Overlap/Physiology Flashcards
Is Spironolactone and Lasix (Furosemide) contraindicated?
NO!!!
Spironolactone is an Aldosterone antagonist
ALD makes Na go into the blood and water follows -> at the collecting tube at the expense of K
Lasix: loop diuretic -> removes water, urine diluted and more, decrease BP ???
Why does patient #1 have low BP and fast HR?
faster HR to compensate for hypotension???
Why are diuretics so toxic to the kidneys?
Why is it so important to treat acute kidney failure with IV fluids?
Why is fluid so important for the kidney to work?
Possible consequences of ARBs (angiotensin receptor blockers) and ACE inhibitors?
They work on the renal tubules
ARB block:
Angiotensin II: Na+ reabsorption into the blood (water follows, raises BP), loss of K+
blocking Angiotension: reducing BP, keeping K+ in the blood (HYPERKALEMIA bc Aldosterone (blocked) is responsible for Na-K exchange)
ACE inhibitor: blocks conversion from Angiotensin I to Angiotensin II
–> reduce BP, no Aldosterone, less Na+. less K+ loss (secretion, Na+/K+ exchange) -> HYPERKALEMIA
Why may patients with chronic kidney disease suffer from hyperkalemia?
NORMAL: kidney counteracts high BP with Na-K exchange -> loss of K+
in CKD:
-K+ secretion (Na-K exchange) doesn’t work as well
-ACE or ARBs cause hyperkalemia (less Na+ to exchange, K+)
Drugs causing Hyperkalemia
ACEi
ARBS
Bactrim
-patients with CKD bc the kidney doesn’t exchange Na and K efficiently to low BP -> K builds up in the blood
What are the consequences of a cardiac injury?
Heart Failure
the ability to pump blood is decreased
-systolic dysfunction -> decreased contractility
-diastolic dysfunction -> decreased filling/compliance
What are the consequences of heart failure?
-End Organ Hypoperfusion
-Pulmonary Edema
-Decreased cardiac output
Symptoms of Endo Organ Hypoperfusion
-less blood is pumped to the organs
-Fatigue
-cyanosis: bluish coloring of the skin (shortage of oxygen)
-cool extremities
-confusion
-renal involvement: kidney injury bc not perfused (tissues suffer from lack of oxygen)
Symptoms of Pulmonary Edema
-Dyspnea (shortness of breath):
decreased cardiac output -> low BP -> kidney wants to raise the BP by increasing fluids in the blood -> more fluid present in the lungs - making it harder to breathe
-orthopnea: shortness of breathe when lying flat
What are the compensation mechanisms of the body for heart failure?
-Left Ventricular Dilation
-activation of the sympathetic nerve system
-RAAS activation
Left Ventricular Dilation
Left Ventricular: main pumping chamber of the heart
the body thinks: a bigger chamber increases the contraction (push) -> DILATION of the LV
How does activation of the sympathetic nerve system help in heart failure?
weak left ventricular contraction -> low cardiac output
it is easier to pump blood through a narrow tube -> so activation of SNS??? -> VASOCONSTRICTION and increase in HR???
How does activation of the RAAS system help in heart failure?
the kidney wants to raise the BP
-sodium retention - moves into the blood
-water retention -> moves into the blood
-Vasoconstriction: through angiotensin II and ADH,
does aldosterone also cause vasoconstriction???
-increase in Preload (increased filling volume of blood in the LV) - HOW does the kidney do that?? -> by increasing blood volume -> more volume means, greater filling of the right ventricle
-increased stroke volume (volume of blood pumped out of the LV) - HOW does the kidney do that??
RAAS causes increased blood volume -> does that cause increased Preload and stroke volume???
Exacerbation of symptoms - Left ventricular Dilatation
-decreased contractility
-mitral regurgitation (LV valve doesn’t close -> backflow of blood)
-atrial fibrillation
-Left atrial enlargement
