Cardiology - HF, HTN, Investigations Flashcards
Cardiovascular investigations categories?
Bedside
Fluids
Imaging
Bedside cardiovascular investigations
History & Examination Risk assessment (smoking, HTN etc.) SpO2 !BP! (standing, sitting, ambulatory), Urine dip, Cardiac monitor
Cardiovascular blood investigations?
Blood -> cardiac enzymes, BNP, D-dimer, culture!
Cardio imaging?
Functional:
ECG (12-lead, exercise, ambulatory)
Structural: Echocardiography USS CXR CT or Coronary angiogram
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
Left Ventricular Failure
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
Congestive Cardiac Failure
Classification of HF
LVF vs RVF
Systolic vs Diastolic
Acute vs chronic
Low-output vs high-output
LVF causes
MR, cardiomyopathy
dilated, HOCM, CAD/IHD, systemic hypertension
Acute HF
New onset OR
decompensated disease.
LVF causes
BODY:
MR, cardiomyopathy
(dilated, HOCM, CAD/IHD, systemic hypertension)
RVF causes
LUNGS: LVF Pulmonary HTN Lung disease valve disease - TR
Systolic HF causes
IHD, MI, cardiomyopathy
results in decreased CO (ineffective ventricular contraction)
Diastolic HF casues
constrictive pericarditis
cardiac tamponade
restrictive cardiomyopathy
(haemochromatosis amyloid/sarcoid, IHD/hypertrophy)
results in increasing filling pressures (ineffective ventricular relaxation)
High-output HF causes?
anaemia
pregnancy
hyperthyroidism
sepsis
results in normal or high cardiac output BUT fails to meet increased
What is Congestive Cardiac Failure?
LVF + RVF
LVF clinical features?
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
RVF features?
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
LVF signs O/E?
Pleural effusion Bibasal crepitations Cardiomegaly, displaced apex, S3 RV heave Murmurs - aortic valve
RVF signs O/E?
Increased JVP
Hepatomegaly (pulsatile)
Pitting oedema
Murmurs - mitral valve
Investigations specific for HF?
BNP (B-type Natriuretic peptide)
Echo Doppler
Both are diagnostic.
When do you check for BNP in blood in HF?
Only when patient has no MI history
No Hx of MI -> BNP -> Echocardiogram
Investigations for patient with HF and MI history.
Echocardiogram. BNP not needed.
Hx MI -> Echocardiogram
What is BNP?
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.
Normal BNP. HF?
HF unlikely
High BNP. HF?
Cannot diagnose. Refer for Doppler TTEcho
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
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
Management of HF
- Lifestyle Interventions/Prevention – stop smoking, reduce salt, optimize weight & nutrition, Flu immunisation, assess lipids
- Treat underlying Cause/Exacerbating Factors e.g. hypertension, anaemia, thyroid disease, infection, dysrhythmia, valve disease
- Avoid Exacerbating factors - NSAIDs, verapamil
- DRUGS!
HF Drugs
- ACEi + BBs
- ARB (if dyspnoea with less than ordinary activity persists)
+ Spironolactone (dyspnoea at rest or MI last month)
- ARB (if dyspnoea with less than ordinary activity persists)
- Digoxin + CRT
(Cardiac resynchronisation therapy)
(*Other:
Diuretics e.g. Furosemide - symptoms relief
Aspirin/Anticoagulants – Hx CHD, VTE
Amlodipine – coexistant HTN)
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.
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.
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.
What is mild HF?
Comfortable at rest
Dyspnoea present with ordinary activity
NYHA II (New York Heart Assoc. Classification of HF)
What is moderate HF?
Dyspnoea with less than ordinary activity; limiting
NYHA III
What is severe HF?
Dyspnoea at rest
NYHA IV
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
Hypertension definition?
Essential HTN is defined as BP ≥140/90 mmHg, with no secondary cause identified
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
Cardiovascular events - consequences of HTN
Stroke - ischaemic and haemorrhagic MI HF Chronic Kidney Disease Peripheral Vascular Disease Cognitive decline Premature death
Types of HTN
Primary (essential)
Secondary
Causes of primary HTN?
Unknown cause (95%)
Salt
Chronic stress
hormones
Causes of secondary HTN?
- Renal disease:
- Intrinsic 75% -> glomerulonephritis, PAN, PCKD, chronic pyelonephritis
- Renovascular 25% -> Renal Artery Stenosis - Endocrine - Cushing’s, Conn’s, phaeochromocytoma, acromegaly, hyperparathyroidism
- Other - coarctation, pregancy, steroids, OCP
PAN - polyarteritis nodosa
PCKD - polycystic kidney disease
HTN symptoms:
Asymptomatic
Headache +/- visual disturbance = malignant HTN
HTN signs:
End-organ damage: Hypertensive retinopathy Proteinuria LVH High BP!!!
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)
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
Malignant HTN management?
Malignant Hypertension/Phaeo -> URGENT referral for specialist care
Secondary HTN management?
Secondary Hypertension -> Look for and treat underlying cause
Primary HTN management
- Lifestyle management
2. Anti-hypertensives
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)
Optimal HTN
<120/<80 mmHg
Normotensive
<140/<90
Stage 1 HTN
> 140/>90
Stage 2 HTN
> 160/>100
Severe HTN (stage 3)
> 180/>110
Isolated systolic HTN
> 160/<90
Malignant HTN?
> 200/>130
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
Anti-hypertensives: Step 2?
ACEi + CCB
ARB if ACEi not tolerated
Anti-hypertensives: Step 3?
Add diuretic (bendroflumethaizide) (So ACEi + CCB + Diuretic)
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
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.
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
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
ACEi side efects?
COUGH
High K
Renal failure (RAS)
angio-odema
ARB side effects?
vertigo,
utricaria,
pruritis
CCB side effects?
ANKLE-OEDEMA,
FLUSHES,
HEADACHE,
gum hyperplasia,
Thiazides side effects?
LOW K (ECG changes/ arrhythmia) LOW NA (confusion)
Spironolactone side effects?
High K
Gynaecomastia
B-blocker side effects?
Bronchospasm
Heart failure
lethargy
Malignant Hypertension complications?
CCF or Enchephalopathy
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.
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
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,
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
Stable angina investigations?
Angina Pectoris [Stable]
1. Bedside – History & Examination
- Fluids – Bloods: FBC (anaemia), U&E, glucose, lipids, thyroxine
- Imaging –
Resting 12-lead ECG (normal, flat/inverted T-waves, Deep Q waves, LBBB)
Exercise ECG
Stress ECG
Which investigation is the most appropriate to confirm diagnosis of IHD?
Exercise ECG
Tests for people unable to exercise?
Stress myocardial perfusion imaging
or Stress Echo
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
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
When should you stop an exercise test?
Rapidly dropping ST segment
BP drop with exercise
Severe chest pain
Arrhythmias
Severity assessment and risk stratification of MI tests?
CT coronary angiogram - non-invasive
Coronary angiogram - invasive
ACS investigations?
History & exam, BP, SpO2
Risk assessment!
Bloods: toroponin! FBC UandE, glucose, lipids (same as before)
ECG (resting)
Risk assessment of ACS?
Age
Gender (male)
CVS risk factors (smoking, diabetes, HTN, dyslipidaemia)
Typical/atypical angina (typical = increased likelihood)
+GRACE risk model
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.
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
Troponin test time intervals?
1st troponin on arrival
2nd 3h later
When does troponin rise?
3-12h post MI
Troponin peak?
24-48h post MI
Troponin decline?
5-14 days
DVT investigations?
Wells score
D-dimer
USS - proximal leg vein
DVT investigation: D-dimer negative?
PE unlikely
DVT investigation: D-dimer positive?
USS of proximal leg vein
DVT investigation: D-dimer positive, USS negative?
Repeat tests 6-8 days later
DVT investigation: D-dimer positive, USS positive?
Treat as DVT
Difference between DVT and PE investigation?
DVT - USS
PE - CTPA (or V/Q scan if unavailable)
D-dimer used equally in both
What is D-dimer?
Fibrin degradation product, present in the blood after clot is degraded by fibrinolysis
D-dimer sensitivity/specificity?
HIGH sensitivity
LOW specificity - because it has high levels in pregnancy, malignancy and post-op
Infective endocarditis (IE) definition?
Inflammation of inner tissue (endocardium) of heart, typically the valves, caused by an infectious agent.
Patient with fever + new murmur?
Infective endocarditis until proven otherwise
Classification of IE?
Acute - endocarditis on normal valves (50%)
Subacute - endocarditis on abnormal valves
Epidemiology of IE?
50% acute
F>M
50% patients >60yo (in US)
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%)
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
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)
IE symptoms?
Fevers/ chills, night sweats, weight loss, arthralgias, headache, dyspnoea, chest pain, weakness
Acute: acute HF + emboli, fever, tachycardia, fatigue
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)
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
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)
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)
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
Duke’s criteria requirements to diagnose IE?
2 major OR
1 major + 3 minor OR
all 5 minor criteria
IE management?
Antibiotic therapy - complicated
Surgery if indicated
*IE surgery indications?
heart failure, valvular obstruction, repeated emboli, fungal endocarditis, persistent bacteraemia; myocardial abscess; unstable infected prosthetic valve
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
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
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
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.
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
