EXAM 2 Flashcards
(334 cards)
Heart failure
(Pump failure)
The heart muscles (myocardium) weakens and enlarges causing decreased ability to pump the blood through the heart and into the systemic circulation.
Congested Heart failure
They have now become fluid volume overload (SOB, gain weight, edema) /
Compensatory mechanisms fail and the peripheral tissues and lungs become congested (fluid overload)
Left-sided heart failure
Left ventricle is not pumping
Pulmonary congested (SOB/shortness of breath), cough, oliguria (400ml output), weight gain
Right sided and left sided typically looks the same
Right-sided heart failure
Right ventricle is not pumping
Peripheral edema, jugular vein distention, and weight gain
They also can have pulmonary edema and crackles, fluid volume over load
Causes of Heart failure
- Chronic HTN (when the heart has to pump harder against the blood vessels that has high pressure in them. When the heart has to work harder, the heart grows
- MI (heart attack): causes damage to heart tissue
- Coronary artery disease (CAD)/atherosclerosis: that means that. The vessels that sits on top oF the heart are not feeding the heart muscles well; so if the heart is not getting enough blood flow into the muscle, then it will start to decline)
Valvular disease: stenosis of the valves; means the valves are tight and the heart has to work harder to push the blood through them; regurgitation means when the valves doesnt close all the way, now the blood flow goes back. So the heart has to pump harder and harder to push that blood forward
-Congenital heart disease
-Aging: as we get older, the heart has to work harder and harder to function
Not everyone gets HF when they get older.
Cardiac Glycosides
We use cardiac glycosides to help improve the contractility of the heart. Make the heart muscle contract more efficiently; they are considered +INTROPES. To increase cardiac output; we perfuse the tissues, & if we perfuse the tissues, our organs work better (in particular our kidneys). They are gonna slow the hR down,
3rd line treatment for pt with HF. /
Inhibit the sodium-potassium pump Increases intracellular sodium leading to increased influx of calcium Causing cardiac muscle fibers to contract more efficiently
Positive Inotrope Negative chronotrope Negative dromotrope Used when other modalities don’t control manifestations
**improve myocardial contractility improves cardiac, peripheral and kidney function due to Increased cardiac output Increased cardiac output decreases preload improving renal perfusion caused decreased edema and promoting fluid excretion
Ianoxin (Digoxin)
A cardiac glycoside
A 2nd line treatment for HF
Used for pt that had Atrial fibrillation/Aflutter rate control (Irregular & rapid Heart rate) or have a low blood pressure
Slows hr down and DOESNT decrease bp
(Ex: if someone has a rapid HR we need something that would lower their hr, but not their bp)
Route: PO/IV
Its a highly protein drug ; means it needs a protein to rest on, if it doesnt have a protein to rest on, they will have active meds floating around; will increase risk of toxicity. ; protein binding power 30%
Small therapeutic window 0.5-2.0ng/ml
When we start to see pts above 2.0, that is when we start to see some toxic side effects such as: bradycardia, anorexia (not eating), N/V, diarrhea, visual changes* (having yellow halos in their visions), confusion, delirium dysrhythmias (ventricular)
Antidote: digibind, ovine: helps reduce levels of digoxin.
Pregnancy category C
You need to Rember that it is excreted by the kidneys. So we may need to lower the dose if the kidney function is not good; can lead to toxicity & pts with thyroid disease alter the metabolism of digoxin so we need to decrease the dose in pt with hypothyroid.
Increases myocardial contraction, increases CO, which increases tissue perfusion and lower HR (decreases AV conduction decreasing HR)
Drug interactions: one of the things we worry about is when pts are on potassium wasting diuretics, they can lose potassium, if they are also on digoxin the digion can get absorbed more readily; which leads to toxicity if they have low potassium levs already. Check potassium levels first before administering.
- cortisones or steroids increases the loss of potassium as well; which increases toxicity
-antacids its gonna decrease the acidity in the stomach, which interferes with the absorption of digoxin. Best to separate the medications by at least an hour.
/
Potassium loss diuretics and increase risk of digoxin toxicity Cortisone solution taken systemically (po,IV) increases hypokalemia increasing risk of toxicity Antacids decrease absorption, stagger doses
Digoxin Nursing considerations
We know that it will decrease HR, so check Hr before
Obtain apical pulse prior to administration
Assess for signs of toxicity (abuses, vomiting, bradycardia ect. )
Monitor digoxin level
Monitor potassium level (why? Low potassium means that increases the absorption of digoxin , which leads to toxicity)
Phosphodiesterase inhibitors
Increase cardiac output
Lower hr & bp; for CHF
Primacor (milrinone)
Inocor
These are + inotropes
Which increase tissue percussions.
**Can use in CHF an improve contractility which increase tissue perfusion, in particular to the kidneys, which will allow th kidneys to get the fluid off.. to help get rid of all of the edema that they are experiencing with CHF.
IV only
For about 24-72 hours (call in a cardiac “tune up”)
Because theses are cardiac select meds, we might see an increase in hr ; watch out for tachycardia. These meds also cause vasodilation, we have a balance act to make sure their bp doesn’t get to low, we are lowering their bp but need to make sure it doesn’t get too low.
/
Primacor (milrinone) Inocor
Positive inotropes that increase stroke volume, cardiac output, vasodilation
IV only 48-72 hours Cardiac dysrhythmia may occur, monitor EKG
Vasodilators
Another agent for heart failure
Decrease venous blood return to the heart, decrease pre load/
**gonna open up the arteries so thats gonna help decrease the workload of the heart,so it doesnt have to work that hard. This will alos help the heart from filing too much (decrease preload)
Arteriolar dilators
Another agent for heart failure
Decrease after load (the heart doesnt have to pump header) increasing cardiac output, increased renal perfusion by dilating arterioles, improve circulation to muscles. ;
ACE inhibitors
Another agent for heart failure
Dilate venues, arterioles, improve renal blood flow, decrease blood fluid volume. Certain ARBS also (Diovan, Atacand)/\
Help improve renal blood flow
Diuretics
Another agent for heart failure
We know we can use to get extra fluid off then have better fluid balance. When there’s better fluid balance, the heart can pump efficiently.
Aldactone (spironolactone)
Another agent for heart failure
Its a potassium sparing diuretic
We use in pts with HF especially low ejection fraction hf.
Blocks the secretion of aldosterone causing decrease fluid retention.
Beta- blockers
Another agent for heart failure
As long as pt doesnt have decompensated HF we can use. Bb will help heart work more efficiently.
Natrecor
Another agent for heart failure
Inhibits ADH (prevents body from holding on to extra fluid) help with vasodilation, diuresis (Acute CHF),
BiDil (hydralazine and isorbide dinitrate) :thats a meds that help them with getting renal blood flow or blood flow to the kidneys to help get the fluid off .
Angina
Chest pain, tightness, radiating to left arm and or neck
Is when someone expernce chest pain (chest pain, burning). It means the heart is not getting sufficiently amount of blood flow, due to plague (ex: blood clot) being in the arteries or coronary spasm (arteries constrict and cause a temporally constriction of blood flow).
If restrict the blood flow in the arteries that are feeding the heart muscles, thats how it’ll get ischemia, which causes chest pain. (Then can lead to a heat attack.)
What are the 3 types of angina?
Classic (stable)
Unstable (preinfarct)
Variant (prinzmetal, vasospasm)
Classic (stable) Angina
Person knows what causes their angina; they can predict it.
Ex: person goes for a walk, gets to top of hill, he develops angina then he walk back home.
/
Occurs with stress or exertion (physical effort)
Unstable (preinfarct) angina
Occurs frequently with progressive severity unrelated to activity.
Progresses
Ex: the man that walks to the top of the hill, if the angina starts to happen before he gets to the top of the hill, that means something changed, its unstable; its gotten worst. He feels dizzy, SOB while walking.
Basically change in the symptoms
Now, if someone suddenly develops angina anaad never experienced it before, it is unstable because they went form nothing to something.
Variant (prinzmental, vasospasm)
Occurs during rest.
Typically the most alarming kind, because it can send someone into cardiac arrest because we have sudden blockage in the heart, usually caused by a vasospasm.
Nonpharmacologic measures to control angina
- avoid heavy meals: helps decrease the pressure on the heart, especially at night.
- avoid smoking & vaping: every puff causes vasoconstriction; then lead to angina
- avoid strenuous exercise: when we know someone who has angina or cardiac disease, we dont want to over do it
- avoid extreme temperatures: avoid being outside in less than 40-degrees for 20mins or so …or in 80 degree or more..puts workload on the heart and causes damage (ex: shoveling snow should be avoided)
- avoid emotional upset
- rest and relaxation techniques.
Antianginal drugs
Increase blood flow by increasing O2 supply (vasodilation) or decreasing O2 demand/ decreasing the heart’s need for oxygen.
Three types of antianginals
Nitrates
Beta-blockers
Calcium Channel Blockers