10. Heart Failure Flashcards
Define heart failure.
A complex clinical syndrome of signs and symptoms that suggest the efficiency of the heart as a pump is impaired.
The heart is unable to deliver blood at a rate that meets the metabolic demands.
What are the 2 broad categories of heart failure?
- Systolic failure: the ability of the heart to pump blood around the body is impaired.
- Diastolic failure: the heart is pumping blood effectively but is relaxing and filling abnormally.
What is the difference between systolic and diastolic failure?
Systolic = impaired left ventricular contraction
Diastolic = impaired left ventricular relaxation
Give the major types of heart failure.
Systolic/diastolic, low output/high output, left/right
Name the different classifications of HF.
Briefly describe the pathophysiology of heart failure.
When the heart fails, compensatory mechanisms attempt to maintain CO. As HF progresses, these mechanisms are exhausted and become pathophysiological.
What is the most common cause of heart failure?
Ischaemic heart disease.
Give 5 causes of heart failure.
- Commonest cause: IHD.
- Hypertension (pulmonary)
- Cardiomyopathy.
- Excessive alcohol.
- Obesity.
- Valvular disease (commonly aortic stenosis)
- Pericardial causes e.g. pericarditis, effusion
- Myocarditis
- Arrythmias (commonly AF)
Why are men more commonly effected by heart failure than women?
Women have ‘protective hormones’ meaning they are less at risk of developing heart failure.
What are the compensatory mechanisms in heart failure?
- Sympathetic system.
- RAAS.
- Natriuretic peptides.
- Ventricular dilation.
- Ventricular hypertrophy.
Explain how the sympathetic system is compensatory in heart failure and give one disadvantage of sympathetic activation.
The sympathetic system improves ventricular function by increasing HR and contractility = CO maintained.
BUT it also causes arteriolar constriction which increases after load and so myocardial work.
Explain how RAAS is compensatory in heart failure and give one disadvantage of RAAS activation.
Reduced CO leads to reduced renal perfusion; this activates RAAS. There is increased fluid retention and so increased preload.
BUT it also causes arteriolar constriction which increases after load and so myocardial work.
What is the counter regulatory system to RAAS?
ANP/BNP hormones.
What hormones does the heart produce?
ANP and BNP.
What are the functions of ANP and BNP?
- Increased renal excretion of Na+ and therefore water.
- Vasodilators.
- Inhibit aldosterone release.
What metabolises ANP and BNP?
NEP.
Why can NEP inhibitors work for heart failure treatment?
NEP metabolises ANP and BNP. NEP inhibitors can therefore increase levels of ANP and BNP in the serum.
Give 3 properties of natriuretic peptides that make them compensatory in heart failure.
- Diuretic.
- Hypotensive.
- Vasodilators.
Describe the ventricular remodelling seen in heart failure
Initial dilatation.
Hypertrophy, loss of myocytes, increased interstitial fibrosis.
Give the 4 cardinal signs of HF.
- Exertional dyspnea / SOBOE (breathlessness worsened by exertion)
- Orthopnoea
- Paroxysmal Nocturnal Dyspnoea
- Peripheral oedema (swollen ankles and swelling in the legs)
- Fatigue
- Cold peripheries
Give 2 signs of RHF.
- Raised JVP
- Basically, right-sided HF is to do with the vena cava + venous return - the blood can’t return back to the heart - so there’s a backlog/backflow - back down the veins - so causing oedema - Ascites.
- Hepatomegaly may be seen
Give 5 signs of left heart failure.
- Pulmonary crackles; and wheeze
- Added heart sounds (3rd and 4th) and murmurs.
- Displaced apex beat.
- Tachycardia.
- Raised JVP (jugular venous pulse)
Give 3 symptoms of heart failure.
- Exertional dypnoea.
- Orthopnoea (SOB on lying down).
- Paroxysmal nocturnal dyspnoea.
- Fatigue.
- Oedema.
- Weight loss.
- Wheeze.
Why might someone with HF feel breathlessness upon exertion?
- Pulmonary Congestion due to LVF → accumulation of intra-alveolar fluid results in stimulation of juxtacapillary J receptors (CNX Innervation), causing rapid + shallow breathing
- Decreased pulmonary compliance
- Increased airway resistance
Why might someone with HF feel tired / have fatigue?
Due to reduced CO.
Iron deficiency anaemia.
Why might someone with HF feel breathless when lying down?
Due to pulmonary oedema.
Dyspnoea in the recumbent position → congestion redistributes from lower limbs into the pulmonary circulation → nocturnal cough relieved by sitting upright and patients sleep on a lot of pillows.
Common in those with ascites and co-morbidities.
Why might someone with HF have peripheral oedema?
- Decreased venous pressure.
- RAAS activation -> sodium and H2O retention.
Why might someone with HF have tachycardia?
Due to activation of the sympathetic system.
Why might someone with HF have dyspnoea/SOB?
Activation of the RAAS by decreased renal perfusion (due to low CO) - salt/water retention - peripheral/pulmonary congestion
Why might someone with HF have episodes of suddenly waking up at night with a severe attack of shortness of breath and cough (PND)?
Acute episodes of shortness of breath + cough (and wheeze) at night → occurs 2-3 hours after lying down and persist after sitting upright (distinct from orthopnoea) (patient may feel like they’re drowning upon waking).
Occurs due to increased pressure in bronchial arteries resulting in airway compression → increased airway resistance.
Why might someone with HF exhibit Cheyne Stokes breathing / respiration?
Decreased sensitivity of the Respiratory Centres to CO2 → delays in detecting increasing Pa(CO2) and decreasing Pa(O2) results in increasing hypercapnia.
Sudden detection then results in hyperventilation, which then results in apnoea + hypocapnia.
(Cyclical breathing / Apneustic Breathing)
Describe the NHYA classification of HF.
Class I = HF present but no limitation
Class II = mild limitation (comfort at rest, fatigue and dyspnoea on normal physical activity)
Class III = marked limitation (comfort at rest, dyspnoea on gentle physical activity) - moderate HF
Class IV = symptomatic at rest (SOB at rest), exacerbated by any physical activity (all activity causes discomfort)
List 2 major criteria on the Farmingham criteria for HF diagnosis.
Mnemonic: SAW PANIC
- S3 heart sound - gallop.
- Acute pulmonary oedema.
- Weight loss.
- Paroxysmal nocturnal dyspnoea.
- Abdominojugular reflux.
- Neck vein distension.
- Increased cardiac shadow on CXR (cardiomegaly).
- Crepitations (crackles heard in lungs).
List 2 minor criteria on the Farmingham criteria for HF diagnosis.
Mnemonic: HEART ViNo
- Hepatomegaly.
- Effusion, pleural.
- Ankle oedema bilaterally.
- exeRtional dyspnoea.
- Tachycardia.
- Vital capacity decrease by 1/3rd.
- Nocturnal cough.
What might be observed upon physical examination for HF?
- Laboured Breathing (acute LVF) → difficulty completing sentences
- BP → High BP in early HF (compensatory Frank-Starling), low BP in late/chronic HF
- Low Pulse Pressure → decreased SV
- Sinus Tachycardia (increased SNS activity) → peripheral vasoconstriction (= peripheral cyanosis + cool fingertips)
- Respiratory System → rales/crepitations, expiratory wheeze (cardiac asthma), pleural effusion
- Cardiovascular System → S3 gallop, left parasternal heaving (RVF), sustained apical heaving (LHF), inferolateral shift of apex beat (LVF)
- Abdominal → hepatomegaly (if pulsatile = tricuspid regurgitation), ascites, slight jaundice, LFTs
- Oedema → tibial or sacral
- Cachexia → loss of muscle mass due to increasing basal metabolic rate, increased cytokines (TNF), intestinal vein congestion
- Elevated JVP (must examine the internal JV [not external] as internal connect directly to RA and without valves)
What investigations might you initially do in someone who has the signs/symptoms suggestive of HF?
- ECG.
- Find underlying cause. - CXR - might show cardiac enlargement.
- Bloods (BNP - B type natriuretic peptide levels)
- Raised levels indicate heart failure.
- If normal: HF is excluded. - Echocardiography.
What are 5 features of heart failure seen on CXR?
ABCDE:
- Aleveolar oedema (bats wings)
- Kerly B lines (interstitial oedema)
- Cardiomegaly
- Dilated upper lobe vessels
- pleural Effusion
You have done an ECG, CXR and blood tests on a patient who you suspect might have HF.
These have come back abnormal.
What investigation might you do next?
An echocardiogram.
Describe the medical management of HF.
Loop diuretics (furosemide) ± spironolactone ± thiazide.
ACE inhibitors (or ARB).
Beta blockers.
± digoxin, vasodilators (e.g. hydralazine)
What is the first line treatment for heart failure?
ABAL:
- ACE inhibitor (e.g. ramipril titrated as tolerated up to 10mg once daily)
- Beta Blocker (e.g. bisoprolol titrated as tolerated up to 10mg once daily)
- Aldosterone antagonist when symptoms not controlled with A and B (spironolactone or eplerenone)
- Loop diuretics improves symptoms (e.g. furosemide 40mg once daily)
Give an example of an ACE inhibitor that is commonly used in HF.
Perindopril.
Name 4 beta blockers that are used in the treatment of heart failure.
- Metoprolol.
- Bisoprolol.
- Carvedilol.
- Nebivolol.
Why are beta blockers good in chronic heart failure?
They block reflex sympathetic responses which stress the failing heart.
What drugs might you give to someone with HF for symptom relief?
Diuretics: thiazides (bendroflumethiazide) and loop diuretics (furosemide).
They promote Na and so H2O excretion.
Name 2 nitrates that are used pharmacologically.
- Isosorbide mononitrate.
- GTN spray.
How do nitrates work in the treatment of heart failure?
They are vaso/venodilators. They reduce preload and so BP.
Give 3 potential side effects of nitrates.
- Headache.
- Syncope.
- Tolerance.
What is cor pulmonale?
Right sided heart failure caused by respiratory disease
Describe the pathophysiology of cor pulmonale.
Increased pressure + resistance in the pulmonary arteries -> pulmonary hypertension -> RV hypertrophy + dilation -> RV unable to effectively pump blood out of the ventricle and into the pulmonary arteries -> leads to back pressure of blood in the RA, the vena cava and the systemic venous system.
What is the most common cause of cor pulmonale?
COPD
Give 4 causes of cor pulmonale.
- COPD is the most common cause
- Pulmonary Embolism
- Interstitial Lung Disease
- Cystic Fibrosis
- Primary Pulmonary Hypertension
Describe the presentation of cor pulmonale.
- Mainly asymptomatic
- SOB - the most common one
- Peripheral oedema
- Exertional dyspnea
- Syncope
- Chest pain
Give 4 signs of cor pulmonale.
- Hypoxia.
- Cyanosis.
- Raised JVP (due to a back-log of blood in the jugular veins).
- Peripheral oedema.
- 3rd heart sound.
- Murmurs (e.g. pan-systolic in tricuspid regurgitation).
- Hepatomegaly due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)
