Heart Failure Flashcards
Give 5 clinical pieces of evidence that someone may have a heart structural/functional abnormality
- ECG
- Echocardiogram
- Cardiac murmur
- Raised natriuretic peptide
- Cardiomegaly
What are the 3 ways Heart failure can be classified?
- Acute vs Chronic
- L side vs R side (or congestive = both)
- Reduced vs Preserved ejection fraction (or both)
What’s the difference between a reduced and preserved ejection fraction?
A reduced EF: Heart cannot pump properly
Therefore there is an issue in systole and the EF becomes less than 40%
A preserved EF: Heart cannot fill properly
Therefore it’s an issue in diastole and the EF remains above 40%
Name 3 things that could cause the body to demand a higher output from the heart, what could cause a lowered output?
Demanding a higher output:
- Pregnancy
- Anaemia
- Hyperthryoidism
Heart is producing a lowered outout: any cardiovascular problem
LName 3 other things that could cause this
Main causes: Coronary heart disease, hypertension
Others: cardiomyopathy, AV valvular disease, arrythmias
What is the main cause of R sided Heart failure?
Try to name 5 other things that could cause this
Main cause: Left sided Heart failure eventually backs up and affects the Right side
- Pulmonary embolus
- Chronic lung disease
- RV infarction
- Shunts: Atrial or ventricular septal defect
- Pulmonary and tricuspid regurgitation
What is the latin term for what occurs in the R side of the heart during R sided heart failure
Cor pulmonale: R sided hypertrophy due to disease in the pulmonary vessels or lungs
What 3 factors help to increase the stroke volume?
- Decreased afterload
- Increased preload
- Increased contractility
What are 3 pathologies that could increase the preload and 2 things that could increase an afterload?
Increasing the preload
- Hypervolemia
- Valve regurgitation
- Heart failure
Increasing the afterload:
- Hypertension
- vasoconstriction
How does the ventricular output change from excercise to heart failure?
Excercise: Dilation of blood vessels (metabolic vasodilators) decreases the afterload and makes ventricular output more efficient in pumping out their end-diastolic volume
Heart failure: The more severe it becomes the more contractility decreases, decreasing ventricular output
What is an ejection fraction, how is it calculated and what should it be normally?
Ejection Fraction: the % of blood that gets pumped out of the heart after each diastolic filling
Calculated:
Amount pumped out/Total ventricular volume at end of diastole
Normal: 55-75%
Where would an oedema occur in L and R sided Heart Failure?
L sided: pulmonary oedema
R sided: peripheral oedema
What are 4 things that could cause a preserved ejection fraction?
Problems with ventricular filling…
- L ventricular hypertrophy
- Restrictive cardiomyopathy
- Coronary heart disease
- Tamponade: fluid accumulation in the pericardial space compressing on the heart
What are the 2 main causes of a reduced ejection fracion? Name 2 ways you could acquire each
Issues pumping blood…
1. Impaired contractility: coronary heart disease, chronic volume overload, and bonus: dilated cardiomyopathy
- Increased Afterload: severe hypertension, aortic stenosis
Give 5 symptoms of LEFT Ventricular failure
- Orthopnea
- Paroxysmal nocturnal dyspnoea
- Nocturnal cough is pink and frothy
- Breathless on exertion
- Weight loss, muscle wasting and fatigue!
Give 5 symptoms of RIGHT ventricular failure
- swollen ankles
- fatigue
- Dysopnea
- Anorexia: gut or liver congestion
- Nausea
Name 4 signs of R ventricular failure
- Pitting oedema
- Raised JVP
- Hepatomegaly (liver may also be pulsating)
- Ascites: fluid accumulation in the peritoneal cavity/abdomen
What is the basic mechanism that forms an oedema?
Hydrostatic
How is staging classified for heart failure? List the stages and their brief characteristics
Heart failure is staged depending on how functional the heart still is
Class 1: no symptomatic limitation of physical activity
Class 2: Mild physical limitation, symptoms when doing ordinary physical activity, i.e; running, weights, etc
Class 3: Marked physical limitation, symptoms when doing ordinary daily activity, i.e; walking, chores
Class 4: severe discomfort and inability to carry out any physical activity without symptoms, symptoms at rest
How is the prognosis for Heart failure?
Generally poor as it can be treated but not cured, class 4 has an 80% mortality rate after 3 years
What are the 3 compensatory mechanisms the body tries to bring the CO back to normal?
- Ventricular remodelling
- Starling law mechanism
- Neurohormonal alterations
Describe the starling law mechanism
Since HF decreases CO and stroke volume:
This decreases the amount of blood being pumped out of the ventricle - which causes an accumulation of blood within the ventricle
This stretches the cardiac myocytes, helps them contract harder and brings the SV and CO back up
When are neurohormonal alterations activated and what are their 2 overall goals?
Activated in response to a low CO
Aim to:
1. Increase systemic vascular resistance as this brings up the BP (BP = CO X TPR) which (through somewhat unknown mechanisms) brings up the CO (involves increasing peripheral venous pressure and decreasing central venous pressure)
- Increase the preload by retaining salt and water
What does the sympathetic nervous system do as a neurohormonal alteration?
Baroreceptors located in the aortic arch and carotid sinus sense a low CO and increase the sympathetic activity:
- Vasoconstriction
- Increased HR
- Increased contractility via adrenaline
What does the RAAS system lead to as a neurohormonal alteration?
Inevitably RAAS leads to fluid retention to help increase the preload:
1. Results in Angiotensin II which increases thirst and arterial vasoconstriction
- Angiotensin II also produces aldosterone which retains Na+ and Excretes K+ and H+
How can neurohormonal alterations become an issue chronically? (4 things)
- Vasoconstriction can lead to increased wall stress and decrease contractility as well as eventual hypotension
- Increasing HR also increases the heart’s metabolic demands (working harder, needs more oxygen)
- Increasing TPR leads to an afterload so high that SV and CO are reduced further (producing further hypotension)
- An increasing volume due to fluid retention causes further pulmonary and peripheral congestion
What does ADH/Vasopressin do as a neurohormonal alteration? When is it released?
Released in response to hypovolaemia:
Increases water retention: increasing volume and preload
What 2 things activate the start of RAAS?
- Sympathetic NS
- Reduced renal blood flow
Both activate Renin to be produced/secreted from JGA cells in the kidney
What are the benefits of B type natriuretic peptide (BNP) and when are they secreted?
Secreted in response to increased Cardiac pressure/being stretched
Work to balance the effects of RAAS:
- Increase excretion of Na+ and water
- Vasodilation
- Decrease renin and action of angiotensin II
What are the 3 main components to Ventricular Remodelling and what is the eventual outcome?
- Hypertrophy
- Fibrosis
- Apoptosis
Eventually, the myocytes become so stretched and damaged that the ventricle wall is weak and thin. This can result in backflow of blood into the L atrium and pulmonary vessels
What are 6 kinds of investigations you could do for heart failure?
- Echo: can look at heart structure
- ECG
- N terminal pro BPN: secreted by myocardial cells in response to increased volume and pressure
- Chest Xray
- Full Blood count
- Test kidney function: U&E and eGFR before prescribing meds that might alter kidney function
Why is N terminal pro-BPN not always reliable?
It’s highly sensitive but has low specificity, as various things can cause it to be raised and it might be decreased in obesity, African-Caribbean origin, and with certain medications
What levels of NT proBPN might lead you to consider chronic heart failure in a patient?
400-2000 mg/l
What is the principle of conservative heart failure management? What are 4 things you could implement
Patient education
- reducing excessive salt and alcohol
- increasing aerobic exercise
- decreasing CV risk factors: smoking
- Use a multidisciplinary team to make sure all available treatment options are considered
What is the main goal in medical management of heart failure? List 4 drugs that can be given
The main goal is symptomatic improvement and to delay the progression of heart failure in order to reduce mortality
- Loop diuretics; furosemide
- Beta-blockers: inhibit sympathetic response
- Nitrates: veno and vasodilation
- ACE inhibitor: reduces fluid retention
What are 3 main surgical interventions that can be done to manage heart failure?
- implantable defibrillator
- implantable pacemaker
- Cardiac surgery: includes heart transplant, mechanical assist devices, valve surgery, revascularisation
Try to list 8 things you would provide as immediate treatment for heart failure
- Loop diuretics
- Oxygen
- Sit patient up
- morphine to reduce anxiety (but careful of the resp rate)
- Vasodilator
- Vasopressor: induces vasoconstriction and elevates mean BP
- Assess ABC hypoxia, hypercarbia (high CO2 levels), metabolic acidosis
.8. Inotropes: decrease cardiac contractility
What defines acute heart failure? List 5 symptoms and 7 signs
Acute Heart failure is the sudden onset of symptoms
Symptoms: severe SOB, sweating, nausea, anxious, dry or productive (wet and chesty) cough
Signs: Hypotension, edema, crackles, S3, raised JVP, tachycardia, orthopnea
