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Phase 2a > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Describe a bicuspid aortic value?

A
  • Go undetected initally
  • Lead to aortic stenosis/regurgitation
  • Treatment = surgically with valve replacement
  • Affects 1% of live births, usually associated with other developmental issues
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2
Q

Describe atrial septal defect?

A

2 types of hole
1. Primum: presentation is earlier, may involve AV valves and effects lower atrial septum

  1. secundum: may be asymptomatic until adulthood when heart compliance is reduced, higher atrial septum

LEFT TO RIGHT SHUNT

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3
Q

Describe ventricular septal defects?

A

Larger holes = more problems in infancy
Smaller = asymptomatic but increase IE risk
Large pan systolic murmur
Smaller hole = louder murmur
Medically treated as hole may close spontaneously then surgical repair before Eisenmengers

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4
Q

What is Eisenmengers Sydrome?

A

Shunt reversed due to development of pulmonary hypertension
Causes deoxygenated blood to go back around the body
Once PHTN is high enough for reversal only heart transplant is curative

Cyanosis, clubbing, HF, syncope ,high RBC

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5
Q

What is this a typical history of?

A 24-year-old gentleman comes to see you for a routine check-up. On auscultation of his back you notice a systolic murmur over his left shoulder blade. Further CV examination shows a radio-femoral delay with a weak femoral pulse bilaterally. The BP in his right arm is 130/85 but in the left arm is 100/67

A

Coarctation of the Aorta

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6
Q

Describe Coarctation of the aorta

A

Aorta is narrowed at the site of the ductus arteriosus

Associated with biscuspid aortic valve and turners syndrome

Severe - blocked aorta

Mild - Raised bp and systolic murmur

Radiofemoral delay BP in right arm>left arm

Both need repairing surgically or stent but risk of aortic aneurysm after repair

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7
Q

What is this a typical history of?

Mother comes to see you. Her two year old has been having episodes where he gets restless and cries for no reason, however as soon as he is allowed to squat down the crying stops. He is a bit underweight for his age and on examination you notice a bit of clubbing.

A

Tetralogy of Fallot

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8
Q

Describe tetralogy of fallot?

A

Most common cyanotic cardiac disorder (3-6 in 100,000) with the highest survival to adulthood

After closure of the ductus arteriosus infants will become progressively more cyanotic as there is less flow to the lungs,

RIGHT TO LEFT SHUNT

Chest xray may show boot shaped heart

Toddlers may squat and infants become cyanotic

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9
Q

What are the 4 features of a tetralogy of fallot?

A
  1. VSD
  2. Pulmonary stenosis
  3. RV hypertrophy
  4. Overriding aorta
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10
Q

Two main problems with IHD?

A
  1. Gradual narrowing of coronary arteries

2. Risk of plaque rupture within coronary arteries

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11
Q

What are the risk factors for IHD?

A 
Modifiable: 
Smoking 
Obesity
Exercise
Diet 
Cocaine

Clinical:
HTN
Diabetes
Hyperlipidaemia

Non modifiable:
Age
Gender

Psychosocial:
High demand, low control jobs

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12
Q

What are the symptoms of IHD?

A

Typically central or left sided pain

May radiate to the jaw or left side of the arm

Often describe as heavy or constricting ‘elephant on my chest’

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13
Q

Investigation of ischaemic heart disease?

A

Cardiac enzymes

ECG

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14
Q

Treatment if IHD?

A 
MONA 
Morphine 
Oxygen 
Nitrates 
Aspirin
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15
Q

Management of IHD?

A

Prevent worsening
Revascularise if there has been an MI
Treat pain

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16
Q

Anterior IHD:

Which leads?
Which coronary artery?

A

V1-V4

Left anterior descending

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17
Q

Inferior IHD:

Which leads?
Which coronary artery?

A

II, III, aVF

Right coronary

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18
Q

Lateral IHD:

Which leads?
Which coronary artery?

A

1, V5-V6

Left circumflex

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19
Q

What is this a typical history of?

A 68 year old gentleman presents with a 1 month history of tight-chestedness and dyspnoea when he walks his dog. This resolves itself once he sits down and has a break for 10 minutes. It sometimes radiates to his jaw, especially when he has been walking uphill.

A

Stable Angina

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20
Q

Risk factors for stable angina?

A 
Age 
Smoking 
Family history 
Dibetes Meillitus 
Obesity 
Physical activity 
Stress
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21
Q

Symptoms of stable angina?

A

Chest pain brought on by exertion but rapidly resolves with rest and GTN

May radiate to arms, jaw, back and neck

May be exacerbated by emotion

May also get some dyspnoea, palpitations or syncope

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22
Q

Investigations for stable angina?

A

ECG - usually normal, may show ST depression and T wave inversion

Bloods - anaemia

CXR - check heart size

Angiogram - gold standard, shows luminal narrowing

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23
Q

Treatment for stable angina?

A

Lifestyle - eat less move more stop smoking

Medical - control hypertension and diabetes

Symptomatic relief - nitrates e.g. GTN spray

Drugs - B blockers, statin, aspirin, ACEi, ivabradine

PTCA - stenting or ballooning the narrowing, risk of restenosis or thrombosis, less invasive

CABG - good prognosis but longer recovery

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24
Q

What is unstable angina?

A

Acute coronary syndrome that is defined by the absence of biochemical evidence of myocardial damage

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25
Q

Aetiology of unstable angina?

A
  • brought on by trivial provocation or for no apparent reason
  • may have crescendo pattern
  • 50% of patients with unstable angina will get an infarction within 30 days if it is left untreated
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26
Q

Symptoms of unstable angina?

A

Chest pain or pressure

Pain radiating anywhere in upper body

Sweating

Dyspnoea

Nausea

Vomiting

Dizziness or sudden weakness

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27
Q

Investigation of unstable angina?

A

FBC = anaemia aggravates it
Cardiac enzymes = excluded infarction as troponin normal
ECG = when in pain shows ST depression
Coronary anigography

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28
Q

Treatment of unstable angina

A

Similar to stable but more direct

Use antiplatelet agents and anticoagulants to break up clots and prevent new ones

Add in nitrates, BB and CCBs

CABG and PCTA are both viable options once the lesion has been identified as may develop into a full STEMI

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29
Q

What is a myocardial infarction?

A

Plaque rupture leads to a clot forming which then occludes one of the coronary arteries causing myocardial death and inflammation

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30
Q

Symptoms of myocardial infarction?

A

Acute central chest pain radiating to jaw and shoulder lasting >20mins

Nausea

SoB

Palpitations

(Some are silent > DM+ old)

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31
Q

Signs of MI?

A

Clammy and pale
4th heart sound
Pansystolic mumur
May later develop peripheral oedema

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32
Q

Acute management of STEMI?

A

Do a 12 lead ECG, give O2 if sats <94%

Establish IV for bloods and enzymes

Brief histor, BP, JVP, murmurs, signs of CCF

Aspirin 300mg PO

Morphine 5-10mg IV and an anti ememtic

(MONA and refer for PCI or thrombolysis if not CI)

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33
Q

What is the subsequent management of an MI?

A

Aspirin - 75mg OD reduces the risk of repeat by 29%

Beta blocker - long term risk reduces risk by 25% ( CI = verapamil)

ACEi

Statin

Address modifiable risk factors!!

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34
Q

What advice would you give post MI?

A

Return to work after 2 months, encourage exercise and no air travel for 2 months

Diet high in oily fish, fruit and veg, low in saturated fats

Exercise: regular daily exercise

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35
Q

What is this a typical history of?

A 67-year-old man comes to see you complaining of cramping pain in his left calf when he gets back from walking uphill to the shops. On examination you notice both his legs are cold and hairless, with an increased capillary refill time in the left but not the right.

A

Peripheral arterial disease

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36
Q

Symptoms of peripheral arterial disease?

A

Cramping in calves, thighs and buttocks that is relived with rest

(signs are the 6 Ps)

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37
Q

What are the 6 Ps of limp ischaemia?

A
  1. Pain
  2. Pallor
  3. Pulselessness
  4. Parethesis
  5. Paralysis
  6. Perishing cold
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38
Q

What are the signs of limb ischaemia?

A

Absent pulses
Punched out ulcers
Postural colour change (Buergers test)

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39
Q

Explain buergers test?

A
  1. Patient supine, elevate legs to 45 degrees for 1-2 mins, observe colour, pallor indicated ischaemia

(occurs when peripheral arterial pressure is inadequate to overcome gravity)

  1. Sit patient up, hang legs over side of bed at 90 degrees, as gravity aids blood flow

Blue first as deoxygenated blood passes through ischaemic tissue

Then red due to reactive hyperaemia from post hypoxic vasodilation

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40
Q

What investigations are carried out for peripheral limb ischaemia?

A

Exclude DM, arteritis, anaemia, renal disease

ABPI - normal is 1-1.2, PAD is 0.5 to 0.9

Colour duplex USS - quick and non invasive, can show vessels and blood flow within them

MR/CT angiography - identify stenosis and quality of vessels

Blood tests - raised CK MM shows muscle damage

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41
Q

What is the management of peripheral limb ischemia?

A

Risk factor modification - quit smoking, treat HTN, lower chloesterol, improve DM

Medications - antiplatelet - clopidogrel is first line

Excercise programs - reduce claudication by improving blood flow

PTA or surgery if severely stenosed

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42
Q

What is this a typical history of?

Despite your advice, the gentleman from earlier comes in a few weeks later complaining of left foot pain at rest which is relieved by hanging it out of the side of the bed at night.

A

Critical Limb ischemia

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43
Q

Describe critical limb ischemia?

A

May be due to a thrombosis, emboli, graft occlusion or trauma

Deep duskiness of limb + sudden deterioration shows arterial occlusion NOT gout or cellulitis

If not revascularised in 4-6 hours then limb loss

Surgical emobolectomy or local thrombolysis

Ulcers more likely on limbs with poor blood supply, healing takes longer due to poor perfusion of lumb and therefore hampers the healing process

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44
Q

What is this typical of?

34 year old male presents to GP with chest pain. What do you want to know?
–	S = central, retrosternal 
–	O = 3 days ago 
–	C = sharp
–	R = left shoulder 
–	A = SOB, cough, hiccups 
–	T = constant 
–	E = made worse on inspiration, relieved by leaning forwards 
–	S = 7/10
A

Pericarditis

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45
Q

What is the most common cause of pericarditis?

A

Viral infections = Coxsackie B

Other viral infections include EBV and mumps

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46
Q

What are the other causes of pericarditis?

A

Bacterial = pneumonia, rheumatic fever, TB, strep, staph
Post MI = Dresslers sydrome
Autoimmune

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47
Q

What is the management of pericarditis?

A

Treat the cause
NSAIDS
Corticosteroids for symptomatic relief
Manage complications

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48
Q

What is cardiac failure?

A

A clinical sydrome rather than one specific disease - a symptomatic condition where breathlessness, fluid retention and fatigue are associated with a cardiac abnormality that reduces cardiac output

A state where the heart is unable to satisfy the needs of the metabolising tissues

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49
Q

What are the causes of heart failure?

A

Ischaemic heart disease (most common)
Cardiomyopathy
Hypertension

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50
Q

Describe systolic heart failure?

A

Failure to contract
EF = <40%
IHD, MI, CM

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51
Q

Describe diastolic heart failure?

A

Inability to relax and fill
EF>50%
Constructive pericarditis, cardiac tamponade, hypertension

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52
Q

Describe the pathophysiology of heart failure?

A

One the heart begins to fail, compensatory changes begin to occur

As the HF progresses, these compensatory changes become overwhelmed and pathological

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53
Q

What compensatory changes occur in heart failure?

A

Sympathetic stimulation = increases afterload by causing peripheral vasoconstriction

RAAS = increases salt and water retention, increases the afterload and preload (increased volume and vasocontriction)

Cardiac changes = Ventricular dilation, myocyte hypertrophy

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54
Q

Describe the mechanism of heart failure?

A
  1. Increased preload
    (failure of heart means more blood is left in the ventricles after systole = increased preload)

Stretching of myocardium maintaining CO

  1. Increased afterload
  2. Salt and water retention
    (reduced cardiac output leading to decreased renal perfusion activating RAAS)
  3. Myocardial remodelling
    (in response to ischaemia myocyte damage etc. Hypertrophy, loss of myocytes and increased interstitial fibrosis)
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55
Q

What are the symptoms of left sided cardiac failure?

A
  • exertional dyspnoea
  • fatigue
  • PND
  • Nocturnal cough - pink frothy sputum
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56
Q

What are the signs of left sided cardiac failure?

A
  • Cardiomegaly
  • 3rd and 4th heart sounds
  • Crepitations in the lung bases
  • Weight loss
  • Reduced BP
  • Tachycardia
  • Cool periphery
  • Heart murmur
57
Q

What are the symptoms of right sided heart failure?

A
  • Peripheral oedema
  • Ascites
  • Nausea
  • Anorexia
58
Q

What are the signs of right sided heart failure?

A
  • Raised JVP
  • Hepatomegaly
  • Pitting oedema
  • Ascites
59
Q

What investigations would you carry out for heart failure?

A

Bloods = B type Natiuretic peptide: FBC, LFTs, U=E, BNP. TFTs

Cardiac enzymes = Creatinine Kinase, Troponin i, troponin T

CXR

ECHO

60
Q

What is the treatment for acute heart failure?

A 
100% oxygen 
Nitrates - GTN spray 
IV opiates - diamorphine 
IV furosemide - reduce fluid overload 
Consider inotropic drug
61
Q

What is the treatment for chronic heart failure?

A

ABCD

A. ACE inhibitors - Ramipril 
B. Beta blockers - Atenolol 
C. CCB and other vasodilators - amlodipine, hydralazine 
D. Diuretics + digoxin - 
Spironolactone = aldosterone antagonist 
Furosemide = loop diuretic
62
Q

What is the management of heart failure?

A

Lifestyle = education, obesity control, diet, smoking cessation, cardiac rehab

Symptomatic = Loop diuretics - furosemide

Disease altering = 
ACEi 
BB
Aldosterone agonists 
Digoxin
63
Q

What is atrial fibrillation?

A

Most common arrhythmia - 5-10% of patients are >65

Atrial activity is chaotic and mechanically ineffective

64
Q

What causes atrial fibrillation?

A

Heart failure, hypertension, thyrotoxicosis

Any condition causing raised arterial pressure

65
Q

Describe the pathophysiology of atrial fibrillation?

A

Atrial activiation 300-600min

Only a proportion of these impulses are conducted to the ventricles (due to the refractory period of the AVN)

HR = 120-180

66
Q

Symptoms of atrial fibrillation?

A 
Asymptomatic 
Palpitations 
Fatigue 
Heart failure 
5x risk of stroke, embolism due to thrombus formed in the atrium
67
Q

What is used for rate control in atrial fibrillation?

A

Beta blockers (atenolol)
CCB (verapamil, diltiazem)
Digoxin

68
Q

What is used for rhythm control in atrial fibrillation?

A

Electrical DC cardioversion

Amiodarone = anti arrhythmia medication

Anticoagulation with warfarin - target INR - 2-3

69
Q

What does Atrial fibrillation look like on an ECG?

A

Irregularly irregular
F waves
No clear P waves
ORS is rapid and irregular

70
Q

What is atrial flutter?

A

Often associated with AF

Atrial rate = 300bpm

Ventricular rate = 150bpm

ECG = sawtooth flutter waves (F waves)

Rx = radiofrequency catheter ablation

71
Q

What is AV nodal re entry tachycardia?

A

Commonest type of SVT

There is a ‘ring’ of conducting pathways in theAV node of which the limbs have different conducting times and refractory periods

This allows a re-entry circuit and impulse to produce a circus movement tachycardia

On ECG = p waves are either not visible, or seen immediately before QRS complex

QRS is a normal shape because the ventricles are activated normally, down the bundle of His

72
Q

What is AV reciprocating tachycardia?

A

Accessory pathway connecting the atria and the ventricles - capable of antegrade or retrograde conduction (in some cases both)

73
Q

What is Wolf Parkinson White syndrome?

A
  • Best known type of AVRT
  • There is an accessory pathway (bundle of Kent) between the atria and the ventricles
  • ECG = shows evidence of the pathway, if path allows some of the atrial depolarisation to pass quickly before it goes through the AVN
  • Early depolarisation of part of the ventricle = shortened PR interval and a slurred start to the QRS (delta wave) and the QRS is narrow
  • Patients are also prone to atrial and occasionally ventricular fibrillation
74
Q

What is sinus bradycardia?

A

<60bpm

75
Q

Extrinsic causes of bradycarida?

A

Treat the underlying cause!

  • Drug therapy
  • Hypothyroidism
  • Hypothermia
  • Raised inter cranial pressure
76
Q

Intrinsic causes of bradycardia?

A

Treat with atropine or temporary pacing in acute causes

  • Acute ischaemia
  • Infarction of the SAN
  • Sick sinus sydrome
77
Q

What is sick sinus syndrome?

A

Bradycardia caused by the intermittent failure of the SAN depolarisation due to the failure of the sinus node to propogate to the atria (sinoatrial block)

If symptomatic - permanent pacemaker insertion

78
Q

Where can the heart be blocked?

A
  1. Block in the AVN or bundle of His

2. Block in the lower conduction system

79
Q

Describe first degree heart block?

A

If R is far from P then you have FIRST DEGREE

Delayed AV conduction = PR interval prolonged >0.2s
Asymptomatic = no treatment

Caused by

  • Acute ischemia
  • Hypokalemia
80
Q

Describe second degree heart block? (I)

A

Longer, longer, longer DROP then you have a WENCKEBACH

  • Progressive PR interval prolongation, until a P wave fails to conduct and a QRS is dropped, then cycle repeats itself
  • Lightheadedness, dizziness, syncope
81
Q

Describe second degree heart block? (II)

A

If some Ps don’t get through then you have a MOBITZ TYPE II

  • Same PR interval but QRS is dropped
  • Chest pain, SOB, postural hypotension
82
Q

What is the difference between mobitz type I and type II?

A

In Mobitz type I the PR interval progressively lengthens until an impulse is blocked

In Mobitz type II the PR interval is prolonged but constant with an occasional impulse being blocked

83
Q

Describe third degree heart block?

A

WiLLiM MaRRoW

  • Causes = all atrial activity fails to conduct to the ventricles
  • ECG = P waves and QRS are independent - ventricular contractions are sustained by spontaneous escape rhythm
  • Rx = IV atropine (acute) or permanent pacemaker insertion
84
Q

What would a right bundle branch block look like?

A

MaRRoW
M in V1
W in V6

Cause = PE, IHD, ASD and VSD

85
Q

What would a left bundle branch block look like?

A

WiLLiaM
W in V1
M in V6

86
Q

What can cause heart block>

A

Coronary artery disease

Cardiomyopathy

Fibrosis in the conducting tissues

87
Q

What is hypertension?

A

Raised blood pressure

Can have primary (95%) or secondary origin

Secondary origins e.g. CKD, Conn’s syndrome, pregnancy

88
Q

If someone is over 55 OR of Black African-Carribean origin what would be the first line of treatment in hypertension?

A

CCB

calcium channel blocker

89
Q

If someone is under 55, and not Black African-Carribean origin OR had type 2 diabetes what would be the first line of treatment?

A

ACEi or ARB

90
Q

What would the second line of treatment for hypertension be?

A 
First line (ACEi OR ARB / CCB) 
\+  add either CCB if on A or A/ add A or A if on CCB  OR add a thiazide like diuretic
91
Q

What would third line of treatment be for hypertenison?

A

ACEi or ARB + CCB + thiazide like diuretic

92
Q

What would be fourth line of treatment for hypertension?

A

ACEi or ARB + CCB + thiazide like diuretic
+

Low dose spironolactone
Alpha or beta blocker

93
Q

What lifestyle changes for HTN?

A
  • Stop smoking
  • Low fat diet
  • Reduce alcohol and salt
  • Increase exercise + reduce weight if obese
94
Q

Describe aortic stenosis?

A

Symptoms occur when valve area is 1/4 of the normal (normal = 3-4cm2)

Types = supravalvular, subvalvular, valvular

Aetiology: congenital bicuspid valve, degenerative calcification, rheumatic disease

95
Q

How does aortic stenosis present?

A

Syncope
Angina
Dyspnoea
Heart failure

Old person who is SAD AS

96
Q

What are the physical signs of aortic stenosis?

A

Pulsus pardus an pulsus tardus

Heart sounds - soft or absent, S4 gallop due to LVH

Ejection systolic murmur - crescendo - decrescendo character

97
Q

What investigations would you carry out for aortic stenosis?

A

Echocardiography - diagnostic
ECG
CXR - LVH calcified aortic valve

98
Q

Management of aortic stenosis

A

General = dental care/hygiene - IE prophylaxis in dental procedures

Surgical = valve replacement, if not medically fit for surgery - transcatheter aortic valve replacement

99
Q

What is mitral regurgitation?

A

Backflow of blood from the LV to the LA during systole

100
Q

Describe the pathophysiology of mitral regurgitation?

A

Exertion dyspnoea
Palpitations
Fatigue

101
Q

What are the signs of mitral regurgitation?

A

Pansystolic murmur at the apex radiating to the axilla
Soft S1
Displaced hyperdynamic apex

102
Q

Investigations for mitral regurgitations?

A

Echocardiogram
CXR - englarged LA and LV
ECG

103
Q

Management of mitral regurgitation?

A

Vasodilator - ACEi e.g. hydralazine

Rate control for AF - BB, CCB, digoxin

Anticoagulation for AF and Flutter

Diuretics to control symptoms

Surgery for deteriorating symptoms - aim to replace the valve

104
Q

Describe aortic regurgitation?

A

Leakage of blood into the left ventricle during diastole due to ineffective coaptation or aortic cusps

Aetiology - RF, IE, bicuspid aortic valves

105
Q

Pathophysiology of aortic regurgitation?

A

Combined pressure and volume overload = left ventricle dilation and LVH

106
Q

What is the presentation of aortic regurgitation?

A
  • Exertional dyspnoea
  • Orthopnoea
  • Paroxysmal nocturnal dyspnoea
107
Q

Signs of of aortic regurgitation?

A
  • Collapsing water hammer pulse
  • Wide pulse pressure
  • Displaced hyperdynamic apex beat
  • Early diastolic murmur
108
Q

What are the notable eponyms of aortic regurgitation?

A 
Corrigans signs 
De Mussets sign 
Durioziez's sign 
Austin flint murmur 
Traube's sign
109
Q

Investigation of aortic regurgitation?

A

Echocardiogram
ECG
CXR - cardiomegaly

110
Q

Management of aortic regurgitation?

A

Medical - vasodilators, ACEi only if symptomatic or HTN

Surgical - Replace valve before LV dysfunction

111
Q

Describe mitral stenosis?

A

Obstruction of the left ventricle inflow that prevents proper filling during diastole

Causes = Rheumatic, IE, mitral annular calcification, congential

112
Q

Presentation of mitral stenosis?

A

Dyspnoea, fatigue, palpitations, chest pain

113
Q

Signs of mitral stenosis?

A 
Malar flush on cheeks 
Low volume pulse 
Tapping, non displaced apex beat 
Rumbling, mid diastolic murmur
Loud opening S1
114
Q

Investigations for mitral stenosis?

A

Echocardiogram
CXR - LA enlargement
ECG - AF and LA englargement

115
Q

Management of mitral stenosis

A

If in AF, rate contril
Anticoagulate with warfarin
Diuretics
Percutaneous mitral ballon valvotomy

116
Q

What is shock?

A

Circulatory failure resulting in inadequate organ perfusion

Low BP - systolic <90mmHg

117
Q

What are the different types of shock?

A
  1. SEPTIC: infection with any organism - acute vasodilation from inflammatory cytokines

2, ANAPHYLATIC: Type-I mediated hypersensitivity, release of histamine

  1. NEUROGENIC: Spinal cord injury, epidural or spinal anaesthesia
  2. HYPOVOLAEMIC: Bleeding, trauma, rupture, AA, GI bleed
118
Q

Define SIRS?

A

Systemic Inflammatory Response Sydrome (SIRS) is defined as

Temp >38 degrees or <36 degrees

Tachycardia >90bpm

Respiratory rate >/= 20 breaths per minute OR PACO2 <4.3kPA

WBC >12 x 10^9

119
Q

Describe the sepsis continuum?

A

SIRS

Sepsis = SIRS + presumed or confirmed infectious process

Severe sepsis = sepsis with end organ failure

Septic shock refractory hypotension

120
Q

Management of septic shock?

A

ABC = airways, breathing, circulation

Investigations and treatment - depend on the cause

Note: in septic shock, take blood cultures before antibiotics

121
Q

What is dilated cardiomyopathy?

A

Dilated cardiomyopathy is a progressive disease of the heart muscle that is characterised by ventricular chamber enlargement

Third most common cause of heart failure and most frequent reason for heart transplantation

122
Q

Symptoms and signs of dilated cardiomyopathy?

A

Fatigue
Dyspnoea on exertion
Orthopnoea, paroxysmal nocturnal cough
increasing oedema/weight

S3 gallop 
Tachycardia 
Tachypnoea 
Irregular BP 
Balloon shape heart on chest Xray
123
Q

Pathology of dilated cardiomyopathy?

A

Enlarged, heavy, dilated heart, possible cardiac weight of up to 900g

Histology shows variable atrophy and hypertrophy

Increased interstitial tissue

Occasional inflammatory cells

124
Q

Investigations for dilated cardiomyopathy?

A
  • Complete blood count
  • B-type natriuretic peptide assay
  • Chest radiography
  • Echocardiography
  • Cardiac magnetic resonance imaging (MRI)
  • Electrocardiography (ECG)
125
Q

What is restrictive cardiomyopathy?

A

Poor dilation of the heart restricts the eventual ability of the heart to take on blood and pass it on to the rest of the body

126
Q

Describe a heart with restrictive cardiomyopathy?

A

Firm enlarged heavy heart with diffuse infiltration of the protein into the myocytes bloody vessels and valves

ECG would be low voltage

127
Q

Describe hypertrophic cardiomyopathy?

A

Many mutations recognised involving B myosin, myosin binding protein C, troponin T, titin

Some mutations are associated with clinical feature=
B myosin: cardiac hypotrophy and dysrhythmia
Troponin T: sudden death

128
Q

What is the pathophysiology of aortic dissection?

A

Tear in the tunica intima of the wall of the aorta

129
Q

What are the associations / risk factors with aortic dissection?

A
  • Hypertension: most important risk factor
  • Trauma
  • Collagens (marfans syndrome)
  • Turners and Noonans syndrome
  • Pregnancy
  • Syphillis
130
Q

What are the features of aortic dissection??

A
  • Chest pain, typically severe, radiated through to the back and tearing in nature
  • Aortic regurgitation
  • Hypertension
  • Other features may result from the involvement of specific arteries e.g. coronary arteries
  • Majority of patients have no or non specific ECG changes, in a minority of patients ST segment elevation may be seen in inferior leads
131
Q

What investigations would be carried out for an aortic dissection?

A

History and physical examination

Imaging studies - chest radiography is first line, CT is the definitive test

Electrocardiography

Full blood count, serum chemistry, cardiac markers

132
Q

What management for aortic dissection?

A

Surgical treatment - area of the aorta with intimal tear is resected and replaced

Medical treatment - antihypertensives and narcotics

133
Q

Who is screened for AAA?

A

Men over 65

134
Q

Which groups suffer with aortic aneurisms?

A

Those who suffer with standard arterial disease

Those with connective tissue disorders e.g. Marfan’s

135
Q

Symptoms of AAA?

A

Pulsing sensation in the stomach like a heart beat

Stomach pain that does not go away

Lower back pain that does not go away

136
Q

What are the symptoms of a burst AAA?

A

Sudden, severe pain in the tummy or lower back

Dizziness

Sweaty, pale and clammy skin

A fast heartbeak

SoB

Syncope

137
Q

Investigations for AAA?

A

Screening
CT of the abdomen
Ultrasound of the abdomen

138
Q

What is the management of AAA?

A

Surgery:

  • Symptomatic aneurysms (80% annual mortality if untreated)
  • Increases size about 5.5.cm
  • Rupture (100% mortality without surgery)

Phase 2a (13 decks)

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