Cardiovascular Flashcards
(162 cards)
1
Q
What bacteria is responsible for rheumatic valve disease?
A
Streptococcus pyogenes
2
Q
What are the three leaflets of the aortic valve called?
A
Right
Left
Non-coronary
3
Q
What are three causes of aortic stenosis?
A
Age (wear and tear –> calcification)
Rheumatic valve disease
Congenital
4
Q
Describe the murmur associated with aortic stenosis
A
Ejection systolic murmur
Radiates to the right upper sternal edge, suprasternal notch and carotids
5
Q
What is the progressive effects of aortic stenosis?
A
Increased LV cavity pressure –> pressure overload –> LV hypertrophy
6
Q
What are the symptoms of aortic stenosis?
A
SOB Chest pain Pre-syncope Syncope Reduced exercise capacity
7
Q
What are the causes of aortic regurgitation?
A
Degenerative Rheumatic valve disease Aortic root dilation Systemic disease Endocarditis
8
Q
Give examples of systemic diseases that can result in aortic regurgitation
A
Marfan’s syndrome
Ehler Danlos syndrome
Ankylosing spondylitis
SLE
9
Q
What is the effect of aortic regurgitation?
A
Blood pushed into aorta In diastole, the valves are incompetent Blood flows back into LV Volume overloaded LV dilation
10
Q
What are the symptoms of aortic regurgitation?
A
SOB
Reduced exercise capacity
11
Q
What is the prevalence of people having a bicuspid aortic valve rather than a tricuspid aortic valve?
A
1-2%
12
Q
What are people with a bicuspid aortic valve prone to developing?
A
Premature dysfunction
13
Q
Describe the mitral valve
A
Fibrous annulus - this can become dilated which pulls the valve leaflets apart
Anterior and posterior leaflets - anterior do the most work
Chordae tendinae and papillary muscles
14
Q
What is the nomenclature of the anterior and posterior leaflets of the mitral valve?
A
A1, A2, A3
P1, P2, P3
15
Q
What is the major cause of mitral stenosis?
A
Rheumatic valve disease
16
Q
What is the effect of mitral stenosis?
A
Pressure overload
Dilated LA
AF
17
Q
Other than AF, what are the two other potential effects of mitral stenosis?
A
Pulmonary hypertension
Secondary right heart dilatation
18
Q
What are the symptoms of mitral stenosis?
A
SOB Palpitations Chest pain Haemoptysis Right heart failure symptoms (pitted oedema, ascites etc)
19
Q
What is the effect of mitral regurgitation?
A
Volume overload in both LA and LV
LA and LV dilation
Pulmonary hypertension and secondary right heart dilation
AF
20
Q
What are the symptoms of mitral regurgitation?
A
SOB
Palpitations
RHF symptoms
21
Q
Who is most likely to develop pathology of the pulmonary valve?
A
Children and young adults
22
Q
What are the causes of tricuspid valve pathologies?
A
Pulmonary hypertension
IVDU
Endocarditis
23
Q
How should valvular disease be assessed?
A
History Examination - murmur BP ECG ECHO - valvular dysfunction CT MRI Exercise tolerance test, CPET, Stress ECHO
24
Q
What medical treatments can be used in the management of valvular disease?
A
Diuretics - reduce overload on heart
Mainly surveillance - watch and wait
25
What are the different surgical options for the management of valvular disease?
Valve repair
Valve replacement
Mechanical
Tissue
26
What type of valve replacement requires warfarin?
Mechanical
27
What are the two procedures that can be used in the management of valvular disease?
TAVI (transcatheter aortic valve intervention)
| Valvuloplasty
28
When can valvuloplasty be used?
Role in mitral valve disease
Mainly young people with RVD
Buy time before valve replacement
29
What is the risk of stroke associated with AF?
5-fold increase compared to general population
30
What percentage of the population have AF?
1.5-2% (prevalence is increasing with the ageing population)
31
Give examples of conditions that predispose to or encourage the progression of AF
```
HTN
Symptomatic HF
Valvular heart disease
Cardiomyopathies
ASDs
Coronary artery disease
Thyroid dysfunction
Obesity
DM
COPD
Sleep apnoea
Chronic renal disease
```
32
What symptoms are associated with AF?
Asymptomatic
Palpitation
Dyspnoea
(rare: chest pain, syncope)
May present with the complications of AF (stroke/peripheral emboli)
33
What type of pulse is associated with AF?
Irregularly irregular
34
What are the three types of AF?
Paroxysmal
Persistent
Permanent
35
Describe paroxysmal AF
Intermittent
Starts and stops
Can last from 30s to over 24hrs at a time
36
Describe persistent AF
Requires intervention to terminate the arrhythmia (IV antiarrhythmic drug or DC cardioversion)
37
Describe permanent AF
Continually there, won't try to restore sinus rhythm
38
What ECG changes are associated with AF?
Absence of P waves
| Irregular QRS complex
39
Describe the ECG changes associated with AF
Atria aren't contracting as a synctium
Different cells are contracting at different rates
There are multiple entry circuits
Ventricles have a variable rate dependent upon which impulses are able to pass through the AV node --> Bundle of His --> activate the ventricles
40
Describe atrial flutter
Re-entry around the tricuspid valve
Atria contracting at a rate of 250-300bpm
Saw-tooth pattern on ECG
41
On what ECG leads can a saw-tooth pattern be seen during atrial flutter?
Inferior leads II, III and aVF
42
What are the haemodynamic effects of AF and atrial flutter?
Loss of cardiac output
Atria are not beating in a coordinated fashion so blood clots may form in the atria --> break off --> thrombus can emboli to the brain, kidneys etc
43
What are the treatment aims in AF?
```
Prevention of stroke
Symptom relief
Optimum management of concomitant cardiovascular disease
Rate control
+/- correction of rhythm disturbance
```
44
What are the essential investigations for a patient with AF?
ECG - confirm arrhythmia
ECHO - structural heart disease
Thyroid function tests
LFTs
45
What is the target HR for a patient with AF who is:
a) asymptomatic
b) symptomatic
Asymptomatic: <110 bpm
Symptomatic: <80 bpm
46
If a patient doesn't have cardiac failure, how should their AF be managed?
```
Beta blocker (bisoprolol 2-5-5mg OD or atenolol 25-50mg BD)
OR
Ca antagonist (verapamil 120-240mg BD)
```
47
What is the second line treatment for a patient with AF who does not have HF?
Digoxin
48
What scoring system can be used to ascertain a patient's risk of having a stroke?
CHA2DS2-VASc
| out of 9
49
What are the components of the CHA2DS2-VASc scoring system?
```
Congestive heart failure/LV dysfunction
HTN
Age >/= 75 (2pts)
DM
Stroke/TIA/thrombo-emobolism (2pts)
Valvular disease
Age 65-74
Female sex
```
50
What should the INR target be for a patient with AF?
2-3
51
What is the risk of an INR >3?
Increased risk of intracranial bleed
52
What is the risk of an INR <2?
Increased risk of stroke
53
What treatment for AF requires INR measurements?
Warfarin
54
What are the new oral anti-coagulants that can be used in the management of AF?
Dabigatran - thrombin inhibitor
Rivaroxaban - factor Xa inhibitor
Apixaban - factor Xa inhibitor
Edoxaban - factor Xa inhibitor
55
Who should be referred for specialist assessment?
Patients who are symptomatic despite adequate rate control
Younger patients <60
Inadequate rate control despite beta-blocker/Ca antagonists + digoxin
Structural heart disease on ECHO
Co-existing HF
56
How can rhythm control be managed in patients with AF?
Direct current cardioversion
Antiarrhythmic drugs
Catheter ablation
57
What are class 1 antiarrhythmic drugs?
Na channel blockers
(Flecainide 100mg bd
Propafenone 150-300mg bd)
58
What are class 3 antiarrhythmic drugs?
K channel blockers --> prolong action potential duration/QT interval
Sotalol 80mg bd
Amiodarone 200mg OD
59
Give an example of a multichannel blocker that can be used in the management of AF
Dronedarone 400mg bd
60
Which veins can be the trigger of paroxysmal AF?
Pulmonary veins
61
What are the two ways of performing catheter ablation?
Radiofrequency current (burning)
Cryo-ablation (freezing)
62
In what patient group is catheter ablation more effective?
Structurally normal hearts
| Minimal heart disease
63
In what proportion of patients is catheter ablation curative in:
a) paroxysmal AF?
b) persistent AF?
Paroxysmal - 65-80%
| Persistent - 50-60%
64
Define endocarditis
Inflammation of the endocardium which results in vegetation formation and ultimately damage to the cusps of the valves
65
What are the components of the endocarditis vegetation?
```
Fibrin mesh
Platelets
White blood cells
Red blood cell debris
Organisms
```
66
Give some example microorganisms that can cause endocarditis
```
Staph. aureus
CoNS
Strept. viridans
HACEK
Coliforms
```
67
Describe HACEK
5 gram negative bacteria which cause endocarditis
Relatively rare
Culture negative endocarditis
68
What are the three classifications of endocarditis?
1. Native valve endocarditis
2. Endocarditis in IVDUs
3. Prosthetic valve endocarditis
69
What microorganisms commonly cause NVE?
S.viridans (oral flora --> transient bacteraemia caused by brushing teeth --> underlying valve disease)
Staphylococcus
70
What microorganisms commonly cause Endocarditis in IVDUs?
S.aureus
E.coli
Pseudomonas
Fungal endocarditis
71
What microorganisms commonly cause PVE?
Staphylococcus endocarditis eps CoNS
E.coli
Pseudomonas
Fungal endocarditis
72
What risk factors are associated with NVE?
Underlying valve abnormalities
Aortic stenosis
Mitral valve prolapse
73
Describe aortic stenosis
Narrowing of the aortic valve
Age-related calcification (50%)
Calcification of congenitally abnormal valve (30-40%)
Rheumatic fever (10%)
74
Briefly describe how Rheumatic Fever can cause NVE
Group A Strept or Strept. progenes infection
Contains streptolysin O toxin
Infection from streptococcus pyogenes --> strept. throat
Partially or untreated liberates the streptolysin toxin
Toxin attracts ASO antibodies
Causes destruction of streptolysin toxin
Protein of heart valves is similar to that of streptolysin toxin
Ab attack the heart valves
Stenosis/regurgitation
75
In IVDU endocarditis, what valve is most commonly affected?
Tricuspid
76
Describe the acute clinical features associated with endocarditis
Patient appears very sick
Progressive valve destruction and metastatic infection
S.aureus and gram negative bacteria
77
Out of all congenital heart defects, what percentage are atrial septal defects?
10%
78
What type of atrial septal defect is the most common, and what does this result in?
Secundum (80%)
| Patent foramen ovale
79
What type of ASD results in an atroventricular septal defect?
Primum
80
What is the physiological effect of an ASD?
Abnormal mixing of blood
Blood flows path of least resistance (LV --> RV = left-right shunt)
Increased volume in RV (blood from RA and from LV)
RV dilates to accommodate blood
Will eventually fail --> Right Ventricular Failure
81
What symptoms are associated with ASD?
Often asymptomatic
Murmur --> ECHO --> diagnosis
Stretching of RA --> vulnerable to supraventricular arrhythmias such as AF/atrial flutter (palpitations, SOB, signs of peripheral heart failure)
May present with stroke (thrombus passes from RHS - LHS of heart --> carotid arteries --> stroke)
82
If a young person has a stroke, what should they be investigated for?
ASD
83
What are the O2 sats like in a patient with ASD?
Normal
84
What is coarctation of the aorta?
Narrowing of the aorta generally at the site of the ductus arterioles insertion
85
What is the physiological implication of coarctation of the aorta?
LV has to pump harder to force blood through the narrowing
LV hypertrophy
LVF
Collateral vessels may develop to bypass blood flow around the narrowing
86
Describe the presentation of coarctation of the aorta
Severe narrowing --> poor peripheral perfusion (cold feet, claudication, abdominal angina)
Symptoms of pre-coarctation HTN (before coarctation, the BP is very high --> headaches and nose bleeds)
87
When performing a CV examination on a patient with coarctation of the aorta, what signs would you expect to see?
Discrepancies in limb BP (lower limb BP is lower than upper limb BP - should. be the other way around)
Radio-femoral delay
Continuous murmur
Normal O2 sats
88
Describe transposition of the great arteries
Aorta and pulmonary arteries switch
Aorta comes off RV
Pulmonary arteries come off LV
89
What is the physiological effect of transposition of the great arteries?
Two separate circulations - incompatible with life
Systemic circulation:
Deoxygenated blood --> RA --> RV --> AORTA --> systemic circulation
Pulmonary circulation:
Oxygenated blood --> LA --> LV --> PULMONARY ARTERIES --> lungs
90
Describe foetal circulation
Receives oxygenated blood from placenta --> IVC --> RA
Lungs under-developed therefore high pressure
Blood follows path of least resistance --> foramen ovale --> LHS of heart
(Some blood may pass into pulmonary circulation but most of this blood will pass into the aorta via the ductus arteriosus)
91
Describe what happens at birth to the components of the foetal circulation
First breath
Change in pressure in heart and lungs
Within a few hours, foramen ovale and ductus arteriosus will close
92
Neonates with transposition of the great arteries depend on what for survival?
Patent ductus arteriosus and foramen ovale
93
In a neonate with transposition of the great arteries, what needs to be administered at the time of birth and why?
IV prostaglandins
Maintains patency of the foramen ovale and the ductus arteriosus - allows mixing of blood - allows time for surgical intervention
94
Describe the surgical intervention for transposition of the great arteries
Historically - atrial switch (baffle connects SVC, IVC and mitral valve to LV --> remove atrial septum = O2 blood ---> atrial septum --> RA --> RV --> aorta --> systemic circulation)
Now: arterial switch (cut aorta and pulmonary arteries --> switch them over and reconnect ie pulmonary arteries to RV; aorta to LV)
95
What complications are associated with atrial switch?
RV dilates due to increased blood volume
RVF
+ Tricuspid regurgitation --> compounds RVF
96
What complications are associated with arterial switch?
Pulmonary arteries supplies coronary arteries --> occlusion/stenosis --> MI/sudden death post op
97
What are the components of Tetralogy of Fallot?
1. VSD
2. Overriding aorta
3. Right outflow tract obstruction
4. Right ventricular hypertrophy
98
Tetralogy of Fallot is a _____ abnormality
cyanotic
99
How is Tetralogy of Fallot treated?
```
IV prostaglandins to maintain patency
BT shunt (improves blood supply to lungs)
Complete repair
```
100
What is associated with a patient who has had a BT shunt to treat Teratology of Fallot?
Unrecordable BP in that arm
101
After a complete repair of Teratology of Fallot, what will happen eventually?
Pulmonary regurgitation (needs replacing)
Increased pressure in RV --> RV hypertrophy --> RVF
Increased pressure in RV is transmitted to RA --> dilatation of RA --> vulnerable to Arrhythmia (AF/atrial flutter)
102
Describe univentricular heart
Only have one functional ventricle
103
What is the most common cause of an univentricular heart?
Tricuspid atresia
104
In treating an univentricular heart, if it is not feasible to produce two ventricles from the ventricle, what circulation needs to be created?
Fontan circulation
105
Describe Fontan circulation
Ventricle is dedicated to systemic circulation
| Venous blood supply directly supplies the pulmonary arteries (deoxygenated blood does not pass through the heart)
106
What problems are associated with a Fontan circulation?
Pulmonary circulation is dependent upon sufficient pressure to supply the lungs
Univentricle needs to supply enough pressure in order to push the blood into the lungs
The lungs need to be at a low pressure (must have low vascular resistance)
107
Describe an aortic stenosis murmur
Low pitch ejection systolic murmur
| Aortic area and radiates up into neck
108
Describe an aortic regurgitation murmur
High pitch early diastolic murmur
| Left sternal edge with patient sat forward in expiration
109
Describe a mitral stenosis murmur
Low pitch mid systolic murmur
| Heard at apex with patient on left side
110
Describe a mitral regurgitation murmur
High pitch pan-systolic murmur
| Apex radiating to axilla
111
Describe a tricuspid stenosis murmur
Rare
| Diastolic murmur at left sternal edge
112
Describe a tricuspid regurgitation murmur
Soft high pitch pan systolic murmur at left sternal edge
| Increases during inspiration
113
Describe a pulmonary stenosis murmur
Soft ejection murmur in pulmonary area
114
Describe a pulmonary regurgitation murmur
Soft early diastolic murmur in pulmonary area
115
Define heart failure
The inability of the heart to keep up to the demands of the body. This is due to inadequate cardiac function due to damage of the heart that prevents it from pumping effectively
116
Give some causes of HF
```
Coronary artery disease
HTN
Idiopathic
Toxins (alcohol, chemo)
Valve disease
```
117
Define Ejection Fraction
EF = SV/Total left ventricle volume
118
What are the two classifications of HF depending on EF?
HF-REF: EF = <40% (systolic HF)
| HF-PEF: EF= >40% (diastolic HF)
119
Describe HF-REF
Ventricles can't pump blood hard enough during systole
More often seen in younger men
Associated with coronary aetiology
120
Describe HF-PEF
Not enough blood fills into the ventricles during diastole
More often seen in older female patients
Associated with a HTN aetiology
121
What are the two types of congestion associated with HF?
Acute (decompensated)
| Chronic (congested)
122
Describe Chronic HF
Present for a period of time
| May have been acute or may become acute
123
Describe Acute HF
Usually admitted to hospital
Worsening of chronic
Can be new onset 'de novo'
124
Describe the pathophysiology of HF
The body interprets the reduced cardiac function as a reducing circulating volume
Activation of SNS, RAAS, BNP to increase fluid retention
Fluid overload --> exacerbates the reduced cardiac function
125
In LVHF, where does the fluid back up and what symptoms does this cause?
Fluid backs up into lungs --> pulmonary HTN and oedema
Dysnpnoea
Orthopnoea (lying flat --> more venous blood flow into heart --> worsens congestion)
Crackles on auscultation
126
What type of pulse may be felt in severe LVHF? What is the mechanism behind this pulse?
Pulsus alternans (alternating strong and weak pulse in the periphery)
Reduced EF --> reduced SV --> more blood in ventricle
At next systole:
Increased myocardium stretch --> increased strength of myocardial contraction --> increased strength of systolic pulse
127
Where does fluid back up into in RVHF and what are the symptoms?
Fluid backs up into body
Raised JVP
Hepatosplenomegaly
Ascites
Pitted oedema
128
Why does a new S3 heart sound occur with chronic HF?
Dilation of the ventricles causes remodelling of the atria in order to accommodate the high filling pressure
S3 is heard (due to volume overload)
129
What type of tachycardia occurs in advanced HF? And what are the results?
Resting sinus tachycardia (reduced tissue perfusion)
```
Patient is:
Cool
Pale
Cyanotic extremities
Diaphoresis (due to hypotension)
Narrow pulse pressure (reduced SV)
```
130
Describe the classification of HF
New York Associated Functional Classification
Class 1: Symptoms only during extreme exertion
Class 2: Symptoms during moderate exertion
Class 3: Symptoms during mild exertion
Class 4: Symptoms at rest
131
What investigations are required for all patients with HF?
```
Bloods: FBCs, U&Es, Cr, urea, LFTs, urate
Natriuretic peptides - BNP
ECG
ECHO
CXR
```
132
Why is BNP important in the investigation of HF?
BNP low = exclude HF
| BNP raised = HF possible diagnosis --> ECG + ECHO to confirm
133
What further tests might be required in a patient with HF?
```
Coronary angiography
Exercise test
Ambulatory ECG monitoring
Myocardial biopsy
Genetic testing
```
134
Describe the basic treatment algorithm for HF
Beta Blocker + ACEi (ARB if unable to tolerate ACEi) + mineralocorticoid receptor antagonist (spironolactone/epenelone)
135
What specialist meds can a cardiologist start a patient with HF on?
Sacubitril/Valsartan + Beta blocker + mineralcorticoid receptor antagonist
136
What is the aim of treatment in patients with HF?
Increase life expectancy
| Reduce rate of hospital admissions
137
Why are ARNI drugs useful in HF management?
Angiotensin receptor neprilysin inhibitor
Inhibits breakdown of neprilysin
Increases natriuretic peptide
Vasodilation, natiuresis, diuresis, inhibition of pathological growth/fibrosis
Inhibits AT1 receptor
138
What are the two devices that can be used to increase survival in HF?
Defibs - shock out abnormal heart rhythms
| CRT - synchronise the RHS and LHS of heart
139
How is it decided if a patient should either get a Defibs or CRT fitted?
More severe symptoms + narrow QRS --> defib
| More severe symptoms + broad QRS --> CRT
140
Describe the MoA of Ivabradine
Inhibits depolarisation of SA node
| Decreases rate of hospitalisation
141
Define HTN
Persistent elevation in arterial BP of >140/90mmHg
142
What is the optimum BP?
<120/<80mmHg
143
What is normal BP?
120-129/80-84mmHg
144
What is high-normal BP?
130-139/85-89mmHg
145
What is grade I HTN?
140-159/90-99mmHg
146
What is grade 2 HTN?
160-179/100-109mmHg
147
What is grade 3 HTN?
>/=180 over >/= 100 mmHg
148
What is isolated systemic HTN?
>/= 140/<90 mmHg
149
Give some risk factors for the development of HTN
```
Non-modifiable:
Age
Gender
Ethnicity
Genetic factors
```
```
Modifiable:
Diet
Physical activity
Obesity
Alcohol excess
Stress
```
150
Give some secondary causes of HTN
Endocrine: phaechromocytoma, hyperaldosteronism, thyroid disorders
Vascular: coarctation of the aorta
Renal: renal artery stenosis
Drugs: NSAIDs, herbal remedies, cocaine, exogenous steroid use
Other: Obstructive Sleep Apnoea
151
How is HTN diagnosed?
2 readings 5 mins apart/2 separate occasions
152
What out of office BP measurements can be taken?
24hr ambulatory - night-time dippers/non-dippers (non-dippers increased CV risk)
Home BP monitoring - 2-3 readings, 2x a day, 4-7 days
153
How does hyperthyroidism affect BP?
Increased SBP
154
How does hypothyroidism affect BP?
Increased DBP
155
How can CV risk be ascertained in patients with HTN?
```
ASSIGN score (>20 = 20% CV risk in 10 years)
Q-risk
```
156
What examinations are useful in a patient with HTN?
```
Measure BP in both arms
Weight/BMI
Xanthelasma
Pulses
Oedema
Rashes
Heart - murmur
Abdomen - renal masses
Vascular bruit - kidneys, carotids
Eyes
```
157
What initial investigations should be organised in a patient with HTN?
```
U&Es
Glucose/HBA1c
Lipid profile
TFTs
LFTs
Urine dipstick ± ACR/PCR
12 lead ECG
```
158
What additional investigations may be useful for a patient with HTN?
```
Renin-aldosterone
24h catecholamines
ECHO
Renal US
MRA renal
```
159
What lifestyle factors can be beneficial in reducing a patient's BP?
```
Increased exercise
Reduce Na intake
Reduce alcohol intake
Smoking cessation
DASH diet - more fruit and veg, more wholegrain, less processed food
```
160
What is the target BP in the management of HTN?
<140/90
| <130/80 - if tolerant
161
Describe the treatment algorithm for HTN
<55: ACEi/ARB
>55 or black African/Caribbean: Ca channel blocker
ACEi/ARB + Ca channel blocker
ACEi/ARB + Ca channel blocker + thiazide diuretic
Resistent HTN:
ACEi/ARB + Ca channel blocker + thiazide diuretic + (diuretic/alpha blocker/beta blocker)
162
What is a side effect of amlodipine?
Ankle swelling
