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Hjertemedisin > Hjertesvikt - Amboss > Flashcards

Hjertesvikt - Amboss Flashcards

1
Q

Hva mener man med hjertesvikt?

A
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2
Q

Hva mener man med kronisk hjertesvikt (“congestive heart failure”)?

A
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3
Q

Hva er venstresidig hjertesvikt?

A
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4
Q

Hva er høyresidig hjertesvikt?

A
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5
Q

Hva er global hjertesvikt?

A
One-sided HF commonly progresses to biventricular HF.
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6
Q

Hva mener man med kronisk kompensert hjertesvikt?

A

Hjertesvikt med stabile symptomer

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7
Q

Hva er akutt dekompensert hjertesvikt?

A
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8
Q

Hva er systolisk/diastolisk dysfunksjon?

Hjertesvikt

A
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9
Q

Hvordan er epidemiologien til hjertesvikt?

Amerikansk data

A
Due to differences in the prevalence of cardiovascular risk factors and social determinants of health. HF is also the most common cause of hospitalization in this age group.
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10
Q

Hvilken kardiovaskulær etiologi kan hjertesvikt (HS) ha?

A
Hemochromatosis can also cause restrictive cardiomyopathy.
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11
Q

Hvilke endokrine/metabolske etiologier kan gi HS?

A
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12
Q

Hvilke pulmonale etiologier kan føre til HS?

A

KOLS

Pulmonal arterie hypertensjon; cor pulmonale

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13
Q

Hvilke substanser (toksiske) etiologier kan føre til HS?

A
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14
Q

Hvilke andre etiologier kan føre til HS?

Ikke kardiovaskulær, endokrin, pulmonal eller toksisk

A
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15
Q

Hva er de tre vanligste årsaken til HS?

A

The three major causes of HF are CAD, hypertension, and diabetes mellitus.

Patients typically have multiple risk factors that contribute to the development of HF.

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16
Q

Hvordan klassifiserer man hjertesvikt ut fra venstreventrikkels ejeksjonsfraksjon?

A

The ejection fraction is preserved because both the LV end-diastolic volume and stroke volume are reduced.

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17
Q

Hvordan klassifiserer “American College of Cardiology/American Heart association” (ACC/AHA) HS?

A

Patients with stage C HF will always remain categorized as such, even if they become asymptomatic (i.e., NYHA class I) with treatment.

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18
Q

Hva er “NYHA” klassifikasjon?

HS

A

The “New York Heart Association” (NYHA) classification system is used to assess limitations in physical activity and symptoms of patients with symptomatic HF (i.e., ACC/AHA stages C and D); it helps determine treatment eligibility and prognosis.

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19
Q

Hva bestemmer hjerteminuttvolum (“cardiac output”)?

A

Cardiac output, which is stroke volume times heart rate, is determined by three factors:

  • Preload
  • Afterload
  • Ventricular contractility
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20
Q

Hva er den underliggende patologiske mekanismen ved HFrEF?

A
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21
Q

Hva er den underliggende patologiske mekanismen ved HFpEF?

A

Although systolic heart failure and diastolic heart failure have similar pathophysiological characteristics, symptoms are less pronounced in the latter.

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22
Q

Hva er den underliggende patologiske mekanismen ved venstresidig HS?

A
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23
Q

Hva er den underliggende patologiske mekanismen ved høyresidig HS?

A
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24
Q

Hva forteller denne?

A

Pressure-volume loops of the left ventricle in systolic and diastolic dysfunction

*The pressure-volume (P-V) loop in systolic dysfunction (yellow): *

Loss of contractility in systolic dysfunction reduces the slope of the line depicting the end-systolic P-V relationship.

Therefore, the end-systolic volume (top left corner of P-V loop) appears increased compared to the normal P-V loop (green).

The end-diastolic volume (bottom right corner of P-V loop) is also increased because of normal venous return to a high end-systolic volume.

This higher end-diastolic volume partially increases the stroke volume via the Frank-Starling mechanism.

*The P-V loop in diastolic dysfunction (blue): *

Increased stiffness of the ventricle in diastolic dysfunction means that the line depicting the diastolic P-V curve is shifted upwards and to the left.

For any given diastolic volume, the ventricular pressure is higher in a dysfunctional heart compared to a healthy heart (green loop), and the end-diastolic volume is reduced compared to a healthy heart (bottom right corner of P-V loop).

Reduced end-diastolic volume with preserved ejection fraction means that the end-systolic volume (top left corner of P-V loop) will be reduced compared to a heart with normal diastolic function.

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25
Q

Hva er konsekvensene av dekompensert HS?

A

The hydrostatic pressure in the capillaries becomes greater than the oncotic capillary pressure, causing fluid to leak into the interstitium and alveoli.

Orthopnea; A sensation of shortness of breath that occurs upon lying down and is relieved by sitting up. Left ventricular failure is a common cause.
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26
Q

Hva viser preparatet?

A

Hepatic congestion (nutmeg liver)

Liver (sagittal section; lateral view)

Yellow streaks of fat and speckles of dark spots can be seen throughout the hepatic tissue.

These findings are consistent with hepatic congestion. The dilated liver sinusoids appear as dark spots. The lack of nutrient supply to the hepatocytes surrounding the central vein leads to additional atrophy and fatty degeneration, causing the liver to resemble a nutmeg seed – hence the name “nutmeg liver.”

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27
Q

Hvilke kompensatoriske mekanismer “settes igang” ved HS?

A

Baroreceptors detect changes in blood pressure and release catecholamines.

And, to a lesser degree, the afferent arterioles.

An increase in preload also leads to an increase in cardiac output via the Frank-Starling mechanism.

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28
Q

Fyll inn

A

Pathophysiology of heart failure

Reduced cardiac output results in the activation of compensatory mechanisms (i.e., ADH and BNP production, activation of the renin-angiotensin system and sympathetic nervous system) in an attempt to restore cardiac output.

Cardiac remodeling and increases in afterload both have a negative effect on cardiac output. Increases in heart rate and preload have a positive effect on cardiac output. The net effect of these compensatory mechanisms may be sufficient to restore cardiac output. If not, the cycle repeats.

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29
Q

Fyll inn

A

Renin-angiotensin-aldosterone system

Flowchart summarizing the biochemical and physiological effects of the renin-angiotensin-aldosterone system

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30
Q

Hvilke symptomer oppstår ved HS?

Generelle

A

In the supine position, cardiac output increases and renal vasoconstriction decreases, leading to an increase in filtered urine and nocturia.

Due to an increase in sympathetic tone.

An S3 gallop indicates rapid ventricular filling, while an S4 gallop indicates ventricular hypertrophy (reduced compliance). Other heart sounds may indicate valvular disease as a potential cause of HF.

https://www.med.umich.edu/lrc/psb_open/html/repo/primer_heartsound/primer_heartsound.html

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31
Q

Hvilke kliniske tegn oppstår ved venstresidig HS?

A

Predominant signs of left-sided heart failure

Initially exertional dyspnea; as HF progresses, also dyspnea at rest

In severe cases or acute decompensated heart failure

Supine position at night increases pulmonary venous congestion

Caused by the build-up of fluid in alveoli

Caused by cardiomegaly

In advanced HF

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32
Q

Hvilke kliniske tegn forekommer ved høyresidig HS?

A

Predominant signs of right-sided heart failure

Primarily of the feet and calves

Caused by stretching of the liver capsule

Also seen in biventricular heart failure

Kussmaul sign; A sign characterized by distention of the jugular veins during inspiration (due to elevation of jugular venous pressure). Can be seen in patients with constrictive pericarditis, restrictive cardiomyopathy, right ventricular infarction, and tricuspid stenosis.
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33
Q

Hva viser bildet?

A

Pitting edema of lower leg

The tissue is markedly edematous above the line to which the patient’s sock had previously been pulled up. After applying pressure to the pretibial area, the residual indentation characteristic of pitting edema becomes visible.

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34
Q

Hva viser bildet?

A

Edema

In this patient with kidney and heart failure, edema of the foot indicates interstitial accumulation of fluids.

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35
Q

Hva er definisjonen av “High-output” hjertesvikt?

A

Heart failure secondary to conditions associated with a high-output state, in which cardiac output is elevated to meet the peripheral tissue oxygen demands

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36
Q

Hvilken etiologi har “High-output” HS (HoHS)?

A

Conditions that result in a high-output state are rarely the sole cause of HF; patients usually have a preexisting cardiac condition that reduces ventricular reserve.
In a high-output state, the heart cannot meet the additional demand, leading to heart failure.

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37
Q

Hva er patofysiologien til HoHS?

A
38
Q

Hvilke symptomer kan oppstå pga. HoHS?

A

High-output HF is commonly associated with signs of low-output HF.

39
Q

Hvordan diagnostiserer man HoHS?

A
40
Q

Hva viser bildet?

A

High output cardiac failure

X-ray chest (AP view) of a patient with an arteriovenous fistula

Generalized enlargement of the cardiac silhouette is accompanied by prominent upper lobe pulmonary vessels (examples indicated by arrowheads) and widespread parenchymal air space opacities (green overlay).

In the setting of a high-flow arteriovenous fistula, an increase in preload from the shunting of blood from the left-sided circulation into the right-sided circulation can result in increased cardiac output. Increased workload may eventually lead to high-output cardiac failure.

41
Q

Hvordan behandler man HoHS?

A
42
Q

Hvilke generelle prinsipper gjelder når man skal diagnostisere HS?

A

Multiple conditions can mimic HF and/or impact therapeutic decisions, e.g., anemia or kidney or liver failure.
No single laboratory finding, imaging study, or clinical feature either excludes or is diagnostic for HF.

43
Q

Hvilke anamnestiske spørsmål bør være med ved mistanke om HS?

A

Obtain a three-generation family history in patients with cardiomyopathy.

44
Q

Hvilke us. bør gjøres ved mistanke om HS?

A
45
Q

Hva kjennetegner BNP/NT-proBNP?

A

BNP and NT-proBNP should not be used interchangeably when establishing trend values for a patient.

These figures have a negative predictive value of 94–98%.

ARNI therapy can increase BNP levels, but decrease NT-proBNP levels.

Normal BNP or NT-proBNP levels do not exclude HF. Always consider the complete clinical picture.

46
Q

Hvilke blodprøver bør man ta ved mistanke om HS?

A

Elevated creatinine may indicate cardiorenal syndrome.

E.g., increased mortality rates, length of hospital stay, and rehospitalization

Changes in cardiac biomarkers such as high-sensitivity cardiac troponin (cTn) can help to establish a prognosis in patients with chronic HF. Using multiple biomarkers (e.g., BNP and cTn) might be more helpful than using a single one.

47
Q

Når er det indikasjon for å gjøre trantorakal ekkokardiogram?

Hjertesvikt

A
48
Q

Hva er funn ved transtorakal ekko ved HS?

49
Q

Når er det indikasjon for rtg. thx ved hjertesvikt?

A

All patients with suspected HF; especially useful in AHF

50
Q

Hva er funn ved rtg.thx ved HS?

A

Chest X-ray has a limited sensitivity and specificity for HF

51
Q

Hva viser bildet?

A

Left ventricular enlargement

X-ray chest (PA view)

The cardiac silhouette is enlarged, with the left heart border displaced laterally (green overlay) from its normal position (green outline) as a result of left ventricular enlargement.

52
Q

Hva viser bildet?

A

Left ventricular enlargement

X-ray chest (lateral view)

The prominent convexity of the posterior border of the cardiac silhouette (green overlay; normal cardiac silhouette indicated by green outline) represents left ventricular (LV) enlargement (indicated by arrow). There is no obliteration of the retrosternal space (red overlay) to indicate right ventricular (RV) enlargement.

53
Q

Hva viser bildet?

A

Cardiogenic pulmonary edema

X-ray chest (AP view; erect) of a patient with cardiogenic pulmonary edema

Enlargement of the cardiac silhouette is accompanied by widening of the vascular pedicle. There is extensive parenchymal interstitial (examples indicated by arrowheads) and air-space edema. Air-space edema is most pronounced in the lower lung zones (green circles).

Vascular pedicle width (VPW; cf. illustration): distance between a vertical line drawn from the point at which the superior vena cava intersects the right main bronchus and a second vertical line drawn through the origin of the left subclavian artery. The VPW (white lines) is normal or narrowed in capillary permeability edema, normal in acute heart failure, and widened in chronic heart failure, fluid overload, and renal failure.

54
Q

Hva viser bildet?

A

Hydrostatic pulmonary edema

X-ray chest (AP view)

The cardiac silhouette is enlarged (hatched green overlay) and the perihilar air space opacities (green overlay) have a bat wing, or butterfly, configuration. Linear interstitial opacities representing Kerley A lines (orange dashed lines) radiate from the hila to the apices and Kerley B lines (white dashed lines) are seen in the lateral mid zones. The costophrenic angles are blunted (arrows) from bilateral pleural effusions.

These features are characteristically seen in cardiogenic pulmonary edema.

55
Q

Hva viser bildet?

A

Constrictive pericarditis

Chest x-ray (lateral view)

A thickened pericardial contour is visible from the apex to the upper cranial half of the heart, indicating fibrosis of the outer layer of the heart (green overlay).

Additional findings include a wedge-shaped, extensive opacity in the basal portion of the left lung, consistent with pleural effusion (green hatched overlay) and increased perihilar lung markings (red overlay), consistent with pulmonary congestion.

56
Q

Når er det indisert å ta EKG ved HS?

A

All patients with suspected HF

57
Q

Hvilke funn gjør man på EKG ved HS?

A

Impaired systolic function leads to congestion in the ventricle and compensatory hypertrophy.

As the ventricle becomes more congested, blood flow backs up, leading to atrial stretch and enlargement and consequent P wave abnormalities.

58
Q
A
59
Q

Hva viser EKG-et?

A

ECG in left ventricular hypertrophy

12-lead ECG (paper speed: 25 mm/s)

  • Heart rate: ∼55/min
  • Regular sinus rhythm
  • Normal cardiac axis: positive (+) QRS complex polarity in leads I, II, and III
  • Broad and bifid P waves (P): referred to as “P mitrale” and suggestive of left atrial enlargement
  • SV2 (S) + RV5 (R) >3.5 mV: meets Sokolow-Lyon criteria for left ventricular hypertrophy
  • Left ventricular strain pattern: ST depression (ST) with T-wave inversion (T) in left-sided leads I and V4–V6

Positive Sokolow-Lyon criteria and left ventricular strain pattern are characteristic of left ventricular hypertrophy.

60
Q

Hvilke andre us. kan være indisert ved mistanke om HS?

A

ECG-gated CT may be used as an alternative in patients with contraindications to MRI.

In decompensated HF, the extraction of oxygen by peripheral tissue is increased, indicating that cardiac output is not high enough to meet the oxygen demand.

Identifying the specific cause of HF is crucial because it allows for tailored treatment in addition to GDMT.

61
Q

Hva viser snittet?

A

Heart failure cells in decompensated heart failure

Photomicrograph of lung tissue (H&E stain; high magnification)

Accumulations of hemosiderin-laden macrophages (siderophages, examples indicated by blue overlay) within alveoli can be seen. Additionally, there are alveoli filled with erythrocytes (examples indicated by red overlay).

Siderophages in pulmonary alveoli (heart failure cells) suggest decompensated heart failure.

62
Q

Hva viser snittet?

A

Pulmonary alveolar edema

Photomicrograph of lung tissue (H&E stain; 400x magnification)

There is accumulation of fluid in the alveoli in the center (green overlay). On the left, there are normal alveoli filled with air (black dashed outlines).

The finding of fluid-filled lung alveoli is consistent with pulmonary alveolar edema.

63
Q

Hva viser snittet?

A

Sloughed epithelial cells of bronchus

Here we can see sloughed epithelial cells of the bronchus.
Often, this is an artefact that occurs as a result of fixation and tissue preparation.

64
Q

Hva viser snittet?

A

Bronchial wall

The structure of this bronchus is as follows (from internal to external):

  • Respiratory epithelium
  • Smooth muscle
  • Support scaffolding with vasa privata, elastic fibers and (here) also
    peribronchial connective tissue
65
Q

Hva viser pilen til?

A

Bronchial gland

Bronchial glands are seromucous and can be found only in the trachea and bronchi, not in the bronchioles.

66
Q

Hva viser snittet?

A

Congested pulmonary vein

In left sided heart failure, acute pulmonary blood stasis (regardless of the cause) leads to pulmonary edema.
Wide, full vessels are noticeable throughout the whole sample and even with the smallest magnification. This is pathological and a sign of blood stasis.

67
Q

Hva ser man i dette snittet?

To ting

A

Blått:

Blocked capillary

In the alveolar walls we can find widened capillaries with a caliber (marked here) that differs significantly from healthy pulmonary capillaries.
This transudate is related to higher hydrostatic pressure within the vessels, for example with left sided heart failure. More examples of enlarged, congested capillaries can be found directly below this annotation.

Rød pil:

Transudate

A classic sign of an acute pulmonary edema is the eosinic red transudate within the alveoli.
The transudate has a low protein content and contains few cells.

68
Q

Hva viser snittet?

A

Air-filled alveolar region

Even with a transudate, air filled alveolar areas filled can still be found.

69
Q

Hva viser snittet?

A

Interlobular septum

This structure composed of connective tissue represents an interlobular septum. With interstitial pulmonary edema, these septa are often thickened. Radiologically, these septa can be seen as Kerly B lines.

70
Q

Hva kan sputumprøver av pas. med HS vise?

A

Sputum analysis in patients with pulmonary edema may show heart failure cells (hemosiderin-containing cells).

  • Pulmonary venous congestion may result in intra-alveolar bleeding.
  • Macrophages that subsequently phagocytose the erythrocytes are called “heart failure cells.”
  • These cells may also be detected in the sputum of patients with pulmonary infarction, vasculitis, or aspiration of blood.
71
Q

Hvilke kardiovaskulære diff.diagnoser har man til HS?

A
72
Q

Hvilke pulmonale diff.diagnoser har man til HS?

A
73
Q

Hvilke andre årsaker er diff.diagnoser til HS?

Ikke kardiovaskulær, pulmonal

A
74
Q

Hvilke komplikasjoner kan oppstå pga. HS?

A

Akutt hjertesviktsforverring

Kardiorenalt syndrom

Arytmier:

  • Especially those associated with tachycardia

Sentral søvnapné

Kardiogent sjokk

Slag; pga. av økt risiko for arterielle tromber (spesielt ved atrieflimmer)

Kronisk nyresvikt

Kardiell cirrhose:

  • A complication of right-sided heart failure characterized by cirrhosis due to chronic hepatic vein congestion.
  • Associated with “nutmeg liver” (diffuse mottling on imaging due to ischemia and fatty degeneration).

Kronisk leggsår pga. venøs stase.

75
Q

Hva er definisjonen på kardiorenalt syndrom?

A

A complex syndrome in which renal function progressively declines as a result of severe cardiac dysfunction

76
Q

Hvordan er epidemiologien til kardiorenalt syndrom?

A

Forekommer hos ca. 30% av pasientene med akutt dekompensert hjertesvikt

77
Q

I hvor mange typer klassifiserer “American Heart Association” kardiorenalt syndrom?

A

5 ulike typer

78
Q

Hva kjennetegner type 1?

KR-syndrom

A
79
Q

Hva kjennetegner type 2?

KR-syndrom

A
80
Q

Hva kjennetegner type 3?

KR-syndrom

A
81
Q

Hva kjennetegner type 4?

KR-syndrom

A
82
Q

Hva kjennetegner type 5?

KR-syndrom

A
83
Q

Hva er patofysiologien ved kardiorenalt syndrom?

A
84
Q

Hvordan diagnostiseres KR-syndrom?

A
85
Q

Hva er behandlingen ved KR-syndrom?

Hvordan er prognosen?

A
86
Q

Hvilke faktorer er assosiert med en dårlig prognose?

Hjertesvikt

A

The prognosis depends on the patient, type and severity of heart disease, and adherence to GDMT and nonpharmacological interventions.

Risk stratification scales may be used to determine prognosis (e.g., CHARM and CORONA risk scores).

Especially useful for establishing the prognosis in hospitalized patients upon admission and discharge

87
Q

Hvordan er 1-årsoverlevelsen baser på NYHA-klasse?

Hjertesvikt

A
88
Q

Hvordan bør man legge opp legemiddelbehandlingen ved kronisk hjertesvikt?

A

Alle pasienter med nedsatt venstre ventrikkelfunksjon (ejeksjonsfraksjon < 40 %) bør behandles med ACE-hemmer, alternativt angiotensinreseptorblokker, betablokker, aldosteronantagonist og natriumglukose transporter 2 (SGLT2)-hemmer med mindre det foreligger spesifikke kontraindikasjoner.
Diuretika gis ved symptomer eller tegn på overvæsking.

ACE-hemmer og betablokker må trappes langsomt opp.

ACE-hemmer byttes ut med sakubitril-valsartan ved vedvarende symptomer.

Den samme medikamentelle behandlingen bør vurderes ved lett nedsatt ejeksjonsfraksjon (40–50 %).

Pasienter med bevart ejeksjonsfraksjon (≥ 50 %) har ikke dokumentert effekt av medikamentell behandling utover SGLT2-hemmer.
Diuretika har ofte god symptomatisk effekt også hos disse pasientene.

Det er viktig å behandle årsak til hjertesvikten der dette er mulig, for eksempel ved hypertensjon eller avleiringssykdom.

89
Q

Hvilke generelle tiltak bør settes i gang som et ledd i hjertesviktbehandlingen?

A

Der det foreligger en delvis reversibel årsak til hjertesvikten (koronarsykdom, hypertensjon, arytmi, korrigerbare klaffefeil, stoffskiftesykdom osv.) er det viktig at dette avdekkes og behandles.

Komorbiditet som diabetes, nyresykdom, lungesykdom og overvekt bør også behandles.

Røykestopp, saltrestriksjon og vektreduksjon er viktig ved hjertesvikt.

Saltrestriksjon betyr forsiktighet med ekstra salttilsetning i kostholdet og at man unngår salt ferdigmat og prosesserte kjøtt- og fiskevarer.

Væskerestriksjon, for eksempel maksimalt 1500 ml drikke/døgn kan være nødvendig dersom overvæsking er sentralt.
Daglig vekt er viktig for å avdekke ev. økende væskeretensjon.

Manglende terapirespons tilsier henvisning til spesialist eller innleggelse.

God hjertesviktbehandling er oftest et samvirke mellom fornuftig livsstil og bruk av mange legemidler.
Dette forutsetter god pasientforståelse og oppfølging fra behandlende lege.

Ved de fleste norske sykehus er det nå hjertesviktpoliklinikker hvor hjertesviktpasienter bør henvises i henhold til nasjonale retningslinjer.

Regelmessig fysisk aktivitet fremmer livskvaliteten ved hjertesvikt.
Dette skyldes ikke bedring i hjertets pumpeevne, men en bedret perifer utnyttelse av oksygen.

90
Q

Hvilke typer medikamenter bør brukes ved HS?

91
Q

Kilder?

Hjertemedisin (25 decks)

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