Heart Failure Flashcards
What is heart failure?
Condition in which the heart is unable to pump sufficiently to maintain blood flow to meet the body’s needs
What is the main cause of heart failure? Name some other causes
Ischaemic heart disease (IHD)
Other causes: Hypertension Dilated cardiomyopathy (pathogen/drugs/alcohol/poisoning/pregnancy/idiopathic) Vascular heart disease/congenital Restrictive cardiomyopathy eg amyloidosis Hypertrophic cardiomyopathy Pericardial disease High output heart failure Arrhythmias (ie AF)
What are the LV end systolic and diastolic volumes?
Systolic~75ml
Diastolic ~ 150ml
*therefore ejection fraction 50%
What 4 factors effect cardiac output?
HR
Aortic and peripheral impedance (after load-ie increase in BP)
Myocardial contractility (reduced = less CO)
Venous capacity (LV preload, nothing going in= nothing coming out)
What effect does an increased end diastolic pressure have on cardiac output?
Increases it to a point
*the force developed in muscle fibre depends on the degree to which the fibre is stretched
What is left ventricular systolic dysfunction?
Increased LV capacity but reduced LV cardiac output
It is the thinning of the myocardial wall due to fibrosis and necrosis of myocardium and activity of matrix proteinases
What are the further complications of LV systolic dysfunction?
Mitral valve incompetence (LA-> LV, cusps don’t change in size so as the walls of LV stretch the valve cusps get pulled apart)
Neuro-hormonal activation (the heart is more exposed to hormones (ie adrenaline) therefore there is a higher risk of MI)
Cardiac arrhythmias (electrical impulses effected, bundle branch block= LV and RV contract at different times. Potential life threatening)
What are the structural heart changes that can occur to cause Heart failure?
- Loss of muscle
- Uncoordinated or abnormal myocardial contraction (see on an ECG)
- Changes to ECM: increase in collagen (type 3 5% becomes type 1 at 25%) and slippage in myocardial fibre orientation
- Change of cellular structure and function: myocytolysis and vacuolation of cells, myocyte hypertrophy, SR dysfunction, changes to Ca2+ availability and/or receptor regulation
How can a MI lead to heart failure?
The heart remodels to protect itself. The myocytes have no remodelling capacity
How does hypertrophy cause heart failure?
Hypertrophy- reduced volume within LV so LV enlarges (dilates) so cardiac output is maintained
What are the two neuro-hormonal systems that are targetted by drug therapy to treat HF?
Sympathetic NS
RAAS
How does HF affect the sympathetic NS?
The SNS tries to compensate for the heart.
Baroreceptor-mediated response
What are the early compensatory mechanism performed by the Sympathetic NS to deal with HF?
The whole idea is to improve CO:
- Cardiac contractility (increase inotropy)
- Arterial and venous vasoconstriction
- Tachycardia
What are the long term deleterious effects that the sympathetic NS can have when it is trying to compensate for HF?
- Beta-adrenergic receptors are down-regulated /uncoupled
- Chronic exposure to noradrenaline can be bad because; it can induce cardiac hypertrophy/myocyte apoptosis and necrosis via alpha receptors, it can induce up regulation of the RAAS
Ultimately what are the results of sympathetic activation in heart failure?
Myocardial hypertrophy
Decreased contractility
Myocyte damage
Which substance in the RAAS is responsible for causing damage when someone has HF? What two receptors does it work on?
Angiotensin II
Works on AT1R and AT2R
What does AT1 receptor do when activated by angiotensin II?
Causes vasoconstriction
This is what causes the problems when someone already has HF
How is the RAAS commonly activated in HF?
- Reduced renal blood flow
2. SNS induction of renin from macula densa
What effects do angiotensin II have on the body?
- Potent vasoconstrictor
- Promotes LVH and myocytes dysfunction
- Promotes aldosterone release
- Promotes Na+/H2O retention
- Stimulates thirst by central action
All work to increase CO
What hormones are released form the heart during heart failure and why?
ANP and BNP
They work to oppose the RAA system because they are released when the heart is stretched
What is another name for AHD?
Vasopressin
In heart failure, what happens to the levels of ADH?
It is increased (want to increase BP and increase CO)
Name some hormones that are associated with HF?
Endothelin
Prostaglandins (stimulated by NA and RAAS)
Nitric oxide (usually potent vasodilator produced by endothelial cells- not produced when someone has HF)
Bradykinin (stimulates production of Prostaglandins and vasodilation)
Tumour necrosis factor (a-TNF) depresses myocardial function
What is a key feature of someone who has HF?
Oedema (pitting)
What can pulmonary oedema cause?
Breathlessness
What is oedema?
Excessive volume of fluid within tissues (interstitial and intracellular)
What effect does HF have on the capillary hydrostatic pressure?
It increases it
In heart failure there is an increase in peripheral arterial resistance, by what mechanisms does this happen? (4)
- SNS
- RAAS
- Reduced NO
- Increased endothelin
Alteration in vascular tone exacerbates the clinical deterioration of someone which HF
If you have reduced skeletal muscle blood flow (like in HF) what are the consequences?
- Reduction in skeletal muscle mass (cachexia): affects all muscles including limbs and respiratory eg diaphragm (leads to increasingly laboured breathing)
- Abnormalities of structure and function
*this all contributes to fatigue and exercise intolerance
In early Hf what maintains the Glomerular filtrate rate (GFR)?
Haemodynamic changes at glomerulus
How does severe HF cause a rise in serum urea and creatinine levels? How is this made even worse?
Severe HF = Renal blood flow falls = Reduced GFR = Rise in urea and creatinine
Made worse by treatment inhibiting the action of Angiotensin II
How can HF cause anaemia?
Reduced kidney perfusion = Reduced erythropoietin = Reduced level of RBC production = Anaemia
What is heart failure with preserved ejection fraction (HFpEF)?
When someone has heart failure but the CO is still maintained.
It is seen in about 50% of the cases of HF
Key factors: frequently elderly and female and often history of hypertension/ diabetes/ obesity
Normal LV function with concentric remodelling
What is the pathology of the HFpEF?
Heart doesn’t relax in diastole
Which can lead to impaired diastolic filling
Therefore LV filling becomes dependent on high LA pressure
RV dysfunction can result from high LA and PA pressures
=
Triggers neuro-hormonal activation as per systolic HF
What are the different types of HF?
Left sided HF
Right sided HF
Biventricular (congestive) cardiac failure
Or you can characterise it into:
Left ventricular systolic dysfunction (LVSD)
Heart failure with persevered ejection fraction (HFpEF)
What are the signs and symptoms of someone with L sided HF?
Fatigue, exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea (PND)
As it progresses you will see: Tachycardia Cardiomegaly (displaces apex beat) 3rd and 4th heart sound Functional murmur of mitral regurgitation Basal pulmonary crackles Peripheral oedema
What causes right HF?
Chronic lung disease
PE/pulmonary hypertension
- the most frequent cause is secondary to left heart failure= congestive HF
- *it is possible but uncommon to see right heart failure alone
What are the symptoms and signs of right HF?
Fatigue, dyspnoea, anorexia and nausea (build up of fluid in liver) Increased Jugular venous pressure Tender, smooth hepatic enlargement Dependent pitting oedema Ascites Pleural effusion
