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
