Congestive Cardiac Failure Flashcards
What is the most likely cause of heart failure?
Heart failure is the most likely cause due to the combination presence of dyspnoea, oedema, elevated JVP, basal crepitations and enlarged liver.
What is dyspnea?
Dyspnoea - by definition refers to a state where the subject is uncomfortably aware of his/her breathing. It is usually associated with either the increase in the work of breathing - associated with reduced lung compliance (stiff lungs) or increased respiratory rate. It is therefore a non-specific symptom and may occur in diseases pertaining to the cardiovascular, respiratory systems or in the presence of severe anaemia. Review the causes of dyspnoea in these systems.
What are the symptoms of R heart failure? L heart failure?
Ankle oedema, hepatomegaly and elevated JVP = right heart failure
Bibasal crepitations = left heart failure.
What’s the term used to describe breathlessness that is worse when lying down?
Orthopnoea is shortness of breath that occurs when lying flat causing the person to have to sleep propped up in bed or sitting in a chair. It is often a symptom of left ventricular failure and/or pulmonary oedema.
Why does orthopnea occur?
Orthopnoea occurs because the normal pooling of blood in the lungs in the supine position is added to a chronically congested pulmonary vasculature; the increased venous return cannot be compensated for by the left ventricle.
The components of the Jugular Venous Waves: the “A”, “C” and “V” waves. Why and where in the cardiac cycle do they occur?
Waves
a – pre-systolic: produced by right atrial contraction
c - bulging of the tricuspid valve into the right atrium during ventricular systole (isovolumic phase)
v – occurs in late systole; increased blood in the right atrium from venous return
The a and v waves can be identified by timing the double waveform with the opposite carotid pulse. The a wave will occur just before the pulse and the v wave occurs towards the end of the pulse.
Descents
x – a combination of atrial relaxation, downward movement of the tricuspid valve and ventricular systole
y – the tricuspid valve opens and blood flows into the right ventricle
What do you understand by the term “Grade 4 murmur”?
A Grade 4 murmur is a loud murmur with a palpable thrill. Based on the intensity of a murmur it may be classified into the four following grades:
Grade 1: The murmur is heard only on listening intently for some time.
Grade 2: A faint murmur that is heard immediately on auscultation.
Grade 3: A loud murmur with no palpable thrill.
Grade 4: A loud murmur with a palpable thrill.
What should you keep in mind when assessing the significance of a murmur note?
A soft ejection murmur may not signify organic pathology
A new murmur is always significant
A loud murmur associated with a thrill is always abnormal
Diastolic murmurs are always abnormal
What is the Frank-Starling curve?
Describes the relationship between the volume of blood in the heart at the end of diastole (known as the pre-load or end-diastolic volume) and the force of contraction of the ventricle. In the normal heart, if myocardial fibres are stretched by an increased volume of blood, there will be an increase in the force and velocity of the contraction.
A failing heart has reduced contractility. This increases the end diastolic volume. Initially the heart will try to respond by increasing the force of contraction. However a greater end diastolic volume is required to give the same force of contraction. The graph is shifted to the right. Eventually a critical point will be reached where the heart can no longer respond to increasing end diastolic volumes and it will decompensate- stroke volume will decrease with further increases in end diastolic volume. The increased venous pressure causes fluid to leak out of the blood into the alveolar interstitial fluid resulting in pulmonary oedema.
- Acidosis + anaesthetic agents = decreased contractibility
- Catecholamines + calcium = increased contractibility
Coronary heart disease and hypertension are the most common causes of heart failure in the UK. What other causes of heart failure do you know?
Ischaemic heart disease accounts for around 40% of all causes of heart failure in the UK. It is useful to categorise other causes of heart failure into the following:
- Structural causes: Valvular disease such as aortic regurgitation, aortic stenosis, mitral regurgitation and mitral stenosis.
- Congenital heart disease: ASD, VSD, inherited cardiomyopathies.
- Rate-related causes: uncontrolled atrial fibrillation, thyrotoxicosis and anaemia (causing a high output state), heart block (causing a low output state)
- Pulmonary causes: COPD, pulmonary fibrosis, recurrent pulmonary emboli, and primary pulmonary hypertension cause right sided heart failure which in turn can cause congestive cardiac failure.
- Alcohol and drugs: Some chemotherapy drugs are cardiotoxic
- Pericardial disease: chronic pericarditis (caused by tuberculosis, lupus, viruses).
- Autoimmune disease: such as amyloidosis and sarcoid.
- Miscellaneous: Pregnancy-induced cardiomyopathy, acute viral myocarditis
What are 4 causes of mitral regurgitation?
- Rheumatic heart disease
- Ischaemic heart disease - associated with papillary muscle rupture
- Valvular vegetations - as in patients with endocarditis
- Physiological mitral valve regurgitation due to dilated left atrium
What is “ejection fraction”?
A measurement of how much blood is being pumped out of the heart with each contraction. It is expressed as a percentage. (i.e. stroke volume/end diastolic volume). A normal ejection fraction is 50 – 70%.
Explore the statements “because the duration of atrial fibrillation is not clear, a rate control strategy using medical therapy would be preferred at this stage” and “never cardiovert someone who has been in AF for more than 48 hours unless it’s going to be life-saving” in greater detail.
In atrial fibrillation, blood flow will be turbulent, with possible areas of decreased flow or stasis of blood in the atria. This can cause clots to form, and the risk is significantly greater after a patient has been in atrial fibrillation for longer than 48 hours. Therefore, if normal sinus rhythm was restored by cardioverting the patient, the clots could be dislodged and there is a risk of causing an embolic stroke. Therefore, if the onset of atrial fibrillation is not known, or the patient has been in atrial fibrillation for longer than 48 hours, cardioversion (a “rhythm control” strategy) is not recommended. In these circumstances a safer approach would be to control the rate with appropriate medication and anti-coagulate the patient. If appropriate, cardioversion can be attempted at a later date once the patient is fully anti coagulated and an echocardiogram has excluded the presence of thrombi.
Who does cardiac failure affect and what is it likely preceded or associated with?
Usually affects > 75y (1:200 - 50-60y; 1:10 - 80+)
Preceeded or associated with AF (usually in elderly)
What does Reynold’s number represent?
The chance that blood flow will be turbulent
What is the physiology of how murmurs are produced?
- Decreased viscosity of blood
- Decreased radius of vessels/valve
- Increased velocity of blood through morphogenically normal structures
- Regurgitation across incompetent valve
Name an example for each murmur mechanism
Decreased viscosity of blood -> Anemia
Decreased radius of vessels/valve -> Valvular stenosis, coarctation of aorta, ventricular septal defect
Increased velocity of blood -> Hyperdynamic states (i.e. sepsis, hyperthyroidism)
Regurgitation across incompetent valve -> valvular regurgitation
How are murmurs graded?
Grade 1 - 6
1: Barely audible
2: Soft, but easily heard
3: Loud
4: Associated with thrill
5: Very loud, heard without full contact of stethoscope
6: Audible without stethoscope
What are the 3 basic shapes of murmurs?
- Crescendo-decrescendo (i.e. AS)
- Uniform (i.e. MR)
- Decrescendo (i.e. AR)
1 + 2 = systolic murmur
3 = diastolic murmur
Name the 2 most important diagnostics for acute heart failure
- Serum BNP
- normal if < 100ng/l or NT-proBNP < 300ng/l - Doppler 2D echo
- Looking for cardiac abnormalities
What is the treatment for acute heart failure?
- IV diuretics
- B-blocker (not atenolol!)
- ACE-i/ARB + aldosterone antagonist (LVEF < 45%)
- TAVI/surgical replacement if AS
- Surgical valve repair if MR
Outline the cardiovascular continuum
- Risk factors
- Atherosclerosis/LVH
- CAD
- Myocardial ischemia
- Coronary thrombosis
- MI
- Arrhythmia/loss of muscle
- Remodelling
- Ventricular enlargement
- CHF
- Death
HF prevalence increases > 55y
Name 12 causes of heart failure
- Ischemia (CAD, AMI) - 40%
- HTN
- Diabetes (diabetic cardiomyopathy)
- Valvular (AS, MR)
- Tachycardia induced (uncontrolled AF)
- Toxins/drugs (alcohol, doxorubicin - anticancer)
- Infective (viral myocarditis - affects young)
- Endocrine (thyrotoxicosis, phaeochromocytoma)
- Dilated cardiomyopathy (idiopathic, pregnancy)
- Genetic (hypertrophic obstructive cardiomyopathy)
- Pulmonary (COPD, pulmonary fibrosis, PE)
- Autoimmune (Sarcoidosis, amyloidosis)
What is the most common presenting symptom of HF?
SOB
- Exertion/rest
- Paroxysmal nocturnal dyspnea
- Orthopnea
Fatigue/loss of energy
Name 6 signs of heart failure
- Pulmonary oedema/pleural effusion
- Increased JVP
- Pitting oedema
- Ascites
- Tachycardia
- S3 gallop
How is a diagnosis of heart failure made?
- Symptoms of HF +
- Signs of HF +
- Objective structural/functional cardiac abnormality at rest (i.e. cardiomegaly, S3, ECG)
HF is always secondary to another cause
What investigations can diagnose HF?
- Bloods -> FBC, Hematinics (iron, B12, folate), U+E (CRF), TFTs, Glucose, LFTs (pulm. congestion), Troponin I
- ABGs
- Brain Natriuretic Peptide (BNP)
- Secreted by ventricles of heart in response to excessive stretching of heart muscle cells
- Increased levels = worse outcome - Chest xray
- ECHO (info relating to LVEF - normal ~60%)
- ECG (i.e. AF, arrhythmias)
What are the 2 categories of HF patients?
- HF presenting with preserved LV function (EF > 45%)
2. HF presenting with reduced LV function (EF < 45%)
What may LVH indicate?
- HTN
- Aortic stenosis
- HOCM - hypertrophic obstructive cardiomyopathy
What is the treatment for heart failure?
In EF < 45%:
- Diuretic
- ACE-i/ARB
- B-blocker
- Aldosterone antagonist
- Devices: CRT/ICD
In EF > 45%:
- Diuretic
- Treat the co-morbidity/underlying cause (i.e. HTN, DM)
What is CRT? ICD?
CRT = cardiac resynchronization therapy
- Improves synchronicity between LV + RV
ICD = implantable cardioverter defibrillator
- Detects and treats ventricular arrhythmias
What is the action of ACE inhibitors?
- Decrease LVH and remodelling
- Decrease vasoconstriction thus increasing venous capacity
- Decrease H2O and Na retention
Why do ACE inhibitors cause a dry cough as a side effect?
Bradykinin is broken down by the ACE enzyme in the lung. Bradykinin causes a cough and because ACE inhibitors prevent ACE from converting AT1 to AT2 bradykinin isn’t broken down.
Which b-blocker is NOT licensed for use in heart failure?
Atenolol
Two days later Dr. Armstrong is again on duty in the Emergency Department. She is asked to review a 36year old lady who has collapsed at home. The triage note states that she has been unwell for the past couple of days with fever and breathlessness. She has been taking paracetamol because she thinks she developed a chest infection after having her tooth removed the previous week.
Considering potential causes, what key factors might you ask in a focused presenting complaint history?
- What were the exact circumstances of the collapse this morning?
- Was there loss of consciousness? How long did it last for? What were you doing at the time of the collapse? Was it witnessed? Was there any change in skin colour? Was there any seizure activity? Is there a family history of sudden death?
- Preceding dizziness in the past few days? Describe it
- Duration of period of being unwell
- Fevers - ?measured. ?pattern
- Breathlessness – since when? Trigger? Any previous problems with breathing or respiratory conditions
- Associated cough? Haemoptysis?
- Associated chest pain?
- Exactly what type of dental work did you have done?
- Were you given antibiotics at the time or since?
- Any previous heart conditions?
- Foreign travel?
- IVDU?
- Could she be pregnant? LMP?
What are the peripheral stigmata of infective endocarditis?
- Petechiae - Common but nonspecific finding (remember to look at the mucosa)
- Subungual (splinter) haemorrhages - Dark red linear lesions in the nail beds
- Osler nodes - Tender subcutaneous nodules usually found on the distal pads of the digits
- Janeway lesions – Non-tender maculae on the palms and soles
- Roth spots - Retinal haemorrhages with small, clear centres; rare and observed in only 5% of patients.
When considering a potential diagnosis of infective endocarditis, there are specific diagnostic criteria.
What are these called and how is the diagnosis made?
Modified Duke criteria for diagnosis of infective endocarditis are the clinical criteria and requires either of the following:
- 2 major criteria
- 1 major and 3 minor criteria,
- 5 minor criteria.
Major Criteria:
1. Positive blood culture for IE: typical micro-organism consistent with IE from two separate blood cultures.
- Evidence of endocardial involvement:
- Positive echocardiogram for IE:
- Oscillating intra-cardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomical explanation; or
- Abscess; or
- New partial dehiscence of prosthetic valve); or
- New valvular regurgitation (worsening or changing of pre-existing murmur not sufficient).
Minor Criteria:
1. Predisposition: predisposing heart condition or intravenous drug use.
- Fever: temperature >38°C.
- Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhages and Janeway’s lesions.
- Immunological phenomena: glomerulonephritis, Osler’s nodes, Roth’s spots and rheumatoid factor.
- Microbiological phenomena: positive blood culture but does not meet a major criterion as noted above or serological evidence of active infection with organism consistent with IE.
- PCR: broad-range PCR of 16S (polymerase chain reaction using broad-range primers targeting the bacterial DNA that codes for the 16S ribosomal subunit).
- Echocardiographic findings consistent with IE but do not meet a major criterion as noted above.
What does blood culture-negative IE (BCNIE) refer to?
This refers to IE in which no causative micro-organism can be grown using the usual blood culture methods. BCNIE can occur in up to 31% of all cases of IE and most commonly arises as a consequence of previous antibiotic administration.
What signs are assumed to show endocarditis until proven otherwise?
Fever + new murmur
What is the commonest organism of acute infective endocarditis on normal and prosthetic valves?
Strep. viridans + Staph aureus = normal valves
Staph epidermidis = prosthetic valves
What are risk factors for infective endocarditis on normal valves?
- Skin breaches (i.e. dermatitis, IV lines, wounds)
- Renal failure
- Immunosuppression
- DM
What are risk factors for infective endocarditis on abnormal valves?
- Aortic/mitral valve disease
- Tricuspid valves in IV drug users
- Coarctation of aorta
- Patent ductus arteriosus
- Ventricular septal defect
- Prosthetic valves
What are the septic signs of infective endocarditis?
- Fever
- Rigors
- Night sweats
- Malaise
- Weight loss
- Anemia
- Splenomegaly
- Clubbing
What are immune complex deposition signs of infective endocarditis?
- Vasculitis
- Microscopic hematuria
- Glomerulonephritis
- AKI
- Roth spots (boat-shaped retinal hemorrhage with pale centre)
- Splinter hemorrhages
- Osler’s nodes
- Janeway lesions
What are the pathognomonic signs of infective endocarditis
Janeway lesions + osler’s nodes
What investigations should you do if suspecting infective endocarditis?
- Blood cultures
- Do 3 sets at different times from different sites at peak of fever - Blood tests (FBC, U&E, Mg2+, LFTs)
- Normochromic, normocytic anemia
- Neutrophilia
- High ESR/CRP
- Rheumatoid factor positive - Urinalysis
- For microscopic hematuria - Chest x-ray
- Cardiomegaly
- Pulmonary oedema - ECG
- Look for heart block - ECHO
- TTE may show vegetations only if >2mm
- TOE better for mitral lesions + aorta root abscess devo - CT
- To look for emboli (spleen, brain, etc)
What is the treatment for infective endocarditis?
Blind therapy - native valve/prosthetic valve implanted > 1y:
- Ampicillin, flucloxacillin + gentamicin
- Vancomycin + gentamicin (if penicillin allergy)
- Meropenem + vancomycin (if thought to be gram neg.)
Blind therapy - prosthetic valve:
- Vancomycin + gentamicin + rifampicin
Staphs - native valve:
- Flucloxacillin for > 4wks
- Vancomycin (if allergic/MRSA)
Staphs - prosthetic valve:
- Flucloxacillin + rifampicin + gentamicin for 6wks (review need for gentamicin after 2wks)
- Vancomycin + rifampicin + gentamicin (if allergic/MRSA)
Streps - fully sensitive to penicillin:
- Benzylpenicillin 1.2g/4h IV for 4-6wks
Streps - less sensitive to penicillin:
- Benzylpenicillin + gentamicin
- Vancomycin + gentamicin (if allergic/penicillin resistant)
Enterococci:
- Amoxicillin + gentamicin
- Vancomycin + gentamicin for 4wks (if allergic)
HACEK organisms (Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella): - Ceftriaxone for 4wks/6wks if prosthetic valve
Fungal:
- Amphotericin (for candida)
- Voriconazole (for aspergillus)
What are the HACEK organisms?
Hemophilus Actinobacillus Cardiobacterium Eikenella Kingella
How does electrical conduction move throughout the heart?
SA node -> AV node -> Bundle of His -> Purkinje fibres -> ventricles
What is the speed of cardiac AP? Why is it this speed?
300ms (its long!)
- This stops re-excitation and fibrillation because of the long refractory period
What does the QT segment represent in regards to cardiac AP?
The plateau of the cardiac AP
What is the resting AP for cardiac muscle?
-80/90mV (negative with respect to the ECF)
What are the 5 phases of the AP?
- Rapid depolarization (entry of Na+ into cells via voltage-dependent activation channels - 10ms)
- Early repolarization
- Plateau phase (slow repolarization)
- Repolarization (fast repolarization)
- Resting membrane potential restored
What currents are associated with the different phases of cardiac AP?
Na+ current -> depolarization
Ca2+ current -> plateau
K+ current -> repolarization
How do arrhythmias arise?
Different refractory periods among cells in the heart. They are prevented by fast conduction velocity and uniform activation by Purkinje fibres.
Arrhythmias arise if the ventricle has pacemaker activity
Where does the electrical activity originate from in the heart?
The heart is a myogenic pump.
Electrical activity originates in the SA node. The backup pacemaker activity is in the AV + Purkinje fibres
What are the 2 broad categories of arrhythmias?
- Abnormal pacemaker/triggered activity
- Early afterdepolarization (EADs) -> decreased outward K+ current (prolonged AP depolarization) leads to longer plateau phase (Ca2+ current) -> Long QT syndrome -> can be either genetic or acquired (i.e. drugs - anticancer, antihistamines)
- Delayed afterdepolarizations (DADs) -> Ca2+ overload (HF) -> spontaneous Ca2+ release from SR -> activates depolarizing membrane currents
- Re-entrant Arrhythmias
- Common post. MI
- Produced by: (a) Unidirectional block; (b) Slow conduction (refractory period must be over once re-entry occurs - common in myocardial ischemia/MI); (c) Short AP (produces short refractory period - MI)
Explain excitation-contraction coupling
Underpinned by systolic Ca2+ transient
At rest = 0.1uM = intracellular [Ca2+] (1:10 000 of that in ECF)
Depolarization = 1uM
- This rise in intracellular Ca2+ levels = cardiac muscle contraction
Ca2+ binds to troponin
Actin + myosin slide over each other = purposeful contraction
What are the sources of Ca2+ for cardiac muscle contraction?
- Intracellular stores -> Sarcoplasmic reticulum
- SR released via ryanodine receptors (RyR) - Outside of cells via L-type Ca2+ channels
Calcium-induced Calcium Release:
L-type Ca2+ channel from outside cell allows extracellular calcium to bind to RyR -> releases intracellular Ca2+
How is Ca2+ removed from the cytoplasm?
- SERCA (back into SR)
- Increased levels of intracellular Ca2+ cause the phosphorylation of phospholamban and the association of this protein with SERCA (sarco/endoplasmic reticulum Ca2+-ATPase) - Na-Ca2+ exchange (out of cell)
- 3 Na+ in for 1 Ca2+ out
How does the heart respond when there’s SNS stimulation?
SNS stimulation = increased contractibility of the heart
Positive inotropic + lusitropic (relaxation of the contraction) effects of catecholamines
B-adrenergic stimulation = less time for heart to fill between contractions thus increased L-type Ca2+ current = increased Ca2+ trigger + loading of cells
= increased SERCA + SR Ca2+ via phosphorylation of phospholamban
- increased Ca2+ to be released
What is the treatment for heart failure with LVEF < 45%?
First-line:
- Offer both ACE inhibitors/ARB + b-blockers
- Consider HYDRALAZINE + NITRATE if intolerant to ACE/ARBs
Second-line add to above:
- Aldosterone antagonist
- ARB
- Hydralazine + nitrate (esp. in ppl of African/Caribbean origin)
If symptoms persist:
- Digoxin
- CRT (pacing with/without defibrillator)
- Consider ICD
What is the treatment for chronic AF?
- Anticoagulation
- Rate control: B-blocker or rate-limiting Ca2+ channel blocker
- If above fails, add digoxin, then consider amiodarone
- Don’t give b-blockers with verapamil - Rhythm control: Elective DC cardio version, Elective pharmacological cardio version (FLECAINIDE/IV AMIODARONE)
- Paroxysmal AF: SOTOLOL or FLECAINIDE PRN
What are the components of the CHADS-2 score?
Diabetes Hypertension Congestive heart failure Age > 75y History of previous stroke or TIA
What class of drug is rivaroxiban?
Direct factor Xa inhibitor
Practice prescribing a loop diuretic as a once only oral dose for a patient with worsening pedal oedema, selecting from the list below. The time is now 6pm. The patient has no known drug allergies.
Furosemide 40mg, Oral
What is the Frank-Starling mechanism?
A greater end-diastolic volume would increase the contractile strength of the ventricles and will increase stroke volume.
Remember, SV is proportional to Preload (EDP which is stretching the walls of the ventricles to their greatest geometrical dimensions)
This occurs because: the myocardium is more stretched due to a greater volume thus their sarcomere length will increase and there will be an increased sensitivity to Ca2+ thus leading to a much stronger contraction.
What is the underlying cause of pulmonary oedema? Peripheral oedema?
Pulmonary oedema -> L sided heart failure
Peripheral oedema -> R sided heart failure
During an ABCDE assessment, what is important to remember when putting someone on oxygen?
- Oxygen should be 15L in a non-rebreathe mask to start
- Sit patient upright
- If needed (I.e. broncospasm) use nebulisers with B2-agonists
What investigations should you perform for someone you suspect has heart failure?
- ECG -> dysrhythmias
- ECHO -> LV function
- Troponins
- Chest x-ray -> pulmonary oedema
- BNP -> heart failure
- FBC -> infection, anemia
- U+E -> kidney function
- ABG/VBG -> lactate, acid-base balance
- Serum glucose
- CRP
What is the difference between high output heart failure and low output heart failure?
High Output:
The normal heart ails to maintain normal or increased output in conditions like anemia, hyperthyroidism, pregnancy. Usually R sided failure occurs followed by L sided failure with presence of shortened circulatory time
Low Output:
Heart fails to generate adequate output in conditions like cardiomyopathy, valvular heart disease, tamponade, and bradycardia
List 9 causes of wide QRS
- LBBB/RBBB
- Ventricular tachycardia
- Wolff-Parkinson White syndrome
- Torsades des Pointes (sinusoidal VT)
- Ventricular fibrillation
- Drugs (I.e. tricycline OD)
- Hypothermia
- Complete heart block (would have bradycardia)
How would you treat acute heart failure?
- Furosemide (reduces breathlessness, decreased LV filling pressure)
- Aspirin
- Clopidogrel
- Fondaparinux
- Digoxin
- Vasopressors (increase cerebral partial pressure) I.e. noradrenaline
- Alpha agonist = vasoconstriction without increase in heart rate - Inotropes (increase contractility of heart) I.e. Dobutamine
- Driving heart that’s not oxygenated = could increase strain on the heart, thus should be used secondary to vasopressors
