Heart failure Flashcards
Define heart failure
HF is a complex clinical syndrome in which the heart is unable to maintain a CO adequate to accommodate metabolic demands & venous return
Define CO, EF & SR
EF refers to ejection fraction which the proportion of blood ejected during each heartbeat, normal range of 50-70%
Describe the EF equation
EF=stroke volume/end diastolic volume x100
Define chronic and acute HF
Chronic is long-term, gradual reduction in heart function
Acute: sudden onset of reduction in heart function, likely to be caused by an MI or papillary muscle rupture
Define HFrEF & HFpEF
HFrEF: refers to HF with a reduced EF which indicates systolic dysfunction, indicates impaired ejection/contractility, range of 50-70% is normal
HFpEF: refers to HF with a preserved ejection fraction, this indicates diastolic dysfunction which is impairment in filling & relaxation
Name causes for HF
- Ischemic HD
- Cytotoxins
- Viruses/bacteria
- Hypertension
- Idiopathic cardiomyopathy
- prolonged arrhythmias
- valvular disease
Describe the new york heart association classification system
Class I: no symptoms, can carry out daily activities
Class II: slight limitations of physical activities resulting in fatigue, SOB or palpitations, but comfortable at rest
Class III: identifiable limitations of physical activity, but mild activity causes fatigue, SOB & angina, fine at rest
Class IV: cannot carry out physical activity without discomfort, shows symptoms of cardiac insuffciency
Describe the ACC heart failure classification system
A (bottom): involves those at high risk e.g., diabetics, family history and those with hypertension
B: involves asymptomatic left ventricular dysfunction e.g., valvular disease or previous MI
C: involves symptomatic HF patients that have a know structural HD & have SOB, fatigue etc
D (top): refers to end-stage HF patients, in which show prominent symptoms despite medical therapy
A pyramid diagram that increases in structural disorders and symptoms as well as severity as you go up, shows evolution and progression to HF
Describe the cause of systolic and diastolic dysfunction in HF
Systolic: heart cannot pump effceintly due to myocardial damage/injury, such as an MI or ischaemia
Diastolic: The heart’s inability to relax properly, leading to impaired filling during diastole, often seen in conditions like hypertension or hypertrophic cardiomyopathy.
Describe the body’s response to decreased CO due to HF
The body’s homeostatic mechanisms of RAAS & SNS are activated to restore perfusion to vital organs
Describe the influence of the SNS on HF
In response to poor perfusion of vital organs the SNS becomes activated & releases adrenaline to cause vasoconstriction, increased HR & contractility. This helps short term, however can also worsen HF due to an increased workload on the heart & increased oxygen demand for myocardium
SNS causes MAP to increases as SR, HR & total peripheral resistance increase due to vasoconstricion and increased HR due to release of adrenaline
Describe the influence of the RAAS on HF
Reduced BP triggers the release of renin from the kidneys due to a lack of perfusion. This triggers the conversion of angiotensin 1 to angiotensin 2 which triggers aldosterone release. Adosterone acts on the collecting ducts and increases the retention of sodium & water to increase BP & preload,
However this can cause fluid retention, oedema & increased workload on the heart
MAP increases due to an increase in SR, HR & total peripheral resistance
Describe the influence of NAP release on HF
Are peptide that are released when the heart becomes damaged, we use these as biomarkers to diagnose & assess HF severity
This is released in HF as pumping ability becomes compromised leading to increased preload and hypertrophy
ANP is released to indicate increased stretching in the atrias, normally due to fluid overload
BNP is released from the ventricles due to increased ventricular wall stress & increased preload, it has diuretic and vasodilatory properties
CNP is involved in vascular homeostasis, e.g., CNS, it does have vasodilatory properties
Describe the neurohormonal response to impaired cardiac performance
- Increased salt & water retention
Short term: increased preload
LT: pulmonary congestion - Vasoconstriction
ST: maintains BP to perfuse vital organs
LT: Increases cardiac energy expenditure and increases workload on heart reducing it’s efficiency as a pump - Sympathetic stimulation
ST: Increases HR & EF
LT: increases strain on heart and cardiac energy expenditure
Describe the structural effects of persistent strain on the heart
Changes in the hearts size, shape & structure occur due to increased stressors placed on the myocardium
- Hypertrophy: myocardium begins to thicken in response to increased workload, this can help maintain CO, but hypertrophied muscle becomes less efficient over time and can lead to dilation
- Dilation: ventricles become dilated which results in reduced contractile function & impaired filling of the heart
- Myocardial fibrosis: as the heart undergoes stress, myocardium may be replaced by fibrous tissue which impairs contractility & relaxation, impairs pumping ability of the heart
3.
Describe venous congestion/pulmonary congestion
VC: refers to blood backing up to the lungs (LSHF) due to a reduction in pumping efficiency of the heart. This can lead to pulmonary oedema or peripheral oedema
This can cause symptoms such as swelling, SOB , bloat
Describe the frank-starling mechanism on HF
it states that the more the heart muscle is stretched (up to a certain point), the stronger the force of contraction, increased venous return increases the degree of stretch
In HF patients myocardium is weakened & therefore increased preload causes the heart to stretch beyond optimal length, the sarcomeres in the myocardium are no longer in their ideal range for effective contraction, and the heart’s ability to contract strongly is impaired.
This leads to a reduced ejection fraction and further worsening of heart failure.
The Frank-Starling mechanism becomes less effective, and the heart can no longer compensate adequately for the failing pumping action.
What are the determinants on ventricular functions
- Afterload
- Preload
- Wall thickness
- Valve efficiency
- Contractility
- HR
Describe the effect of preload & afterload on VF
Preload refers to the volume of blood filling the ventricles at the end of diastole, in HF patients they have an increased preload due to frank-starling mechanism & to increase SR, however increased preload can lead to blood backflow causing pulmonary congestion
Afterload refers to the pressure required of the ventricles to overcome for blood to be pumped out, HF patients having a higher afterload results in a reduced SR & increases myocardial workload
Describe the effect of contractility & HR on VF
Contractility (inotropy) refers to the ability of the myocardial fibers to contract independently of preload & afterload. In HF patients contractility is increased to increase CO & SR to allow efficient perfusion of organs, but this leads to an increased workload on the heart
Describe the effects of hypertrophy & ventricular volume on VF
Hypertrophy occurs due to an increase in workload this can initially compensates the heart from stress, but leads to impaired filling and reduced O2 supply
VV refers to the total volume of blood in the ventricles during a cycle phases, Excessive volume may lead to dilation of vessels and myocardium which can cause decreased contractility effciency
Describe the hemodynamic effect on left-sided HF
- Reduced LVEF leads to less blood pumped into systemic circulation leading to a EF
- LVEDP increases due to LV dysfunction, blood backs up to LA & pulmonary veins increasing LVEDP as LV fails to empty properly, this reflects an increased filling pressure
- Pulmonary congestion is caused by high LVEDP due to backflow of blood to PV’s creating an increase in pressure in the pulmonary capillaries. If pressure exceeds threshold then fluid can leak out causing oedemas
- Decrease in CO due to reduced EF leading to hypoperfusion of organs, the body attempts to compensate by using SNS & RAAS, but this increases workload on the heart
Describe the symptoms and physical signs of LSHF
Symptoms:
1. Dyspnea
2. Cough
3. Fatigue
4. Tachycardia
5. Haemoptysis
signs:
1. pulmonary oedema
2. S3 gallop
3. Pleural effusion
4. Basilar rates (abnormal lung cracking)
Describe the hemodynamic effect on right-sided HF
- Decreased RVEF as the RV fails to pump blood into the pulmonary circulation
- Elevated RVEDP due to increased filling pressure of the RV due to backflow of blood into RA
- Venous congestion: leads to oedema, liver enlargement & ascites
- A decreased CO leads to a reduction in systemic perfusion & leads to activation of complimentary mechanisms e.g., SNS & RAAS
Describe the symptoms and physical signs of RSHF
Symptoms: abdominal pain, anorexia, nausea, bloating and swelling
Signs: JVD, peripheral oedema, liver enlargement & abdominal jugular reflex
Describe the consequences of decreased MAP (mean arterial pressure)
A decreased MAP means less blood is available to perfuse vital organs, including the heart itself. This forces the heart to work harder to maintain adequate circulation, increasing the workload on the already compromised heart.
Worsening cardiac function: In heart failure, the heart is already pumping less efficiently, and lower MAP further strains the heart muscle. This can worsen symptoms of HF
