Cardiology - HF, HTN, Investigations Flashcards
(119 cards)
1
Q
Cardiovascular investigations categories?
A
Bedside
Fluids
Imaging
2
Q
Bedside cardiovascular investigations
A
History & Examination Risk assessment (smoking, HTN etc.) SpO2 !BP! (standing, sitting, ambulatory), Urine dip, Cardiac monitor
3
Q
Cardiovascular blood investigations?
A
Blood -> cardiac enzymes, BNP, D-dimer, culture!
4
Q
Cardio imaging?
A
Functional:
ECG (12-lead, exercise, ambulatory)
Structural: Echocardiography USS CXR CT or Coronary angiogram
5
Q
A 55 year old gentleman with a history of systemic hypertension presents to A&E with breathlessness on exertion & orthopnoea. Examination reveals cardiomegaly & a displaced apex beat to the left.
Myocardial Infarction Left Ventricular Failure Constrictive pericarditis Right Ventricular Failure Congestive Cardiac Failure
A
Left Ventricular Failure
6
Q
A 62 year old gentleman presents with fatigue, breathlessness & anorexia. On examination his JVP is noted as being elevated, he has hepatomegaly & swollen ankles.
Myocardial Infarction Left Ventricular Failure Constrictive pericarditis Right Ventricular Failure Congestive Cardiac Failure
A
Congestive Cardiac Failure
7
Q
Classification of HF
A
LVF vs RVF
Systolic vs Diastolic
Acute vs chronic
Low-output vs high-output
8
Q
LVF causes
A
MR, cardiomyopathy
dilated, HOCM, CAD/IHD, systemic hypertension
9
Q
Acute HF
A
New onset OR
decompensated disease.
10
Q
LVF causes
A
BODY:
MR, cardiomyopathy
(dilated, HOCM, CAD/IHD, systemic hypertension)
11
Q
RVF causes
A
LUNGS: LVF Pulmonary HTN Lung disease valve disease - TR
12
Q
Systolic HF causes
A
IHD, MI, cardiomyopathy
results in decreased CO (ineffective ventricular contraction)
13
Q
Diastolic HF casues
A
constrictive pericarditis
cardiac tamponade
restrictive cardiomyopathy
(haemochromatosis amyloid/sarcoid, IHD/hypertrophy)
results in increasing filling pressures (ineffective ventricular relaxation)
14
Q
High-output HF causes?
A
anaemia
pregnancy
hyperthyroidism
sepsis
results in normal or high cardiac output BUT fails to meet increased
15
Q
What is Congestive Cardiac Failure?
A
LVF + RVF
16
Q
LVF clinical features?
A
Effects on lung in LVF: Dyspnoea Poor exercise tolerance fatigue orthopnea paroxysmal nocturnal dyspnoea nocturnal cough (+/- pink frothy sputum) wheeze (cardiac asthma) nocturia, cold peripheries, weight loss, muscle wasting
+VENOUS CONGESTION leading to FLUID ACCUMULATION in both LVF and RVF
17
Q
RVF features?
A
Systemic effects in RVF: Peripheral oedema ascites facial engorgement pulsation in neck and face (TR) Nausea, anorexia, epistaxis(nose bleeding)
+VENOUS CONGESTION leading to FLUID ACCUMULATION in both LVF and RVF
18
Q
LVF signs O/E?
A
Pleural effusion Bibasal crepitations Cardiomegaly, displaced apex, S3 RV heave Murmurs - aortic valve
19
Q
RVF signs O/E?
A
Increased JVP
Hepatomegaly (pulsatile)
Pitting oedema
Murmurs - mitral valve
20
Q
Investigations specific for HF?
A
BNP (B-type Natriuretic peptide)
Echo Doppler
Both are diagnostic.
21
Q
When do you check for BNP in blood in HF?
A
Only when patient has no MI history
No Hx of MI -> BNP -> Echocardiogram
22
Q
Investigations for patient with HF and MI history.
A
Echocardiogram. BNP not needed.
Hx MI -> Echocardiogram
23
Q
What is BNP?
A
Secreted by ventricular myocardium, related to LV pressure – reflects Myocyte stretch.
Increases GFR and decreases renal NA resorption.
can rule out HF but not diagnose - Echo still needed.
24
Q
Normal BNP. HF?
A
HF unlikely
25
High BNP. HF?
Cannot diagnose. Refer for Doppler TTEcho
26
Why is an Doppler Echo important in HF diagnosis?
Accesses cause and heart function:
Cause - valve diesease, MI
Function - systolic/diastolic LV function, ejection fraction
27
HF CXR findings?
```
ABCDE
A - Alveolar oedema (Bat's wings)
B - Kerley B lines (interstitial oedema, horizontal lines above costophrenic recesses)
C - Cardiomegaly
D - Dilated prominent upper lobe vessels
E - pleural Effusion
```
28
Management of HF
1. Lifestyle Interventions/Prevention – stop smoking, reduce salt, optimize weight & nutrition, Flu immunisation, assess lipids
2. Treat underlying Cause/Exacerbating Factors e.g. hypertension, anaemia, thyroid disease, infection, dysrhythmia, valve disease
3. Avoid Exacerbating factors - NSAIDs, verapamil
4. DRUGS!
29
HF Drugs
1. ACEi + BBs
2. + ARB (if dyspnoea with less than ordinary activity persists)
+ Spironolactone (dyspnoea at rest or MI last month)
3. Digoxin + CRT
(Cardiac resynchronisation therapy)
(*Other:
Diuretics e.g. Furosemide - symptoms relief
Aspirin/Anticoagulants – Hx CHD, VTE
Amlodipine – coexistant HTN)
30
A 62 year old man, 3 months after an MI, taking aspirin, atenolol and simvistatin, whose echocardigram shows worsening left ventricular function. Select the single most appropriate means of reducing cardiovascular risk
```
Spironolactone
Anticoagulation Thearpy
Sublingual Gtn
ACE inhibitor therapy
Furosemide
```
ACE inhibitor therapy
First line treatment is with an ACE inhibitor which reduces morbidity and mortality associated with the condition. All patients with LV dysfunction should receive ACE inhibitors, whether symptomatic or not.
31
The same 62 year old man whose echocardigram shows worsening left ventricular function. Returns reporting no improvement in symptoms. He's on aspirin, atenolol, simvastatin and an ACEi. He had an MI 3 months ago. What other treatment should he be given?
```
Spironolactone
Β-Blocker
Hydralazine/nitrate combo
Digoxin
ARB
```
ARB
ARBs are second line treatment for mild-moderate HF. Spironolactone would be given if he was moderate-severe OR had an MI in the past month.
32
After 3 months, the gentleman returns reporting that after a few weeks of symptom relief his exercise tolerance has reduced and now he is breathless at rest. What further therapy should be included (he's on aspirin, atenolol, simvastatin ACEi and an ARB
```
Spironolactone
Β-Blocker
Hydralazine/nitrate combo
Digoxin
ARB
```
Digoxin
Third line treatment for HF. Cardiac Resynchronisation Therapy should also be considered.
33
What is mild HF?
Comfortable at rest
Dyspnoea present with ordinary activity
NYHA II (New York Heart Assoc. Classification of HF)
34
What is moderate HF?
Dyspnoea with less than ordinary activity; limiting
NYHA III
35
What is severe HF?
Dyspnoea at rest
NYHA IV
36
When is a hydralazine/nitrate combo used in HF treatment?
It's second line - after ACEi and BBs.
| Given for moderate-severe HF in Afro-Carribeans
37
Hypertension definition?
Essential HTN is defined as BP ≥140/90 mmHg, with no secondary cause identified
38
HTN epidemiology?
Disease risk associated with blood pressure - continuous relationship.
Above 115/70mmHg, the risk of cardiovascular events doubles for every 20/10mmHg rise in blood pressure
39
Cardiovascular events - consequences of HTN
```
Stroke - ischaemic and haemorrhagic
MI
HF
Chronic Kidney Disease
Peripheral Vascular Disease
Cognitive decline
Premature death
```
40
Types of HTN
Primary (essential)
| Secondary
41
Causes of primary HTN?
Unknown cause (95%)
Salt
Chronic stress
hormones
42
Causes of secondary HTN?
1. Renal disease:
- Intrinsic 75% -> glomerulonephritis, PAN, PCKD, chronic pyelonephritis
- Renovascular 25% -> Renal Artery Stenosis
2. Endocrine - Cushing's, Conn's, phaeochromocytoma, acromegaly, hyperparathyroidism
3. Other - coarctation, pregancy, steroids, OCP
PAN - polyarteritis nodosa
PCKD - polycystic kidney disease
43
HTN symptoms:
Asymptomatic
| Headache +/- visual disturbance = malignant HTN
44
HTN signs:
```
End-organ damage:
Hypertensive retinopathy
Proteinuria
LVH
High BP!!!
```
45
Bedside HTN investigations and diagnosis?
Blood pressure measurement (lol) - sitting and standing
(OSCE:
Standardise the environment and provide a relaxed, temperate setting
Measure Blood pressure in BOTH arms - re-measure if difference > 20mmHg
> 140/90 mmHg ⇄ Repeat later in consultation ( if different repeat a 3rd time) [Record the LOWEST]
Offer ABPM (ambulatory BP measurement) for diagnosis)
46
Investigations for end-organ damage?
```
Fundoscopy (retinopathy)
Estimate CVS risk (QRISK2)
Urine dip (haematuria, proteinuria)
Urinalysis (albumin:creatinine ratio)
Bloods (glucose, U&E, Creatinine, eGFR, Serum total & HDL cholesterol)
ECG (LVH, previous MI)
or Echo
```
47
Malignant HTN management?
Malignant Hypertension/Phaeo -> URGENT referral for specialist care
48
Secondary HTN management?
Secondary Hypertension -> Look for and treat underlying cause
49
Primary HTN management
1. Lifestyle management
| 2. Anti-hypertensives
50
HTN classification?
```
Optimal (<120/<80)
Normotensive (<140/<90)
Stage 1 HTN (>140/>90)
Stage 2 HTN (>160/>100)
Stage 3 (severe) HTN (>180/>110)
Isolated systolic (>160/<90)
Malignant HTN (>200/>130)
```
51
Optimal HTN
<120/<80 mmHg
52
Normotensive
<140/<90
53
Stage 1 HTN
>140/>90
54
Stage 2 HTN
>160/>100
55
Severe HTN (stage 3)
>180/>110
56
Isolated systolic HTN
>160/<90
57
Malignant HTN?
>200/>130
58
Anti-hypertensives: Step 1?
ACEi (lisinopril - <55yo) OR
CCB (Nifedipine >55yo or Afro-Caribbean )
```
Stage 1 Hypertensives with:
End-organ damage
CVS/Renal Damage
Diabetes
10-year CVS risk > 20%
≥ Stage 2 Hypertensives
```
GOAL = <140/90
<130/80 in Diabetes
< 150/90 if aged >80
59
Anti-hypertensives: Step 2?
ACEi + CCB
| ARB if ACEi not tolerated
60
Anti-hypertensives: Step 3?
```
Add diuretic (bendroflumethaizide)
(So ACEi + CCB + Diuretic)
```
61
Anti-hypertensives: Step 4?
Increase diuretic dose OR*
Spironolactone (low dose) OR**
Alpha/Beta-Blocker
* Depending on K level (K-sparing)
* * Not tolerated/ contraindicated/ ineffective
62
A 40 year old man with diabetes, proteinuria and hypertension of 148/98 mmHg
```
Β-blocker
Calcium Channel Blocker
Losartan
ACE-I
Thiazide Diuretic
```
ACE-I
This man has concomitant diabetes and chronic renal disease and stage 1 hypertension. The first line treatment is monotherapy with an ACE-inhibitor. ACE inhibitors are renoprotective and decreases the progression of proteinuria in diabetics.
63
The same gentleman after 3 months of the treatment you gave him (ACEi) returns for a review and you find his blood pressure is now 150/100. What treatment would you add in
```
Β-blocker
Calcium Channel Blocker
Losartan
ACE-I
Thiazide Diuretic
```
Calcium Channel Blocker
64
The same gentleman, again, after another 3 months of treatment (ACEi + CCB) returns and you find his blood pressure is now 150/100. What treatment would you now add in.
```
Β-blocker
Calcium Channel Blocker
Losartan
ACE-I
Thiazide Diuretic
```
Thiazide Diuretic
65
ACEi side efects?
COUGH
High K
Renal failure (RAS)
angio-odema
66
ARB side effects?
vertigo,
utricaria,
pruritis
67
CCB side effects?
ANKLE-OEDEMA,
FLUSHES,
HEADACHE,
gum hyperplasia,
68
Thiazides side effects?
```
LOW K (ECG changes/ arrhythmia)
LOW NA (confusion)
```
69
Spironolactone side effects?
High K
| Gynaecomastia
70
B-blocker side effects?
Bronchospasm
Heart failure
lethargy
71
Malignant Hypertension complications?
CCF or Enchephalopathy
72
How to treat malignant HTN?
First line -> IV labetalol
This is a hypertensive emergency with BP >210/130.
Guidelines indicate the goal is to reduce MABP by no more than 25% in the first hour, then if stable, to 160/100 or less within the next 2 to 6 hours.
73
A 53 year old lady with hypertension was on an antihyperstive treatment by you, but has developed a dry cough and refuses to take the drug anymore. He is otherwise well. What is the Culprit?
```
Β-blocker
Calcium Channel Blocker
Losartan
Spironolactone
ACE-I
```
ACE-I
```
ACEi SEs:
COUGH
High K
Renal failure (RAS)
angio-odema
```
74
A few months down the line the same lady, has had more medication added to control his hypertension. She now presents to you complaining of ankle swell. O/E you find bilateral ankle oedema. What is the culprit?
```
Β-blocker
Calcium Channel Blocker
Losartan
Spironolactone
ACE-I
```
Calcium Channel Blocker
```
Side effects:
ANKLE-OEDEMA,
FLUSHES,
HEADACHE,
gum hyperplasia,
```
75
A 45 year old gentleman with difficult to control hypertension presents to your practice for an annual review of his medication. On examination you notice gynaecomastia. What is the culprit?
```
Β-blocker
Calcium Channel Blocker
Losartan
Spironolactone
ACE-I
```
Spironolactone
SEs:
high K
Gynaecomastia
76
Stable angina investigations?
Angina Pectoris [Stable]
1. Bedside – History & Examination
2. Fluids – Bloods: FBC (anaemia), U&E, glucose, lipids, thyroxine
3. Imaging –
Resting 12-lead ECG (normal, flat/inverted T-waves, Deep Q waves, LBBB)
Exercise ECG
Stress ECG
77
Which investigation is the most appropriate to confirm diagnosis of IHD?
Exercise ECG
78
Tests for people unable to exercise?
Stress myocardial perfusion imaging
| or Stress Echo
79
What does exercise ECG show?
Disease severity increases with degree of ST segment depression
Shows crude correlation between exercise capacity and post MI diagnosis:
9% mortality in <10min Bruce protocol
2% mortality in >10min Bruce protocol
80
What is Bruce protocol?
A diagnostic test used in the evaluation of cardiac function, developed by Robert A. Bruce
- basically its walking on a treadmill which gradually increases in speed and incline while you're plugged into an ECG.
Ventilation is also measured
81
When should you stop an exercise test?
Rapidly dropping ST segment
BP drop with exercise
Severe chest pain
Arrhythmias
82
Severity assessment and risk stratification of MI tests?
CT coronary angiogram - non-invasive
| Coronary angiogram - invasive
83
ACS investigations?
History & exam, BP, SpO2
Risk assessment!
Bloods: toroponin! FBC UandE, glucose, lipids (same as before)
ECG (resting)
84
Risk assessment of ACS?
Age
Gender (male)
CVS risk factors (smoking, diabetes, HTN, dyslipidaemia)
Typical/atypical angina (typical = increased likelihood)
+GRACE risk model
85
What is the GRACE risk model?
Web-based tool that can be used to predict in-hospital and post-discharge MORTALITY or MI in patients following an initial ACS.
86
What does the GRACE risk model take into account?
ECG ST changes and Q waves
Heart rate, SBP, Creatinine, elevated biomarkers
Hx of CCF and MI
87
Troponin test time intervals?
1st troponin on arrival
| 2nd 3h later
88
When does troponin rise?
3-12h post MI
89
Troponin peak?
24-48h post MI
90
Troponin decline?
5-14 days
91
DVT investigations?
Wells score
D-dimer
USS - proximal leg vein
92
DVT investigation: D-dimer negative?
PE unlikely
93
DVT investigation: D-dimer positive?
USS of proximal leg vein
94
DVT investigation: D-dimer positive, USS negative?
Repeat tests 6-8 days later
95
DVT investigation: D-dimer positive, USS positive?
Treat as DVT
96
Difference between DVT and PE investigation?
DVT - USS
PE - CTPA (or V/Q scan if unavailable)
D-dimer used equally in both
97
What is D-dimer?
Fibrin degradation product, present in the blood after clot is degraded by fibrinolysis
98
D-dimer sensitivity/specificity?
HIGH sensitivity
| LOW specificity - because it has high levels in pregnancy, malignancy and post-op
99
Infective endocarditis (IE) definition?
Inflammation of inner tissue (endocardium) of heart, typically the valves, caused by an infectious agent.
100
Patient with fever + new murmur?
Infective endocarditis until proven otherwise
101
Classification of IE?
Acute - endocarditis on normal valves (50%)
| Subacute - endocarditis on abnormal valves
102
Epidemiology of IE?
50% acute
F>M
50% patients >60yo (in US)
103
Casues of IE?
```
Acute:
Dermatitis
IVDU
renal failure
organ transplantation
DM
post-op wounds
```
```
Sub-acute:
aortic or mitral valve disease,
tricuspid valve in IVDU,
coarctation,
patent ductus arteriosus,
Ventricular Septal Defect,
prosthetic valves (10-30%)
```
104
IE patophysiology?
Turbulent blood flow -> endothelial damage to valvular surfaces ->platelets and fibrin adherence to underlying collagen -> prothrombotic millieu.
Bacteraemia -> colonisation of thrombus -> Mature infective vegetation
105
IE offending organisms?
Streptococcus viridans - >35%, naitive, non-IVDU
Staphylococcus Aureus - IVDU
Staph. Epidermidis - prosthetic valves
Others; enterococci, coagulase-negative staph, Coxiella burnetii, chlamydia, fungi (candidia, aspergillus,hisoplasma)
106
IE symptoms?
Fevers/ chills, night sweats, weight loss, arthralgias, headache, dyspnoea, chest pain, weakness
Acute: acute HF + emboli, fever, tachycardia, fatigue
107
IE signs?
SCIE:
Septic: fever, rigors, night sweats, anaemia, clubbing, anorexia
Cardiac: new murmur!
Immune Complex deposition: vasculitis, acute renal failure (microscopic haematuria, glomerulonephritis), Roth spots, splinter haemorrhages, Osler's nodes (painful)
Embolic - other organ abscesses, Janeway lesions (painless)
108
IE investigations?
History and exam, CVS risk assessment, fundoscopy
Bloods = BLOOD CULTURE x3!!! (+ FBC, ESR/CRP, U&E, Mg+)
Urinalysis
ECG
ECHOCARDIOGRAM!
(Transthoracic TTE or trans-oesophageal TOE. TOE more sensitive)
+ Duke's criteria
109
Duke's Criteria?
Used to make a clinical diagnosis of IE
Needs 2 major OR 1 major + 3 minor OR all 5 minor criteria
Major:
- Typical IE organisms in 2 separate cultures OR persistently +ve (eg. 3 cultures >12h apart)
- Endocardium involved (+ve Echo* OR new valvular regurgitation)
* vegetations, abscess, dehiscence of prosthetic valve
Minor:
- Predisposition (cardiac lesion, IVDU)
- Fever >38C
- Vascular/immuno. features (Splinter haemorrhage, Roth spots (fundoscopy), microscopic haematuria, janeway lesions, osler’s nodes)
- +ve blood culture (not major)
- +ve Echo (not major)
110
Minor Duke's criteria?
Minor:
- Predisposition (cardiac lesion, IVDU)
- Fever >38C
- Vascular/immuno. features (Splinter haemorrhage, Roth spots (fundoscopy), microscopic haematuria, janeway lesions, osler’s nodes)
- +ve blood culture (not major)
- +ve Echo (not major)
111
Major Duke's criteria?
Major:
- Typical IE organisms in 2 separate cultures OR persistently +ve (eg. 3 cultures >12h apart)
- Endocardium involved (+ve Echo* OR new valvular regurgitation)
* vegetations, abscess, dehiscence of prosthetic valve
112
Duke's criteria requirements to diagnose IE?
2 major OR
1 major + 3 minor OR
all 5 minor criteria
113
IE management?
Antibiotic therapy - complicated
| Surgery if indicated
114
*IE surgery indications?
heart failure, valvular obstruction, repeated emboli, fungal endocarditis, persistent bacteraemia; myocardial abscess; unstable infected prosthetic valve
115
30 year old women returning from holiday. Sudden onset chest pain with shortness of breath, coughed blood. She has no other lung disease. What investigation would you do to confirm diagnosis?
```
12-lead ECG
CT Pulmonary Angiogram
D-dimer
Spirometry
Chest X-ray
```
CT Pulmonary Angiogram
Suspect PE. The key word is "confirm" so not D-dimer
116
A 35 year old lady presents with severe pain in her right calf. She has recently returned from a family holiday in Australia. She is taking no other medication other than the OCP. What investigation would you do first.
```
INR
Proximal Leg Vein USS
D-dimer
FBC
Thrombophilia screen
```
D-dimer
Then USS
117
An 80 year old man with a history of ischaemic heart disease trips over a paving stone & fractures his hip. An ambulance takes him to A&E. 1 hour after arrival, he develops crushing central chest pain. Select the single most appropriate investigation
```
V/Q Scan
Cardiac Troponin
Chest X-ray
Coronary Angiogram
Transthoracic Echo
```
Cardiac Troponin
118
50 yr old man attends A&E with SOB, fever and hyperdynamic regular pulse of 100. BP 160/60 mmHg. He has a murmur at the left sternal edge. On further enquiry it is found he attended for a routine dental procedure 2 months ago. Which 2 of these investigations could you use to confirm diagnosis.
```
CT Pulmonary Angiogram
Urinalysis
Blood Cultures
Fundoscopy
TOE Echocardiogram
```
Blood Cultures
TOE Echocardiogram
Any patient presenting with fever and a new murmur should always make you think of bacterial endocarditis.
119
A lady with no history of a previous heart attack is complaining of swelling in her legs which goes all the way up to her thighs, and she feels may be extending into her lower stomach. She says she feels depressed and thinks these are side-effects of the medications she is on. You notice that she has pulsation in her neck and her face appears engorged.
```
Echocardiogram
BNP
CT Angiogram
Coronary Angiogram
Chest X-ray.
```
Echocardiogram
This lady has RHF. The key investigation is a TTE coupled with Doppler flow studies which allows quantification of systolic and diastolic function and calculation of the EF.
CXR and & ECG may show changes but are not Diagnostic
