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41 Cards in this Set
- Front
- Back
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the two major divisions of the cardiovascular system |
pulmonary circulation and systemic circulation |
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regulation of cardiac output |
cardiac output = HR x stroke volume (volume of blood pumped/heartbeat |
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regulation of articular pressure (AP) |
-systolic pressure is ABP during ventricular contraction -diastolic pressure is ABP of ventricular relaxation |
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control of mean arterial BP |
BP= CO x total peripheral resistance (TPR) Baroreceptors - respond to variance in BP located in aortic arch and carotoid |
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Hormonal control of vascular system |
epinephrine and nonepinephrine - Renin- Angiotensin System aldosterone antidiuretic hormone (ADH) atrial natriuretic peptide (ANP) |
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Epinephrine and nonepinephrine |
hormonal control of vascular system catchecholamines released in response to activation of sympathetic NS. constriction or dilation |
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renin-angiotensin system (RAAS) |
hormonal control of vascular system •produced by the Kidney. Renal baroreceptors sense a change in BP and release renin to increase or decrease blood pressure. If BP is high = release of renin is decreased. If BP is low: release of renin is increased |
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aldosterone |
hormonal control of vascular system- sodium reabsortion •:circulates to the kidney and causes cells to increase sodium reabsorption. An increase in plasma volume will increase blood pressure ** where salt goes water will follow |
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antidiuretic hormone (ADH) |
hormonal control of vascular system- •potent vasoconstrictor to increase blood pressure |
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atrial natriuretic peptide (ANP) |
hormonal control of vascular system- hormone released by right atrium when there is an increase in BP - works on kidney to increase in the excretion of salt |
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1. heart rate is controlled by: 2. rate is increased by: 3. rate is decreased by: |
1. ANS 2. sympathetic branch acting on beta1 adrenergic receptors in SA node. 3. parasympathetic acting through muscarinic receptors in SA node |
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constriction of blood vessels are regulated solely by the: |
symapthetic system |
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what is cardiac output? how is it measured |
CO is measured CO= SV x HR average adult is 5mL/ min heart rate= controlled by ANS |
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define preload? |
preload is the end diastolic pressure (the pressure inside the left ventricle before contraction) |
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afterload |
arterial pressure left ventricle must overcome to eject blood |
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stroke volume is determined by |
1 myocardial contractility 2 cardiac preload 3. cardiac afterload |
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starlings law of heart |
CONTROL OF STROKE VOLUME BY VENOUS RETURN FOR PHARMA- SYSTEMIC FILLING PRESSURE (FORCE THAT RETURNS BLOOD TO HEART) BLOOD VOLUME AND VENOUS TONE CAN BE ALTERED BY DRUGS law states that force of ventricular contraction is proportional to miscle finer length (up to a point). As fiber length increases (ventricular diameter) there is a corresponding increase in contractile force. ie- left ventricular contraction (output) is able to match with volume of blood delivered by veins. if venous return increases - CO increases as well. stretch a rubber band too much over time it will stretch out and not go back to original shape |
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ARTERIAL PRESSURE is determined by |
arterial pressure is driving force that moves blood thru arterial side of the sytemic circulation. AP= PR (perphieral resistance) x CO ***peripheral resistance is regulated primarily thru constriction (vasoconstriction on periphery) and dilation of arterioles to major organs***** |
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FACTORS THAT DETERMINE VENOUS RETURN |
1. auxiiary mm pumps 2. resistance to flow btw peripheral vessels and R atrium 3. R atrial pressure - elevation of which will impede venous return |
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under normal conditions AP is regulated by |
1. ANS- (responds rapidly: by baroreceptor reflex / short-term control = constriction of arterioles, veins and accelerated HR), S teady state control: regulation by adjusting CO and perphieral resistance) 2. the renin- angiontensin-aldosterone system (RAAS) (morse slow to respond hours or days to influence AP) 3. kidneys (responsible for long-term control takes days or weeks to adjust). |
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MAP equation |
(diastolic x 2) + systolic /3 = mean aterial pressure |
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lifestyle modifications for hypertension |
*decrease in salt intake - detailed DASH eating plan (dietary restrictions) alcohol restriction *aerobic exercise smoking cessation maintenance of K and Ca |
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what are DIURETICS ? |
diuretics are used to increase output of urine used for 1) tx of hypertension 2) mobilization of edematous fluid assoc with: heart faliure, cirrhosis, or kidney disease and to prevent renal failure |
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Overview of kidney |
ANATOMY 1. main functional unit is the nephron 2. 4 regions: glomorous, proximal convoluted tubule, loop of Henle, distal convoluted tubule Physio- 3 basic functions of diuretics cleansing of ECF, ad maintence of acid-base balance and excretion of metabolic wastes and foreign substances
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how diuretics work |
1. MOA: blockade of sodium and chloride reabsorption- block H20 reabsorption - causes lower BP 2. site of action: proximal tubule produces greatest diuresis 3. adverse effects: hypovolemia, acid/balance imbalance, electrolyte imbalances - sodium and **potassium*** |
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PROTOTYPES: Loop Diuretics: Furosemide (Lasik) Thiazide Diuretics: Hydrochlorothiazide Potassium- Sparing Diuretics: spironolactone, triamterene |
how do they work? mechanism of action |
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diuretics work by: |
MOA: block reabsorption of NA+ and chloride (don't allow to na and cl to leave tubule to make medulla more salty for water to follow, instead- thereby changing osmotic pressure within nephron- this causes water and solutes to be retained for excretion) *the amount of Na and Cl blocked dictates the amount of urine produced - as the amount of solute becomes less as it continues through nephron - diuretics that act early have opportunity to block greatest amount of solute reabsorption Adverse: diuretics interefere normal operation of kidney so can cause hypovolemia (from exccessive fluid loss), acid-base imbalance, and altered electrolytes - these can be minimized by using short-acting, timing of drug admin - so kidneys can rest |
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loop diuretics (high-ceiling) |
prototype: furosemide (lasik) most freq prescribed MOA: ascending loop of Henle, by blocking reabsorption so Na and Cl (prevents passive reabsorption of h2O PHARMoKINetics- oral, IV and IM- oral: diuresis onset 60 mins for 8 hrs, IV lasik: onset w/in 5 mins, lasts for 2 hrs (critical situations) 10-20 mg/min- repeat in 1 or 2 hours if needed therap usage: pulmonary edema assoc. with congestive HF, edematous states, hypertension that cannot be controlled with reg diuretics) adverse: hyponatremia: excessive Na loss, hypochloremia - chloride loss, dehydration- water loss (signs of: dry mouth unusual thirst, and oliguria (little pee output) - hypotension, hyperglycemia, hypokalemia< k value drops below 3.5, ototoxicity (pt can go deaf), hyperuricemia (gout) D/D interactions: digoxin (sever loss of K: monitor closely), ototoxic drugs (gentamicin), lithium, anti-hypertensive drugs, NSAIDS (attenuate diuretic) |
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nursing implications for lasik |
the will void- have access to bathroom get baseline data- BP sititing and supine, wt, pulse, resp, electrolytes monitor BP 90 or below - hold and call provider strict I/O, daily wt measure decerase in edema, auscultate lungs for CHF teaching: eat K rich foods, monitor wt, PO lasts 8 hours: how to take so they are not getting up all night |
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thiazides (benzothiadiazides) |
similiar to loop diuretics: increase renal excretion of sodium, chloride, K and H2O, ALSO- elevate plasma levels of uric acid and glucose, difference: maximum diuresis is much lower than loop (loop can be effective where there is scant urine, thiazides cannot), needs adequate kidney fnction ineffective if GFR is less than 15-20 mL/min |
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HCTZ - hydrochlorothiazide (Microzide) hydrodiuril???/ |
thera use: most widely used drug for use in essential hypertension (bp can be controlled by drug alone), mobilizing edema assc with CHF, heapatic disease, renal disease, diabetes blocks reabsorption of sodium and chloride in early segment of the distal convoluted tubule- begins 2 hrs after oral, peaks in 4-6 hours, persists 12 hrs, drug excreted unchanged in urine adverse: category B, same as loop except for ototoxicity, use in pregnancy and Bmilk D/D: same as loop, digoxin increased levels, augments hypertensive meds, increases levels of lithium |
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potassium sparing diuretic |
prototype: spironolactone (aldactone) 2 responses: produce modest increase urine ouput and produce a decrease in K excretion, rarely used alone- often used to counteract loop or thiazides K loss 2 subcategories: aldosterone antagonist, nonaldosterone antagonists |
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spironolactone (aldactone) |
MOA: blocks action of aldosterone in distal nephron (aldo. acts to promote Na uptake in exchange for K) inhibition has opposite effect blocks synthesis of new proteins (req for transport of k and na) does not stop old ones from doing job. so effects are not seen until life cycle of old completed 1 o 2 days retention of K and increased secretion of NA pharmK: effects take up to 48 hrs to develop MNI: watch Na levels and K levels thera use: hypertension, edema HF reduces mortility and hospital admission, primary hyperaldosteronism, PMS, polycystic ovaries, acne Adverse: hyperkalemia >5 mEq/L, benign and malignant tumors, endocrine effect (ITS A CORTCOSTERIOD)- test D/D thiazides and loops, k supplements, salt substitutes (potassium-chloride), ACEinhibitor, angiotensin receptor blockers and direct renin inhibitors |
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osmotic diuretics (mannitol) |
MOA:promotes diuresis by creating osmotic force that inhibits passive reabsorption in nephron- increased urine output pharmK: must be given parenterally. IV active in 30-60 mins for 6-8 hrs indications: prophylaxsis for renal faliure, reduction if intracranial pressure, IOP adverse: edema (caution w pts with heart disease) pulls fluid from spaces, HA, nausea, fluid electrolyte imbalance |
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4 families of Drugs acting on Renin- Angiotensin- ALdosterone System (RAAS) |
angiotensin-converting enzyme ACE inhibitors, angiotensin-converting enzyme blockers (ARB), direct renin inhibitors (DRI), and aldosterone antagonists |
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RAAS basic physiology |
RAAS plays important role in regulating BP, blood volume, fluid and electrolyte balance. it mediates pathophysio changes assoc with hypertension, hf, and MI. exerts effects through angiotensin II and aldosterone HOW IT WORKS- kidneys sense decrease in BP, kidneys release renin, renin is converted to angiotensin I by enzyme angiotensinogen angio I in converted to angio II by ACE, angio II stimulates release of aldosterone from adrenal cortex, aldosterone causes NA and H2o retention and increases BP (by increasing blood volume) |
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angiotensin I and angiotensin II actions |
polypeptides- angio I is precursor of angio II and has weak biological effect. Angio II performs in all processes regulated by RAAS: vasoconstriction (in arterioles) causes BP to rise, release of aldosterone, alteration of cardiac and vascualar structure |
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actions of aldosterone |
regulation of blood volume and BP pathological cardiovascular effects |
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angio- aldosterone system |
regulation of BP by renin-angio-aldo system, regulates BP in situation of hemorrhage, dehydration, or Na depletion, by: constricting renal blood vessels and acting on kidney to promote retention of na and h2o and excretion of K |
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ACE inhibitors - captopril |
INdications: hypertension, heart faliure, MI, diabetic and nondiabetic nephropathy, used to prevent adverse cardio events: MI, stroke, and death in pts of high cardio risk. adverse: cough (most common reason for discontinuing tx, factors increase advance age, female, asian), angioedema, first dose hypotension- a precipitous drop in BP to minimize first dose should be low, diuretics temp discontinued , (NI) bp monitored) , fetal injury, hyperkalemia, dysegia bad taste in mouth, renal faliure, neutropenia D/D- diuretics, antihypertensive agents, drugs that raise K level, lithium |
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ACE inhibitors |
love them |
