Module 2 Flashcards
What are the determinants of stroke volume?
Preload, afterload, and myocardial contractility
What is preload
Ventricular wall tension at the end of diastole (approximated by end diastolic volume or pressure)
What is afterload
Ventricular wall tension during contraction; force that must be overcome to eject blood from the ventricle (often approximated by systolic ventricular (or arterial) pressure)
What is contractility (inotropic state)
Property of the heart muscle that accounts for changes in strength of contraction, independent of preload or afterload. Reflects chemical or hormonal influences
Stroke volume
Volume ejected from the ventricle during systole
SV= end diastolic volume - end systolic volume
Ejection fraction (EF)
Fraction of end-diastolic volume ejected from the the ventricle during each systolic contraction
EF = SV / end diastolic volume
Normal is 55%-75%
Cardiac output
CO= SV x HR
Volume of blood ejected from ventricle per minute
Compliance
Passive length-tension properties.
Intrinsic property of a chamber that describes its pressure-volume relationship during filling. Reflect ease of difficulty the chamber can be filled
How is heart failure different than congestive heart failure
Heart failure is defined at the inability of the heart to pump blood forward into the arterial system at a rate necessary to meet metabolic demands
Congestive heart failure is a complex of signs and symptoms (syndrome) that arises when heart failure occurs. Dominated by blood and retained fluid contesting in the venous system.
What are the 6 categories of heart failure?
- Increase in the resistance of ejection of blood from ventricles (increased afterload)
- An increase in the volume of blood to be pumped.
- Impairment of atrial emptying
- Reduced myocardial contractility (impaired systolic fn)
- Reduced myocardial relaxation (impaired diastolic fn)
- Increased demand for blood by peripheral tissue (high output HF)
What factors can increase resistance to the ejection of blood from the ventricles (afterload)
Arterial hypertension
Aortic or pulmonary semilunar valve stenosis
Subaortic stenosis
Coarctation of the aorta
What causes an increase in blood volume (preload)
Left to right shunts (congenital)
Regurgitation of any of the 4 heart valves
What can impair atrial emptying
Atrial tutors
Mitral and tricuspid valve stenosis
Atrial thrombosis
What can reduce myocardial contractility
Ischemia from CAD
Myocardial infection
Myocyte disarray of hypertrophic cardiomyopathy
Myocardial injury
What can reduce myocardial relaxation?
Causes: those that prevent the myocardium form expanding (tamponade, constrictive pericarditis)
And those that make the myocardial muscle less compliant (ischemic heart disease, hypertrophy of myocardium)
Low-output heart failure
When cardiac output falls below normal and cannot meet the minimal metabolic demands of the body, even at rest.
Causes: Myocardial ischemia, MI, and cardiac arrhythmias.
High-output heart failure
(Less common)
When CO is excessive but heart is unable to meet increased demand for oxygenated blood.
Appears at the onset of physiological or pathological stresses that require a compensatory increase in CO.
Forward failure
Hypotheses to explain the effects of HF by reduced tissue perfusion that occurs and by the compensatory mechanisms.
Reduced brain perfusion results in confusion, dizziness,, loss of consciousness. Reduced muscle perfusion = weakness, fatigue
Decline in renal perfusion triggers retention of salt and water, alleviates fall in CO, but causes vascular congestion and edema.
Backward failure
Hypothesis that attributes the affects of heart failure to the heart inability to pump the blood from the venous system.
Blood damming behind the failing heart.
Congestion of venous and capillary beds leading to edema and partly responsible for the kidneys retaining fluid.
Left sided heart failure
(LHF)
Most common (30x) due to high pressure gradients across the valves and higher workload.
Most result from MI, valvular disease, hypertension.
IN LHF blood accumulates upstream in left atrium and pulmonary vasculature. Pressure in pulmonary capillaries rise, fluid escapes to interstitium and accumulates in alveolar spaces causing pulmonary edema.
Right-sided heart failure (RHF)
Usually follows LHF bc of increased pulmonary pressure = increased right heart afterload. Cor pulmonale (hypertrophy of right v) causes RHF from pulmonary hypertension arising from destruction of lung tissue (bronchitis, emphysema, pneumoconiosis) Also RHF is caused from large pulmonary emboli, MI's, diffuse myocarditis, pulmonary vascular sclerosis accompanying congenital HD.
Signs of RHF
Systemic venous congestion and edema, splenic enlargement, peripheral edema, ascites Elevated RA pressure Abdominal pain Oliguria Peripheral pitting edema
Signs of LHF
Pulmonary congestion and edema. Elevated pulmonary wedge pressure Rales Chronic productive cough Frothy sputum Hemopytysis (spitblood) Dyspnea Orthopnea Cheyne stokes respiration. (Lying flat = hard to breath) Paroxysmal nocturnal dyspnea Air hunger Tachycardia Skin pallor or cyanosis Fatigue
Bilateral HF
Both sides of the heart fail at the same time.
Causes: toxic conditions, infections, radiation injury, diffuse malignancies, pericardial disease, myocardial ischemia, arrhythmias.
Sometimes a result of progression from unilateral HF.
Compensatory responses to heart failure
- Decline in CO (forward failure) resulting in reduced tissue perfusion, tissue hypoxia, cyanosis, and weakness
- Backed up blood in vessels supplying the heart (backward failure) causing venous congestion, hypertension and edema
- Compensatory responses to restore CO and maintain adequate perfusion of the tissues
Acute compensatory responses to HF
-Increase HR (raising CO)
-Release of calcium from SR to myocadial cells
- venous vasoconstriction (decrease blood vol in venous system and improving venous return)
-arteriolar vasoconstriction (raising peripheral resistance to blood flow raising arterial blood pressure.
Release of epinephrine, angiotensin II, and ADh (vasoconstrictors)
Chronic compensatory responses to heart failure.
Slower in onset typically longer in duration
- fluid retention, raising blood vol
-chamber dilation
Myocardial hypertrophy in response to dilation, increased workload or both
Increase erythropoiesis to compensate for tissue hypoxia.
What mechanisms underlie fluid retention
Cardiac output declines -> arterial BP falls -> peripheral vasoconstriction -> abrupt decline in glomerular filtration pressure and renal blood flow -> decreases globular filtration -> decrease urine output ->provoke the release in renin from renal afferent arterioles -> activates angiotensin II (vasoconstrictor) -> raises peripheral resistance and increases venous tone -> improves blood return to heart
Angiotension II also promotes uptake of sodium and water into blood from distal convoluted tubule with action of aldosterone and direct action on tubular cells.
ADH is also released
Chamber dilation mechanisms.
With atrial pressure rising with increased venous return to the heart more blood is returned to ventricles which undergo passive dilation.
If heart is damaged by ischemia myocardial stretching promotes hypertrophy of cells which through protein synthesis add new sarcomeres and chambers enlarge significantly
Myocardial hypertrophy
Provoked by volume and pressure overload.
Pressure overload - muscle mass increases to provide force to overcome addition resistance to flow-> wall thickens -> wall becomes stiff, diastolic fn may be impaired. Pressure overload also compromises coronary blood flow.
Volume overload- increase in cardiac workload - heart mass is increased, wall width remains constant.
Increased erythropoiesis
When heart fails and tissue are deprived of blood and oxygen for a period of time erythropoietin is released causing an increase in RBC synthesis. This raises blood viscosity.
Cardiac decompensation can occur with a viscous cycle of fluid retention and dilation.
