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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
Q

dilated cardiomyopathy causes

endstage cardiovascular disease

A

htn

valvular heart disease

cad/mi

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26
Q

dilated cardiomyopathy causes

systemic disease

A

sle/ra

scleroderma

polyarteritis nodosa

dermato-myositis

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27
Q

dilated cardiomyopathy causes

toxins-mediated

A

alcohol

cocaine

radiation

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28
Q

dilated cardiomyopathy causes

other causes

A

myocarditis

tokosubo cardiomyopathy

perpartum cardiomyopathy

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29
Q

dilated cardiomyopathy

CAD/MI

A

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

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30
Q

Dilated Cardiomyopathy

HTN

A

HTN
Increase cardiac workload

Left Ventricular Hypertrophy

Diastolic dysfunction

Ventricular Dilatation

Systolic Dysfunction

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31
Q

dialted cardiomyopathy

valvular heart disease

A

Aortic regurgitation

Increase in EDV/preload

Increase in cardiac workload

Left Ventricular Hypertrophy

Left ventricular dilatation

Systolic dysfunction (very quickly gets to here)

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32
Q

infective myocarditis

A

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

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33
Q

non infective myocarditis

toxic myocarditis

A

Chemotherapy
Doxorubicin (Adriamycin)

Heavy metals (copper, iron, lead)

Lithium

Malaria drugs

Radiation causing inflammation and fibrosis

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34
Q

non infective myocarditis

Autoimmune/ CTD associated Myocarditis

A

Giant Cell Myocarditis
PM/DM
SLE/RA

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35
Q

cocaine and myocardium

A

May cause vasospasm leading to MI

May cause arrhythmia

May cause drug-induced myocarditis/cardiomyopathy due to released catecholamines

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36
Q

alcoholic cardiomyopathy

A

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

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37
Q

peripartum cardiomyopathy

A

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

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38
Q

takostubo cardiomyopathy

fun facts

A

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

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39
Q

takostubo cardiomyopathy

A

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
Q

hypertrophic cardiomyopathy

Genetic (hocm)

A

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
Q

HOCM clinical manifestation

A

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
Q

valsalva manuever

A

decreaes venous return to heart

decreases volume of blood in heart

easier to obstruct with less blood in the heart so murmur increases

43
Q

non genetic cardiomyopathy

A

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
Q

non genetic cardiomyopathy

symptoms

A

Related to diastolic dysfunction
SOB
Edema

Related to Obstruction
Syncope
Chest Pain

45
Q

Restrictive cardiomyopathy

overview

A

Characterized by impaired filling causing predominantly diastolic dysfunction

Primary genetic forms are uncommon

Secondary forms are due to other conditions

46
Q

restrictive cardiomyopathy causes

A

Infiltrative disease
Amyloidosis
Sarcoidosis

Systemic storage diseases
Hemochromatosis
Glycogen Storage Diseases

Metabolic disorders

Fibrotic
Radiation
Scleroderma

Endomyocardiac
Loffler’s endocarditis
Endomyocardial Fibrosis

47
Q

pulmonary htn

A

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
Q

primary pulmonary htn is

A

idiopathic

49
Q

secondary pulmonary htn is

A

other reasons

50
Q

pulmonary htn means

A

right side heart

51
Q

pulmonary arterial htn causes

A

idiopathic/familial

portal htn

drugs/toxins mediate

left to right shunt

ctd

hiv infection

52
Q

pulmonary htn causes du to left heart disease

A

lvh/lah disease

valvular disease

53
Q

pulmonary htn cor pulmonale causes

A

copd

sleep disorders

ild

alveolar hypoventilation disorders

54
Q

pulmonary htn other cause

A

due to chronic thrombotic/embolic disease

55
Q

idiopathic pulmonary htn (primary)

A

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
Q

pulmonary htn left to right shunt

A

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
Q

drug associated pulmonary htn

A

Fenfluramine (weight loss pill)
Direct effect on pulmonary vasculature
Secondary effect via right sided valvular heart disease

Amphetamines

Cocaine

58
Q

pulmonary htn/right heart failure due to left heart problems

A

left ventricular failure

increase lv volumes/pressures

increase la volumes/pressure

increase artery pressure

r vent hypertrophy

r vent failure

59
Q

cor pulmonale

A

Most common cause of pulmonary HTN

these are backwards:

RV Failure
RV Hypertrophy
Increase RV after-load
Pulmonary Hypertension
Pulmonary Disease
60
Q

pulmonary embolism

A

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
Q

high output failure

A

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
Q

beriberi disease

A

thiamine deficiency

dry

wet is chf

63
Q

CHF Clinical manifestation left sided heart failure

A

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
Q

chf clinical manifestation right sided heart failure

cor pulmonale

A

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
Q

symptoms of chf

backward failure

A 
Left heart failure
Pulmonary edema
   SOB, cough (frosty)
   PND
   Orthopnea
   Pleural effusions
66
Q

symptoms of chf

right heart failure

A

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
Q

symptoms of chf

forward failure

A

Mostly in left heart failure

Hypotension

Weakness

Exercise intolerance

End organ damage

Cardiac ischemia

Watershed infarcts

   Renal failure

   Bowel ischemia

   Shock liver
68
Q

new York heart association functional classification

A

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
Q

stages of heart failure

stage a

A

At high Risk for Heart Failure, but without structural heart disease

70
Q

stages of heart failure

stage b

A

Structural Heart Disease, but without symptoms or signs of heart failure

71
Q

stages of heart failure

stage c

A

Structural Heart Disease, with prior or current symptoms of heart failure

72
Q

stages of heart failure

stage d

A

Refractory Heart Failure Requiring specialized intervention

73
Q

chf physical findings

vs

A

BP may be low in advanced CHF

Tachycardia is often present

Tachypnea and hypoxia in severe cases

74
Q

chf physical findings neck

A

Jugular Vein Distention

Hepato-jugular (Abdominal-jugular) reflux

Thyroid enlargement in toxic goiter may be present

75
Q

chf physical findings

lungs

A

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
Q

chf physical finding

heart palpation

A

PMI is displaced if LV is enlarged

Parasternal lift (heave) if RV is enlarged

Arrhythmia is common

77
Q

chf physical findings

heart auscultation

A

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
Q

chf physical findings

abdomen

A

shifting dullness is the good test for ascites

79
Q

CHF PHYSICAL FINDINGS LE

A

EDEMA

80
Q

chf ekg finding

A

lvh

rvh

biventricular hypertrophy

corpulmonale

afib

ventricular ectopy

81
Q

v1 up

A

rvh

post mi

rbbb

82
Q

ekg cor pulmonale

A

up in v1

very tall p wave in lead II

83
Q

ventricular ectopy ekg

A

triplet pvcs occur in groups of three can get doublets etc

84
Q

chf diagnostic tests bnp

A

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
Q

bnp

A

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
Q

heart failure chest cray

A

cardiomegaly

fuzzy hilum

basal congestion

pleural effusion

kerley b lines

87
Q

echocardiogram

main test for chf

mogaskin nucleotides you putin

A 
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
Q

chf meds

A

ARBs

Digoxin

b -Blockers

Aldosterone antagonists

Nitrates

hydralazine

89
Q

ARBs

A

Decrease after-load

Improve symptoms and mortality

90
Q

Digoxin

A

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
Q

b -Blockers

A

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
Q

WHY B BLOCKES WORK IN HEART FAILURE

A

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
Q

Aldosterone antagonists

A

Diuretic and a final piece of the renin-angiotensin-aldosterone axis

Decreases mortality in severe heart failure

94
Q

Nitrates

A

Decrease preload and somewhat after-load

Improve symptoms of acute CHF

In combination with hydralasine improve mortality in African-Americans

95
Q

hydralazine

A

decrease afterload

if you cant tolerate acei bc of renal failure

96
Q

overview of chf meds

A

All mortality improvements are for CHF patients with decrease systolic function/ejection fracture

CV Exam III (17 decks)

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