Session 11- Heart failure Flashcards
What are the three key factors in determining stroke volume?
- Preload
- Afterload
- Contractility
What are the two major groups of heart failure?
- Systolic dysfunction -> Decreased ejection fraction due to an abnormality of ventricular emptying
- Diastolic dysfunction -> Abnormalities of diastolic relaxation
What are the two main causes of systolic dysfunction?
- Impaired myocardial contractility
- Excessive afterload
What effect can loss of contractility have on myocytes?
- Destruction of myocytes
- Abnormal myocyte function
- Fibrosis
How does afterload cause a decreased ejection fraction?
-Increased resistance to flow
What effect does systolic dysfunction have on SV?
-Decreases it
Why does the end diastolic volume increase in systolic dysfunction?
-Decreased ejection fraction -> Larger end systolic volume -> normal venous return added to increased ESV -> Increased end diastolic volume
If the EDV is increased in systolic dysfunction, why does this not increase SV?
-The initial problem of decreased contractility/increased afterload is still present
Why does pulmonary congestion and oedema occur in left systolic dysfunction?
-Increased EDV -> Increased pressure in LV -> increased pressure in LA -> increased pressure in pulmonary veins and capillaries -> increased hydrostatic capillary pressure -> transudate moves into pulmonary interstitium ->Pulmonary oedema and congestion
What are the common causes of diastolic dysfunction?
- Impaired diastolic dysfunction haha
- Increased stiffness of ventricular wall
What type of injury would cause impaired relaxation and stiffness?
-Acute myocardial infarction leading to fibrosis and scar tissue
Why is the RV susceptible to damage caused by sudden increases in afterload?
-Thin walled chamber which is used to pumping blood against a low pulmonary vascular resistance
What is the most common cause of RHF?
-LHF which increases pulmonary resistance and thus the af-terload of- the RV
Besides LHF, what is the most common cause of isolated RHF?
-Increased afterload due to diseases of the lung parenchyma or pulmonary vasculature eg lung disease, pulmonary hypertension, valvular disease
What effects and why does RHF directly have effect on the systemic system? (not compensatory mechanisms)
-Increased pressure in RV due to high afterload -> increased pressure in RA and congestion due to higher pressure in RV -> congestion of systemic veins -> increased hydrostatic pressure causes oedema -> hepatomegaly as first organ back and liver becomes saturated with blood -> possible ascites due to increased hydrostatic pressure
How does starlings law participate in compensatory mechanisms of systolic dysfunction LHF? What are its limitations?
- Decreased ejection fraction -> SV decreased -> normal venous return adds to increased ESV -> increased end diastolic volume -> causes the heart to contract harder as preload is greater increasing SV
- In severe HF with a great decrease in contractility of the heart, the heart cannot eject anymore blood than the maximum it can, despite increasing EDV
What are the three main compensatory neurohormonal mechanisms activated in response to decreased CO?
- The sympathetic nervous system
- Renin-Angiotensin-Aldosterone System
- Increased ADH
What effect do compensatory mechanisms have on vascular resistance and why?
-Increase vascular resistance in order to maintain arterial bloodf-low and thus perfusion to the tissues as bp=COxTPR and if CO is decreased then TPR needs to be raised
What is compensatory heart failure?
-When the fall in SV, however decreased CO is counteracted by an increase in HR and an increase in TPR through compensatory mechanisms, so the impairment is asymptommatic or mild
What overall effect do compensatory mechanisms have on sodium and water retention and why does this occur?
-Increase Na and H2O retention in order to increase blood volume and thus increase BP and also increase SV through starling’s law of filling of the heart
What two organs sense a fall in CO and how?
- Brain through baroreceptors in carotid sinus and aortic arch
- Kidney through juxtaglomerular apparatus
What leads to the activation of SNS after a fall in CO?
- Baroreceptors in carotid sinus and aortic arch detect fall in CO and decrease their firing rate to the medulla
- Causes an increase in sympathetic outflow and diminish in parasympathetic
What are the immediate consequences of increasing SNS in LHF?
- Increase in HR
- Increase in ventricular contractility
- Vasoconstriction of vessels through af-adrenoreceptors
What is the reason for activating the SNS in LHF?
- Counteract fall in CO by increasing HR and force
- Increase TPR through vasoconstriction to maintain bp
Why is venoconstriction helpful in HF?
-Less capacitance in veins -> higher venous return to heart -> f-rank starlings law
What mediates the RAAS?
-Release of renin
Where is renin secreted from?
-Juxtaglomerular cells of the kidney
What causes secretion of renin?
- Decreased renal artery perfusion pressure secondary to low CO
- Direct stimulation of JGA by SNS through b2-adrenoreceptors
What is the function of renin?
-Cleaves circulating angiotensinogen to angiotensin I
What happens to angiotensin I when synthesised?
-Rapidly converted to angiotensin II through proteolytic cleavage by ACE
What are the main functions of angiotensin II?
- Vasoconstrictor which increases TPR to maintain bp
- Increase intravascular volume through stimulating thirst receptors in hypothalamas and stimulating the adrenal cortex to increase aldosterone secretion to increase Na retention by the kidney and thus increase water reabsorption
Where does aldosterone promote sodium reabsorption?
-Distal convoluted tubule
What is the benefit of increasing intravascular volume in LHF?
-Maintain bp and increase CO through starlings law
Where is ADH (vasopressin) secreted from?
-Posterior pituitary
What causes increased ADH secretion in HF?
-Baroreceptors detect fall in BP and relay to brain
Why is increased secretion of ADH beneficial in HF?
- Increases thirst
- Increases aquaporin channels means increased water retention
- Increased blood volume
- Maintains BP and starlings law increases CO
What are the consequences of chronic activation of RAAS?
-Increasing intravascular volume -> initially increases EDV which tries to increase SV, however this increases pressure in chambers causing the pressure in the previous system to increase leading to oedema
ie in LHF, increased pulmonary capillary hydrostatic pressure = oedema
in RHF, increased systemic congestion and hydrostatic pressure leading to peripheral oedema and hepatosplenomegaly and ascites
What causes activation of brain and kidney compensatory mechanisms in RHF?
-Decreased ejection fraction from RV -> decreased pulmonary flowf-> decreased filling of LV -> decreased CO f-> fall in bp detected by baroreceptors causing activation of SNS and ADH secretion -> reduced flow to JGA causes activation of RAAS, in addition to SNS acting on b-adrenoreceptors
What effect does chronic activation of SNS have in LHF?
- Chronic vasoconstriction increases the afterload which the already failing left ventricle has to contract against, may therefore decrease SV further
- Increased HR increases metabolic demand of heart which can further reduce contractility
- Continuous exposure to NA results in downregulation of b-adrenoreceptors and upregulation of inhibitory g-proteins resulting in a negative inotropic response
What are the two types of natriuretic peptide?
- Atrial natriuretic peptide
- B-type natriuretic peptide
What causes the release of ANP?
-Atrial distention
When is BNP produced?
-When ventricular myocardium is subjected to haemodynamic stress eg in heart failure or MI
What are the functions of natriuretic peptides?
Ultimately oppose compensatory mechanisms
- Excretion of Na and water
- Vasodilation
- Inhibition of renin secretion
- Antagonists of angiotensin effects on aldosterone and ADH
What are possible causes of impairment of ventricular dysfunction in HF?
- Loss of myocytes from cellular necrosis (Ischaemic heart disease MI/CAD)
- Impaired function of living myocytes through mechanical wall stress resulting in dilation of the wall leading to mechanical and electrical uncoupling
- Impaired function of myocytes through altered expression of contracile proteins by inflammatory cytokines
What are the common factors which precipitate compensated or asymptomatic HF to develop into a clinical manifestation?
- Increased metabolic demand and thus cardiac workload eg fever, infection, anaemia, exercise
- Increasing preload -> diet high in Na, excess fluid
- Increasing afterload -> hypertension
- Conditions which impair contractility -> MI, negative inotropic meds
How would a tachyarrhythmia precipitate HF?
-Decreased diastolic ventricular filling and increased myocardial O2 demand
What is the most common clinical manifestation of LHF?
-Breathlessness on exertion
What causes breathlessness in LHF?
- Pulmonary oedema results in reduced pulmonary compliance due to compression of the walls of the bronchi and alveoli, increasing the resistance to airflow, and the reduction in the available number of- alveoli
- Reduced blood flow to overworked respiratory muscles lead to atrophy
What effect does HF have on skeletal muscle?
- Decreased CO -> decreased tissue perfusion -> atrophy of skeletal muscle including diaphragm
- Fatigue and weakness
Why would HF cause dulled mental status?
-Decreased cerebral perfusion
Why would HF cause impaired urine output?
-Decreased renal perfusion -> high pressure not maintained and needed for glomerular filtration
Why would nocturia happen in HF?
-Bloodflow to kidney re-established when supine, promoting renal perfusion and diuresis
Why does hepatomegaly occur in RHF?
-Liver becomes engorged with blood
Why does nausea and anorexia occur in RHF?
-Oedema within the gastrointestinal tract
Why would a patient with RHF gain weight despite having a decreased appetite?
-Accumulation of interstitial fluid due to systemic congestion and RAAS/ADH
Why do pateints with severe HF appear cachexia?
-Poor appetite and metabolic demands of increased effort in breathing
Why would a patient appear diaphoretic?
-Sweating due to increased SNS-> activation of sweat glands
Why are the extremities of patients with uncompensated LHF often cool?
-Chronic vasoconstriction of the peripheries
Why can sinus tachycardia occur in HF?
-Increased sympathetic NS
Why does crackling in the lungs occur with HF?
-Pulmonary oedema -> air bubbling through fluid
Why can wheezing occur in HF?
-Narrowed airways due to oedema
What are causes of increased afterload which can precipitate LHF?
- Hypertension
- Atheroscleosis
- Aortic stenosis
- Hypertension
What are causes of increased preload which can precipirate LHF?
- Mitral regurgitation
- Aortic regurgitation
What is heart failure?
-The inability of the heart to pump blood at a sufficient rate to meet the metabolic demands of the body
What is high-output HF?
-The demand of- the body outweighs the hearts ability
Briefly describe the classes of HF
- Class i-> asymptommatic
- Class ii-> Slight limitation to physical activity
- Class iii-> Marked limitation of physical activity
- Class ivf-> inability to carryout physical activity without symptoms, possible symptoms at rest
How is the pulmonary and systemic vascular congestion treated in HF?
- Fluid restriction
- Dietary Na restriction
- Diuretics
What groups of drugs are used to increase CO and tissue perfusion?
-Vasodilators and positive inotropic drugs
Describe the structural changes in the heart after an MI
- Necrosis and scarring
- Heart remodels around scar as it is thin and weak
- Heart becomes asymmetrically dilated
Why is the mitral valve effected in systolic dysfunction?
-LV becomes dilated and the valve becomes incompetent as it does not close tightly
Describe the structural changes which occur in the heart in diastolic and systolic HF
- Heart undergoes hypertrophy due to increased workload
- Overtime the muscle wears which results in dilation and thinning in a symmetrical manner
Why does contraction become uncoordinated and abnormal in HF?
- Muscle damage results in loss of muscle and dilation
- This decreases mechanical and electrical coupling resulting in uncoordinated contraction
- ECM increases in collagen and myocardial fibre orientation slips
What receptor does Aii cause the compensatory mechanisms through?
-AT1R
What is the effect of- angiotensin II acting on AT2R?
-Increased nitric oxide production which is a vasodilator
List some signs and symptoms of LHF
- Breathlessness (dyspnoea)
- Fatigue
- Tachycardia
- Cardiomegaly (displaced apex beat)
- Functional murmur of mitral regurgitation
- Peripheral oedema
- Basal pulmonary crackles
What are the signs and symptoms of RHF?
- Fatigue
- Dyspnoea
- Anorexia and nausea
- High JVP
- Hepatomegaly and ascites
- Pitting odema
List the common pharmacological treatments of HF
- Diuretics -> reduce blood volume
- ACE inhibitors -> inhibit angiotensin ii -> decrease blood vol and vasoconstriction
- Nitrates -> vasodilator to reduce afterload
- B-blockers -> decrease HR and f-orce of- contraction to decrease metabolic demand
What is the known side effect of an ACE inhibitor?
-Dry cough due to blocked effect of bradykinin
