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Hayders Phase 2A > Cardio > Flashcards

Cardio Flashcards

1
Q

What does an atherosclerotic plaque consist of

A

Necrotic core
Connective tissue
Fibrous cap
Lipids

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2
Q

Which layer of the vessel does athlersclerotic plaque form

A

Intimal layer of arteries

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3
Q

Mechanism of clot formation: step 1

A

Formation of fatty streak. In first 2 decades.
LDL deposited in intimal layer. Gets modified into oxidised LDL.
Causes endothelial damage that secretes chemoattractants. Monocytes and T lymphocytes.
Modified LDL taken up by macrophages that become lipid ladent macrophages.
Fatty streak formed of:
Lipid Ladent macrophage and T lymphocytes

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4
Q

Athlesclerotic clot forming. After fatty streak. Step 2

A

Formation of intermediate lesions.
Macrophages become foam cells.
Platelet adhere
T lymphocytes and foam cells secrete interferons that causes smooth muscle cells to accumulate.
Foam cells. T lymphocytes. Smooth muscle cells and platelets

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5
Q

Atherosclerotic clot formation step 3

After intermediate lesions

A

Formation of plaque.
Foam cells die and form necrotic core
Platelets secreting platelets derives growth factors that’s causes smooth muscle proliferation and progresses into fibrous cap
Fibrous cap has collagen- strength- and elastin- flexible

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6
Q

Atherosclerotic clot is constantly growing and reciding. What are the 2 main complications that could cause

A

1 lumen narrowing- plaque stenosis. Covers 50-75% of coronary=SCAD. Or peripheral vascular disease

2plaque rupture. Atherothrombotic occlusion.
Exposure of basement membrane. Activated massive clotting cascade= infarcts. Either in location or downstream. Causes ACS or stroke

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7
Q

Where are atherosclerotic plaque likely to form

A

Areas of turbulent flow. Bifurcation. Changes in diameter or thickness

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8
Q

Outcomes of a plaque

A

Plaque erosion- emboli. Causes infarct. Second most prevalent cause of coronary thromboses

Athlersclerotic aneurysm. Rupture of a AAA

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9
Q

Risk factors for atherosclerotic plaque

A 
Hypertension 
Diabetes M
Obesity
Family history 
Hyperlipidemia 
Age 
Smoking
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10
Q

Stable angina pathophysiology

A

Coronary artery’s are low resistance and microvessles have variable resistance

Atherosclerotic plaque forms
Perfusion dropped.
Dilation of small vessels as much as possible to normalise flow.

During exertion. Required perfusion increases.
Small vessels unable to dilate anymore as they are maximally dilated.
Required flow in normal Q=3m/s. In exertion Q=15m/s
Anginal pain

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11
Q

Anginal chest pain typical qualities

A

Central crushing chest pain radiating to jaw and arm.
Pain onset by exertion.
Pain improves with rest or GTN

3=typical anginal pain
2=atypical
1= non anginal

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12
Q

What is the rating of anginal pain compared against

A

CAD risk probability.

Compares score with age to asses likeliness of ACS

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13
Q

Investigation after assessing risk of angina

A

Low risk. Move onto another differential
Medium risk- stress echo or exercise test.
Very high risk then progress to management of SCAD

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14
Q

Primary prevention of angina/atherosclerosis

A

Reduce risk factors, Obesity, diet smoking
Statins
Antihypertensives
Better control of diabetes

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15
Q

Secondary prevention of angina

A

Same as primary prevention plus anti platelets. Aspirin and clopidogrel

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16
Q

First line management of SCAD

A

Symptomatic -GTN PRN and how to use it

Disease modifying.
B blockers, or CCB.
(These are first line and reduce symptoms)
Antiplatelet

Preventative
Antihypertensives- CCB or ACEi
Information on lifestyle
Statins

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17
Q

What can aggravate angina

A

Exertion
Large meal
Emotion
Weather

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18
Q

Name B blockers used for angina and ACS and their CI/ SE

A

Bisoprolol
Atenolol
For anginal

Atenolol
Propranolol
Metopranolol
For post MI

CI- asthma. Prinzmetal angina. COPD. High doses in HF. Bradycardia

SE fatigue. Hypotension, bradycardia, sexual dysfunction

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19
Q

what are CCB
name a few types
method if action
and their uses

A

Amlodipine
L-Type CCB
smooth muscle dilators (-ve Ionotropic)
These are arterodilaters. Reduced after load and energy needed to produce same CO. Reduces heart workload.

Use in coronary spasm( prinzmetal angina)

Cause odema in legs since they are arterodilaterers. CI in HF

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20
Q

give an example of a Short acting nitrates and its method of action

A

GTN sublingual

Venodilators

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21
Q

give an example of a long acting nitrates and its method of action

A

Veno and arterio dilators
Nicorandil
HCN channel slower
Ivabidrine

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22
Q

Surgical management for angina

A

Pericuteanous coronary intervention.

Indications are poor response to meds. Previous MI

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23
Q

Treatment to include with PCI

A

Drug illuding stents

Dual antiplatlet

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24
Q

Prinzmetal angina
ECG changes
Cause and treatment

A 
Coronary artery spasm 
Shows ST elevation as pain occurs and subsided with it
Pain occurs at rest 
CCB Amlodipine 
Long acting nitrates ivabridine. 
CI: B blockers and aspirin
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25
Q

ECG of SCAD

A

Normal or ST Depression plus T Wave inversion

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26
Q

Aspirin and clopidogrel drug class

A

COX inhibitor and GP2b3A agonist

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27
Q

Type of chest pain associated with ACS and presentation

A 
Central crushing chest pain. Radiating to jaw and arms. 
Persistent pains. 
SOB 
Palpitations 
Nausea and sweating
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28
Q

Patients presents with suspected ACS

Investigations

A

12 lead ECG
Cardiac enzymes
Bloods FBC U&E Glucose Lipids
CXR looks for oedema, HF sign, cardiomegaly

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29
Q

Name cardiac enzymes

A

Troponin
Creatine kinase
Cardiac isoenzyme
Lactate dehydrogenase

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30
Q

Signs of ACS

A

Distress, anxiety, pallor, sweatiness

Bp HR up or down
4th heart sounds.

Signs of HF( oedema JVP 3rd heart sounds)
Pansytolic murmurs (papliary muscle dysfunction)
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31
Q

Complications of ACS on presentation

A

Syncope, low BP
Oedema
Epigastic pain
Vomiting

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32
Q

Emergency treatment if ACS

A 
MONA 
Morphine 
Antiemetic 
Oxygen if hypoxia 
Nitrates. GTN
Antiplatlets- aspirin 300mg
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33
Q

Results for NSTEMI/UA ECG

A

Normal
ST Depression
T wave inversion
Both of the above

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34
Q

ACS ECG shows NSTEMI/UA

Troponin=-ve

A

-ve cardiac enzymes=UA
No permanent damage occurred
No necrosis

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35
Q

ACS NSTEMI/ UA with +ve cardiac enzymes and T wave

A

Suggests NSTEMI. There could be necrosis

T wave inversion also shows necrosis

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36
Q

ACS without stemi treatment

A

Dual antiplatelt therapy

Anticoagulation (antithombosis) LMWH or warfarin

Anti ischemia agent (anginal treatment)
B blockers (not biseprolol) or CCB + GTN
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37
Q

General management for ACS

A 
Antiplatelet
Anticoagulation 
Bed rest for 48 hours 
continue B blockers 
Secondary prevention
Antihypertensives 
Aldosterone antagonist if evidence of HF
Statins 
Better DM 
Stop smoking 
Exercise 
Diet
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38
Q

Assessing risk for ACS NSTEMI/UA

A

Grace score

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39
Q

Surgical treatment for NSTEMI/UA

A

Unstable= PCI is CABG

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40
Q

STEMI ECG

And results

A 
T wave peaking pointy
St elevation 
T inversionI
Deep Q wave- suggests full thickness infarct 
Weeks after Q&T wave still show

New LBBB pattern

Troponin and enzymes elevated
Creatine kinase

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41
Q

Management for STEMI

A

Reperfusion therapy.
If patient presents within 90 minutes of STEMI then PCI
Followed by dual antiplatelet

After 90 mins to 12 hours then fibrolytic therapy. Alteplase/reteplase tpa
Rescue PCI if fibrolytic.

Give them anti coagulation

Post 12 house- dual antiplatlet+ anticoagulation

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42
Q

Complication of MI

A 
Atrial or ventricular arrhythmia
LBBB
Heart failure occurs in 40%
mural thrombi
drsslers
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43
Q

Pt presents with signs and symptoms of MI but ECG and chest X-ray are clear. Describe the pain as tearing. What is differential

A

Suspect Dissection. Use emergency CT. correct in surgery

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44
Q

Stages of hypertension

A

Stage 1 140/90
Stage 2 160/100
Severe 180/110

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45
Q

Requirement to treat hypertension

A

If stage 1 plus organ damage

Stage 2 or severe

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46
Q

Diagnosing hypertension

A 
Ambulatory blood pressure monitor if elevated 
Biochemistry 
U&E LFT FBC GFR glucose 
Fundiscope for hypertensive retinopathy 
HBA1C
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47
Q

Treating hypertension pharmacological

A

Over 55 or Afro cardibean = CCB
Under 55 anything else = ACEi

ACEi untolerated then ARB
Then B blockers
Then CCB
Then thiazides like diuretics

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48
Q

Treating hypertension conservative

A

Main 3
Lose weight
Drink less booze (booze BP)
Reduce salt intake

Smoking, reduced stress. Coffee

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49
Q

Hypertension prevalence

A

One quarter of adults and half of those over 60

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50
Q

Complications of hypertension

A

Biggest one is stroke
MI Aneurism renal dysfunction heart failure

CI: oral contraception and antidepressants
Medication stopped before surgery

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51
Q

Hypertrophic cardiomyopathy.
inheritance pattern
prevalence
pathophysiology

A

Autosomal dominant
Prevalence 1 in 500
Mutations cause hypertrophy of ventricles and septum
Causing LVOT obstruction

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52
Q

Signs and symptoms of hypertrophic cardiomyopathy

A

Asymptomatic. First symptom can be sudden death. 6%
Signs. Crescendo de crescendo early systolic murmur
Syncope
Dyspnoea
Chest pain

Ejection systolic murmur due to LVOT
Jerky carotid pulse
S4 heart sounds due to crack when atria contract

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53
Q

Causes of ejection systolic murmur

A

Obstruction or stenosis

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54
Q

Pansystolic murmur is a sign of

A

Mitral regurgitation.
VSD

Pansystolic murmur is a fixed volume sounds that’s occurs between S1 and S2 since as blood is ejection it goes up into across: leaky mitral valve, septum

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55
Q

Differentiate HCM and Aortic stenosis since they both have the same ejection systolic murmur

A

Patients does valsalva or stand up from squatting since this (reduces filling) decreases preload so less blood in LV. (reduced CO)
Murmur is louder in HCM since less blood pressing back against ventricle wall so obstruction is larger
Murmur is quieter in aortic stenosis since less blood is leaving past stenosis

56
Q

Investigation for HCM

A

ECG- shows T wave inversion Q wave AF

Gold standard is echo or cardiac MRI

57
Q

HCM treatment

A

Symptomatic treatment
B blockers or CCB vamirpil. Reduce HR cause more filling time so less obstruction

If AF of Vt then add amiodarone plus warfarin
Preventing sudden death
If high risk then Implantable cardiac defibrillator

Screening in relatives

58
Q

Dilated Cardiomyopathy

A

Autosomal dominant

Cytoskeleton abnormality leading to dilated ventricles

59
Q

Presentation of dilated cardiomyopathy

A

Presentation similar to HF since dilation can cause HF

Symptoms SOB
Fatigue

Signs 
oedema 
Raised JVP
Pleural effusion 
S3 heart sound. Physiological in young people sound of blood hitting LV after mitral valve opens. Pathological means dilated ventricle
60
Q

Investigations in Dilated cardiomyopathy

A

Echo- gold stander- shows dilation

CXR

61
Q

Treatment of dilated cardiomyopathy

A

Transplant since 40% mortality in 2 years

Digoxin ACEi ICD diuretics

62
Q

Arrhythmogenic cardiomyopathy details

A

Autosomal recessive
Mutation in Desmosomes causes fibrosis which causes arrhythmia

Presentation is arrhythmia or sudden death

cardiac MRI shows fibrosis

B blocker for symptomatic
Amiodarone
ICD

63
Q

Commonest sites for aneurysm

A 
Abdominal aorta 
Iliac 
Poptial
Femoral
Thoracic
64
Q

Prevalence of AAA

A

5% in over 60

5m=F

65
Q

Screening program for AAA

A

Men aged 65-75 echo

66
Q

Presentation and treatment of AAA

A 
Severe pain 
Epigastic radiating to the back 
Hypotension
Tachycardia 
Anemia 
Sudden death

If small then risk factors and surveillance (every 3 months) small is less than 5.5 cm diameter. If larger than 5.5 or rapidly growing then operate
If large then surgical repair of gortex graft or stent

67
Q

Risk factor of AAA

A 
Age 
Male gender 
Hypertension
Smoking
Hyperlipidemia 
Atherosclerosis
68
Q

Aortic dissection
what is it

presentation

Investigation

Treatment

A

A tear in the intimal layer of artery causing blood to enter medial layer and the intimal layer gets cleared

Rf and causes: ehler danlos syndrome, Marfans (eaker connective tissue) Male over 50

Sudden onset chest pain. Not radiating. Tearing pain 
Pulse defect
Left right BP different 
Syncope, Hyper or Hypotension 
Develop aortic regurgitations
Coronary ischemia and tamponade

ECG, CXR and CT angiography

Surgery is corrective

69
Q

tetralogy of fallots pathophysiology

A

misaligned VSD
overriding aorta
RV hypertrophy
Pulmonary stenosis/block of RVOT

essentially get a Right to left shunt

70
Q

what does maternal alcohol or infection cause

A 
alcohol= septal defect
infection= PDA and valvar defect
71
Q

explain foetal circulation

A

umbilical vein (ligementum teres) to IVC via ductus venosus (ligementum venosus) then foramen ovalue and Ductus arteriosis (ligamentum arteriosis)

72
Q

signs of congenital heart disease

A 
Central cyanosis 
clubbing due to prolonged cyanosis
pulmonary hypertension 
syncope 
eisenmenger syndrome 
growth failure 
squatting
73
Q

explain central cyanosis

A

right to left shunt as complete mixing of ventricular blood- in fallots

74
Q

explain pulmonary hypertension and eisinmenger syndrome

A

SD or VSD (eisinmengers complex) causes left to right shunt which causes increased pressure on pulmonary causing pulmonary hypertension which causes RV hypertrophy which causes right to left shunt

75
Q

fallots presentation

A

Squatting
cyanosis
syncope on exercise

76
Q

fallots treatment

A

O2 if cyanosed
squat as this +PVR -VR -Right to left shunt
B blockers as reduce strain and surgery

77
Q

Ventricular septal defect prevalence

A

most common conginetal heart defect. 1 in 500

78
Q

Ventricular septal defect
presentation, signs, symptoms and murmur
treatment

A

presents with pulmonary plethora (radiological finding, patinet looks pink ), increased perfusion to lungs. symptoms include SOB Tachypnoea Tachycardia cardiomegaly.
pansystoloc murmur, smaller the hole, less serious the disease, more sound
Treatment surgical

79
Q

shunts right to left and left to right

A

left to right is how it usually starts of, except fallots due to overriding aorta, L to R causes pulmonary plethora and pulmonary hypertention which then starts to become R to L which gives cyanosis

80
Q

atrial defect
Interatrial defects

atrioventricular spetal defects

A

L to R shunts, pulmonary plethora, SOB, increased RR and HR

big hole in heart common in downs, breathlessness can get eisinemgers syndrome needs corrective surgery

81
Q

patent foramen ovale is associated with what

A

associated with increased risk of paradoxical embolism from stroke

82
Q

where does ductus arterosis insert into aorta

A

between brachiocephalic and L common carotid

83
Q

coarction of aorta
pathophysiology
signs symptoms complications and diagnoses

A 
Narrowing of aorta at ductus arteriosus
upper body hypertension lower body hypotension 
radiofemoral delay
kidney injury 
scapular bruti, buzz
CT/MRI diagnostic
84
Q

Patent ductus arteriosis
pathophysiology
signs symptoms complications and diagnoses

A

DA in fetus shunts PA to aorta. in adult it shunts from aorta to PA. causes Pulmonary plethora, SOB tachypnoea/cardia low BP.
can cause LA LV dilation and RV hypertrophy
ECHO diagnostic

85
Q

what causes ventricular dilation and hypertrophy

A

dilation is caused when there is excess blood entering the ventricle or atria, this can be due to increased entry or a back flow, as a result the heart dilates to accommodate flow and ends up being too dilated can lead to heart failure as it will stop pumping properly

Hypertrophy is caused when there is excess force to pump against, eg hypertension or increased after load.
PDA is a good demonstrator because there is increased blood flow into the left atria and ventricle there is LA LV dilation and because the pressure in pulmonary artery has increased there is RV hypertrophy

86
Q

bicuspid aortic valve

prevalence and assosiations

A

usually tricuspid, 1-2% it isn’t, its the most common congenital valve defect
associated with coarction and aortic stenosis

87
Q

what causes ventricular dilation and hypertrophy

A

ventricle pumps against pressure= hypertrophy
ventricle overload= dilation
in dilation there is displaced apex beat

88
Q

what does s4 represent

A

contraction of a stiff ventricle, due to HCM, aortic stenosis

89
Q

what does S3 represent

A

contraction of a stiff atria, high pressure atrial contraction against a ventricle, mitral stenosis, dilated cardiomyopathy CHF

90
Q

What is the commonest valvar heart disease and its causes

A

aortic stenosis as caused by Bicuspid aortic valve.

degeneration and calcification, inflammatory proccess or rheumatic heart disease

91
Q

risk factors for aortic stenosis

A 
male 
diabetes 
hypertension 
smoking 
hyperlipidemia
92
Q

pathophysiology of aortic stenosis

A

valve stenosis due to inflammatory process

causes increased after load and LVOT obstruction so LV hypertrophy so LA hypertrophy pulmonary oedema (cardiac failure)

93
Q

presentation of aortic stenosis

A

dyspnoea
angina
syncope on exertion

94
Q

signs of aortic stenosis

A

pulsus tardus - retarded- slow pulse
pulsus parvus -poor, weak pulse
S4- due to hypertrophic ventricle contraction
ejection systolic murmur

95
Q

investigations and diagnoses of aortic stenosis

A

CXR may show calcification
ECG shows Hypertrophy
echo-diagnostic, can see LVOT obstruction

96
Q

2 Treatments for aortic valve stenosis

A

valve replacement or TAVI
trans catheter aortic valve replacement
infective endocarditis prophylaxis
vasodilators are CI since wouldn’t change afterload, would lower BP and cause syncope

97
Q

mitral stenosis pathophysiology what it causes and presentation, treatment

A

caused by calcification, rhematic heart disease or IE
LA hypertrophy, pulmonary oedema - presentation = SOB
pulmonary oedema- RHF
diastolic murmur.
diagnose by echo and treat with replacement valve

98
Q

mitral regugitation

pathophysiology what it causes and presentation, treatment

A

rhematiod heart disease, calcification and IE.
bacflow during systole, causes LA dilation, LV dilation, displaced apex,
progressive HF
SOB oedema fatiuge lethargy
increased risk of IE
pansystolic murmur
replacement

99
Q

Aortic regurgitation pathophysiology what it causes and presentation, treatment

A

LV dilation, Early diastolic decrescendo murmur
causes LVF and this causes symptoms of oedema, chest pain, fatigue, syncope, chest pain due to reduced coronary perfusion
management are vasodilators, B blockers.

100
Q

causes of Heart failure

A

MI
Dilated cardiomyopathy - valve disease
Hypertension
most to least common

101
Q

pathophysiology of HF, compensatory mechanism that try to keep patient alive

A

treat it like you have just lost blood. BP dropped:
RAAS activated, increased fluid reabsorbed=oedema
symathetic system activated adrenaline, positive chronotropic and ionotropic.
constriction of periphral vessles.
increase venous return .
all these do is make situation worst
release of naturetic peptides

102
Q

function of naturetic peptides

A

inhibit ADH inhibit RAAS vasodilators decrease water reabsorption lower BP

103
Q

signs of fluid overload

A 
pulmonary oedema- SOB and orthopnoea 
ascites 
periphral oedema 
hepatomegally 
raised JVP
104
Q

LV HF with preserved EF symptoms

A

SOB, orthopnoe.. fluid overload
fatiugue wheeze,
Nocturnal couch with pink sputum
nocturia- get up to pee, sign that daytime urine filtration is low

105
Q

signs of LVHF

A 
tachycardia, 
S3 and S4
cardiomegaly 
pleural effusion 
fluid overload symptoms(5)
106
Q

what is the classification and staging of heart failure

A

new york heart assosiation classiification
I: asymptomatic
II: slight limitation mild HF
III:Marked limitation Moderate HF
IV: unable to carry out physical activity without discomfort Sever HF

107
Q

Investigation and diagnoses of HF

A 
bloods - Nauturetic peptides 
CXR- cardiomegaly pleural effusion and pulmonary oedema 
ECG- identify cause of MI
Echo- assesmnet of LV function
biochemistry- GFR, U&E Thyroid LFT
108
Q

management of LV HF Pharmacological symptomatic treatment

A

Diuretics
start on thiazide (DCT) diuretic - bedfroflumothiazide
then loop diuretic - Furosemide
lastly aldesterone antagonist- spironolactone

109
Q

management of LV HF Pharmacological control

A

ACEi-ramipril, SE is hypotension so administer v slowly
B Blocker, bisoprolol, Slows HR reduces work load, risk of hypotension so again start slow.
these reverse effect of activated sympathetic drive and RAAS to normalise flow and reduced workload on heart
if HF with AF the Digoxen

110
Q

management of LV HF Pharmacological conservative

A

diet
smoking
weight loss
activity

111
Q

who is at risk of a silent MI

A

Diabetics and Hypotensive patients

112
Q

risk factors for infective endocarditis

A 
previous IE
Had prosthetic valve replacement 
congenital heart defect 
IVDU
Bad dental health 
VSD PDA, any abnormal heart structure or valve disease
113
Q

3 pathogens that can cause IE

A

Strep Viridans
Staph aureus
Enterococci

114
Q

2 factors that lead to IE

A

Abnormal cardiac structure and bateremia

115
Q

cause of Complications of IE

A

IE causes platelet and fibrin or bacterial accumulation.
these can be projected distally into anywhere in the body causing peripheral stigmata.
think of IE as a Heart disease that’s ejecting gunk everywhere

116
Q

Complication/signs of IE

A

Stroke, AKI, PE or Peripheral stigmata:
petechiae, red spots
splinter haemorrhage, spots under nails
Oslers nodes- tender subcutaneous nodules in digits
Janeways lesions- nontender subcutaneous nodes in digits
Roth spots on fundescope- retinal infarct

117
Q

Criteria used to diagnose IE

A

Modified dukes criteria

118
Q

Investigations for IE

A 
Echo cardiogram is gold standers 
Transeosphageal echo if looking at prosthetic valves 
Blood cultures 
FBC= low Hb high WBC
High CRP High U&E
CXR= pulmonary odema or PE
ECG=PR elongation/heart block
Increased INR
119
Q

Treatment for IE

A

Initially IV antibiotics then continue oral antibiotics for 4-6 weeks
antibiotics- Benzlypenicilin & gentamyosin
MRSA= Vancomyosin
surgery if extensive
treat any complications

120
Q

Prevention of IE

A

Good dental care, education of Risks like surgery and non medical procedure like tattoo and piercings

121
Q

3 Diseases that class as Pericarditis

A

acute pericarditis
pericardial effusion & Cardiac tamponade
constrictive pericarditis

122
Q

What is acute pericarditis and its cause

A

Inflammation of pericardium often idiopathic or due to viral Coxsackie B- Enterovirus
or post MI as Dressler’s syndrome

123
Q

Diagnoses of acute pericarditis

A

2 out of these 3
characteristic chest pain
friction, pericardial rub
ECG changes

124
Q

define pericardial chest pain

A

sharp central retrosternal and pleuritic- worst by movement and inspiration, made better by leading forwards . radiates to back and shoulder due to phrenic involvement

125
Q

ECG changes of Pericarditis

A

PR depression and diffuse or wide ST elevation

126
Q

signs and symptoms of pericardial effusion

A

Signs of PE or tamponade- Dysponea
cough, dry
hiccups
plus pericarditis signs

127
Q

Investigations in Pericadial effusion

A

CXR- normal or effusion
troponin- normal
ECG- main diagnostic

128
Q

difference between ECG of STEMI and pericarditis

A

STEMI- ST elevation is convex upwards
Pericardits - ST elevation is Concave upwards+ PR Depression
remember if you had an MI you’d be conVEXED too

129
Q

Management for pericardial effusion or acute pericarditis

A

treat underlying issue.

NSAIDs or Colchoicne- reduces reoccurrence

130
Q

cardiac tamponade

signs symptoms investigation and management

A

Dysponea, raised JVP Pulsus paradoxis
muffled S1 and S2. Tachycardia but hypotensive
ECG and Echo diagnostic
if small, manage like pericarditis if large then urgent draining

131
Q

constrictive pericarditis

what is it how is it diagnosed and whats the treatment

A

calcification of pericardium
causes heart failure
diagnosed by CT or MRI
surgical treatment

132
Q

causes of soft S1

A

Mitral regurgitation

133
Q

causes of loud S1

A

mitral stenosis

134
Q

causes of soft S2

A

Atrial Stenosis

135
Q

What does S3 in old person suggest

A

Dilated ventricle

Hayders Phase 2A (10 decks)

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