Pathophysiology of Cardiac Failure Flashcards
How is CO calculated?
HR x SV
What two factors is preload determined by?
EDV
Venous return
Define afterload.
Force the contracting heart must generate to eject blood from the heart
What two factors determine afterload?
Vascular resistance
Ventricular wall tension
(think…T = PR, therefore P is going to be determined by T & R)
What is inotropy (for the purposes of the CVS)?
Myocardial contractility
Define myocardial contractility.
The sympathetic mediated change of cardiac muscle
What direct effect does increased myocardial contractility have?
Increases CO
Does myocardial contractility refer to the speed of contraction of the force at which the contraction is generated?
Force
Which ion influences myocardial contractility?
Ca2+
What chemical mediator is L-type Ca2+ channel opening facilitated by?
cAMP
What inhibits Na+/Ca2+ exchange?
Cardiac glycosides, e.g. digoxin
Outline the New York Heart Association Classification of Heart Failure.
Classes 1 - 4
Class 1 = no limitation of physical activity; no fatigue, dyspnea (shortness of breath) or palpitations
Class 2 = slight limitation of physical activity; ordinary activity results in fatigue, dyspnea or palpitations
Class 3 = marked limitation of physical activity; less than ordinary activity results in fatigue, dyspnea or palpitations
Class 4 = unable to carry out any physical activity without discomfort; fatigue, dyspnea or palpitations at rest
What is the difference between systolic and diastolic dysfunction with regard to ejection fraction and EDV (and hence SV)?
Systolic: ejection fraction @ 40% as opposed to normal 50-65%
Diastolic: no change in ejection fraction
Systolic: EDV only increases if volume overload affecting conditions; if caused by contractility or pressure overload affecting conditions, same EDV
Diastolic: EDV decreases due to decreased filling, leading to decreased SV and decreased CO
Systolic: impaired contraction
Diastolic: impaired relaxation
What does systolic dysfunction result from?
Conditions that affect:
- Contractility
- Volume overload
- Pressure overload
What causes diastolic dysfunction?
Impedance of ventricular expansion
Increased wall thickness
Delayed diastolic reaction
Increased HR
How is SV calculated?
EDV - ESV
What is ascites?
An accumulation of fluid in the abdominal cavity
What can be an issue in heart failure patients when going from a standing position to a supine lying position?
Blood redistributed from the lower limbs can backup and cause congestion in the lungs
What can left heart failure cause?
Congestion in the lungs
Decreased cardiac output
Bearing in mind what left heart failure causes, what are some signs and symptoms of this condition?
Orthopnea Cough with frothy sputum Paroxysmal nocturnal dyspnea Cyanosis Hypoxia
What can right heart failure cause?
Congestion in the peripheral tissues
Liver congestion
GI tract congestion
Bearing in mind what right heart failure causes, what are some signs and symptoms of this condition?
Impaired liver function Anorexia GI distress Weight loss Oedema Ascites
What are some causes of right ventricular dysfunction?
Pulmonary hypertension Valve damage/stenosis/incompetence Cardiomyopathy Infarction Left ventricular failure Congenital heart defects
How can left ventricular failure lead to right heart dysfunction (failure)?
Since afterload of right ventricle is significantly increased due to congestion in the lungs, pressure required for right ventricle to pump blood to the pulmonary system is also significantly increased –> increased pulmonary pressure, so right heart failure is very possible
What are some causes of left ventricular dysfunction (failure)?
Hypertension (TPR increase)
Acute MI
Aortic or mitral valve stenosis or regurgitation
What is the function of cardiac failure compensatory mechanisms?
Involved in hypovolaemia
What is the chain of events that makes the Frank-Starling compensatory mechanism problematic?
Increased vascular volume
- -> increased EDV
- -> increase in muscle stretch & O2 consumption
- -> change in preload (length - tension curve)
- -> sarcomere beyond optimal length and SV decrease
What is the chain of events that makes the Sympathetic Activity compensatory mechanism problematic?
Tachycardia, vasoconstriction and decreased perfusion of non-essential tissues
- -> blood directed towards tissues that it is essential to oxygenate
- -> increased TPR & renin release
- -> increased workload of the heart
- -> damage to myocytes & ischaemia
- -> decreased contractility
- -> desensitisation of Beta (but not Alpha) receptors
Where are beta receptors predominantly situated?
The heart
Where are alpha adrenoreceptors predominantly situated?
The vasculature
What is the chain of events that makes the Renin-Angiotensin compensatory mechanism problematic?
Focus on blood volume:
Decrease in renal blood flow
–> renin release
–> increased angiotensin II formation
–> increased vasoconstriction & aldosterone release
–> increased Na+ & water reabsorption
–> oedema & increased congestion
Why can fibroblasts and collagen deposits sometimes be found in the ventricles in cardiac failure patients?
Angiotensin II and aldosterone are involved in inflammatory responses leading to deposition of collagen and fibroblasts in the ventricles
What is the result of deposition of collagen and fibroblasts in the ventricles?
Increased stiffness
Decreased contractility
–> Myocardial remodelling and progressing dysfunction
What 4 physiological CV parameters need to be targeted in cardiac failure treatment and what change needs to take place to each?
Increase CONTRACTILITY
Decrease PRELOAD and/or AFTERLOAD –> decrease CARDIAC WORKLOAD
- by relaxing vascular smooth muscle
- by reducing blood volume
Inhibit Renin Angiotensin Aldosterone System (RAAS)
Prevent inappropriate increase in HR
