Heart Failure (CVS) Flashcards
Define heart failure
Heart failure may be defined as a clinical syndrome where the heart is unable to generate sufficient CO to meet the metabolic needs of the body.
aka congestive heart failure (CHF).
Can’t pump enough blood baso.
What is the functional classification of HF?
Systolic HF = Heart failure with reduced ejection fraction
Diastolic HF = Heart failure with preserved ejection fracture
These two specifically always refer to left sided HF
Describe HFrEF and causes
This is systolic left HF. This occurs when there is impaired vent contraction in systole resulting in reduced ejection fraction as the vents can relax and fill but cannot eject enough (rEF is <40%)
Causes: IHD, dilated cardiomyopathy, myocarditis, arrhythmias
Describe HFpEF and causes
This is diastolic left HF (pEF >50%) The LV has preserved systolic function however the LV is unable to relax and fill properly due to stiffness resulting in inadequate filling in diastole.
Causes: left ventricular hypertrophy (e.g. due to chronic hypertension), hypertrophic cardiomyopathy, cardiac tamponade, constrictive pericarditis
Difference between left sided HF and right sided HF
LHF = left side is affected first/primary. Blood builds up in the left heart as it is not ejected out (both in rEF and pEF) and backs up into the lungs -> pulmonary oedema.
Describe right sided HF and brief aetiology
RHF = Often secondary to LHF (commonest cause).
The incr pulm pressure causes incr resistance against the right heart contraction. The right heart then compensates with vent hypertrophy.
However, isolated RHF can also occur and is often secondary to lung diseases such as pulmonary hypertension and pulmonary emboli - in these cases the HF is referred to as cor pulmonale
Describe the NYHA classification
This classifies HF based on severity of symptoms
Class 1 (no limitation): ordinary physical activity does not cause undue fatigue, dyspnea or palpitations
Class II (mild limit): ‘’ causes fatigue, dyspnea, palps, or angina
Class III (moderate limit): comfortable at rest, less than ordinary activity causes above symptoms
Class IV (severe limit): symptoms at rest, any phys acticity incr discomfort
Difference between low output HF and high output, which is more common
Low-output is much more common than high-output.
Low-output occurs when CO = reduced due to a primary problem with the heart and the heart is unable to meet the body’s needs.
High-output = normal CO, but there is an increase in peripheral metabolic demands that the heart is unable to meet.
What are the risk factors for HF?
Advancing age (>65 years old)
Hypertension
Diabetes
Causes/Main risk factors of the causes
Describe starling’s law pathophysiology of HF
The pathogenesis of heart failure is complex and follows from mechanisms that result in a failure of cardiac output.
One mechanism is the altered starling’s law. Due to poor contraction, ESV increases. Usually, this incr stretch so incr SV. However, this doesn’t happen in HF as much and the curve flattens out and drops. This is due to the relationship between cardiomyocyte stretch and contractility being altered.
Describe compensatory mechanisms in the pathophysiology of HF
In HF, neurohormonal compensatory mechanisms develop which are initially helpful but eventually become detrimental and contribute to the development of symptoms.
The drop in CO is what leads to compensatory mechanisms - incr in SNS activity, RAAS, vasopressin activity.
Average of HF diagnosis in UK?
75
Commonest causes of HF in europe and north america?
CAD, hypertension and valvular disease.
Significant cause of HF in south america?
Chagas disease, but rare in europe and north america
What are the symptoms of Left HF?
LHF causes pulm congestion/oedema (bc blood/pressure backs up) and systemic hypoperfusion.
Fatigue!
Shortness of breath on exertion (
Orthopnea
Paroxysmal nocturnal dyspnea
Nocturnal cough (+/- pink frothy sputum)
You might get RHF symptoms if its progressed to that
What clinical signs of left HF may be found in exam?
Tachypnea
Bibasal fine crackles on auscultation of the lungs
Cyanosis
Prolonged capillary refill time
Hypotension
What are the symptoms of right HF?
Ankle swelling (bilateral)
Weight gain
Abdominal swelling and discomfort
Anorexia and nausea
What are the clinical signs of right HF found during examination?
Raised JVP
Pitting peripheral oedema (ankles to thighs to sacrum)
Tender smooth hepatomegaly
Ascites
Transudative pleural effusions (typically bilateral)
What is a common symptom for all types of HF?
Clinical signs can be diff in dif types of HF, but all of them tend to have fatigue
Overall typical clinical features of HF? (not specific to left or right)
short of breath, bilateral ankle swelling, fatigue, weight change
Raised JVP, basal crepitations and peripheral oedema
(bc LHF can cause RHF, so all symptoms show)
What are the differential diagnoses for sus HF?
COPD, Pneumonia, PE, cirrhosis, pulm fibrosis, nephrotic syndrome,
Renal failure (fluid retention, peripheral overload) - difference is by looking at other symptoms/signs
Liver failure (fluid retention and peripheral overload esp ascites) - diff is signs (liver has diff e.g. jaundice)
What is the first line investigation for chronic HF? What differentials can we cut out?
N-terminal pro B type natriuretic peptide (NT proBNP) and BNP blood tests
(the substances themselves have diff functions, but indicate HF)
What are the high, raised and normal levels of NTproBNP and time referral for each?
High level = >2000pg/ml. Refer urgently for specialist assessment incl transthoracic echo, to be seen within 2 weeks)
Raised levels = 400-2000 (refer and TT echo within 6 weeks)
Normal = < 400 (HF diagnosis is less likely)
Why is NT proBNP elevated in HF?
ProBNP is released by the ventricles in response to stretch and then cleaved into BNP and NT-proBNP. This is normal e.g. in exercise.
In HF, there is increased stretch and strain tf a lot is released which is why high levels occur.
Causes of elevated BNP/NTproBNP
Lung disease e.g. COPD/PE, Kidney disease, cirrhosis, diabetes, age
(COPD does incr level mildly, but HF has much higher incr - i think)
So if it reaches high levels - likely to be HF so overall, high levels indicate HF
What are the other investigation tests for sus HF?
12 lead ECG (show ischemic changes or arrhythmias) in all pts
Other bloods (U and E for renal function bc meds, LFTs to see if hepatic congestion, TFTs for hyperthyroidism, glucose and lipid profile for modifiable CVS RFs)
Chest X rays - HF findings are ABCDEF (alveolar oedema, kerley B lines, cardiomegaly, upper lobe blood diversion, pleural effusions, fluid in the horizontal fissure)
How is the transthoracic echo interpreted to diagnose HF?
Confirms presence and degree of vent dysfunction (i.e. HF). It measures LV ejection fraction and shows heart structure.
It classifies HF:
EF< 40% = HFrEF so systolic dysfunction)
EF = 41-49% = HFmrEF (mildly)
EF> 50% but has raised BNP = HFpEF so diastolic dysfunction
What is the conservative management for HF?
Weight loss if BMI> 30
Smoking cessation
Salt
Cardiac rehab (personalised exercise programme)
What is the first line therapy for chronic HFrEF?
ACE inhibitor (e.g. ramipril) AND beta blocker (e.g. bisoprolol)
However, each drug needs to be given one at a time (once stable on first drug, you can give the other)
ARBs can be used instead of ACEi if has cough (side effect). Avoid ACEi if has valvular heart disease until specialist assessed). If intolerant to both - hydralazine
These drugs are done for HFrEF (not really used for pEF as insufficient evidence that they help)
What are the main medical treatments given for HF?
ACEi and BB (1st line for rEF)
Aldosterone antagonist (2nd ‘’)
Loop diuretics (both if fluid overload)
‘ABAL’
What medication is given if symptoms persist in HFrEF treated with ACEi and BB?
Aldosterone antagonist e.g. spironolactone
Second line treatment
Potassium should be monitored bc both ACEi and Ald antag cause hyperkalaemia
aka MRA
What is the management of HFpEF?
Manage co morbidities such as hypertension, afib, IHD, diabetes (lifestyle change)
Give loop diuretics to relieve fluid overload symptoms (e.g. pulm/peripheral oedema) e.g. flurosemide
Offer personalised exercise based cardiac rehab programme unless the condition is unstable
What is third line therapy for HFrEF?
If symptoms persist, consider these. This should be initiated by a specialist.
Consider:
SGLT2 inhibitor e.g. flozin
Replace ACEi with Sacubitril valsartan
Ivabradine
Hydralazine nitrate (Esp if afro-caribbean)
Digoxin (esp if has AF)
Cardiac resynchronisation therapy (indication = ECG shows widened QRS complex) (baso a type of pacemaker)
Mnemonics for medication of HFrEF?
BASH - BB, ACEi, spironolactone, hydralazine (all improve mortality)
ABAL - ACEi, BB, Aldos antag, Loop diuretic (diuretic doesnt improve mortality but helps symptoms)
Others meds that are offered to people with HF?
Annual flu vaccine
One off pneumococcal vaccine
What are complications of HF?
Afib
Blood clots - PE or stroke
Impaired kidney or liver function
Muscle wasting
Depression
Describe acute heart failure
Sudden onset or worsening of HF symptoms
Either new onset with no past history of HF - de novo HF
OR decompensation of chronic HF tf with history - decompensated AHF (more common)
Presents after 65 year usually
What are the symptoms and signs of acute HF?
Breathlessness, reduced exercise tolerance, oedema, fatigue
Cyanosis, tachycardia, raised JVP, Displaced apex beat, bibasal crackles or wheeze, S3 sound
This will be sudden onset
Investigations for acute HF?
Bloods, CXR, Echo, raised BNP
same as chronic baso
What is the emergency management for acute HF?
Stabilise the patient:
Sit patient up - reduces venous return
High flow O2 therapy (aiming sats>94%)
Loop diuretics - IV furosemide 40mg and more doses if needed
Morphine - as vasodilator
