Week 4 Module 3B
Cardiac Part 2 of 2 Outline
Applied Pathophysiology - Concordia St. Paul
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NUR 376 Applied Pathophysiology
Week 4 Module 3B Cardiac Part 2 of 2 Outline
by Rhaeven Ortiz
This week you will be learning about valve disorders and heart failure (HF). There are hints through this outline for your heart failure
assignment.
• Learning Objectives:
o Identify risk factors and preventative measures for left and right heart failure.
o Differentiate the pathophysiologic mechanisms of left and right heart failure.
o Compare/contrast and provide rationales for the clinical manifestations of left and right sided heart failure.
o Explain pulmonary dysfunction in heart failure.
o Differentiate between two major types of valvular dysfunction.
o Explain the pathophysiology of valvular dysfunction including the consequences.
• Ch. 17
o Review pages 400-408
▪ Left ventricular ejection fraction - percentage of blood propelled out of the left ventricle with each contraction.
▪ Box 17-1 (in pharm you will learn why we give certain meds)
▪ Cardiac Output = HR x SV
HR = number of ventricular contractions per minute; avg is 70 bpm
SV = mLs of blood ejected per ventricular contraction; in health individual it is ~70 mL
Amount of blood that the heart pumps out of the left ventricle each minute
▪ Preload - volume of blood at the end of diastole or the volume of blood that enters the right atrium from the
venous system
▪ Afterload - amount of resistance that the ventricle must overcome in order to pump blood out of the heart;
workload of the left ventricle, or resistance exerted by the pressure within the aorta against the left ventricle.
The greater the systemic arterial vascular resistance, the greater the afterload against the left ventricle.
▪ Cardiac Contractility
• Inotropic vs chronotropic
Inotropic Versus Chronotropic Function of the Heart. The inotropic function of the heart refers to the force of
contraction of the cardiac muscle. The heart’s contractility can be influenced by the amount of calcium
available for interaction between the actin and myosin filaments of the cardiac muscle fibers. Sympathetic
stimulation can increase force of contraction, which is referred to as a positive inotropic effect.
Chronotropic function refers to heart rate (HR). When digitalis is administered, it decreases HR by slowing
conduction of impulses through the atrioventricular (AV) node; therefore, it has a negative chronotropic
effect. Beta-adrenergic blocking agents antagonize the SNS effect on the heart by slowing impulses at the
sinoatrial (SA) node, also a negative chronotropic effect. Conversely, epinephrine, an adrenergic or
sympathetic stimulant, has positive inotropic and positive chronotropic effects on the heart. Under the
influence of epinephrine, the heart has a greater force of contraction and increased heart rate.
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▪ Frank-Starling Law (box 17-3)
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▪ The mechanism behind edema (may need to refer back to ch. 7)
• Starling’s
• Hydrostatic pressure
• Osmotic pressure
Edema refers to the abnormal accumulation of fluid in the interstitial space (the area between cells in tissues), often leading
to swelling. To understand the mechanism behind edema, it’s essential to look at Starling’s forces, which govern the movement of
fluid between the capillaries and the interstitial space. The main factors involved in this fluid movement are hydrostatic pressure and
osmotic (oncotic) pressure.
1. Starling’s Forces:
Starling’s law of capillaries describes the balance between the pressures driving fluid out of capillaries and
those pulling it back in. There are two main pressures involved:
• Hydrostatic pressure: This is the pressure exerted by the fluid within the capillaries. It pushes water
and solutes out of the blood vessels and into the surrounding tissues. It is typically higher at the arterial
end of capillaries and lower at the venous end.
• Osmotic pressure (oncotic pressure): This is the pressure exerted by proteins (mainly albumin) in the
blood, which tends to pull water back into the capillaries from the interstitial space. Osmotic pressure
remains relatively constant throughout the length of the capillary.
2. Hydrostatic Pressure:
This is the force exerted by blood against the walls of the capillaries. It is highest at the arterial end of the
capillary and lower at the venous end. When hydrostatic pressure is high, it pushes fluid out of the
capillaries and into the surrounding tissue.
In conditions where hydrostatic pressure increases (e.g., in congestive heart failure or venous obstruction),
more fluid is forced out into the interstitial space, potentially leading to edema.
3. Osmotic Pressure:
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