test 2 part 2 Flashcards
(25 cards)
Cardiac Failure caused by
any condition that decreases ability of heart to pump enough blood to satisfy body’s needs
Decreased contractility due to decreased coronary blood flow
Damaged heart valves
Pericardial disease
Vitamin B deficiency
Primary heart muscle disease
How a person responds to an acute myocardial infarction (or other decrease in cardiac function) depends on (2)
How bad the cardiac insult is (i.e. how much does the person’s cardiac function curve shift down from normal) and how much cardiac reserve is left.
Whether enough cardiac function is left so kidneys are able to maintain a normal balance between intake and output (i.e. maintain a relatively normal circulating blood volume).
Cardiac reserve
Normal
5-13 L/min is 260% increase
Cardiac reserve
hypereffective
5 L/min to 25 L/min is 500% increase
Cardiac reserve
Hypereffective PLUS Hypertrophy
5 L/min to 30 L/min is 600% increase
what causes a decrease in the reserve of the heart
Any condition that results in a hypoeffective heart
symptoms of a patient with hypoeffective heart
Immediate shortness of breath – can be
extreme (not able to supply tissues with needed blood supply)
Extreme muscle fatigue (muscle ischemia)
Extreme increase in heart rate (created by increase in sympathetic tone)
Cardiac reserve can be tested by
-stress test, either physical
or chemical
Severe coronary thrombosis and severe valvular disease
-have no cardiac reserve and the CO isn’t high enough to support them at normal operation
Normal renal function depends on
-the ability of the
body to maintain a normal
MAP and CO.
If heart/body are not able to
maintain a normal MAP and
CO the kidneys will
-continually retain salt and
fluid. Renin-angiotensin
system play major role in this mechanism.
Initial response to acute moderate failure (myocardial infarction)
- cardiac function curve moves down
- no change in venous return
- CO drops
- RAP increases
ANS response to acute moderate failure
Within seconds, the circulatory reflexes begin to
kick in (Baro, Chemo, and CNS response)
Both the cardiac and venous function curves are
affected
-increased heart rate and contractility
-Increased venous constriction increases mean systemic filling pressure
-CO increases
-RAP increases
-patient is okay
Chronic stage of acute moderate failure
- CO still too low so kidneys begin to retain salt and water
- heart begins to recover
- CO increase
- RAP increases
- Since CO normal, renal function returns to normal so no further increase in CBV
effect of the cardiac and venous function curves by chronic stage acute moderate failure
Shift cardiac function curve up as damaged tissue heals increasing overall performance
Shift venous function curve to right as mean systemic filling pressure increases
Shift slope of venous function curve up as veins stretched by increased volume
What if the failure is severe?
If the failure is severe enough, person’s heart/system will not be able to compensate
If kidneys continue to hold onto salt and water, the person’s heart and cardiovascular system will quickly decompensate.
Decompensated cardiac failure (renal output is not normal and there is NO further increase in cardiac function)
Kidneys continue to hold onto salt and water
CBV continues to increase
Mean systemic filling pressure continues to increase
Venous function curve continues to move to the right
RAP continues to increase pushing cardiac performance farther to right on curve
End result is cardiac deterioration and development of cardiogenic shock
Pharmacological treatment of sever failure
Increase cardiac function -inotropic agents -increase BP to increase coronary Q -Vasodilator/inotropic combination to increase cardiac performance and reduce SVR Increase urine output Decrease salt and water intake
Treat original cause of cardiac failure
Re-establish blood flow to ischemic heart -Drugs that breakdown clots -Balloon angioplasty -Stents -Coronary artery bypass grafts Repair / replace damaged valve Replace the heart
Left side failure with normal right side function will increase overall volume in the pulmonary circulation
Produces increase in mean pulmonary filling pressure
Produces increase in mean pulmonary capillary pressure
Once pulmonary edema begins to form, the volume of fluid can increase so rapidly that the patient can “drown” in 20 to 30 minutes
when does peripheral edema begin to form
Peripheral edema begins to form during the compensatory stage when reduced renal function results in an increase in CBV and an increase in the mean systemic filling pressure
causes of increase in CBV
Decreased glomerular filtration rate Activation of renin-angiotensin system Increased aldosterone secretion Increase sympathetic tone -Constriction renal afferent arterioles -Stimulates increased renal tubular reabsorption of salt and water -Stimulation of renin release -Stimulation of antidiuretic hormone release
Pulmonary edema can be lethal
As fluid leaks into interstitial spaces and alveoli, ability to transfer oxygen is compromised
Decreased oxygen in the blood means less oxygen available to the heart which exacerbates the decrease in cardiac function
Decreased oxygen in the blood leads to peripheral vasodilation and an increase in venous return
how to treat pulmonary edema
Fix the left hearts function