WK3 - Heart Failure Flashcards
Compare the difference in Tx for treating heart failure between 1972 and 2010.
1972 - “the earlier the bed rest is instituted after onset of cardiomyopathy, the greater the benefits expected”
2010 - “regular Ex is a safe and effective Tx modailty in most CHF patients, partially reversing some maladaptations in myocardial and skeletal muscle function = improves physical fitness and quality of life and perhaps reduced mortality”
Comment on the prevalence of heart failure in Aus.
2.1%/y - 511,000
- 67k new cases
158,000 admissions/y
61,000 HF deaths/y
3.1bil in healthcare/y
+146,000 / 10y
657,000 cases by 2025
- the incidence on HF is increasing every year
Comment on the prevalence of HF in QLD.
98k cases/y
- 12,600 new cases
30k admissions/y
11,900 HF-related deaths/y
- 1,700 deaths within 1y Dx
$600mil in healthcare /y
- 402mil in hospital care
+35,000 cases/10y
133,000 cases by 2025
1/3 - 2/3 HR admissions are preventable. T or F?
True
* Failure to adhere to prescribed therapy
– Pharmacological and non-pharmacological
- Failure to recognise and seek early Tx for escalating
Sx of CHF.
– Poor discharge planning and follow up.
– lack of social support, isolation, depression, cognitive impairment, multiple co-morbidities.
What is the typical trajectory of chronic heart failure?
- Dx
- responding to Tx
- clinical instability
- poor Tx response
- death
- support and palliative care can bring patients back to stage 2
- sudden death can occur after 1. between 2&3 and after 3.
Provide the pathophysiology of heart failure.
- heart unable to pump at rate that is adequate for metabolising tissue (organs/muscles)
- inability of LV to pump blood adequately can be due to failure of systolic or diastolic function
Define chronic heart failure.
- a complex clinical syndrome with typical signs and Sx (e.g. dyspnoea, fatigue) that can occur at rest or on effort.
- secondary to an abnormality of cardiac structure/function that impairs ability of heart to fill with blood at normal pressure or eject blood sufficient to fulfill needs of metabolising organs.
What are the causes of heart failure?
- long-term hypertension
- CAD
- MI
^^ 60% of causes
*chronic arrhythmias - valve problems
- long term alcohol/drug issues
- heart abnormalities present at birth
- drug SE e.g. chemo
- viral infections - HIV and flu
- idiopathic - unknown causes
What are secondary changes in the body that lead to heart failure?
- degeneration/loss of cardiomyocytes
- replacement with scarring and fibrosis
- impaired myocardial contractility and valve competence
What are the hemodynamic changes that lead to heart failure?
- decreased CO during Ex (or at rest)
- elevated LV filling pressures
- compensatory ventricular overload
- elevated pulmonary and central venous pressures
What are the secondary organ changes that lead to heart failure?
- major derangement in skeletal muscle metabolism
- impaired vasodilation
- renal insufficiency leading to Na+ and water retention
What is the difference between systolic and diastolic heart failure?
Systolic - HR with reduced EF (HRrEF)
* inability of cardiac myofibrils to contract/shorten against load, leading to reduce EF
* loss of muscle, usually due to MI
* loss of contractility
DIASTOLIC = HR with preserved EF (HRPEF)
* abnormal increase in resistance to filling LV
* stiff or non compliant chamber that is partially unable to expand as blood flows during diastole
* increased ventricular pressure, higher than noral filling pressures
SV for both sit below normal at 50mL
How does the heart compensate to maintain function?
- increase HR - maintain CO with reduced SV
- increase blood volume - use hormones and nerve signals to reduce blood flow to kidneys = retain Na+ to increase water retention
- cardiac remodelling - hypertrophy/chamber enlargement to cope with extra workload
–> heart = stretched, less contractile = decreases efficiency of contraction = reduced amount of blood circulation.
What are the heart’s compensatory mechanisms?
- autonomic nerves - increased sympathetic adrenergic activity
- hormonal - renin-angiotensin-aldosterone system
- ventricular remodelling - dialtion and hypertrophy
What is the SNS response?
- most immediate
- stimualte beta-adrenergic receptors to elevate HR and increase contractility to augment SV = greater CO
- epinephrine and norepinephrine = increased HR, contractility, vasoconstriction to increase CO
However also causes…
* increased preload, afterload, ventricular remodelling, hypertrophy, myocardial necrosis
* all advance HF overtime
* may trigger arrhythmias and sudden death
What is triggered/activated by a decrease in Q, systemic BP and kidney perfusion?
- caused by myocardial dysfunction - ischaemic heart disease, MI, valve disease, HTN, arrhythmias etc
- activates baroreceptors (LV, carotid artery and aortic arch)
–> vasomotor regulatory centres in medulla stimulated = SNS activated
–> increase catecholamines (adrenaline) = vasoconstriction to increase afterload, BP and HR for ventricular remodelling
What is the RAAS system?
renin-angiotensin-aldosterone system
* regulation BP and water balance
* triggered by initial drop in kidney perfusion = increase Na+ and water absorption
= increased preload, afterload and contractility via
* increase blood volume, systemic filling pressure and venous return
- blood volume low = kidney secrete renin
- renin stimulates angiotensin I production -> converted to angiotensin II (powerful vasoconstrictor)
- angiotensin also stimulates secretion of hormone aldosterone from adrenal cortex = kidney tubules to retain Na+ and water = increased blood volume
What causes ventricular remodelling?
- abnormal pressure and volume overload = myocardial hypertrophy
Overtime may cause further impairment of pump performance due to…
* impaired systolic pump - impaired muscle function/collagen growth
* diastolic compliance changes - thickened ventricular walls
Hypertrophy alters cardiac function by depressant effect on ventricular compliance, rate and contraction force.
What does ventricular remodelling involve?
- myocyte hypertrophy = large abnormal cells = cannot contract efficiently
eventually causes…
* increased LV mass
* changes in ventricular shape
* impaired contractility
* despite larger size, ventricle becomes less effective = increased chamber wall stress and O2 need
What happens during ventricular dilation?
*ventricles dilate =spherical geometry
* Occurs as diastolic filling increases over time to augment contractility via increased preload (Frank-Starling Mechanism)
* LV dilation results in energetically unfavourable configuration
Explain heart failure progression.
Compensatory mechanisms:
* SNSactivation
* RAAS
* ventricular remodelling
Causes a shift to right of ventricular function curve, reflecting more pronounced increase in ventricular filling pressure with no further increase in cardiac performance.
What are the Sx of HF?
- SOB
- feet/legs oedema
- weight gain or bloating
- tiredness
- appetite loss
- faintness or dizziness
- heart palpitations
- chest pain
- dry irritating cough
What are the classifications of HF stages?
New York Heart Association (NYHA)
- Class I – asymptomatic HF
– No limitations to PA - Class II – mild HF; slight limitation of PA.
– Ordinary PA =fatigue, palpitations, dyspnoea or angina - Class III – moderate HF;
– Less than ordinary PA leads to Sx - Class IV – severe HF;
– Sx at rest
Ex intolerance is the hallmark feature of HF. T or F?
True!
1. reduced pulmonary reserve
2. reduced cardiac reserve
3. skeletal muslce dysfunction
4. other factors: obesity, anaemia, unhealthy diet, peripheral vascular dysfunction, impaired autonomic regulation
How is HF Dx?
- chest x-ray - enlarged heart
- echo - EF <50%
- angiogram - CAD and LV function
- blood test - brain natriuretic peptide >500 = likely HF
