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Finals > CVS > Flashcards

CVS Flashcards

1
Q

Define aortic dissection

A

Where there is a break in the lumen of the aorta that causes blood to flow between the layers of the wall creating a false lumen.

Most commonly affects around the ascending aorta and aortic arch.

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2
Q

What is the presentation of aortic dissection?

A
  • Tearing chest pain of sudden onset
  • Radiating to back
  • HTN
  • Hypotension as the dissection becomes more severe
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3
Q

What is the management of aortic dissection?

A 
Type A (ascending aorta):
- surgical management but manage HTN to between 120-100 systolic

Type B (descending aorta):
Supportive
Manage HTN with IV labetalol

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4
Q

What are the possible end results of atherosclerosis?

A
  • Angina
  • Acute coronary syndrome
  • TIA
  • Strokes
  • Peripheral arterial disease
  • Chronic mesenteric ischaemia
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5
Q

Define peripheral arterial disease

A

PAD results from atherosclerosis and narrowing of the arteries supplying the limbs and periphery

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6
Q

Define critical limb ischaemia

A

is the end stage of peripheral arterial disease where there is an inadequate supply of blood to a limb to allow it to function normally at rest

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7
Q

Define intermittent claudication

A

is the symptom of having ischaemia in a limb during exertion that is relieved by rest. it is typically a crampy, achy pain in the calf muscles associated with muscle fatigue when walking beyond a certain intensity.

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8
Q

What is Leriche’s syndrome and what is the clinical presentation?

A

Associated with occlusion in the distal aorta or proximal common iliac artery

Clinical triad:

  • thigh/buttock claudication
  • Absent femoral pulses
  • Male impotence
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9
Q

What are the examination findings in peripheral vascular disease?

A 
Weak peripheral pulses
Pallor
Cold
Skin changes
Buerger's test
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10
Q

What are the investigations in peripheral vascular disease?

A

ABPI (>0.9 normal)
Arterial doppler
Angiography (CT or MRI)

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11
Q

What are the 6P’s in critical limb ischaemia

A 
Pain
Pallor
Paraesthesia
Pulselessness
Paralysis
Perishing cold
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12
Q

What is the management of intermittent claudication?

A
  • Lifestyle changes to reduce risk factors
  • Optimal medical tx for comorbidities
  • Medical treatments: Atorvastating 80mg, Clopidogrel 75mg, naftidrofuryl oxalate (vasodilator).
  • Surgical treatments: angioplasty and stenting, bypass surgery
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13
Q

What is the management for critical limb ischaemia?

A 
Urgent referral to vascular 
Analgesia
Urgent revascularisation by:
- angioplassty and stending
- bypass surgery
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14
Q

What are the causes of primary and secondary hypertension?

A

Primary has no particular cause

Secondary: ROPE
- Renal diseease
Obesity
Pregnancy induced
Endocrine
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15
Q

What are the complications of HTN?

A 
Ischaemic heart disease
Cerebrovascular accident
Hypertensive retinopathy
Hypertensive nephropathy
Heart failure
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16
Q

What are the investigations done in order to assess for end organ damage in HTN?

A

Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage

Bloods for HbA1c, renal functiona nd lipids

Fundus examination for hypertensive retinopathy

ECG for cardiac abnormalities

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17
Q

What is the medical options of HTN?

A 
ACE inhibitor 
Beta blocker
Calcium channel blocker
Diuretic (thiazide like)
ARB
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18
Q

What is the medical management ladder in HTN?

A

Step 1:

  • Aged less than 55 and non-black use ACE inhibitor
  • Aged over 55 or black use Calcium channel blocker

Step 2: A+C or A+D or C+D (if black use ARB instead of A)

Step 3: A+C+D

Step 4: A+C+D+additional

Additonal: if K+ <4.5mmol then spironolactone. If >4.5 alpha or beta blocker

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19
Q

Give the pathophysiology of venous ulcers

A

Occurs due to pooling of blood and waste products in the skin secondary to venous deficiency (varicose veins, DVT, phlebitis etc)

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20
Q

What are the distinguishing features of venous ulcers?

A
  • Odematous flushed skin
  • Hyperpigmentation to skin
  • Varicose eczema
  • Tend to be larger
  • Irregular boarder
  • More likely to bleed
  • Pain relieved by elevation and worse on hanging
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21
Q

What is the management of venous ulcers?

A

Treat underlying cause
Good wound care
Tissue viability nurse
Plastic surgery input

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22
Q

Define Patent ductus arteriosis

A

The ductus arterosus normally stops functioning within 1-3 days of birth but when it doesn’t it’s called patent ductus arterosus.

It can be due to maternal infections such as rubella or genetic. Prematurity is a key risk factor.

Small PDA can be asymptomatic throughout childhood and present with heart failure like symptoms later in life.

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23
Q

Describe the pathophysiology of patent ductus arteriosus

A

pressure in the aorta is higher than that in the pulmonary vessels, so blood flows from the aorta to the pulmonary artery.

This creates a left to right shunt where blood from the left side of the heart crosses to the right side increasing the pressure in the pulmonary vessels thus causing pulmonary hypertension leading to right sided heart strain.

Pulmonary hypertension and right sided heart strain lead to right ventricular hypertrophy.

The increased blood flowing through the pulmonary vessels and returning to the left side of the heart leads to left ventricular hypertrophy.

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24
Q

Describe the presentation of the patent ductus arteriosus

A

Can be picked up during newborn examination if a murmur is heard but may also present with:

  • SOB
  • difficulty feeding
  • poor weight gain
  • LRTI
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25
Q

What murmur is heard with a patent ductus arteriosus?

A

A normal first heart sound with a continuous crescendo-decrescendo “machinery” murmur

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26
Q

How is a patent ductus arteriosus diagnosed?

A

confirmed by echo

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27
Q

Describe the management of patent ductus arteriosus

A

typically patients monitored until 1 year of age using echos.

After 1 year, highly likely that PDA will close spontaneously and trans-catheter or surgical closure can be performed.

Indomethacin

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28
Q

Give the pathophysiology of atrial septal defects

A

ASD leads to shunt with blood moving from left to right.

This means blood continues to flow to the lungs and pt does not become cyanotic but increased flow to right side leads to right sided overload and right heart strain.

This can lead to right heart failure and pulmonary hypertension.

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29
Q

What are the different types of atrial septal defects?

A
  1. Ostium secondum where the septum secondum fails to fully close leaving a hole in the wall
  2. Patent foramen ovale, where the foramen ovale fails to close
  3. Ostium primum where the septum primum fails to filly close. This tends to lead to atrioventriculalr valve defects .
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30
Q

What are the complications of atrial septal defects?

A

Stroke with VTE**
AF or atrial flutter
Pulmonary HTN or R sided HF
Eisenmenger syndrome

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31
Q

Give the presentation of atrial septal defects

A

mild-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border with fixed split second heart sound.

May be asymptomatic and present later with dyspnoea, HF or stroke.

Childhood symptoms are:
SOB
Difficulty feeding
Poor weight gain
 LRTI
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32
Q

What is the management of atrial septal defects?

A

Refer to paeds cardio

Surgically closing with a transvenous catheter closure or open heart surgery.

Anti-coagulants to reduce risk of clots and stroke in adults

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33
Q

What is the condition association and pathophysiology of ventricular septal defects?

A

Commonly associated with Down’s syndrome and Turner’s syndrome.

Left to right shunt leads to right sided overload, R HF and increased flow into the pulmonary vessels.

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34
Q

Describe the presentation of ventricular septal defects

A 
Typically asymptomatic but if symptomatic: 
Poor feeding
Dyspnoea
Tachypnoea
Failure to thrive
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35
Q

What are the examination findings in ventricular septal defect?

A

pan-systolic murmur more prominently heard at the left lower sternal border in the third and fourth intercostal spaces.

There may be a systolic thrill on palpation

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36
Q

What are the causes of a pan-systolic mumur?

A

Ventricular septal defect
Mitral regurg
Tricuspid regurg

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37
Q

What is the management of ventricular septal defects?

A

Can be corrected surgically using a transvenous catheter closure via the femoral vein or open heart surgery.

There is an increased risk of infective endocarditis therefore prophylactic antibiotics should be considered during surgical procedures

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38
Q

Define tetralogy of fallot

A

There are four coexisting pathologies:

  • Ventricular septal defect
  • Overriding aorta
  • Pulmonary valve stenosis
  • Right ventricular hypertrophy
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39
Q

Give the pathophysiology of tetralogy of fallot

A

Overriding aorta and pulmonary stenosis encourage blood to be shunted from the R heart to the left causing cyanosis.

Right ventricular hypertrophy develops due to increased resistance leading to right to left cardiac shunt.

Blood bypasses the lungs and thus cyanosis occurs. The degree to which this happens depends on severity of pulmonary stenosis.

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40
Q

What are the risk factors for tetralogy of fallot?

A

Rubella infection
Increased age of the mother
Alcohol consumption in pregnancy
Diabetic mother

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41
Q

What are the investigations and findings in tetralogy of fallot?

A

Echo
Doppler flow studies
CXR showing boot shaped heart due to R ventricular thickening
Ejection systolic murmur

42
Q

Describe the presentation of tetralogy of fallot

A

Severe cases will present with HF before 1 year and S+S

Signs and symptoms:
Cyanosis
Clubbing
Poor feeding
Poor weight gain
Ejection systolic murmur heard loudest in the pulmonary area
"tet spells"
43
Q

What are “tet spells”

A

intermittent symptomatic periods where the right to left shunt becomes temporarily worsened precipitating a cyanotic episode.

44
Q

What are the treatment options for tet spells?

A

Squat/knees to chest

Medical:

  • Supplementary oxygen
  • B blockers
  • IV fluids
  • Morphine
  • Sodium bicarbonate
  • Phenylephrine infusion
45
Q

What is the management of tetralogy of fallot?

A

Neonates: prostaglandin infusion to maintain ductus arteriosus.

Total surgical repair by open heart surgery is the definitive treatment but mortality is around 5%

46
Q

What is ebstein’s anomaly and the conditions that it is associated with?

A

Where the tricuspid valve is set lower in the R side of the heart causing a bigger right atrium and a smaller R ventricle.

Associated with cyanosis and Wolf-parkinson-white syndrome

47
Q

Describe the presentation of ebstein’s anomaly?

A
  • evidence of HF
  • gallop rhythm heard on auscultation
  • cyanosis
  • SOB/ tachypnoea
  • Poor feeding
  • Collapse or cardiac arrest
48
Q

What are the investigations and their findings for ebstein’s anomaly?

A

ECG:

  • arrhythmias
  • R atrial enlargement
  • RBBB
  • L axis deviation

CXR:

  • cardiomegaly
  • R atrial enlargement

Echo to confirm diagnosis and assess severity

49
Q

What is the management of ebstein’s anomaly?

A

Medical:

  • treat arrhythmias and HF
  • Prophylactic antibiotics to prevent infective endocarditis

Definitive management is by surgical correction of underlying defect

50
Q

What are the risk factors for infective endocarditis?

A
  • rheumatic valve disease
  • prosthetic valves
  • congenital heart defects
  • IVDU
  • others: recent piercings
51
Q

What are the causative organisms of Infective endocarditis?

A

Staph aureus is now the most common cause. Also common in acute presentation and IVDUs

Staph epidermidis commonly colonise indwelling lines and is most common in patients following prosthetic valve surgery

52
Q

What are the signs of tricuspid regurgitation?

A

pan-systolic murmur (louder on inspiration)
prominent V waves in JVP
pulsatile hepatomegaly
left parasternal heave

53
Q

What are the causes of tricuspid regurgitation?

A 
Right ventricular infarction
Pulmonary HTN
Rheumatic heart disease
Infective endocarditis
Ebstein's anomaly
Carcinoid syndrome
54
Q

What is acute pericarditis?

A

Inflammation of the pericardium. It is one of the differentials of any patient presenting with chest pain

55
Q

What are the signs and symptoms of acute pericarditis?

A

Chest pain: may be pleuritic. Often relieved by sitting forward

Non-productive cough

Dyspnoea

Flu-like symptoms

Signs:

  • Pericardial rub
  • tachypnoea
  • tachycardia
56
Q

What are the causes of acute pericarditis?

A
  • viral infections (coxsackie)
  • Tb
  • Uraemia
  • trauma
  • post MI, dressler’s syndrome
  • connective tissue disease
  • hypothyroidism
  • malignancy
57
Q

What are the investigations and their findings for acute pericarditis?

A

ECG changes:

  • saddle-shaped ST elevation
  • PR depression

Transthoracic echo

58
Q

What is the management of acute pericarditis?

A
  • treat underlying cause

- combination of NSAIDs and colchicine is now first line

59
Q

What is the causes of constrictive pericarditis?

A
  • any cause of acute pericarditis

- especially Tb

60
Q

What are the features of constrictive pericarditis

A
  • dyspnoea
  • RHF: elevated JVP, ascites, oedema, hepatomegaly
  • JVP shows prominent x and y descent
  • pericardial knock - loud S3
  • Kussmaul’s sign is positive
61
Q

What is seen on CXR for constrictive pericarditis?

A

Pericardial calcification

62
Q

What is the definition of aortic stenosis?

A

Narrow aortic valve that restricts from blood flow from the left ventricle into the aorta.

Aortic valve is usually made up on 3 leaflets but in aortic stenosis, they can have anywhere between one - four leaflets.

63
Q

Describe the presentation of aortic stenosis

A

May be asymptomatic and found incidentally or:

  • chest pain
  • dyspnoea
  • syncope

symptoms are typically worse on exertion

64
Q

Describe the signs of aortic stenosis

A

Ejection systolic murmur heard loudest at the aortic area

  • it has a crescendo-decrescendo character
  • radiates to the carotid.

Other signs:

  • ejection click
  • palpable thrill
  • slow rising pulse and narrow pulse pressure
65
Q

What are the causes of aortic stenosis?

A
  • Degenerative calcification (>65)
  • Bicuspid aortic valve (<65)
  • William’s syndrome
  • post-rheumatic disease
  • subvalvular: HOCM
66
Q

What is the investigation and management for aortic stenosis?

A

If asymptomatic, then observe patient

if symptomatic, valve replacement

ECHO is the gold standard investigation for diagnosis

67
Q

Give the features of aortic regurgitation

A
  • early diastolic murmur: intensity increased by handgrip manoeuvre
  • collapsing pulse
  • wide pulse pressure
  • Quincke’s sign
  • De musset’ s sign
68
Q

What are the causes of aortic regurgitation?

A

Rheumatic fever
Infective endocarditis
Connective tissue diseases (RA/SLE)
Bicuspid aortic valve

69
Q

What are the causes of mitral stenosis?

A

RHEUMATIC FEVER
Mucopolysaccharidoses
Carcinoid
Endocardiall fibroelastosis

70
Q

What are the features of mitral stenosis?

A 
Mid-late diastolic murmur 
Loud S1, opening snap
Low volume pulse
Malar flush
AF
71
Q

What can be seen on CXR for mitral stenosis?

A

L atrial enlargement

72
Q

What can be seen on echo for mitral stenosis?

A

normal cross sectional area of the mitral valve is 4-6sq cm. A ‘tight’ mitral stenosis implies a cross sectional area of <1sq cm

73
Q

Give the pathophysiology of mitral regurgitation

A

When blood leaks back through the mitral valve on systole. Myocardium can thicken over time and eventually go into irreversible HF

2nd most common valve disease after aortic stenosis

74
Q

What are the risk factors for mitral regurgitation?

A 
Female
Lower body mass
Age
Renall dysfunction
Prior MI
Prior mitral stenosis or valve prolapse
Collagen disorders
75
Q

What are the causes of mitral regurgitation?

A
  • following coronary artery disease or MI, as a result of damage to its supporting structures
  • mitral valve prolapse: when the leaflets of the mitral valve are deformed so the valve doesn’t close properly
  • Infective endocarditis
  • Rheumatic fever
  • Congenital
76
Q

What are the symptoms of mitral regurgitation?

A

Most are asymptomatic, but if there is:

  • fatigue
  • SOB
  • oedema
77
Q

What are the signs of mitral regurgitation?

A
  • pansystolic murmur
  • described as ‘blowing’
  • heard best at the apex and radiating into the axilla
78
Q

What are the investigations and findings in mitral regurgitation?

A

ECG: borad P wave, indicative of atrial enlargement

CXR: cardiomegaly with enlarged left atrium and ventricle

Echo: Crucial to DIAGNOSIS

79
Q

What are the treatment options in mitral regurgitation?

A

Medical management in acute cases:

  • nitrates
  • diuretics
  • positive inotropes
  • intra-aortic balloon pump

If HF:
- ACEi, B-blockers and spironolactone

In acute, severe: surgery

Repair over replacement has lower mortality and higher survival rates but if not possible then replace with either artificial or a pig valve.

80
Q

Describe the presentation of myocarditis

A
  • usually <50yr
  • 2-3 week hx of viral syx
  • Recent travel?

Symptoms:

  • fatigue
  • chest pain
  • dyspnoea/orthopnoea
  • palpitations, syncope
81
Q

What is the examination findings for myocarditis

A

S3 and S4 gallops
Pericardial rub
Tachycardia

82
Q

What are the investigations and findings for myocarditis?

A

ECG:

  • ST depression or elevation
  • T wave inversion
  • AV node block

Bloods: raised troponin and CK-MB

CXR: enlarged heart and/or HF

Echo: ventricular dilatation and abnormal wall movement

Biopsy: definitive test but v risky so not done often

Cardiac MRI:: useful to differentiate myocarditis and ischemia/infarction

83
Q

What is the management of myocarditis?

A

Acute + haemodynamically stable:

  • supportive care
  • treat underlying cause

If ventricular dysfunction: ACEi/ARB

Acute + haemodynamically unstable:
- IV arterial vasodilator

Refractory/end stage:

  1. Heart transplant
  2. L ventricular assist device
84
Q

Define infective endocarditis

A

A condition caused by infection of the endocardium by bacteria. Most commonly occur at sites of previous damage but can affect normal ones as well. S. Aureus will commonly infect tricuspid valve in IVDU

85
Q

What are the risk factors for infective endocarditis?

A

Valvular damage:

  • previous rheumatic heart disease
  • age related vascular degeneration
  • prosthetic valve

IVDU

86
Q

Describe the signs and symptoms of infective endocarditis

A

Acute presentation:

  • fever and new heart murmur
  • petechiae
  • haematuria
  • cerebral emboli

Textbook signs of IE:

  • janeway lesions
  • Osler’s nodes
  • vasculities
  • thrombocytopaenia
  • malignancy
87
Q

What is the diagnosis of infective endocarditis?

A

MAJOR:

  • positive blood culture for infective organisms on 2 separate tests if >12 hours apart
  • Echo shows strictures, unusual blood flow, abscesses
  • new valve regurgitation

MINOR:

  • fever >38
  • predisposition to IE
  • unusual echo
  • immunological factors present
  • blood culture positive

IE definitely present:

  • 2 major or
  • 1 major, 3 minor
  • 5 minor
88
Q

What are the indications for surgery in Infective endocarditis?

A 
IE resistant to abs 
Fungal disease resistant to tx
IE causing embolic events
IE with CHF
Structural damage on echo
89
Q

What is the presentation of left atrial myxoma?

A

Popping sound in early diastole

Loud 1st heart sound

90
Q

What is the normal cardiac axis?

A

-30 to 90

91
Q

What is used for medical cardioversion?

A

Flecanide

92
Q

What is incorporated in the CHA2DS2-VASc score?

A 
Congestive HF 1
HTN or anti-hypertensives 1
Age >75 2
DM 1
Stroke/TIA previously 2
Vascular disease 1
Age 65-74 1
Sex: Female 1
93
Q

Which artery stemming from the aorta can impact descending aortic dissection?

A

Left renal artery

94
Q

What is nicorandil used for?

A

Angina

95
Q

What is the presentation of cardiac tamponade?

A

Classical features - Beck’s triad:
hypotension
raised JVP
muffled heart sounds

Pulsus paradox

96
Q

What is the stepwise approach to heart failure treatment?

A
  1. ACEi and B-blockers
  2. Aldosterone antagonist
  3. Specialist led: Ivabradine, digoxin, hydralazine + nitrate, sacubitril-valsartan or cardiac resychronisation
97
Q

Which is the only calcium channel blocker licensed for heart failure?

A

Amlodipine

98
Q

What is the mechanism of action of calcium gluconate?

A

Stabilises the myocardium and does NOT lower potassium

99
Q

What is the management of a new BP of >180/120 and no worrying signs?

A

1st line: urgent investigation for end organ damage

100
Q

What is secondary prevention for patients with stroke and AF?

A

Apixaban or warfarin

Finals (20 decks)

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