Cardiac Failure Flashcards
How is RV EDP and LV EDP measured?
RV EDP
- Catheter inserted via a vein across the tricuspid valve
- Measure @ end of diastole, RV EDP = RA EDP = JVP
LV EDP
- Pulmonary ‘wedge’ pressure: catheter from right side of heart wedged into Pulmonary A. and balloon occludes blood flow > measures pulmonary venous pressure
- Measure @ end of diastole, LV EDP = LA EDP = pulmonary venous/wedge pressure
How does fluid leak across capillaries due to ‘Starling forces’
- Tends out at arterial end
- Tends in at venous end
- Excess fluid removed by lymphatics
- Increases in VENOUS pressure causes fluid to leak out and oedema.
What happens if LV EDP is too high?
LA pressure increased, Pulmonary venous pressure increased > fluid pushed out @ pulmonary capillaries > pulmonary congestion (@ around 20-30 mmHg) and manifests as shortness of breath
What happens if RV EDP is too high?
RA pressure increased > JVP/ peripheral venous pressure increased > fluid pushed out @ peripheral capillaries > oedema
What are 3 cardiac failure adaptations and why are they inappropriate?
Triggered by the drop in CO and the activation of the SNS and RAS
- Na+ and water retention: fill up with fluid, oedema
- K+ loss: can trigger arrhythmias
- Vasoconstriction: increases afterload, harder for the heart to work
What are the 3 mechanisms of right heart failure?
Mechanisms of right heart failure
- Global heart disease e.g. cardiomyopathy
- Specific right heart disease e.g. RV cardiomyopathy, pulmonary hypertension, valves, shunts
- Left heart failure e.g. mitral stenosis Pulmonary venous hypertension > pulmonary congestion > chronic hypoxia > Pulmonary vasoconstriction > Pulmonary artery hypertension > right heart failure
What are the 2 patterns of cardiac hypertrophy and what are their physiology?
Concentric
- increased wall thickness w/o LV enlargement
- Often due to pressure overload (more afterload)
- more sarcomeres in parallel
Eccentric
- increased chamber size and normal relative wall thickness
- often due to volume overload (more preload)
- more sarcomeres in series
How can cardiac hypertrophy turn pathological?
In the long term cardiac hypertrophy may decompensate:
- LV dilation: increased LVEDV and LVESV, decreased EF
- reduced systolic function and CO
- Increased LVEDP
- Eventual cardiac failure
How can heart failure result in diastolic dysfunction?
- Thick muscle is stiff (harder to fill heart with blood)
- higher LVEDP required to achieve same LVEDV leading to increased pulmonary venous pressure and pulmonary congestion
- atrial kick more important: susceptible to atrial fibrillation
What are the possible consequences of heart failure?
Epidemiology – increased risk of:
- Ischaemic Heart Disease
- Cardiac Failure
- Atrial fibrillation
- Stroke
Functional – diastolic dysfunction
What are some causes of Right Ventricular Hypertrophy?
- Congenital – e.g. Transposition of Great Arteries
- Pulmonary Hypertension
– lung disease
– pulmonary embolus
– chronic Left heart failure
• Right heart valves
– Pulmonary Stenosis/Regurgitation
– Tricuspid Regurgitation
What are some causes of LVH?
Environmental
– Concentric: pressure overload: high afterload
• Hypertension, Aortic Stenosis
– Eccentric: volume overload: high preload
• Mitral and Aortic Regurgitation, Ventricular Septal Defect
– Following myocardial infarction
– Following cardiac injury – e.g. myocarditis
– Obesity, Diabetes, Renal Failure
– Infiltration
Genetic
– Hypertrophic Cardiomyopathy
– Fabry’s Disease
What happens in hypertrophic cardiomyopathy and what are the consequences?
- Increased LV wall thickness esp. of septum
- Cellular hypertrophy
- Myocyte disarray Consequences:
- LV Outlow tract obstruction
- Diastolic Dysfunction
- Ventricular arrhythmias – sudden death
How is LVH identified?
- Clinical – forceful apex beat, S4, S3
- ECG – tall voltages, T wave inversion
- CXR – large heart in eccentric LVH – may be normal size in concentric LVH
- Echo
- MRI
- Cardiac CT
What is the genetic basis of hypertrophic cardiomyopathy?
- Autosomal Dominant
- Mutation in genes for sarcomere proteins
- Most common
– β cardiac MHC
– cardiac myosin binding protein
– cardiac troponin I & T
What is the mechanism of action and effect of Digoxin on cardiac myocytes?
E.g. Digoxin
- inhibit Na+/K+- ATPase
- increased [Na]i decreases Ca2+ extrusion
- increase Ca2+ in SR
- increase Ca2+ release with each AP
Benefit: Increased contractility @ 25 mins
Risk: dysrhythmia @ 45 mins
What are some of the effects of glycosides in heart failure and what factors increase its toxicity?
- narrow margin of safety, low therapeutic index
- affect all excitable tissues (can trigger ventricular arrhythmias, but used to treat atrial arrhythmias)
increased toxicity with:
- low K+ (decreased competition for binding)
- high Ca2+ (decreased gradient for Ca2+ efflux)
- renal impairment
- oral absorption, t1/2 ~ 40 hr, wrong dose takes a long time to come down
What is the mechanism of action and adverse effects of β-Adrenoceptor agonists and PDE inhibitors?
-Intravenous, short term support for acute heart failure, cardiogenic shock<!--StartFragment-->
Not for long term management
Reduced sensitivity of B1 receptors by:
Decreased B1 R expression
Impaired B1 R coupling
Leading to reduced B1 R agonist sensitivity
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β-adrenoceptor agonists
– NA/A, activate both α- & β-adrenoceptors
– dobutamine, selective β1-adrenoceptor agonist
Phosphodiesterase inhibitors
– Amrinone
Adverse effects for both:
- Increase cardiac work, O2 demand
- Risk of arrythmias
What is the mechanism of action and adverse effects of aldosterone receptor antagonists?
e. g. spironolactone
- Inhibit aldosterone action on cortical and distal tubules
- K+ sparing diuretic
Adverse effects: require close monitoring for hyperkalaemia and renal function
How are β-adrenoceptor antagonists used in heart failure and what are their side effects?
attempts to inhibit the disease process in early stages
β1 blockade (cardiac) metoprolol
- reduces tachycardia, cardiac work
- inhibits renin release and subsequent AngII effects
- protects against receptor downregulation
β1 & α1 blockade (vascular, carvedilol only)
- vasodilation reduces afterload, cardiac work
**Side effects: **
- hypotension, fatigue (cardiac and β2-mediated)
- bronchoconstriction (β2 block – so not in asthma)
- cold extremities (α1-mediated reflex – so not in PVD)
- may cause and/or mask signs of hypoglycaemia (so not in diabetes)
