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CV Exam III > Congestive Geart Failure > Flashcards

Congestive Geart Failure Flashcards

1
Q

CHF syndrome not disease

A

Syndrome is a constellation of signs and symptoms occurring together and characterizing a particular abnormality or condition

The same syndrome may occur with different diseases, which may have distinctly different etiologies and pathogenesis

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2
Q

CHF definition

A

Clinical Syndrome in which an of is responsible for the of the heart to with blood at a rate sufficient to of the metabolizing tissues.

Pump failure

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3
Q

heart failure epidemiology

A

Prevalence is 5,000,000 patients

Incidence is 500,000 patients per year

1 million of hospital admissions a year

50,000 death a year

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4
Q

Pathophysiology of systolic heart failure

A

Myocardial function

How strong the muscle is

Preload (EDV)

The more heart fibers are stretched the more difficult it is for them to contract increasing work/pressures and causing hypertrophy (Starling law)

After-load

Resistance against heart contraction/ejection of blood

Heart rate

Too slow—decreases cardiac output ( decCO = SV x decHR)

Too fast —not enough time to fill ( decCO = decSV x incHR)

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5
Q

pathophysiology of diastolic heart failure

A

Impaired relaxation –functional problem

Ischemia

Impaired compliance (“stiff” ventricle) –anatomical problem related to interstitial fibrosis

Hypertrophy

Hypertension

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6
Q

pathophysiology of high output failure

A

Normal heart function with

increased metabolic demand

Increased peripheral blood flow from decreased PVR

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7
Q

pathophysiology of heart failure

steps

A

heart damage, ventricular overload, decrease vent contraction

tachycardia, ventricular dilation, myocardial hypertrophy

decrease co

decreased renal perfusion

increased na retention

increased osmotic pressure

increased adh

increased water reabsorption

fluid overload edema

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8
Q

heart failure classification

A

Systolic vs. Diastolic Heart Failure

Low Output vs. High Output Heart Failure

Left vs. Right vs. Biventricular failure

Acute vs. Chronic Heart Failure

Forward vs. Backward Heart Failure

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9
Q

systolic heart failure

A

Systolic Heart failure results from inadequate cardiac output (C.O.)/Ejection Fracture (E.F.)
C.O. = S.V. x H.R.
S.V. = E.D.V. –E.S.V.
E.F. = S.V./E.D.V.

we measure the ejection fracion to determin 55 is normal

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10
Q

diastolic heart failure

A

results from inability of the ventricles to relax and fill normally with blood during diastole.

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11
Q

forward vs backward heart failure

A

Relates to clinical manifestations of the heart failure as a result of pump failure

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12
Q

forward heart failure

A

is decrease in perfusion of the organs/tissues down-stream from the heart

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13
Q

backward heart failure

A

is “backing up” of the blood into the organs upstream, increasing hydrostatic pressure, which leads to congestion/edema

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14
Q

left sided heart failure

A 
Left ventricle primarily affected.
Caused by conditions primarily affecting left ventricle
     CAD/MI
     Aortic/Mitral valves problems
     HTN
    Cardiomyopathies

forrward failure symptoms are primarily in systemic circulation (downstream)

Backward failure symptoms/congestion in the lungs (upstream)

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15
Q

right sided heart failure

A 
Right ventricle primarily affected.
Caused by conditions primarily affecting right ventricle
     Pulmonary diseases/cor pulmonale
     Tricuspid/pulmonary valves
     Pulmonary Hypertension
     Pulmonary emboli

Backward failure symptoms/congestion in the systemic venous circulation (upstream)

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16
Q

biventricular heart failure

A

end result of left and right failure

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17
Q

acute heart failure

A

due to a sudden and severe event
Massive MI
Chorda tendinae rupture
 Large PE

Predominantly forward failure

Flash Pulmonary Edema

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18
Q

chronic heart failure

A

Progresses slowly

Has exacerbation

Predominantly backward failure

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19
Q

Causes of high output heart failure

A

Metabolic disorders
thyrotoxicosis

excessive blood flow
anemia
av fistula
beriberi

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20
Q

causes of right heart failure

A

cor pulmonale

pulm art htn

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21
Q

causes of left heart failure

systolic

A

decreased contractility
dilated cmp

increased preload
valvular insufficiency

increased after load
sever acute htn
valvular stenosis

change in heart rate
arrhythmias

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22
Q

causes of left heart failure

diastolic

A

chornic htn

hypertrophi cmp

restrictive cmp

ischemic fibrosis

pericardial diseases

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23
Q

restrictive cardiomyopathy causes

A

infiltrative disorders

storage/metabolic disorders

fibrotic disorders

endomyocardial disorders

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24
Q

hypertrophic cardiomyopathy causes

A

with obstruction

genetic

hypertensive cardiomyopathy

without obstruction

due to aortic stenosis

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25
dilated cardiomyopathy causes endstage cardiovascular disease
htn valvular heart disease cad/mi
26
dilated cardiomyopathy causes systemic disease
sle/ra scleroderma polyarteritis nodosa dermato-myositis
27
dilated cardiomyopathy causes toxins-mediated
alcohol cocaine radiation
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dilated cardiomyopathy causes other causes
myocarditis tokosubo cardiomyopathy perpartum cardiomyopathy
29
dilated cardiomyopathy CAD/MI
Due to death or functional ischemic dysfunction of myocardial tissue due to complete or partial blockage of coronary arteries  Degree of dysfunction depends on the percent of myocardium affected Ischemic cardiomyopathy
30
Dilated Cardiomyopathy HTN
HTN Increase cardiac workload Left Ventricular Hypertrophy Diastolic dysfunction Ventricular Dilatation Systolic Dysfunction
31
dialted cardiomyopathy valvular heart disease
Aortic regurgitation Increase in EDV/preload Increase in cardiac workload Left Ventricular Hypertrophy Left ventricular dilatation Systolic dysfunction (very quickly gets to here)
32
infective myocarditis
One of the main causes of dilated cardiomyopathy ``` Multiple etiological agents Viral (most common) Bacterial Fungal Helminthic ``` Febrile illness or URI frequently precedes cardiac symptoms by few weeks Symptoms can present acutely (fulminant) or gradually more common in young people
33
non infective myocarditis toxic myocarditis
Chemotherapy Doxorubicin (Adriamycin) Heavy metals (copper, iron, lead) Lithium Malaria drugs Radiation causing inflammation and fibrosis
34
non infective myocarditis Autoimmune/ CTD associated Myocarditis
Giant Cell Myocarditis PM/DM SLE/RA
35
cocaine and myocardium
May cause vasospasm leading to MI May cause arrhythmia May cause drug-induced myocarditis/cardiomyopathy due to released catecholamines
36
alcoholic cardiomyopathy
From prolonged chronic alcohol use (at least 10 years of chronic exposure) Due to direct toxic effect of alcohol on myocardium Different from beriberi disease, although thiamine deficiency is frequent in alcoholics
37
peripartum cardiomyopathy
Between last month of pregnancy and first 5 months after delivery Likely due to immune-mediated process (from baby antigen) No preexisting cardiac disease (stay edemic after birth) More than ½ of patients improve within 6 months
38
takostubo cardiomyopathy fun facts
A.K.A. Stress cardiomyopathy A.K.A. Apical Ballooning Syndrome A.K.A. Broken Heart Syndrome Takotsubo” is Japanese name for an octopus trap
39
takostubo cardiomyopathy
Triggered by an acute medical illness or by intense emotional or physical stress ``` Postulated mechanisms include catecholamine excess  coronary artery spasm  microvascular dysfunction  OR dynamic mid-cavity or left ventricular outflow tract obstruction which may contribute to apical balooning. ``` Symptoms are similar to an acute MI CP, SOB, Syncope
40
hypertrophic cardiomyopathy Genetic (hocm)
Group of disorders Myocardial hypertrophy unrelated to any pressure or volume overload Due to different genes mutations Myosin heavy chains  Proteins regulating Calcium handling Most are autosomal dominant Inter-ventricular septum often disproportionally involved Sub-aortic stenosis is often present Mostly causes diastolic, not a systolic dysfunction (vlave normal but thick septum causes narrowing)
41
HOCM clinical manifestation
Affects younger people Symptoms/signs SOB Chest Pain Syncope (often after exercise) (lack of co) Arrhythmias Atrial Fibrillation  Ventricular arrhythmias  Sudden death Systolic murmur along the left sternal border  increases with Valsalva maneuver/upright position decreases with squatting
42
valsalva manuever
decreaes venous return to heart decreases volume of blood in heart easier to obstruct with less blood in the heart so murmur increases
43
non genetic cardiomyopathy
Hypertensive cardiomyopathy Similar to HOCM except for more generalized thickening with no disproportional involvement of the septum Aortic stenosis-related hypertrophy happens bc increased workload
44
non genetic cardiomyopathy symptoms
Related to diastolic dysfunction SOB Edema Related to Obstruction Syncope Chest Pain
45
Restrictive cardiomyopathy overview
Characterized by impaired filling causing predominantly diastolic dysfunction Primary genetic forms are uncommon Secondary forms are due to other conditions
46
restrictive cardiomyopathy causes
Infiltrative disease Amyloidosis Sarcoidosis Systemic storage diseases Hemochromatosis Glycogen Storage Diseases Metabolic disorders Fibrotic Radiation Scleroderma Endomyocardiac Loffler’s endocarditis Endomyocardial Fibrosis
47
pulmonary htn
Pulmonary circulation is a low pressure circulation 20/10 (pulmonary) vs. 120/80 (systemic) Blood flow is the same as in systemic circulation Pulmonary vascular resistance is much less than systemic vascular resistance Pulmonary HTN is increased pressures in the pulmonary circulation
48
primary pulmonary htn is
idiopathic
49
secondary pulmonary htn is
other reasons
50
pulmonary htn means
right side heart
51
pulmonary arterial htn causes
idiopathic/familial portal htn drugs/toxins mediate left to right shunt ctd hiv infection
52
pulmonary htn causes du to left heart disease
lvh/lah disease valvular disease
53
pulmonary htn cor pulmonale causes
copd sleep disorders ild alveolar hypoventilation disorders
54
pulmonary htn other cause
due to chronic thrombotic/embolic disease
55
idiopathic pulmonary htn (primary)
Uncommon (2 cases per million) Females>males 30-50 is predominant age of onset 12-20% is autosomal dominant genetic disorders with incomplete penentrance Mean survival is 2-3 years from diagnosis
56
pulmonary htn left to right shunt
Communication between left and right heart High pressure systemic circulation gets dumped into low pressure pulmonary circulation ``` Due to various heart defects Ventricular septal defect Patent ductus arteriosus  Atrial septal defect Atrioventricular septal defect ```
57
drug associated pulmonary htn
Fenfluramine (weight loss pill) Direct effect on pulmonary vasculature Secondary effect via right sided valvular heart disease Amphetamines Cocaine
58
pulmonary htn/right heart failure due to left heart problems
left ventricular failure increase lv volumes/pressures increase la volumes/pressure increase artery pressure r vent hypertrophy r vent failure
59
cor pulmonale
Most common cause of pulmonary HTN these are backwards: ``` RV Failure RV Hypertrophy Increase RV after-load Pulmonary Hypertension Pulmonary Disease ```
60
pulmonary embolism
Usually originates from lower extremities May also come from upper extremities, abdominal veins, heart Results in increase in pulmonary artery pressure therefore increasing after-load for right ventricle May lead to right ventricular failure
61
high output failure
Normal heart Increase metabolic demand doesn’t match with cardiac output Thyrotoxicosis Excessive blood flow overwhelms normal abilities of the pump Anemia AV fistula Conditions decreasing peripheral vascular resistance (Beriberi, sepsis etc)
62
beriberi disease
thiamine deficiency dry wet is chf
63
CHF Clinical manifestation left sided heart failure
parosyxmal nocturnal dyspnea elevated pulmonary capillary wedge pressure restlessness confusion orthopnea tachycardia exertional dyspnea fatigue cyanosis ``` pulmonary congestion cough crackles wheezed bloodtinged sputum tachypnea ```
64
chf clinical manifestation right sided heart failure | cor pulmonale
fatigue inc peripheral venous pressure ascites enlarged liver and spleen may be secondary to chronic pulmonary problems distended jugular veins anorexia and complaints of gi distress weight gain dependant edema
65
symptoms of chf backward failure
``` Left heart failure Pulmonary edema  SOB, cough (frosty)  PND  Orthopnea  Pleural effusions ```
66
symptoms of chf right heart failure
Lower extremity swelling/edema Anasarca/ascitis/pleural and pericardial effusion Could affect lungs as well End organ damage Congestive hepatopathy/nutmeg liver Splenomegaly with hypersplenism Intestinal congestion leading to GI symptoms
67
symptoms of chf forward failure
Mostly in left heart failure Hypotension Weakness Exercise intolerance End organ damage Cardiac ischemia Watershed infarcts ``` Renal failure  Bowel ischemia  Shock liver ```
68
new York heart association functional classification
Class I: Symptoms with more than ordinary activity Class II: Symptoms with ordinary activity Class III: Symptoms with minimal activity (brushing teeth) Class IIIa: No dyspnea at rest  Class IIIb: Recent dyspnea at rest Class IV: Symptoms at rest
69
stages of heart failure stage a
At high Risk for Heart Failure, but without structural heart disease
70
stages of heart failure stage b
Structural Heart Disease, but without symptoms or signs of heart failure
71
stages of heart failure stage c
Structural Heart Disease, with prior or current symptoms of heart failure
72
stages of heart failure stage d
Refractory Heart Failure Requiring specialized intervention
73
chf physical findings vs
BP may be low in advanced CHF Tachycardia is often present Tachypnea and hypoxia in severe cases
74
chf physical findings neck
Jugular Vein Distention Hepato-jugular (Abdominal-jugular) reflux Thyroid enlargement in toxic goiter may be present
75
chf physical findings lungs
Crackles/rales. Usually bilateral Bi-basilar The higher you can hear them, the worse CHF is Sometimes decrease breath sounds on bases (bc fluid is there) Dullness on percussion Tactile Fremitus Decreased in case of bilateral pleural effusion  Increased in case of alveolar/interstitial edema
76
chf physical finding heart palpation
PMI is displaced if LV is enlarged Parasternal lift (heave) if RV is enlarged Arrhythmia is common
77
chf physical findings heart auscultation
S1may be diminished if LV function is very poor P2 (Pulmonic component of S2 ) may be accentuated when pulmonary hypertension is present. An apical third heart sound (S3) with low EF S4is usually present with diastolic dysfunction Murmurs may indicate the presence of significant valvular disease as the cause of heart failure or the result of it.
78
chf physical findings abdomen
shifting dullness is the good test for ascites
79
CHF PHYSICAL FINDINGS LE
EDEMA
80
chf ekg finding
lvh rvh biventricular hypertrophy corpulmonale afib ventricular ectopy
81
v1 up
rvh post mi rbbb
82
ekg cor pulmonale
up in v1 very tall p wave in lead II
83
ventricular ectopy ekg
triplet pvcs occur in groups of three can get doublets etc
84
chf diagnostic tests bnp
Brain Natriuretic peptide Hormone produced by heart cells (ventricles) Alone with ANP (atrial natriuretic peptide, which is produced by atrial cells) released in response to increased ventricular filling pressures Both BNP and ANP have diuretic, natriuretic and hypotensive effect (compensatory effect in response to increase in ventricular filling pressures) BNP is used as a marker of heart failure
85
bnp
High false positive rates ``` Increased in other conditions Old age Renal failure Cor pulmonale Pulmonary hypertension Pulmonary embolism ``` Doesn’t rule out other causes of dyspnea Chronic elevation in cardiomyopathy doesn’t help with diagnosing exacerbations very sensitive but not specific
86
heart failure chest cray
cardiomegaly fuzzy hilum basal congestion pleural effusion kerley b lines
87
echocardiogram main test for chf mogaskin nucleotides you putin
``` Ultrasound examination of the heart  Looks at Size of the heart chambers Thickness of the walls ``` Contractility Ejection fraction Wall motion abnormality Septal defects (bubble study) Valvular structures and their integrity Intracardiac structures (clots, tumors) Diastolic dysfunction Pulmonary pressures
88
chf meds
ARBs Digoxin b -Blockers Aldosterone antagonists Nitrates hydralazine
89
ARBs
Decrease after-load Improve symptoms and mortality
90
Digoxin
The oldest drug used for CHF Increases contractility Improves symptoms, decrease hospitalizations No effect on mortality May cause arrhythmia Narrow therapeutic index heart blocks and vision changes (yellow)
91
b -Blockers
Used only with low EF Improves symptoms Prolongs life Started only in stable patients Counter-intuitive treatment Usually decrease contractility and C.O. Only 3 beta-blockers have a proven effect on mortality Metoprolol Succinate Carvedilol Bisoprolol
92
WHY B BLOCKES WORK IN HEART FAILURE
Upregulate beta receptors improving inotropic and chronotropic responsiveness of the myocardium >improvement in contractile function. Reduce the level of vasoconstrictors> decrease after-load. Have a beneficial effect on LV remodeling >improvement in LV geometry > increase contractility. Reduce myocardial consumption of oxygen. Decrease the frequency of ventricular premature beats and the incidence of sudden cardiac death (SCD), especially after a myocardial infarction
93
Aldosterone antagonists
Diuretic and a final piece of the renin-angiotensin-aldosterone axis Decreases mortality in severe heart failure
94
Nitrates
Decrease preload and somewhat after-load Improve symptoms of acute CHF In combination with hydralasine improve mortality in African-Americans
95
hydralazine
decrease afterload if you cant tolerate acei bc of renal failure
96
overview of chf meds
All mortality improvements are for CHF patients with decrease systolic function/ejection fracture

CV Exam III (17 decks)

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