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Cardio II Exam 3 > Congestive Heart Failure > Flashcards

Congestive Heart Failure Flashcards

1
Q

CHF

A

Clinical Syndrome in which an abnormality of cardiac structure or function is responsible for the inability of the heart to eject or fill with blood at a rate sufficient to meet the demands of the metabolizing tissues.

“pump failure”

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2
Q

preload and HF

A

systolic failure

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

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3
Q

afterload and HF

A

Resistance against heart contraction/ejection of blood

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4
Q

heart rate and HF

A

too slow = decreased CO

too fast = not enough time to fill (low CO due to very low SV)

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5
Q

components of diastolic dysfunction?

A
  • impaired relaxation

- impaired compliance (stiff ventricle): due to hypertrophy and HTN

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6
Q

high output failure?

A

normal heart function, but due to increased metabolic demands, or increased peripheral blood flow from decreased PVR

  1. Metabolic disorders: thyrotoxicosis
  2. excessive bloodflow: anemia, AV fistula, BeriBeri
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7
Q

pathophys of heart failure?

A

heart damage/ventricular overload/ decreased ventricular contraction –> tachycardia, ventricular dilation, myocardial hypertrophy –> decreased CO –> decreased renal perfusion –> increased sodium retention –> increased pressure –> increased ADH –> increased water reabsorption –> fluid overload/edema –> heart damage

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8
Q

what do chatecholamines do in HF?

A

increased NE and epi seen in CHF –> this is why Beta blockers have shown to be helpful

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9
Q

systolic vs. diastolic HF?

A

systolic HF: results from inadequate CO (SVxHR) or EF (SV/EDV)

  1. Dilated CM = decreased contractility
  2. valvular insufficiency = increased preload
  3. severe acute HTN, valvular stenosis –> increased after-load
  4. arrhtymias = change in HR

diastolic HF: results from inability of ventricles to relax and fill normally w/ blood during diastole

  1. chronic HTN
  2. HOCM
  3. RCM
  4. ischemic fibrosis
  5. pericardial disease
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10
Q

forward vs. backward HF?

A

**forward failure - decrease in perfusion of the organs/tissues downstream of heart
= left HF results in no perfusion (hypotension, weakness, exercise intolerance, end organ damage: cardiac ischemia, renal failure, bowel ischemia, shock liver)

  • *backward failure = backing up of blood into the organs upstream, increasing hydrostatic pressure –> leads to congestion and edema
  • LH backward failure = pulmonary edema
  • RH backward failure = peripheral edema
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11
Q

left sideHF?

A

caused by: CAD/MI, aortic/mitral valve problems, HTN, CMs

forward failure = problems in systemic circulation
backward failure = congestion of lungs

sx: paroxysmal nocturnal dyspnea, elevated pulmonary capillary wedge pressure, pulmonary congestion (cough, crackles, wheezes, blood-tinged sputum, tachypnea), resltessness, orthopnea, tachycardia, exertional dyspnea, fatigue, cyanosis

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12
Q

right sided HF?

A

caused by: pulmonary diseases/cor pulmonale, tricuspid/pulmonary valves, pulmonary HTN, pulmonary emboli

  • results in congestion in systemic circulation (upstream)
    sx: fatigue, increased peripheral resitsnance, ascites, enlarged liver/spleen, may be secondary to chronic pulmonary problems, distended JVP, anorexia/GI distress, weight gain, dependent edema
  • can result in end organ damage: congestive hepatopathy/nutmeg liver, splenomegaly with hypersplenism, intestinal congestion/GI sx
  • can affect lungs as well as 20% of blood is received from bronchial artery off of the aorta
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13
Q

acute vs. chronic HF?

A

acute:
- due to sudden event: MI, chorda tendinae rupture, large PE
- usually forward failure
- flash pulmonary edema (frothy sputum)

chronic: progressess slowly, usually results in backward failure (congestion)

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14
Q

causes of dilated cardiomyopathy?

A
  1. CAD or MI: Due to death or functional ischemic dysfunction of myocardial tissue due to complete or partial blockage of coronary arteries
    - results in an “ischemic cardiomyopathy”
  2. HTN: causes increased workload –> LVH –> diastolic dysfunction –> ventricular dilation –> systolic dysfunction
  3. Valvular Heart Disease:
    aortic regurg –> increased preload/EDV –> increased workload –> LVH –> left ventricular dilation –> systolic dysfunction
  4. Infective myocarditis:
    - a main cause of DCM
    - usually viral, cardiac sx preceded by URI 2 weeks earlier
    - suspect when see young people with DCM
    - will have viral synd. that goes away then developes SOB
    (older people with DCM, think ischemic HD)
  5. non-infective myocarditis
  6. alcoholic cardiomyopathy
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15
Q

non-infective myocarditis

A

results in DCM

1. Toxic MC: 
Chemotherapy 
Doxorubicin (Adriamycin)
Heavy metals (copper, iron, lead)
Lithium – used for bipolar disorders
Malaria drugs
Radiation causing inflammation and fibrosis
  1. AI/CTD associated MC
    Giant Cell Myocarditis
    Polyomyocyties/DM
    SLE/RA
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16
Q

how does cocaine affect 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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17
Q

alcoholic CM?

A
  • type of DCM
  • occurs in prolonged chronic alcohol use (10+ years)
  • alcohol directly affects myocardium
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18
Q

CAD/MI?

A

cause DCM

  1. CAD or MI: Due to death or functional ischemic dysfunction of myocardial tissue due to complete or partial blockage of coronary arteries
    - results in an “ischemic cardiomyopathy”
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19
Q

HTN?

A

cause DCM

2. HTN: causes increased workload –> LVH –> diastolic dysfunction –> ventricular dilation –> systolic dysfunction

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20
Q

aortic regurg?

A

DCM
3. Valvular Heart Disease:
aortic regurg –> increased preload/EDV –> increased workload –> LVH –> left ventricular dilation –> systolic dysfunction

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21
Q

infective myocarditis?

A

DCM
4. Infective myocarditis:
- a main cause of DCM
- usually viral, cardiac sx preceded by URI 2 weeks earlier
- suspect when see young people with DCM
- will have viral synd. that goes away then developes SOB
(older people with DCM, think ischemic HD)

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22
Q

peripartum CM

A
  • type of DCM
  • occurs b/w last month of pregnancy and first 5 mos after delivery
  • likely due to immune-mediated process
  • over 1/2 improve within 6 mos.
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23
Q

Takotsubo CM

A

type of DCM
“stress CM” or “broken heart snd”

  • triggered by acute medical illness or intense emotional/physical stress
    mechanism: stress –> catecholamine xs (NE ) –> coronary aa. vasospasm –> microvascular dysf or dynamic left ventricular outflow tract obstruction which contribute to apical balooning

sx are similar to acute MI: CP, SOB, syncope

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24
Q

HOCM

A
  • genetic hypertrophic CM
  • group of disorders causing myocardial hypertrophy unrelated to any pressure or volume load
  • due to diff. gene mutations: myosin heavy chains, proteins regulating Ca2+ handling
  • most autosomal dominant
  • inter-ventricular septum often disproportionally enlarged
  • sub-aortic stenosis often present
  • mostly causes diastolic, not systolic dysfunction
  • ex. athletes dropping dead during a game
  • patients don’t die from the hypertrophy but from the arry.
25
Q

clinical sx of HOCM?

A
  • affects younger people
    sx: SOB, c/p, syncope after exercise, arrhythmias (a fib, v arr, sudden death)

systolic murmur along left sternal border that increases with valsalva maneuver and decreases with squatting

  • valsalva decreases volume inside of heart, if have lots of hypertrophy, then the lumen is small and blood volume thats decreased makes murmur louder

NOTE: when have aortic stenosis the murmur is louder if there is more blood in it (squatting)

26
Q

valsalva maneuver?

A

The Valsalva maneuver or Valsalva manoeuvre is performed by moderately forceful attempted exhalation against a closed airway –> reduces venous return –> CO remains low

27
Q

non-genetic Hypertrophic CM?

A

hypertensive cardiomyopathy: similar to HOCM except for a more generalized thickening with no disproportional involvemnt of septum
- aortic stenosis related hypertrophy

sx:
- related to diastolic dysfunction, SOB, edema
- related to obstruction: syncope (decrease in CO ), c/p (decreased flow to cardiac aa.)

28
Q

restrictive CM

A
  • impaired filling causing predominantly diastolic dysfunction
  • genetic forms are uncommon, most forms are secondary conditions:
    ex. amyloidosis, sarcoidosis, hemochromatosis, glycogen storage disease, metabolic disorders, radiation, scleroderma. Loffler’s endocarditis, endomyocardial fibrosis
29
Q

pulmonary HTN

A
  • normal pulmonary circulation is 20/10
  • pulmonary HTN is precursor to RHF
  • cor pulmonale = primary pulmonary HTN
30
Q

pulmonary arterial HTN?

A 
idiopathic/familal
portal HTN
drugs/toxins mediated
HIV infection
CTD 
left to right shunt
31
Q

pulmonary HTN due to left heart disease?

A

valvular heart disease

LVH/LAH disease

32
Q

cor pulmonale

A

pulmonary disease –> pulmonary HTN –> increased RV afterload –> RV hypertrophy –> RV failure

ex. COPD, sleep disorders, ILD, alveolar hypoventilation disorders

33
Q

idiopathic pulmonary HTN?

A
  • uncommon, females>males
    age 30-50 onset
  • 12-20% is autosomal dominant genetic disorder
  • mean survival of 2-3 years
34
Q

Left to right shunt?

A

ASD, VSD, PDA, AVSD

  • results in left high pressure being transmitted to right high pressure
  • Esenmenger syndrome: results when the flow reverses due to severe HTN in lungs
35
Q

what weight loss pill is associated w/ pulmonary HTN?

A

fenfluramine weight loss pill –> secondarily causes right sided valvular heart disease

  • also cocaine and amphetamines
36
Q

pulmonary embolism

A

originates from lower extremities –> causes pulmonary HTN and right sided HF

37
Q

thyrotoxicosis

A

causes increase in HR and increase in SV due to thyroid storm which overwhelms the heart –> high output failure

38
Q

anemia

A

causes high output heart failure b/c tissues aren’t being well perfused so heart works harder

39
Q

AV fistula

A

causes high output HF b/c it decreases the peripheral resistance and causes more blood to stay in periphery, so decreased SV means that heart has to increase HR to compensate

40
Q

Beriberi

A

a cluster of symptoms caused primarily by a nutritional deficit in vitamin B1 (thiamine).

wet beriberi causes peripheral tissues to become edematous –> decreased total SV –> results in heart having to work harder –> HOHF

41
Q

** New YOrk Health ASsosocation (NYHA) Functional Class. of CHF ***

A

Class I: Symptoms with more than ordinary activity (extreme exercise)

Class II: Symptoms with ordinary activity (walking upstairs)

Class III: Symptoms with minimal activity

Class IIIa: No dyspnea at rest (can’t click remote control)

Class IIIb: Recent dyspnea at rest (fluctuates)

Class IV: Symptoms at rest

42
Q

Stages of HF ACC/AHA guidelines

A

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

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

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

Stage D: Refractory Heart Failure Requiring specialized intervention

43
Q

physical findings of CHF

A

VS: BP may be low in advanced CHF, tachycardia, tachynpea and hypoxia

Neck: see JVD, hepato-jugular reflux, thyroid enlargment

Lungs: crackles/rales bilaterally, usually bi-basilar (the higher you hear them the worse the CHF)

  • decreased breath sounds at bases
  • dullness to percussion
  • tactile fremitus (decreased in b/l pleural effusion= space surrounding lungs, increased in alveolar interstitial edema)
44
Q

heart changes in CHF?

A

PMI displaced if LV is enlarged

parasternal heave if RV is enlarged

arr. is common

S1 may be diminshed if LV fn is poor

45
Q

P2 accentuated?

A

pulmonary HTN

46
Q

S3

A

present with low EF - due noncompliant ventricle

47
Q

S4

A

present with diastolic dysfunction due to floppy atria

48
Q

which test is better for ascites?

A

shifting dullness:

tympanic on top, dull on bottom, this should shift because water shifts

49
Q

CHF EKG findings?

A

LVH, RVH, biventricular Hypertrophy, atrial fibrillation, PVC’s

cor pulmonale: see RV strain and RVH (upslope of PR), see RAD

look at slides

50
Q

BNP?

A

hormone produced by heart cells in ventricles

used as a marker for HF, but not specific. only can prove that there is prob. not HF if its low

High false positive rates: Increased in other conditions
Old age
Renal failure
Cor pulmonale
Pulmonary hypertension
Pulmonary embolism
51
Q

Kerley B lines

A

often seen on CXR in CHF

52
Q

Diuretics?

A

Loop diuretics
Help with “congestion” part of CHF
Improvement of symptoms, but not mortality (live better, but not longer)
May worsen renal function and cause electrolytes abnormalities

53
Q

ACEIs?

A

Decrease after-load –> increase ventricular function

Improves symptoms and mortality.

54
Q

which groups improve mortality?

A

ACEIs, beta blockers, ARBs, aldo antagonists

nitrates + hydralazine improve mortality in AA’s

55
Q

ARBs?

A

Decrease after-load

Improve symptoms and mortality

56
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
57
Q

beta 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

Why?
Upregulate beta receptors improving inotropic and chronotropic responsiveness of the myocardium and improvement in contractile function.

Reduce the level of vasoconstrictors causing decreased after-load.

Have a beneficial effect on LV remodeling causing improvement in LV geometry 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

58
Q

aldo antagonists

A

Diuretic and a final piece of the renin-angiotensin-aldosterone axis
Decreases mortality in severe heart failure

59
Q

nitrates

A

Decrease preload and somewhat after-load
Improve symptoms of acute CHF
In combination with hydralasine improve mortality in African-Americans

+ hydralazine (decreases afterload)

Cardio II Exam 3 (15 decks)

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