Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
77 Cards in this Set
- Front
- Back
|
How do you find cardiac rate?
|
heart rate x stroke volume
|
|
|
1.What is ejection fraction?
2.What is normal? 3.What does EF tell you about the heart? |
1.the volume of blood ejected during systole
2.~66% 3.how well it functions as a pump |
|
|
1.What is stroke volume?
2. function of what? |
1.Equal to ejection fraction (end diastolic volume - end systolic volume)
2.function of preload, afterload, and contractility |
|
|
What are the etiologies of heart failure? (4)
|
1.myocardial infarction
2.hypertension 3.cardiomyopathy 4.increased work load |
|
|
What is cardiac reserve?
|
the ability of the heart to increase cardiac output during increased activity
|
|
|
1.What is the normal volume of the cardiac reserve?
2.Who is more likely to have a decreased cardiac reserve? |
1. 4.5 - 8 L/m
2. older people |
|
|
Explain the pathogenesis of heart failure. (3)
|
1.impaired filling of the ventricle and/or impaired pumping leads to
2. decreased C.O. which 3. activates the compensatory mechanisms |
|
|
1.Which organ especially compensates for heart failure?
2.can people noramlly keep this going over time? |
1.kidney
2.no |
|
|
What are the clinical manifestations of heart failure?
|
1.none
|
|
|
What are the compensatory responses to HF? (5)
|
1.increased SNS activity
2.activation of the RAAS 3.natriuretic peptides 4.ventricular hypertrophy 5.frank-starling mechanism |
|
|
How does the increased SNS activity work as a compensatory response to HF? (2)
|
1.this increases catecholamine activity (Epi. and NE)
2.this causes vasoconstriction borth arterial and venous |
|
|
1.During increased SNS activity, sotres of what are decreased?
2.what is increased? |
1.stores of Epi and NE
2.afterload is increased (huge amount of resistance and increased ventricle workload over time) |
|
|
What are the arterial effects of increased SNS activity?(2)
|
1.incrased BP
2.redistribution of bloodflow |
|
|
What areas have increased perfusion? (arterial effects of increased sns activity)
|
brain and heart
|
|
|
What are the venous effects of increased SNS activity in the compensatory response to HF?(2)
|
1.increased venous return (increased ventricular volume and stretch and therefore increased preload)
2.+ inotropic effect (increased contractility) |
|
|
Natriuretic peptides (compensatory response to HF) increases the circulating levels of what?
|
ANP and BNP
|
|
|
ANP is release from what cells?
in response to what? What does ANP produce? |
1.atrial cells
2.increased stretch and pressure 3.produces rapid and transient diuresis and moderate loss of K+ in urine |
|
|
Where is BNP stores?
What is secreted in response to? What effects does BNP have? |
1.ventricular cells
2.in response to increase pressure and stretch 3.same as ANP |
|
|
How is the RAAS activated? (5)
|
1.a decrease in renal blood flow causes
2. increased renin secretion which activates 3.angiotensin II that causes 4.vasoconstriction 5. and increased afterload |
|
|
What is the second way the RAAS in activated? (9)
|
1.decreased RBF causes
2.increased renin secretion that activates 3.aldosterone which causes 4.the retention of Na and H2O and this 5.increases venous return which in turn causes 6.increased ventricular volume and stretch 7.increases preload (increases C.O.) |
|
|
1.What causes hypertrophy?
2.what are the short term effetcts (1) 3.what are the long term effetcs(4) |
1.increased workload
2.improved contractility and C.O. 3. -ventricular remodeling with decreased chamber size - reduced diastolic filling - increased ventricular wall tension - myocardial ischemia |
|
|
What is the Frank-Starling Mechanism?
|
a stretching the myocardial fibers and increases force of contraction druing systole
|
|
|
Systolic Failure:
1.decreased what? 2.this can be cuased by? |
1.decreased contractility
2.ischemia heart disease, anemia, valvular insufficiency |
|
|
What are the clinical manifestations of systolic failure? (2)
|
1.decreased cardiac output
2.decreased tissue perfusion |
|
|
1.In diastolic failure, the size of what is decreased?
2.What causes this? |
1. decreased size of ventricle
2.ischemic heart disease, hypertropric cardiomyopathy, mitral stenosis |
|
|
Clinical manifestations of diastolic failure r/t?
|
vascular congestion
|
|
|
With combined systolic and diastolic failure, clinical manifestations are r/t?
|
vascular congestion and decreased cardiac output
|
|
|
How does vascular congestion happen?
|
1.increased ventricular pressure causes
2.increased atrial pressure which in turn cuases 3.increased capillar pressure (vascular oncotic pressure)cuases 4.increased interstitial fluid (lymph drainage) |
|
|
How does decreased cardiac output cause decreased perfusion?
|
decreased cardiac output causes decreased arterial pressure which in turn causes decreased tissue perfusion
|
|
|
What is the etiology of left-sided failure? (3)
|
1.Acute MI
2.cardiomyopathy 3.aortic or mitral valve dysfunction |
|
|
How does left-sided failure cause interstitial pulmonary edema?
|
increased left ventricular pressure causes increased LAP
2.this causes pulmonary venous congestion (backflow into lungs) 3.interstitial pulmonary edema |
|
|
What type of lung sounds would you hear with left-sided failure?
|
lots of crackles
|
|
|
How does left-sided failure cause decreased peripheral tissue perfusion? (3)
|
1.decreased cardiac output causes
2.redistribution of blood to the brain and heart which causes 3.decreased peripheral tissue perfusion |
|
|
What are the clinical manifestations of left-sided failure?(Caused by dyspnea progressing to pulmonary edema) (6)
|
:
1.increased work of breathing 2.DOE 3.orthopnea 4.paroxysmal nocturnal dyspnea 5.non-productive cough 6.rales and pink frothy sputum |
|
|
What is the rales and pink frothy sputum caused by?
|
capillary leakage
|
|
|
What are the cardiac clinical manifestations of left-sided failure? (5)
|
1.tachycardia
2.A-Fib 3.thready pulse (1+) 4.pulsus alterans (forceful then weak) 5.S3 heart sound (ventricular gallop) |
|
|
What are the clinical manifestations of left-sided failure related to the skin? (3)
|
1.pallor
2.cool to the touch 3.cyanosis |
|
|
What are the clincial manifestations of left-sided failure related to muscle? (2)
|
1.fatigue
2.weakness |
|
|
What are the neurological clinical manifestations of left-sided failure? (2)
early or late onset? |
1.confusion
2.insomnia -late onset |
|
|
What are the renal clinical manifestations of left-sided failure? (5)
|
1.decreased GFR
2.increased BUN(in response to fluid changes)/creatine(better indicator) 3.dilutional hyponatremia (solution : solvent ration off) 4.decreased urine Na 5.increased urine Spef. gravity |
|
|
What is the etiology of right-sided failure? (4)
|
1.end-stage lung disease (cor-pulmonale)
2.pulmonic or tricuspid value dysfunction (stenosis or regurgitation) 3. RV MI 4. left-sided HF |
|
|
What does right sided HF cause?
How? |
-systemic venous congestion
-increased RVP causes increased RAP which then causes the congestion |
|
|
What are the clinical manifestations and sequela of systenic venous congestion?(5)
|
1.JVD
2.positive hepatojuglar reflux (lying supine 10-20 press on liver and will see fluid "wave" in jugular) 2. Hepatomegaly 3.peripheral edema fluid weight gain 4.nocturia |
|
|
Diagnosis of Right-sided failure by?
what are the s/s? (4) |
-the s/s
1. elevated BNP and ANP 2.elevated endothelin-1(ET-1) 3.electrocardiography 4.ejection fraction |
|
|
Name/describe the 4 classes of heart failure
|
I.normal activities don't trigger symptoms (diet control fluid vol. diuresis)
II.ordinary activites result in:(fatigues, palpitations, dyspnea, angina) III. less than ordinary actiivtys resulting in symptoms IV. symtpoms at rest |
|
|
What are the primary and secondary etiologies of cardiomyopathy?
|
-primary - unknown
-secondary - MI, pregnancy, viral infection, hypertension |
|
|
What is dilated CMP?
|
progressive cardiac hypertrophy and dilation (of 1 or both ventricles); impaired pumping
|
|
|
What are the etiologies of dilated CMP? (5)
What is the #1? |
1.ischemia #1
2.alcohol 3.myocarditis 4.genetic 5.idiopathic |
|
|
What are the s/s of dilated CMP? (5)
|
1.DOE
2.paroxismal nocturia 3.A-Fib 4.crackles 5.mural thrombi(clot in ventricle that can break off caused by pooling) |
|
|
What is hypertrophic CMP?
|
ventricular hypertrophy, impaired diastolic filling
|
|
|
What is the etiology of hypertrophic CMP?
How fast does it become symptommatic? |
unknown
slowly over time |
|
|
What is hypertrophic CMP the most common cuase of?
Origin? |
-sudden death in the young
-may be familial |
|
|
What are the symptoms if they appear? (3)
|
1.A-fib
2.DOE 3.heart murmur(often discovered in sports physical) |
|
|
What is restrictive CMP?
|
excessively rigid ventricular walls
|
|
|
restrictive CMP endemic where?
|
asia and aftrica
|
|
|
What is the etiology of restrictive CMP? (1)
|
amiloydosis - lay down of fatty substances (immune)
|
|
|
What are the s/s of restrictive CMP? (4)
|
1.dyspnea
2.orthopnea 3.fatigue 4.weakness |
|
|
What is peripartum CMP?
|
LV dysfunction in the last month of pregnanacy to 4 months postpartum
(AI response to hormonal changes, maladaptive resonse to hemodynamic changes) |
|
|
What is the etiology of peripartum CMP?
What are the risk factors? (5) |
-unknown
-1.advanced maternal age 2.african-american race 3.multifetal pregnancy 4.preeclampsia 5.gestational hypertension |
|
|
What is the mortality rate of peripartum CMP?
|
18-56%
|
|
|
What causes valvular disorders?
|
regurgitation back into atria aka insufficiency aka incompetence; stenosis
|
|
|
How does regurgitation occur in valvular disorders?
|
it's a failure of valve leaflets(incomplete opening during diastole) and increased cardiac workload over time
|
|
|
What causes the stenosis in valve disorders?
|
constriction of valve opening, cardiac workload because of smaller diameter; impairs ventricular filling
|
|
|
What is the etiology of ventricular disorders? (4)
|
1.inflammatory
2.infective(endocarditis) 3.congenital (probs. w/ valve). 4.papillary muscles dysfunction (usually with AMI) |
|
|
What is the pathogenesis of valvular disorders?
|
1.restriction of flow between the left atrium and ventricle causes
2.increased LAP which causes 3.LA hypertrophy which causes 4.pulmonary congestion, pulmonary hypertension, then over time causes 5.right heart failure |
|
|
More pathogenesis of valvular disorders?
|
1.,2.,3...
causes tachycardia which causes A-Fib |
|
|
What are the clinical manifestations of stenosis? (5)
|
1.diastolic murmur***#1
2.DOE (backward effects of LHF) 3.tachycardia 4.A-Fib 5.irregular pulse |
|
|
retrograde flow from LV to LA causes...
(Stenosis) |
1.increased ventricular workload to maintain CO which then causes
2.LV dilation and increased contractility 3.LV hypertrophy |
|
|
retrograde flow from LV to LA causes(Stenosis)
|
1.increase LAP
2. which causes LA hypertrophy 3.which causes either pulmonary congestion(pulmonary hypertension)(right heart failure) or trachycardia (A-Fib) |
|
|
What are the clinical manifestations of stenosis? (5)
|
1.weakness and fatigue
2.DOE 3.palpitations 4.pan(holo)systolic murmur (through systole)**** 5.A-Fib |
|
|
What is the etioloty of aortic stenosis?
|
congenital valve malformations, rheumatic heart disease, elderly - artherosclerosis causes changes in valve leaftlets
|
|
|
What is the pathogenesis of aortic stenosis?
|
Obstruction of outflow from LV to aorta which
1.increases resistanche to LV ejection(afterload) 2.This causes increased LVP or increase length of systole 3.increase LVP cuases wall stiffness - LV hypertrophy and then causes 4.increased LVEDP |
|
|
What are the clinical manifestations of aortic stenosis? (6)
|
1.ANGINA***
2. syncope(inadequate blood flow to brain) 3.LV failure 4. ejection murmur (hear during systole) 5.marked fatigue (decreased CO) 6.exertional hypotension |
|
|
What happens in aortic regurgitation?
|
aortic leaflets don't close
|
|
|
What is the etiology of aortic regurgitation? (4)
|
1.endocarditis
2.rheumatic heart disease 3.trauma 5.aortic dissection |
|
|
What is the pathogenesis of aortic regurgitation?
|
retrograde flow from aorta (LV during diastole) which causes
1.LV volume laod which cuases 2.Hypertrophy resulting in 3.LV failure or possibly mV regurgitation -OR- decreased cardiac output, compensatory decreased in peripheral resistance |
|
|
What are the clinical manifestations of aortic regurgication? (early and late)
|
1.Diastolic murmur
2.early - palpitations, fatigue, DOE, widening pulse pressure late- angina, heart failure |
