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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the possible end results of atherosclerosis?

A
  • Angina
  • Acute coronary syndrome
  • TIA
  • Strokes
  • Peripheral arterial disease
  • Chronic mesenteric ischaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define peripheral arterial disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the examination findings in peripheral vascular disease?

A
Weak peripheral pulses
Pallor
Cold
Skin changes
Buerger's test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the investigations in peripheral vascular disease?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 6P’s in critical limb ischaemia

A
Pain
Pallor
Paraesthesia
Pulselessness
Paralysis
Perishing cold
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the management for critical limb ischaemia?

A
Urgent referral to vascular 
Analgesia
Urgent revascularisation by:
- angioplassty and stending
- bypass surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the complications of HTN?

A
Ischaemic heart disease
Cerebrovascular accident
Hypertensive retinopathy
Hypertensive nephropathy
Heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the medical options of HTN?

A
ACE inhibitor 
Beta blocker
Calcium channel blocker
Diuretic (thiazide like)
ARB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the management of venous ulcers?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What murmur is heard with a patent ductus arteriosus?
A normal first heart sound with a continuous crescendo-decrescendo "machinery" murmur
26
How is a patent ductus arteriosus diagnosed?
confirmed by echo
27
Describe the management of patent ductus arteriosus
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
28
Give the pathophysiology of atrial septal defects
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.
29
What are the different types of atrial septal defects?
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 .
30
What are the complications of atrial septal defects?
Stroke with VTE** AF or atrial flutter Pulmonary HTN or R sided HF Eisenmenger syndrome
31
Give the presentation of atrial septal defects
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 ```
32
What is the management of atrial septal defects?
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
33
What is the condition association and pathophysiology of ventricular septal defects?
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.
34
Describe the presentation of ventricular septal defects
``` Typically asymptomatic but if symptomatic: Poor feeding Dyspnoea Tachypnoea Failure to thrive ```
35
What are the examination findings in ventricular septal defect?
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
36
What are the causes of a pan-systolic mumur?
Ventricular septal defect Mitral regurg Tricuspid regurg
37
What is the management of ventricular septal defects?
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
38
Define tetralogy of fallot
There are four coexisting pathologies: - Ventricular septal defect - Overriding aorta - Pulmonary valve stenosis - Right ventricular hypertrophy
39
Give the pathophysiology of tetralogy of fallot
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.
40
What are the risk factors for tetralogy of fallot?
Rubella infection Increased age of the mother Alcohol consumption in pregnancy Diabetic mother
41
What are the investigations and findings in tetralogy of fallot?
Echo Doppler flow studies CXR showing boot shaped heart due to R ventricular thickening Ejection systolic murmur
42
Describe the presentation of tetralogy of fallot
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
What are "tet spells"
intermittent symptomatic periods where the right to left shunt becomes temporarily worsened precipitating a cyanotic episode.
44
What are the treatment options for tet spells?
Squat/knees to chest Medical: - Supplementary oxygen - B blockers - IV fluids - Morphine - Sodium bicarbonate - Phenylephrine infusion
45
What is the management of tetralogy of fallot?
Neonates: prostaglandin infusion to maintain ductus arteriosus. Total surgical repair by open heart surgery is the definitive treatment but mortality is around 5%
46
What is ebstein's anomaly and the conditions that it is associated with?
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
Describe the presentation of ebstein's anomaly?
- evidence of HF - gallop rhythm heard on auscultation - cyanosis - SOB/ tachypnoea - Poor feeding - Collapse or cardiac arrest
48
What are the investigations and their findings for ebstein's anomaly?
ECG: - arrhythmias - R atrial enlargement - RBBB - L axis deviation CXR: - cardiomegaly - R atrial enlargement Echo to confirm diagnosis and assess severity
49
What is the management of ebstein's anomaly?
Medical: - treat arrhythmias and HF - Prophylactic antibiotics to prevent infective endocarditis Definitive management is by surgical correction of underlying defect
50
What are the risk factors for infective endocarditis?
- rheumatic valve disease - prosthetic valves - congenital heart defects - IVDU - others: recent piercings
51
What are the causative organisms of Infective endocarditis?
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
What are the signs of tricuspid regurgitation?
pan-systolic murmur (louder on inspiration) prominent V waves in JVP pulsatile hepatomegaly left parasternal heave
53
What are the causes of tricuspid regurgitation?
``` Right ventricular infarction Pulmonary HTN Rheumatic heart disease Infective endocarditis Ebstein's anomaly Carcinoid syndrome ```
54
What is acute pericarditis?
Inflammation of the pericardium. It is one of the differentials of any patient presenting with chest pain
55
What are the signs and symptoms of acute pericarditis?
Chest pain: may be pleuritic. Often relieved by sitting forward Non-productive cough Dyspnoea Flu-like symptoms Signs: - Pericardial rub - tachypnoea - tachycardia
56
What are the causes of acute pericarditis?
- viral infections (coxsackie) - Tb - Uraemia - trauma - post MI, dressler's syndrome - connective tissue disease - hypothyroidism - malignancy
57
What are the investigations and their findings for acute pericarditis?
ECG changes: - saddle-shaped ST elevation - PR depression Transthoracic echo
58
What is the management of acute pericarditis?
- treat underlying cause | - combination of NSAIDs and colchicine is now first line
59
What is the causes of constrictive pericarditis?
- any cause of acute pericarditis | - especially Tb
60
What are the features of constrictive pericarditis
- dyspnoea - RHF: elevated JVP, ascites, oedema, hepatomegaly - JVP shows prominent x and y descent - pericardial knock - loud S3 - Kussmaul's sign is positive
61
What is seen on CXR for constrictive pericarditis?
Pericardial calcification
62
What is the definition of aortic stenosis?
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
Describe the presentation of aortic stenosis
May be asymptomatic and found incidentally or: - chest pain - dyspnoea - syncope symptoms are typically worse on exertion
64
Describe the signs of aortic stenosis
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
What are the causes of aortic stenosis?
- Degenerative calcification (>65) - Bicuspid aortic valve (<65) - William's syndrome - post-rheumatic disease - subvalvular: HOCM
66
What is the investigation and management for aortic stenosis?
If asymptomatic, then observe patient if symptomatic, valve replacement ECHO is the gold standard investigation for diagnosis
67
Give the features of aortic regurgitation
- early diastolic murmur: intensity increased by handgrip manoeuvre - collapsing pulse - wide pulse pressure - Quincke's sign - De musset' s sign
68
What are the causes of aortic regurgitation?
Rheumatic fever Infective endocarditis Connective tissue diseases (RA/SLE) Bicuspid aortic valve
69
What are the causes of mitral stenosis?
RHEUMATIC FEVER Mucopolysaccharidoses Carcinoid Endocardiall fibroelastosis
70
What are the features of mitral stenosis?
``` Mid-late diastolic murmur Loud S1, opening snap Low volume pulse Malar flush AF ```
71
What can be seen on CXR for mitral stenosis?
L atrial enlargement
72
What can be seen on echo for mitral stenosis?
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
Give the pathophysiology of mitral regurgitation
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
What are the risk factors for mitral regurgitation?
``` Female Lower body mass Age Renall dysfunction Prior MI Prior mitral stenosis or valve prolapse Collagen disorders ```
75
What are the causes of mitral regurgitation?
- 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
What are the symptoms of mitral regurgitation?
Most are asymptomatic, but if there is: - fatigue - SOB - oedema
77
What are the signs of mitral regurgitation?
- pansystolic murmur - described as 'blowing' - heard best at the apex and radiating into the axilla
78
What are the investigations and findings in mitral regurgitation?
ECG: borad P wave, indicative of atrial enlargement CXR: cardiomegaly with enlarged left atrium and ventricle Echo: Crucial to DIAGNOSIS
79
What are the treatment options in mitral regurgitation?
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
Describe the presentation of myocarditis
- usually <50yr - 2-3 week hx of viral syx - Recent travel? Symptoms: - fatigue - chest pain - dyspnoea/orthopnoea - palpitations, syncope
81
What is the examination findings for myocarditis
S3 and S4 gallops Pericardial rub Tachycardia
82
What are the investigations and findings for myocarditis?
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
What is the management of myocarditis?
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
Define infective endocarditis
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
What are the risk factors for infective endocarditis?
Valvular damage: - previous rheumatic heart disease - age related vascular degeneration - prosthetic valve IVDU
86
Describe the signs and symptoms of infective endocarditis
Acute presentation: - fever and new heart murmur - petechiae - haematuria - cerebral emboli Textbook signs of IE: - janeway lesions - Osler's nodes - vasculities - thrombocytopaenia - malignancy
87
What is the diagnosis of infective endocarditis?
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
What are the indications for surgery in Infective endocarditis?
``` IE resistant to abs Fungal disease resistant to tx IE causing embolic events IE with CHF Structural damage on echo ```
89
What is the presentation of left atrial myxoma?
Popping sound in early diastole | Loud 1st heart sound
90
What is the normal cardiac axis?
-30 to 90
91
What is used for medical cardioversion?
Flecanide
92
What is incorporated in the CHA2DS2-VASc score?
``` 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
Which artery stemming from the aorta can impact descending aortic dissection?
Left renal artery
94
What is nicorandil used for?
Angina
95
What is the presentation of cardiac tamponade?
Classical features - Beck's triad: hypotension raised JVP muffled heart sounds Pulsus paradox
96
What is the stepwise approach to heart failure treatment?
1. ACEi and B-blockers 2. Aldosterone antagonist 3. Specialist led: Ivabradine, digoxin, hydralazine + nitrate, sacubitril-valsartan or cardiac resychronisation
97
Which is the only calcium channel blocker licensed for heart failure?
Amlodipine
98
What is the mechanism of action of calcium gluconate?
Stabilises the myocardium and does NOT lower potassium
99
What is the management of a new BP of >180/120 and no worrying signs?
1st line: urgent investigation for end organ damage
100
What is secondary prevention for patients with stroke and AF?
Apixaban or warfarin