

differentials for IE 3

A

SLE
antiphsopholipid syndrome
meningitis

154
Q

what is pericarditis and what can accompany it

A

acute inflammation of pericardium
with or without effusion

155
Q

who does pericarditis usually affect (2)

A

typically affects males 20-50 years old

156
Q

causes of pericarditis (in order of how common) (5)

A

mostly idiopathic
viral infections
trauma eg MI
bacterial infections (mycobacterium tuberculosis)
fungal infections

157
Q

pathophysiology of pericarditis (3)

A
  1. acute inflammation of pericardium
  2. the inflated pericardial layers rub against each other and exacerbate further inflammation
  3. this can lead to exudate building up in the pericardial space
158
Q

what are the two types of effusion that can occur in pericarditis

A

serous or haemorrhagic effusion can occur

159
Q

symptoms of pericarditis (4)

A

chest pain which extends to the left shoulder tip that is worse on inspiration and lying down
fever, dyspnoea, cough

160
Q

what is formed in constrictive pericarditis and what does it impair

A

this is a late complication of acute pericarditis where
granulation tissue formation in pericardium means impaired diastolic filling

161
Q

what is pericardial friction rub and when is it present (2 things to mention about what it sounds like)

A

high pitched scratchy sound heart loudest on the midline during inspiration
pericarditis

162
Q

investigations for pericarditis and results (3) and which one is diagnostic

A

CXR: cardiomegaly due to effusion
ECG: saddle shaped ST elevation and PR depression (diagnostic)
FBC: high ESR and WCC

163
Q

treatment for pericarditis (3)

A

NSAIDs (ibuprofen)
and colchicine for 3 weeks
antibiotics if bacterial TB infection

164
Q

treatment for TB (remember mneumonic)

A

RIPE
rifampin
isoniazid
pyrazinamide (pirate names zinna then mide)
ethambutol

165
Q

complication of pericarditis 3

A

cardiac tamponade
myocarditis
constrictive pericarditis

166
Q

what condition causes pericardial effusion

A

acute pericarditis

167
Q

explain at what point pericardial effusion becomes a medical emergency and what is another name for this

A

when it compromises ventricular filling
cardiac tamponade

168
Q

1 symptom and 3 signs of pericardial effusion

A

soft and distant heart sounds
muffled apex beat
raised JVP (jugular vein pulse)
dyspnoea

169
Q

investigations for pericardial effusion (3)

A

CXR: large globular heart
ECG: low voltage QRD complexes
Echocardiogram (diagnostic)

170
Q

management for treating pericardial effusion (2)

A

treat the underlying cause eg pericarditis
most resolved spontaneously

171
Q

what is cardiac tamponade and how does it affect the ventricles

A

ventricles unable to fill because of accumulation of fluid in pericardial space due to pericardial effusion

172
Q

how is cardiac output reduced in cardiac tamponade

A

accumulation of fluid in pericardial space causes compression of heart chambers which decreases venous return (pressure gradient)
this decreases the filling of the heart and reduces the cardiac output

173
Q

SIGNS not symptoms of cardiac tamponade (4)

A

Beck’s triad:
muffled heart sounds
raised jugular venous pulse
hypotension
pulses paradoxus (large decrease in stroke volume so the systolic blood pressure drops by more than 10mmHg on inspiration)

174
Q

investigations for cardiac tamponade 3 and results of each

A

CXR: large globular heart
ECG: low voltage QRS complexes
Echocardiogram: late diastolic collapse of right atrium

175
Q

treatment for cardiac tamponade

A

pericardiocentesis (drainage of fluids from pericardial space)

176
Q

differential diagnosis for cardiac tamponade

A

Kaussmal’s
also causes a paradoxical increase JVP with inspiration

177
Q

what is medically classed as an abdominal aortic aneurysm 2

A
  1. permanent aortic dilation
  2. diameter over 3cm
178
Q

where does AA occur (1,1) and what is it associated with (1,1)

A

typically infrarenal (below renal arteries) - associated with elderly men
can occur in thoracic aorta- typically associated with Marfans and Ehlers Danlos syndromes

179
Q

risk factors for AAA (4)

A

smoking, obesity, family history, age

180
Q

what is the pathophysiology for AAA (1) and what risk does this increase (1)

A

dilation of all 3 layers of the artery
increased risk of rupture

181
Q

symptoms of AAA (4) and when do these symptoms occur (1)

A

sudden epigastric pain radiating to flank
pulsatile mass in abdomen
hypotension
tachycardia
asymptomatic until rupture

182
Q

investigations for AAA (1st line/ diagnostic) 1 ONLY

A

abdominal ultrasound to look at aorta

183
Q

treatment for AAA if not ruptured yet (2 classifications for different treatment pathways)

A

for asymptomatic and under 5.5cm monitor
for symptomatic and/or over 5.5cm then open surgery/ EVAR- extravascular aneurysm repair

184
Q

treatment for AAA if ruptured (4)- step by step pathway

A

stabilise: ABCDE, fluids, transfusion
AAA graft surgery

185
Q

differential diagnosis for AAA

A

acute pancreatitis

186
Q

what is aortic dissection and what is it due to

A

tear in intima causing blood to ‘dissect’ through the media and the layers
due to mechanical wall stress

187
Q

risk factors for aortic dissection (main, 4)

A

hypertension (main)
family history
trauma
smoking
connective tissue disorder eg Marfans/ Ehlers Danlos sydnrome

188
Q

2 locations of aortic dissection and their classification

A
  1. Sinotubular junction (where aortic root become ‘tubular’ aorta near aortic valve)-most common (location is classed as A)
  2. distal to left subclavian artery in descending aorta (location is classed as B)
189
Q

pathophysiology of aortic dissection and how can it cause organ failure

A

blood dissects through the media and intima and pools in the false lumen
this causes decreased perfusion to end organs which can cause organ shock/ failure

190
Q

symptoms of aortic dissection (6)

A

sudden onset of ripping/tearing chest pain
hypotension
NEW AORTIC REGURGITATION MURMUR
neurological deficit eg fainting
CARDIAC TAMPONADE
DECREASE IN LEFT ARM PERIPHERAL PULSE

A in Aortic= aortic regurgitation murmur
D in dissection= decrease in left peripheral pulse
SS in dissection= syncope (fainting) and sudden onset of ripping/ tearing chest pain
C in dissection= cardiac tamponade
ion in dissection= hypotension

then hypotension

191
Q

investigations and results for aortic dissection (2, gold standard)

A

chest x-ray: widened mediastinum
gold standard is TOE- more sensitive and specific for aortic dissection- shows intimal flap and false lumen
CT angiogram- shows intimal flap and false lumen (for more stable patients)

192
Q

differential diagnosis for aortic dissection (1)

A

MI

193
Q

treatment for aortic dissection (2)
prevention for aortic dissection (2)

A

open surgical repair (for location A) or endovascular aneurysm repair (for location B)
prevention: beta blocker eg labetolol to prevent reflex tachycardia
and sodium nitroprusside vasodilator

194
Q

complications of aortic dissection (4)

A

cardiac tamponade
aortic regurgitation
pre-renal AKI
stroke

A in aortic= aortic regurgitation
R in aortic= (pre) renal AKI
i in aortic= ischaemic stroke
c in arotic= cardiac tamponade

195
Q

what are the two main types of venous thromboemboli

A

DVT and PE

196
Q

risk factors for venous thromboembolism (think about virchows triad)- 4 1 2

A

hypercoagulability (due to pregnancy, obesity, sepsis, malignancy)
venous stasis (due to immobility-causes aggregation of clotting factors)
endothelial injury (smoking, trauma)

197
Q

what is DVT

A

thrombus in deep leg vein

198
Q

compare concern of a DVT above and below the calf

A

if below calf, less concerning as there r many minor veins there
if above calf, this can be life threatening so there r more major veins and occlusion can impede distal flow

199
Q

symptoms of DVT (3)

A

unilateral swollen calf
warm and oedematous veins
blue leg if occlusion of a large vein

200
Q

diagnosis criteria 1 and 2 investigations for DVT. What is the GS

A

diagnosis based on Wells score being 2 or above:
diagnostic test: raised D-dimer and duplex ultrasound (GS)

201
Q

treatment for DVT (2 med and 2 non pharmological) and what is this treatment plan the same as

A
  1. DOAC (LMWH if renally impaired)
  2. utilise mobilisation and compression stockings
    small PE
202
Q

differential for DVT

A

cellulitis

203
Q

what is PE

A

DVT embolisms and lodges in the pulmonary artery circulation

204
Q

how does PE cause right sided failure and what is the medical term for this

A

right ventricle strains to overcome PE
=pulmonary hypertension
=right sided heart failure

cor pulmonale

205
Q

symptoms of PE (7)

A

sudden onset pleuritis chest pain
dyspnoea
tachycardia
hypotension
increase JVP
ankle oedema

206
Q

investigations for PE (4)- 1st line, diagnostic, 1 other and diagnosis criteria

A

first line: high D-dimer
diagnostic: CT pulmonary angiogram (key!)
ECG: sinus tachycardia, new RBBB, S1Q3T3 (large S wave in lead 1, Q wave in lead 3, inverted T wave in lead 3)
Diagnosis based on Well’s score being 4 or above

207
Q

treatment for large PE and how common is this

A

thrombolytic eg alteplase
uncommon

208
Q

treatment for small PE (2) and how common is this (what is the contraindication and what can be given instead)

A

1) heparin given as it works faster, is more potent and has reduced risks of coagulation
2) anticoagulants given ie DOACs like apixiban/ rivaroxiban
contraindication for renal impairment- give LMWH eg dalteparin
more common

209
Q

what is peripheral vascular disease

A

ischaemia of lower limb arteries

210
Q

risk factors for PVD (6)

A

smoking
hypertension
ageing
obesity
chronic kidney disease
type 2 DM

211
Q

what is the classification for acute PVD, when is there pain, how occluded is the lumen and what is the cause of the occlusion

A

intermittent claudification
pain on exertion
partial lumen occlusion
atherosclerotic

212
Q

what is the classification for chronic PVD, when is there pain, and what is there a risk of getting 2

A

critical limb ischaemia
pain at rest
gangrene and infection

213
Q

what occurs when blood supply is occluded (3)

A

irreversible nerve and muscle damage within 6 hours and skin changes r the last to appear, mostly likely gangrenous changes

214
Q

symptoms of PVD (4) and test and positive result for it 1

A

skin changes: colour, cooler and ulcerations
pulsatile regions (due to turbulent blood flow)
burger test positive: elevate leg 45 degrees for 1 min= pallor then reactive hyperaemia

215
Q

why does chronic ischaemic pain occur at night (2) and what can this lead to (2)

A

due to elevation of limb which can further reduce blood supply to the distal part of the limb which can cause tissue loss (ulcers and gangrene)

216
Q

what does ABPI stand for, what is it what is classed as normal and explain what the value for results means

A

ankle brachial pressure index
compares blood pressure in upper and lower limbs as a ratio
0.5-0.9= intermittent claudication
less than 0.5= critical chronic limb ischaemia
absent/0= risk of acute limb threatening ischaemia

217
Q

what are the investigations for PVD (3)

A
  1. ABPI
  2. colour duplex ultrasound imaging- assesses degree of stenosis
  3. CT angiography if surgery is considered
218
Q

treatment for intermittent claudification (2)

A
  1. reduce risk factors eg stop smoking
  2. exercise programme for intermittent which trains through the pain to stimulate collateral blood supply growth
219
Q

treatment for chronic limb ischaemia (1)

A

revascularisation surgery (PCI if small, bypass if longer)

220
Q

treatment for acute limb-threatening ischaemia (1)

A

surgical emergency requires revascularisation within 4-6 hours otherwise there is an increase amputation risk

221
Q

complications of PVD (3)

A

amputation
permanent limb weakness
rhabdomyolysis

222
Q

what usually happens to healthy patients with acute limb ischaemia

A

their body develops collaterals (extra vessels to alternatively vascularise the limb around the faulty blood vessels)

223
Q

what are the 6 Ps and how can they assess the severity of the acute limb ischaemia

A

6 Ps: pulselessness, pallor, pain, persistently cold, paralysis, parasthesia
->the more of these 6 Ps that you have, the more deadly the ischaemia

224
Q

what is tachycardia

A

bpm over 100

225
Q

what are the conditions with tachycardia (5)

A

A fib
atrial flutter
Wolff parkinson white
supraventricular tachycardia
ventricular tachycardia

226
Q

what is bradycardia

A

bpm under 60

227
Q

what are the conditions with bradycardia (6)

A

RBBB
LBBB
primary, secondary and tertiary heart block
sinus bradycardia

228
Q

what 6 arrythmias are there

A

atrial fibrillation
atrial flutter
wolff-parkinson white (AVRT)
long QT syndrome
AV blocks
Bundle branch blocks

229
Q

what is the atrial firing rhythm of atrial fibrillation

A

irregular irregular atrial firing rhythm

230
Q

what is the most common cardiac arrythmia

A

atrial fibrillation

231
Q

causes of atrial fibrillation (4)

A

heart failure
hypertension
secondary to mitral stenosis
sometimes idiopathic

232
Q

risk factors of atrial fibrillation (5)

A

60+
T2DM
hypertension
valve defects eg mitral stenosis
past history of MI

233
Q

explain the pathophysiology of atrial fibrillation and how it increases the risk of thromboembolic events (3)

A
  1. rapid firing rate 300-600 bpm causes atrial spasm (not co-ordinated contraction like normal)
  2. blood is not efficiently pumped to ventricles
  3. this decreases cardiac output and increases the risk of thromboembolic events
234
Q

symptoms of A fib (6)

A

palpitations
irregularly irregular pulse
thromboemboli eg ischaemic stroke
chest pain
SYNCOPE
HYPOTENSION

6 Ps- palpitations, pulse, pain in chest, (hy)potension, (P)FAINTING and thromPoemboli

235
Q

what are the 3 types of atrial fibrillation and what are their patterns

A

paroxysmal (episodic)
persistant (longer than 7 days)
permanent (sinus rhythm unrestorable)

236
Q

diagnostic investigation for atrial fibrillation (1, 3)

A

ECG is diagnostic:
irregularly irregular pulse
narrow QRS (less than 120ms
no p waves (fibrillatory squiggles instead)
acronym= PIQ

237
Q

acute treatment for atrial fibrillation

A

synchronised cardioversion DC (shock heart back into normal rhythm)

238
Q

long term treatment for atrial fibrillation (2 management approaches)

A

medical approach: beta blocker/ CCB eg verapamil and anticoagulation
surgical approach

239
Q

surgical treatment for atrial fibrillation, what is it for

A

radio frequency ablation
intends to prevent future episodes

240
Q

complications of atrial fibrillation (3)

A

heart failure
ischaemic stroke
mesenteric ischaemia

241
Q

what is atrial flutter firing rhythm (2) and compare it for atrial fibrillation (2)

A

irregular organised atrial firing
less common and less severe than atrial fibrillation

242
Q

pathophysiology of atrial flutter 2

A
  1. fast atrial ectopic firing 120-350 bpm
  2. this causes atrial spasm
243
Q

symptoms of atrial flutter (2)

A

dyspnoea
palpitations

244
Q

investigation for atrial flutter (1) and results (2)

A

ECG diagnostic: f wave ‘saw tooth’ pattern, often with a 2:1 blocker (2 p waves for every QRS)

245
Q

treatment for atrial flutter that is acutely unstable

A

DC synchronised cardioversion

246
Q

treatment for atrial flutter that is stable (2) and what is the purpose of these treatments

A
  1. rhythm/ rate control with beta blocker and oral anticoagulation
  2. radio frequency ablation
    to prevent future episodes
247
Q

what is the wolff parkinson white AVRT

A

accessory pathways for conduction= bundle of Kent

248
Q

what is an AVRT

A

means an accessory pathway exist for impulse conduction

249
Q

explain the pathophysiology of the wolff parkinson white arrythmia (syndrome)

A

pre-excitation syndrome (excite ventricle faster than typical pathwa)

250
Q

what is the cause of wolff parkinson white (1)

A

often hereditary

251
Q

what are the symptoms of wolff parkinson white (3)

A

palpitations
dizziness
dyspnoea

252
Q

what are the ECG changes seen in Wolff parkinson white (3)

A

slurred delta waves
short PR interval
wide QRS complex
acronym= QuPiD

253
Q

what is the treatment for wolff parkinson white (3)

A
  1. valsalva manoeuvre and carotid massage
  2. IV adrenaline (temporarily ceases conduction- warn patient it feels like dying)- 6mg then 12mg, then 12 mg and additional doses if unsuccessful
  3. radiofrequency ablation of bundle of Kent
254
Q

what is long QT syndrome and what type of arrythmia does this lead to?

A

congenital channelopathy disorder where mutation affects cardiac ion channels
=ventricular taachycardia

255
Q

what is a typical long QT interval in long QT syndrome

A

QT interval is 480ms +

256
Q

what are the 4 causes of long QT syndrome

A
  1. Romano Ward syndrome (autosomal dominant)
  2. Jerrell Lange Nelson syndrom (autosomal recessive)
  3. hypokalaemia and hypocalcaemia (not inherited)
  4. drugs eg amiodarone and magnesium
257
Q

what are two examples of long QT syndrome

A

torsades de pointes
ventricular fibrillation

258
Q

what is torsades de pointes, what does this look like on an ECG

A

polymorphic ventricular tachycardia in patients with prolong QT

rapid irregular QRS completes which ‘twist’ around baseline

259
Q

what does ventricular fibrillation look like on ECG and what can happen with ventricular fibrillation

A

shapeless rapid oscillations on ECG

patient becomes pulseless and goes into cardiac arrest (no effective cardiac output)


260
Q

what can torsades de pointes do? (2)

A

cease spontaneously
develop into ventricular fibrillation

261
Q

what is the first line of treatment for ventricular fibrillation

A

electrical defibrillation

262
Q

what is primary AV block

A

PR interval prolongation (200ms +) and every P followed by QRS

263
Q

what is the treatment for asymptomatic and symptomatic primary AV block (1, 3)

A

if asymptotic then no treatment
symptomatic treatment= beta blocker eg atenolol, CCB eg verapamil, digoxin to block AVN conduction

264
Q

what are the two types of secondary AV block

A

Mobitz type 1 and 2

265
Q

what is mobitz 1 AV block

A

PR prolongation until a QRS is dropped (PR progressively elongates)

266
Q

what are the causes and treatment of mobitz 1 AV block (4,1)

A

causes: inferior MI, beta blockers/ CCB/ digoxin
treatment only for symptomatic= pacemaker

267
Q

what is mobitz 2 AV block

A

PR interval is consistently prolonged at the same length
with random dropped QRS

268
Q

what are the causes, symptoms and treatment of mobitz 1 AV block (5,3, 1)

A

causes: inferior MI, beta blockers/ CCB/ digoxin, rheumatic fever
symptoms: SOB, chest pain, syncope (triad)
treatment= pacemaker

269
Q

what is a tertiary AV block

A

AV dissociation (complete heart block so atria and ventricles beat independantly of each other

270
Q

what sustains the heartbeat in a tertiary AV block, what is their firing rate and why is this bad

A

ventricular escape rhythm is sustaining the heartbeat
(ventricle pacemakers take over which is bad (firing rate= 20-40bpm))

271
Q

causes of tertiary AV block (3) and treatment (2)

A

acute MI, hypertension, structural heart disease
treatment: IV atropine and permanent pacemaker

272
Q

what is a bundle branch block and what are the two types

A

blocked bundles of His
can either be RBBB or LBBB (right/ left bundle branch block)

273
Q

what happens in a RBBB and in a LBBB

A

RBBB: right ventricle is activated later than left ventricle
LBBB: left ventricle is activated later than right ventricle

274
Q

what are the causes of RBBB (3) and LBBB (2)

A

RBBB: pulmonary emboli, ischaemic heart disease, ventricular septic defect
LBBB: ishcaemic heart disease, valvular disease

275
Q

what is the heart sound and ECG pattern in RBBB

A

wide physiological S2 splitting heart sound
MARROW: M in V1 (R wave), W in V6 (S wave)

276
Q

what is the heart sound and ECG pattern in LBBB

A

reversed S2 splitting heart sound
WILLIAM: W in V1 (r wave), M in V6 (s wave)

277
Q

what is cardiomyopathy and what are the 3 types

A

disease of the myocardium (muscular/ conduction defects)
hypertrophic, restrictive and dilated

278
Q

why is hypertrophic cardiomyopathy significant

A

most common cause of death in young people

279
Q

cause of hypertrophic cardiomyopathy 3

A

cause: familial inherited auto s mutation of sarcomere proteins (troponin T and myosin B), exercise and aortic stenosis

280
Q

pathophysiology of hypertrophic cardiomyopathy

A

thick noncompliant heart causes impaired diastolic filling which decreases cardiac output

281
Q

symptoms of hypertrophic cardiomyopathy (5)

A

chest pain, palpitations, SOB, syncope, may present with sudden death

282
Q

investigations for hypertrophic cardiomyopathy (2 + diagnostic)

A

abnormal ECG, genetic testing, echocardiogram (diagnostic)

283
Q

treatment for hypertrophic cardiomyopathy (3)

A

beta blocker, calcium channel blocker, amiodarone (anti-arrhythmic)

284
Q

how common is restrictive cardiomyopathy

A

rare

285
Q

causes of restrictive cardiomyopathy (3)

A

granulamatous disease (sarcoidosis, amyloidosis), idiopathic, post MI

286
Q

pathophysiology of restrictive cardiomyopathy

A

Rigid fibrotic myocardium fills poorly and contracts poorly= low CO

287
Q

symptoms of restrictive cardiomyopathy (4)

A

dyspnoea, oedema, congestive heart failure, narrow pulse pressure eg 105/95

288
Q

investigations for restrictive cardiomyopathy (2 + diagnostic)

A

ECG, echocardiogram (diagnostic), cardiac atherterisation (definitive)

289
Q

treatment for restrictive cardiomyopathy (1)

A

none
can consider transplant but most patients die within 1 year

290
Q

how common is dilated cardiomyopathy

A

most common cardiomyopathy

291
Q

causes of dilated cardiomyopathy (3)

A

autosomal dominant familial cytoskeletal gene mutation, ischaemic heart disease and alcohol

292
Q

pathophysiology of dilated cardiomyopathy

A

thin cardiac walls do not contract well= decreased cardiac output

293
Q

symptoms of dilated cardiomyopathy (4)

A

dyspnoea, heart failure, atrial fibrillation and thromboemboli

DiLATed

D= dyspnoea
L= heart faiLure
A= atrial fibrillation
T= thromboemboli

294
Q

investigations for dilated cardiomyopathy (1 + diagnostic)

A

ECG, echocardiogram (diagnostic)

295
Q

treatment for dilated cardiomyopathy (1)

A

treat underlying conditions eg AFib and heart failure

296
Q

what can shock be medically classed as?

A

a medical emergency

297
Q

what occurs during shock and what is the risk 3

A

hypoperfusion of tissues which causes tissue hypoxia and risks organ dysfunction

298
Q

what are the 3 types of shock and explain what causes failure in each

A

cardiogenic: heart pump failure, issue with LV

hypovolemic: issue with venous return to heart, reduced preload

distributive: issue with arterial supply to tissues (includes septic, neurogenic and anaphylactic shock)

299
Q

presenting symptoms of shock 6

A

confusion
weak and rapid pulse
REDUCED GLASGOW COMA SCALE
DECREASED URINE OUTPUT
pale, cold skin
hypotension

300
Q

what is the earliest and more accurate indicator of shock

A

increased capillary refill time

301
Q

what are the 4 main organs at risk of failing due to shock

A

kidney
lung
heart
brain

302
Q

what is hypovolemic shock due to

A

due to blood loss (trauma or GI bleed) or fluid loss (dehydration)

303
Q

symptoms of hypovolemic shock (4)

A

clammy pale skin, confusion, hypotension, tachycardia

304
Q

treatment for hypovolemic shock (3)

A

ABCDE, give oxygen and fluids

305
Q

what is septic shock due to

A

due to uncontrolled bacterial infection

306
Q

symptoms of septic shock (4)

A

pyrexic, warm peripheries, bounding pulse, tachycardia

307
Q

treatment for septic shock

A

ABCDE, broad spectrum antibiotic

308
Q

what is cardiogenic shock due to (4)

A

due to heart pump failure, MI, cardiac tamponade and pulmonary emboli

309
Q

symptoms of cardiogenic shock (2)

A

heart failure signs (oedema), increased JVP

310
Q

treatment for cardiogenic shock (2)

A

ABCDE and treat underlying cause

311
Q

what is anaphylactic shock due to

A

IgE mediated type 1 hypersensitivity against an allergen

312
Q

treatment for anaphylactic shock (2)

A

ABCDE and IM adrenaline

313
Q

what is neurogenic shock due to, give an example and what nervous system does it impair

A

due to spinal cord trauma eg road traffic injury
disrupts sympathetic nervous system but the parasympathetic remains intact

314
Q

symptoms of neurogenic shock (4)

A

hypotension, bradycardia, confusion, hypothermia

315
Q

treatment for neurogenic shock (2) and how does it work

A

ABCDE and IV atropine (blocks vagal tone and causes more PNS inhibition and gives more chance for SNS to work)

316
Q

where is rheumatic fever normally found

A

mostly in developing countries in young people

317
Q

what is rheumatic fever

A

systemic response to beta haemolytic group A strep
eg pyogenes

318
Q

what is rheumatic heart disease and how common is this

A

where rheumatic fever affects the heart. 50% of those with rheumatic fever and likely to have rheumatic heart disease

319
Q

what is the pathophysiology of rheumatic fever

A
  1. M protein from S pyogene reach within the valve tissue of the heart
  2. antibodies and cross linking occurs in response to this= autoantibody mediation destruction and inflammation
  3. this typically thickens leaflets causing valve stenosis
320
Q

what valves are affected in rheumatic fever

A

mostly affects mitral valve (70% mitral only, 25% mitral and aortic)

321
Q

3 symptoms, 2 signs of rheumatic fever

A

SYMPTOMS
new murmur (particular mitral stenosis)
pyrexia
athritis

SIGNS:
Sydenham’s chorea (uncoordinated jerky movements)
arthritis
erythema nodosum (swollen fat under skin causing bumps/ patches to look darker/redder than surrounding skin)

322
Q

investigations for rheumatic fever (2) and what would be seen on each

A

chest x ray: cardiomegaly / heart failure (mitral stenosis signs)
echocardiogram: shows extent of valvular damage

323
Q

diagnosis criteria for rheumatic fever

A

diagnosis: Jones criteria
recent S progenies infection
need 2 major/ 1 major and 2 minor symptoms
major= new murmur, arthritis, erythema nodosum, Sydenham’s chorea
minor= pyrexia, increase in ESR/CRP, arthralgia

324
Q

treatment for rheumatic fever 2

A

antibiotics: IV benzyloenecillin immediately then phenoxypenecillin for 10 days

325
Q

what can be given for Sydenham’s chorea that occurs due to rheumatic fever

A

give haloperidol

doll holding peri peri chicken with a halo on top

326
Q

how are structural heart defects diagnosed

A

echocardiogram

327
Q

how common is bicuspid aortic valve defect and what valve does it usually affect

A

most common inherited heart defect
aortic

328
Q

what happens in the bicuspid aortic valve defect

A

bicuspid degenerates faster than normal and will become regurgatative earlier- leads to arotic stenosis/ regurgitation

329
Q

what is atrial septal defect 2 and how does it affect oxygen levels

A

open foramen ovale so blood shunts from left to right, it doesnt- it is non cyanotic

330
Q

compare older and younger people with atrial septal defect

A

older patient have more shunting, causing dyspnoea compared to younger with more compliant hearts

331
Q

what can atrial septal defect lead to 4

A

overloads right hand side circulation= right ventricular hypertrophy
this leads to eisenmenger syndrome (pulmonary hypertension which reversal of shunt which goes from right to left and non oxygen blood is pumped to the body)

332
Q

treatment for atrial septal defect

A

if it doesn’t spontaneously close then use surgical methods

333
Q

what is ventricular septal defect and is this cyanotic

A

left to right shunt in ventricle
non cyanotic (doesn’t affect oxygen levels)

334
Q

what is there a risk of in ventricular septal defect

A

risk of eisenmengers and right ventricular hypertrophy (similar to atrial septal defect)

335
Q

what are the symptoms for a small and large ventricular septal defect (1,3)

A

small VSD= asymptomatic, large= exercise intolerance, failure to thrive, harsh pan systolic murmur

336
Q

treatment for ventricular septal defect

A

spontaneous closure or surgical closure

337
Q

what is an atrioventricular septal defect and what is this assocaited with

A

hole down middle of heart (no atrial or interventricular septum)
with Downs syndrome

338
Q

treatment for atrioventricular septal defect

A

hard to treat

339
Q

what is a patent ductus arteriosus

A

ductus arterioles fails to close post birth causing blood to shunt from aorta to pulmonary trunk

340
Q

what is the risk for a patent ductus arteriosus 1

A

risk of pulmonary overload and eisenmengers

341
Q

symptoms for patent ductus arteriosus (3)

A

dsypnoea, failure to thrive, machine like murmur

342
Q

investigations for patent ductus arteriosus (3)

A

chest x-ray, ECG, echocardiogram

343
Q

treatment for patent ductus arteriosus (2)

A

prostaglandin inhibitor (eg methacin) which may induce closure, otherwise consider surgery

344
Q

what is the tetralogy of fallots pathophysiology and is it cyanotic

A

ventricular systolic defect causes right ventricle outflow obstruction (deoxygenated blood is shunted to the systemic circulation), making it cyanotic

345
Q

investigations for tetralogy of fallot and what do they show (2,1)

A

echo, chest x-ray shows a boot shaped heart

346
Q

what is a behavior of infants with tetralogy of fallot and why do they do this

A

infants often seen in knee to chest squatting position which increases preload and after load and improves cyanosis

347
Q

treatment for tetralogy of fallot

A

treatment: full surgical repair within 2 years of life (this gives a good prognosis if done)

348
Q

what is coarctation of the aorta 1 and what is the pathophysiology of this

A

narrowing of aorta
blood is diverted through proximal aortic arch branches= increased perfusion to upper body vs lower body

349
Q

symptoms of coarctation of aorta (2)

A

scapular bruits (hypertension in collaterals), upper body hypertension

350
Q

investigations for coarctation of aorta and what is seen (2,1)

A

CT angiogram, chest x-ray= ‘notched ribs’= dilated intercostal vessels

351
Q

treatment for coarctation of the aorta (2)

A

surgical repair or stenting

352
Q

what are non-pharmalogical treatments to prevent falls in the future 3

A

compression stockings
sitting-standing slowly, increase oral salt/ fluid intake

353
Q

what is the pharmacological treatment for postural hypotension

A

oral fludrocortisone

354
Q

acute treatment of acute coronary syndrome 5

A

MONAC
morphine
oxygen IF sats under 94
nitrates
aspirin
clopidogrel

355
Q

risk factors for aortic dissection 3

A

cocaine users
connective tissue disorders
smoking

356
Q

what is an alternative to beta blockers that are contraindicated in severe asthma 1

A

verapamil (CCB)

357
Q

what valve is usually affected in IVDU

A

tricuspid

358
Q

what two medications are given to heart failure patients to slow the progression of their heart failure

A

ACEi
beta blockers

359
Q

what are the cardinal signs of heart failure 3

A

orthopnea (difficulty breathing whilst lying down)
ankle oedema
fatigue

360
Q

what is becks triad 3 and what condition is it associated with

A

increased JVP
hypotension
muffled heart sounds
cardiac tamponade

361
Q

what is the 2nd step if one drug is not controlling hypertension for the two categories of people to treat

A

<55 not A/C origin= CCB or thiazide like diuretic eg indapamide can be added
>55 of A/C origin= ACEi or ARB or thiazide like diuretic eg indapamide can be added

362
Q

if a patient is on ACEi and BB already but still symptomatic what should be given to them 1

A

spironolactone

363
Q

what ecg leads look at the lateral aspect of the heart

A

I, aVL, V5, V6

364
Q

what ecg leads look at the anterior aspect of the heart

A

V3-4

365
Q

what ecg leads look at the inferior aspect of the heart

A

II, III, aVF

366
Q

what ecg leads look at the septal aspect of the heart

A

V1-2

367
Q

what ecg leads looks at the LAD

A

V1-4

368
Q

what ecg leads look at the RCA

A

II, III, aVF

369
Q

what ecg leads look at the LCx/ diagonal of LAD

A

I, aVL, V5-6

370
Q

what CHA2DS2VASK score requires anticoagulation for males and females

A

males- 1 or more
females- 2 or more

371
Q

what is the specific treatment for heart failure with reduced ejection fraction and preserved ejection fraction

A

reduced EF (less than 40%): spironolactone
preserved EF (over 40%): furosemide

372
Q

what valve disorder can present several days after an MI

A

acute mitral regurgitation

373
Q

what is the 1st line treatment for IE and what is the GS

A

1- TTE
2- TOE

374
Q

what is dresslers syndrome

A

pericarditis caused by injury to the heart

375
Q

what is a side effect of amlodipine and what alternative can be given to prevent this side effect 2

A

peripheral/ ankle oedema
ace inhibitor (if not already given) and indapamide

376
Q

what is the triad of rheumatic fever presentation

A

polyarthritis, athralgia, erythema marginatum

377
Q

rheumatic fever treatment 2

A
  1. IV benzylpenecillin
  2. phenoxymethylpenecillin for 10 days
378
Q

what is the diagnosis criteria for rheumatic fever called

A

Jones

379
Q

what is the function of furosemide in heart failure

A

symptomatic releif

2A content- Sameera (21 decks)

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