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Emergenze in casa di riposo
Sant’Angelo Lodigiano (LO), 13-14 ottobre 2005
Edema polmonare acuto”
Simone Franzoni
Gruppo di Ricerca Geriatrica
Centro Medico Richiedei - Palazzolo s/O
Arch Intern Med. 2005 Feb 28;165(4):374-8.
Integrating palliative care into heart failure care.
Hauptman PJ, Havranek EP.
Heart failure is a condition for which both palliative care and hospice
care can be appropriate.
The disease's increasing prevalence and predilection for elderly patients
with significant comorbidity underscore the need to integrate these
modes of care with the acute care approach that has dominated heart
failure treatment.
We propose integration of a palliative care approach early in the course
of heart failure treatment and a tiered process for selecting patients for
hospice care.
A transition of the focus to palliative care rather than mortality reduction
should occur over time, when clinical status deteriorates and advanced
therapeutic options become inappropriate or ineffective.
Failure to respond to the need for palliative care puts at risk the mandate
to treat the patient with heart failure during the entire course of illness.
Caso clinico “Edema polmonare acuto”
L.L.L., F, 82 anni,
viene trasferita in Riabilitazione Geriatrica da un
Reparto di Medicina, dove è stata ricoverata per:
“TIA: disartria, deficit di forza arto superiore
sinistro, deviazione rima buccale”.
Richiesta di proseguimento delle cure in ambito
riabilitativo è stata giustificata in base alla presenza di
instabilità posturale.
Familiari descrivono da qualche mese progressivo
declino funzionale e cognitivo.
Anamnesi sociale:
17 anni di scolarità; ex ostetrica, nubile.
Prima dell’evento acuto viveva da sola con aiuto familiare
(anche IADL intra-moenia).
Anamnesi patologica remota:
- ipertensione arteriosa sistemica e diabete mellito II tipo
(in trattamento dagli anni ’90)
- ricovero per frattura femore sx da caduta (osteosintesi,
complicata da piaga da decubito tallone, tromboflebite arto
inferiore e delirium ’95)
- ascesso perianale fistolizzato (toilette chirurgica DH ’97)
Anamnesi patologica remota:
- ricovero per diabete scompensato (IO – insulina),
insufficienza renale cronica, cardiopatia ischemica
cronica, dislipidemia, insufficienza venosa arti inferiori,
deterioramento cognitivo (MMSE 24/30) (’99)
- diagnosi ambulatoriale: steatosi epatica, gastropatia
microerosiva, osteoporosi (’01)
- ricovero per verosimile TIA, encefalopatia
multinfartuale, aterosclerosi TSA (stenosi 40-50% ACI
sx e 30% ACI e ACE dx ’01).
Esami strumentali recenti:
TC encefalo (’01): ”Grossolane alterazioni corticosottocorticali sovra-sottotentoriali, più evidenti in sede
temporo-parietale. Diffusa leucomalacia periventricolare
con aumento volumetrico ex-vacuo cavità ventricolari.
Strutture mediane in asse. Non espansi extracerebrali”.
ECOcardio (’01): ”FE 53%”.
Terapia in atto:
Acido Acetilsalicilico
Perindopril
Atorvastatina
Fenformina+glibenclamide
Ca carbonato+colecalciferolo
1c
1c
1c
1/2+1+1c
1c
Cardioaspirin
Procaptan
Totalip 20
Suguan
Ideos
Esame obiettivo (all’ingresso in RG):
- condizioni generali discrete, tono umore depresso,
decubito indifferente (BMI 32)
- stazione eretta possibile con appoggio, dismetria arti
inferiori, deambula cautelata con evidente zoppia
- varici e discromie arti inferiori, lieve linfedema
- es.neurologico: indenni i nervi cranici, ipertono arti
superiori bilaterale, ROT normali, lieve deficit forza
emisoma sx, Babinski e riflesso palmomentoniero sx
- incontinenza urinaria cronica da urgenza e stress.
NO ipotensione ortostatica
PA 105/65 mmHg
ECG: tachicardia sinusale (FC 115 bpm). BAV I°.
Intervallo QT ai limiti superiori. Asse elettrico equilibrato.
Onda Q in V1-2. Onde T appiattite in V4-6.
Diagnosi d'ingresso:
- Disturbo dell’equilibrio e della marcia a genesi mista:
-encefalopatia multinfartuale. Recente TIA (emisindr.sx)
-dismetria art inferiori (osteosintesi frattura femore sx ’95)
-poliartrosi (rachide e anche)
- Deterioramento cognitivo moderato a genesi mista;
pregresso delirium postchirurgico (’95)
- Ipertensione arteriosa sistemica, grado I, a rischio
cardiovascolare molto elevato
- Cardiopatia ischemica cronica; tachicardia ndd
- Aterosclerosi TSA non emodinamica
- Diabete mellito 2°tipo (IO; in fase di complicanze
sistemiche: insuff.renale cronica, ascesso perianale ’97)
- Dislipidemia II tipo, steatosi epatica, obesità
- Gastropatia microerosiva (’01)
- Insuff.venosa arti inferiori; tromboflebite sx (’95).
Obiettivi:
- Riabilitazione all’equilibrio e alla marcia
- Valutazione decadimento cognitivo
- Monitoraggio valori pressori e compenso
cardiovascolare (tachicardia).
Terapia instaurata all’ingresso:
Acido Acetilsalicilico
1c
Fenformina+glibenclamide
1/2+1+1c
Sinvastatina
1c
Nitroglicerina
1cer
(sospeso antipitertensivo e calcio)
Cardioaspirin
Suguan
Liponorm 20
Nitrodur 10
Diario clinico:
1-2°giornata: tranquilla, parzialmente orientata,
cammina con aiuto, insight rischio caduta
Normale frequenza cardiaca, PA 120/70 mmHg;
sospeso monitoraggio ECG applicato al momento
dell’ingresso.
Si richiede consulenza neuropsicologica, RX ginocchia.
Assessment:
MMSE 14/30
BADL 6/6 perse
Tinetti tot. 8/28
IPN 24.3
GDS 8/15
Barthel 30/100
PPT 4/28
IADL 7/8 perse
3-7°gg: iniziata FKT motoria, FC e PA nella norma. Edemi
declivi (fasciatura compressiva elastica).
8°gg: da alcuni giorni astenia ingravescente e
peggioramento resistenza all’esercizio fisico. FC 108 bpm
aritmico. PA 130/85 mmHg. Es.obiettivo sovrapponibile
all’ingresso. Durante la giornata più episodi di tachicardia
(circa 130 bpm). Monitor per controllo PA, FC e
saturazione O2 (Sat.O2: 88-90% in aria ambiente; 93-94%
in O2 1,5 l/min. Non si applica O2; si richiede RX torace).
ECG: wondering PM. FC 104 bpm. Non alterazioni
significative ripolarizzazione ventricolare.
9°gg: persiste tachicardia, nulla di rilevante all’es.obiettivo
polmonare.
RX torace: focolaio di addensamento parenchimale ,
piuttosto esteso, nei segmenti basali lobo inferiore dx.
Versamento pleurico consensuale lieve. Ampliamento vasi
polmonari centrali, cuore con aumento diametro trasverso.
Riduzione in altezza D11 tendente deformazione a cuneo.
OD: pleuropolmonite basale destra. Lieve versamento
pleurico bilaterale. Stasi piccolo circolo. Crollo
osteoporotico D11.
Richiesti es.ematochimici. Inizia ceftidoxima 2g/die.
11°gg: lieve stato soporoso, persiste astenia. No
leucocitosi neutrofila, solo peggioramento anemia (Hb da 11.6 a
10.6 g/dl). Data l’assenza di dispnea e di reperti obiettivi toracici
significativi non eseguita terapia broncodilatatrice.
11°gg
ore 23:
dispnea acuta, con severo broncospasmo diffuso.
PA 140/70 mmHg. FC 110 bpm. Sat.O2 aa: 84% (95% con
O2 4l/min).
Praticata ripetutamente terapia broncodilatatrice con beta
stimolanti, cortisonici e anticolinergici. Dato aggravarsi
broncospasmo eseguita aminofillina e cortisonico ev.
ore 0.30:
PA 140/90 mmHg, FC 130 bpm, Sat.O2: 94% (3 l/min).
Ridotto broncospasmo, risolta la dispnea.
Si mantiene monitoraggio.
12°gg
ore 8.30:
PA 130/80 mmHg FC 72 bpm; eupnoica, persiste lieve
broncospasmo.
Prosegue terapia broncodilatatrice e si aggiunge
furosemide 25 mg/die.
ore 16:
intensa precordialgia. PA 90/60 mmHg.
ECG: segni ischemia in V4-5-V6.
Si somministra isosorbide dinitrato sbl.
ore 16.30:
persiste precordialgia, ECG invariato. Trasferita in UCC.
ore 22: rientra in reparto.
Consulenza cardiologia:
”Paziente ipertesa, diabetica, affetta da demenza senile,
insuff.renale cronica, recente TIA in trattamento
riabilitativo, inviata per precordialgia.
Non attendibile, riferisce dolore da 3 giorni, ma
successivamente nega. Tranquilla, buon compenso
emodinamico.
PA 130/80 mmHg, ECG RS, BAV I con alterazioni
aspecifiche ripolarizzazione V4-6, peraltro già evidenti
(4/’02). EO: torace MV ridotto basi. Non segni scompenso.
Troponina nella norma. In considerazione lunga durata
sintomatologia e negatività troponina, il dolore non sembra
di origine cardiaca.
Vista l’anamnesi aggiungere diltiazem 60 ½ c x2.
Ricontrollare troponina, domani”.
OD: dolore toracico non cardiaco
13-24°gg:
Persiste grave astenia, non è più in grado di mantenere la
stazione eretta autonomamente e riesce a deambulare
solo con doppio aiuto umano.
Obiettività respiratoria nella norma. Assente precordialgia.
Non è possibile eseguire FKT.
Prosegue con terapia antibiotica (fino in 14°gg); diltiazem
60 ½ c x 2.
PA 95/60 mmHg. FC 100 bpm.
Troponina negativa.
Leucocitosi neutrofila, K 5.6 mEq/l e peggioramento
anemia (Hb 10.3 g/dl).
ECG: persistono onde T negative in V5-6. Positivizzazione
in V4.
RX anche: osteopenia. A sx esiti frattura consolidata collo
femore (vite dinamica). Coxartrosi senza rilevante
compromissione interlinee articolari.
RX ginocchia: gonartrosi bilaterale, calcificazioni arterie
poplitee.
RX torace (controllo): completa scomparsa addensamento
parenchimale e versamenti pleurici.
Si incrementa nitrato transdermico a 15 mg/die.
Dato elevato rischio tromboembolico inizia eparina calcica
s.c. 5000 UI x 2.
25°gg:ore 1.30:
dispnea acuta, rantoli a piccole bolle campi medio-basali
bilateralmente. Edemi declivi.
PA 120/70 mmHg. FC 110 bpm. ECG: non ischemia in atto.
Somministrato metilprednisolone 40 mg e.v. e praticata aerosol
terapia. Posizionato catetere vescicale. O2 terapia 2l/min.
PA 120/70 mmHg, FC 140 bpm. Sat.O2 93%.
ore 2.45:
dopo 100 mg furosemide ev la dispnea si risolve.
PA 100/85 mmHg. FC 108 bpm. Stabile Sat.O2. Diuresi 600cc.
OD: edema polmonare acuto
26°gg:
scarso compenso cv, incremento ponderale 6 Kg rispetto
all’ingresso. Diuresi 2300 cc/24h. Glicemia 500 mg/dl.
Sostituito IO con insulina e nitrato TTS con isosorbide
mononitrato 50 mg/die; prosegue furosemide 40 mg/die.
Aggiunto ciprofloxacina 500 mg x 2. Richiesto ecocardio.
OD: diabete mellito 2°tipo in fase di scompenso
27-30°gg: miglioramento quadro emodinamico, calo 6 kg.
Ecocardio: lieve dilatazione (ipertrofia eccentrica) e
disfunzione sistolica Vsx (FE 40%); non aumentata pressione
telediastolica. Insuff.mitralica moderata. Ipertensione
polmonare (PAPs 40mmHg). Non aumentata PVC.
OD: scompenso sistolico, insufficienza mitralica
moderata, ipertensione polmonare
Sostituito diltiazem con carvedilolo 6,25 mg/die.
Ancora labile compenso glicometabolico, incremento insulina.
31°gg:
febbre (38.1°C). Sostituita ciprofloxacina con imipenem /
cilastatina 500mg x 3. Richiesti es.ematochimici, marker
neoplastici, Rx torace ed ecografia addominale (sindrome
paraneoplastica ?).
34°gg:
RX torace: “sostanzialmente sovrapponibile al precedente”
Ecografia addominale: colelitiasi
Persiste leucocitosi neutrofila, grave anemia (Hb 7.1 g/dl)
CA19/9 34.7(0-34 U/ml), CEA 4.8(0-3.4 ng/ml), TPA,CA15/3 e alfafeto V.N.
Trasferimento in Geriatria per acuti.
39°gg: Diagnosi di trasferimento (dopo 5gg):
- Sepsi da infezione vie urinarie
- Anemia normo/cromica/citica di recente insorgenza (3 emotrasfusioni)
- Gastrite atrofica diffusa, erosioni duodenali, ernia jatale
- Scompenso cardiaco da prevalente disfunzione sistolica
- Cardiopatia ischemica cronica
- Ipertensione arteriosa sistemica
- Recente polmonite basale destra
- Diabete mellito tipo 2 (attuale terapia dietetica)
- Encefalopatia vascolare (recente TIA); decadimento cognitivo
moderato-severo secondario, delirium anamnestico
- Poliartrosi (osteosintesi femorale per frattura ‘95)
- Colelitiasi
- Insufficienza venosa arti inferiori
- Pregresso ascesso perianale fistolizzato (‘97)
Terapia consigliata:
- Imipenem + cilastatina
500 x 4 Tenacid 500
- Isosorbide mononitrato 50
1c
Monocinque R 50
- Carvedilolo 6.25
1c
Dilatrend 6.25
- Omeprazolo 20
1c
Antra 20
- Movicol
2b
- Atem + Pulmaxan
2cc + 1 f x 2
Dieta ipoglucidica.
40-47°gg:
astenia, esegue a fatica i passaggi posturali. Deambula con
doppio aiuto umano per brevi tragitti.
Ematuria con contrazione diuresi e obiettività polmonare
suggestiva di stasi;
ripresa terapia diuretica (furosemide 25 mg) e rimosso catetere
vescicale.
Scarso controllo glicemia, riprende insulina.
Apiressia, compenso emodinamico soddisfacente
(PA 130/80 mmHg. FC 84 bpm).
48°gg:
Sospeso imipenem/cilastatina (dopo 21 gg).
49-57°gg:
ridotta astenia, dispnea assente, apiressia, peso corporeo
stazionario.
Esegue a fatica i passaggi posturali; deambula con singolo
aiuto umano per brevi tragitti.
Sostituita terapia insulinica con IO. Sospesa eparina.
Ridotta furosemide a 12,5 mg/die.
Inizia FKT motoria.
58°gg:
ore 2.30:
dispnea acuta, rantoli a piccole bolle campi medio-basali
bilateralmente. Edemi declivi.
PA 100/60 mmHg. FC 120 bpm. ECG: non ischemia in atto.
Somministrato furosemide 125 mg ev, nitroglicerina ev, O2
terapia 3l/min.
ore 3.00:
dispnea risolta.
PA 90/55 mmHg. FC 102 bpm. Stabile Sat.O2 in aa. Diuresi
800cc.
OD: edema polmonare acuto
59-66°gg:
lieve astenia, dispnea assente (a riposo), apiressia, peso
corporeo – 2 Kg rispetto all’ingresso.
Non sufficiente controllo glicemia, si ritorna a insulina.
Stato funzionale invariato.
Hb 11.4 g/dl, azotemia 68 mg/dl, creatininemia 1.7 mg/dl.
Assessment di dimissione:
MMSE 11/30
GDS 6/15
Val.neuropsicologica indicativa per severo deterioramento
varie funzioni cognitive di tipo prevalentemente degenerativo.
Tinetti tot. 10/28
PPT 9/28
Diagnosi di dimissione:
- Scompenso cardiaco sistolico (NYHA III; intercorrenti episodi di edema
polmonare acuto), insuff.mitralica moderata, ipertensione polmonare
- Cardiopatia ischemica cronica
- Ipertensione arteriosa sistemica, grado I, a rischio cv molto elevato
- Pleuropolmonite basale dx intercorrente con versamento pleurico bilater.
- Sepsi da infezione vie urinarie intercorrente
- Anemia acuta ndd intercorrente (emotrasfusa); pregressa anemia da
disordine cronico
- Diabete mellito 2°tipo in trattamento con insulina e in fase di complicanze
sistemiche: insufficienza renale cronica, ascesso perianale (’97)
- Dislipidemia II tipo, obesità
- Gastrite atrofica diffusa, erosioni duodenali, ernia jatale, colelitiasi
- Insufficienza venosa arti inferiori; pregressa tromboflebite sx (’95).
- Poliartrosi (rachide, anche, ginocchia); crollo osteoporotico D11; dismetria
arti inferiori (esiti osteosintesi per frattura femore sx da caduta ’95)
- Demenza mista associata a disturbo depressivo; delirium postchirurgico
(’95); encefalopatia multiinfartuale; recente TIA (emisindrome sx)
- Disturbo equilibrio e marcia a genesi mista con elevato rischio di caduta
- Incontinenza urinaria cronica mista.
IDS 26/64
GIC IV
Terapia consigliata:
- Isosorbide mononitrato 50
- Carvedilolo 6.25
- Omeprazolo 20
- Ticlopidina
- Humulin R
1c
Monocinque R 50
1c
Dilatrend 6.25
1c
Antra 20
1+1c Opteron
4+4U e 30/70 14U
Dieta per diabetici 1400 KCal/die, calze elastiche
Dopo 6 mesi:
Ricovero in ospedale per acuti per edema polmonare acuto
Incremento ponderale + 8 Kg
Trasferimento in RSA; aggiunta furosemide 25 mg/die
Dopo altri 12 mesi:
Non più episodi di scompenso cardiaco acuto.
Peso non valutabile
Spunti di discussione:
DD: polmonite, broncospasmo, edema polmonare acuto
Ecocardiogramma ?
Approccio farmacologico corretto ?
Catetere vescicale, sempre ?
Erano prevenibili gli ultimi 2 episodi di edema polmonare ?
Monitoraggio dispnea nel paziente demente (FR ?)
Trasferimento in ospedale per acuti ?
CPAP in RSA ?
Prognostic Judgments and Triage Decisions for Patients With Acute
Congestive Heart Failure
Wally R. Smith, MD; Roy M. Poses, MD; Donna K. McClish, PhD; Elizabeth C.
Huber, MD; F. Lynne W. Clemo, MD; Donna Alexander, PhD; and Brian P.
Schmitt, MD (CHEST 2002;121:1610–7)
Study objectives: To determine how well triage physicians judge the probability of
death or severe complications that require treatment only available in an ICU to
maintain life for patients with acute congestive heart failure (CHF).
Patients or participants: Patients were those visiting the emergency department
(ED) with acute CHF, excluding those who already required a treatment only
available in an ICU to maintain life, and those with possible or definite myocardial
infarction. Physician participants were those caring for the patients in the ED.
Measurements and results: We performed chart reviews to ascertain whether each
patient died or had severe complications develop by 4 days. A calibration curve that
stratified these judgments by decile demonstrated that physicians consistently
overestimated this probability (p < 0.01).
Physicians’ judgments were only moderately good at discriminating which patients
would have the outcome (receiver operating characteristic curve area, 0.715).
Conclusions: Physicians drastically overestimated the probability of a severe
complication that would require critical care for patients with acute CHF who were
candidates for ICU admission.
Their judgments of this probability were associated with their triage decisions, as
they should be according to several guidelines for ICU triage. Overestimation of the
probability of severe complications may have lead to overutilization of scarce
critical care resources. Current critical care triage guidelines should be revised to
take this difficulty into account, and better predictive models for patients potentially
requiring critical care should be developed.
(CHEST 2002; 121:1610–1617)
Treatment of acute pulmonary oedema: diuresis or vasodilatation?
Michael Gammage
THE LANCET • Vol 351 • February 7, 1998
Intravenous loop diuretics have formed the mainstay of treatment for acute cardiogenic
pulmonary oedema since the 1960s but in recent years increasing use has been
made of intravenous nitrates as adjunctive therapy for acute and chronic pulmonary oedema.
In 1983 Nelson and colleagues reported a randomised, prospective study of isosorbide
dinitrate infusion versus furosemide infusion that showed similar falls in pulmonary-artery
occluded pressure (equivalent to leftatrial pressure) and suggested that isosorbide dinitrate
resulted in haemodynamically better changes with regard to myocardial oxygen consumption
and peripheral perfusion.
Despite studies such as these, the use of nitrates instead of (rather than as well as) loop
diuretics in the management of acute pulmonary oedema has not become standard practice.
This might relate to the inconvenience of infusion therapy but, until recently, there had been
no randomised, prospective comparison of the two therapies when given as bolus injection
as opposed to infusion.
When given intravenously, furosemide causes rapid venodilation, which results in a decrease
in left and right ventricular end-diastolic pressures; there is, however, still some
disagreement about the extent of this fall in filling pressures in the absence of the diuresis,
which usually starts within 30 min.
Transient rises in blood pressure have been shown to occur with furosemide, probably
because of activation of the sympathetic and reninangiotensin systems, which leads to
increased peripheral vascular resistance and afterload; this effect has the potential to
decrease cardiac output and increase cardiac work, with the possibility of worsening
myocardial and other tissue ischaemia.
Since many patients with acute cardiogenic pulmonary oedema have underlying myocardial
ischaemia or infarction, the initial symptomatic benefit may be followed by detrimental
effects on myocardial perfusion with extension or completion of myocardial necrosis.
Many patients with acute pulmonary oedema are not fluid overloaded before the event, so
redistribution rather than reduction of circulating volume might be a more appropriate
approach.
Theoretically, therefore, nitrates offer many of the advantages but not the disadvantages
associated with intravenous loop diuretics. But can they be as effective and are they as
convenient in an emergency?
In the prethrombolysis era, management of the patient with myocardial infarction and acute
pulmonary oedema was (relatively) simple; sit the patient up in bed, give oxygen, administer
intravenous opioids and furosemide, monitor, and leave for 30 to 60 min.
As the management has become more active, the concept of greater physician involvement
has evolved, but will a bolus injection of isosorbide dinitrate, repeated every 5 min, be a
practical proposition for the busy junior doctor?
The idea of bolus administration of intravenous nitrates is not new but, until recently, most
commercially available preparations were thought suitable for use only by continuous
infusion.The demonstration that isosorbide dinitrate can be given safely as small boluses,
repeated every 5 min as necessary, has the potential to change that perception. In their
randomised, prospective study of 104 patients, Cotter and colleagues have shown, as
secondary
Intravenous isosorbide dinitrate has a rapid onset of action, with peak vasodilatation at 5
min,10–12 but the short elimination half-life (0·6 h) requires frequent repeat dosing when
given by bolus.
Isosorbide-5-mononitrate shares the pharmacological actions of the dinitrate and is the main
active metabolite formed after administration of isosorbide dinitrate,13 but it has a much
longer half-life (5·1 h). The mononitrate therefore seems to represent a better long-acting
nitrate for intravenous bolus use in acute pulmonary oedema.
For intravenous nitrate therapy to displace furosemide for the management of acute
pulmonary oedema, it needs to be effective in a single bolus injection in most cases, must be
safe to use in the presence of moderate hypotension, and must be effective in patients on
chronic long-acting nitrate or diuretic therapy. Bolus isosorbide dinitrate has not yet been
shown to fulfil these criteria; bolus isosorbide mononitrate might, but a large, randomised
prospective comparison with furosemide or a furosemide/isosorbide dinitrate combination is
required.
Does Continuous Positive Airway Pressure by Face Mask Improve Patients With
Acute Cardiogenic Pulmonary Edema Due to Left Ventricular Diastolic
Dysfunction?
Karim Bendjelid, MD, MS; Nicolas Schu¨ tz, MD; Peter M. Suter, MD, FCCP;
Gerard Fournier, MD; Didier Jacques, MD; Samir Fareh, MD; and Jacques-A
Romand, MD
CHEST MARCH, 2005
Objective: Continuous positive airway pressure (CPAP) by face mask is an
effective method of treating severe cardiogenic pulmonary edema (CPE). However,
to our knowledge, no study has provided a precise evaluation of the effects of
CPAP on cardiac function in patients presenting with CPE and preserved left
ventricular (LV) function.
Setting: A 14-bed, medical ICU at a university hospital.
Patients: 9 consecutive patients presenting with hypoxemic acute CPE.
Interventions: All patients were selected for 30 min of CPAP with 10 cm H2O by
mask with fraction of inspired oxygen adjusted for a cutaneous saturation > 90%.
Measurements and results:
in patients with preserved LV systolic function, mean arterial pressure and LV enddiastolic volume were decreased significantly by CPAP (p < 0.04).
In patients with LV systolic dysfunction, CPAP improved LV ejection fraction (p <
0.05) and decreased LV end-diastolic volume (p 0.001) significantly.
Conclusion: CPAP improves oxygenation and ventilatory parameters in all kinds of
CPE. In patients with preserved LV contractility, the hemodynamic benefit
of CPAP results from a decrease in LV end-diastolic volume (preload).
Guidelines on the diagnosis and
treatment of Acute Heart Failure (AHF)
The task force on AHF of the European
Society of Cardiology
March 2005
Patients with AHF have a poor prognosis.
Mortality:
Particularly high in patients with AMI (30% at 12 mo)
Max: 40% at 12 mo
Predictors:
elevated pulmonary capillary pressure, low serum sodium,
increased left ventricular dimension.
Hospitalization:
45% rehospitalized at least once within 12 mo
Definition AHF
As a rapid onset of symptoms and signs secondary to
abnormal cardiac function.
I. AHF decompensated (de novo or decompensation CHF)
symptoms and signs mild and do not fulfil criteria for
cardiogenic shock, pulmonary oedema, hypertensive crisis
II. Hypertensive AHF
symptoms and signs are accompanied by high blood pressure
and relatively preserved left ventricular function with a chest
radiograph compatible with acute pulmonary oedema
III. Pulmonary oedema
verified by chest X-ray, accompanied by severe respiratory
distress, with crackles over the lung and orthopnea,
O2 saturation <90%
IV. Cardiogenic shock
evidence of tissue hypoperfusion induced by HF after
correction of preload. Systolic blood pressure < 90mmHg
and/or low urine output (<0.5 ml/Kg/h), with a pulse rate >
60/min with or without evidence of organ congestion
V. High output failure (arrhythmias, anemia)
high heart rate, warm peripheries, pulmonary congestion, low
blood pressure (sepsi)
VI. Right heart failure
low output syndrome with increased jugular venous pressure,
increased liver size and hypotension.
Diagnosis of AHF is clinical and supported by …
Clinical evaluation
blood pressure, heart rate, external jugular veins, wet rales in
lung fields, peripheral temperature
ECG
rate, rhythm, acute coronary syndrome, atrial-ventricular strain
Chest X-ray
assess pulmonary congestion, infectious lung disease
Laboratory tests
arterial blood gas analysis, pulse oximetry? B-type natriuretic
peptide ?
Echocardiography
ventricular function, pulmonary artery pressure
Causes and precipitating factors in AHF
1) Decompensation of pre-existing CHF (cardiomyopathy)
2) Acute coronary syndromes
(a) myocardic infarction / unstable angina with large extent of
ischaemic dysfunction
(b) mechanical complication of acute myocardical infarction
(c) right ventricular infarction
3) Hypertensive crisis
4) Acute arrhythmia (ventricular tachycardia and fibrillation,
atrial fibrillation or flutter, other supraventicular tachycardia)
5) Valvular regurgitation / endocarditis / rupture of chordae tendinae,
worsening of pre-existing valvular regurgitation
6) Severe aortic valve stenosis
7) Acute severe myocarditis
8) Cardiac tamponade
9) Aortic dissection
Causes and precipitating factors in AHF
11) Non-cardiovascolar precipitating factors
(a) lack of compliance with medical treatment
(b) volume overload
(c) infections, particularly pneumonia or septicaemia
(d) severe brain insult
(e) after major surgery
(f) reduction in renal function
(g) asthma
12) High output syndromes
(a) septicaemia
(b) thyrotoxicosis
(c) anaemia
(d) shunt syndromes
Goals of treatment of the patient with AHF
____________________________________________________________________________
Clinical
↓ symptoms (dyspnoea and / or fatigue), clinical signs, body weight
↑ diuresis, oxygenation
Laboratory
Serum electrolyte and blood glucose normalisation
↓ BUN and/or nomalisation, S-bilirubin, plasma BNP
Haemodynamic
↓ pulmonary capillary wedge pressure to<18 mmHg
↑ cardiac output and/or stroke volume
Outcome
↓ lengh of stay in the intensive care unit, duration of hospitalisation, mortality
↑ time to hospital re-admission
Tolerability
Low rate of withdrawal from therapeutic measures
Low incidence of adverse effects
________________________________________________________________________________
BUN= blood urea nitrogen
Organization of the treatment of AHF
Requires a treatment plan in the hospital system.
Best results are achieved if patients are treated promptly by
expert staff in areas reserved for HF patients.
Should be followed by a subsequent HF clinic programme.
Non-invasive monitoring
Blood pressure (every 5 min. until the dosage of vasodilators,
diuretics, or inotropes has been stabilized), heart rate,
respiratory rate, temperature,
Pulse oximeter (every hour if receiving oxygen therapy), ECG
General therapeutic approach in AHF by findings
on invasive haemodynamic monitoring
Haemodynamic
Characteristic
Suggested therapeutic approach
Cardiac Index
Decreased
Decreased
Decreased
Decreased
Maintained
Pulmonary
Capillary
Wedge Pressure
Low
High or Normal
High
High
High
>85
<85
>85
Vasodilator
(nitroprusside
NTG, fluid
Loading may
become
Necessary)
Consider inotropic
agents
(dobutamine,
dopamine) and
i.v. Diuretics
Vasodilators
(nitroprusside,
NTG) and i.v.
diuretics and consider
inotrope (dobutamine)
Systolic Blood
Pressure
Outline of
therapy
Fluid
loading
i.v. diuretics
if SBP is low,
vasocontrictive
Inotropes
Treatment of AHF - Oxygen and ventilatory assistance
Outcome: adequate levels of oxygenation at the cellular in order to prevent
end-organ dysfunction and the onset of multiple organ failure.
Maintenance of a patient airway is imperative.
Sat.O2: 95-98%
No evidence that giving increasing doses of oxygen results in an improved
outcome.
The use of increased concentrations of oxygen to patients without evidence
of hypoxaemia may cause harm.
RCT suggest that non-invasive ventilation (CPAP, NIPPV) in acute
cardiogenic pulmonary oedema is associated with a significant reduction of
tracheal intubation and mechanical ventilation.
Insufficient data to demonstrate a significant reduction in mortality.
Treatment of AHF
Morphine and its analogues
Severe AHF with restlessness and dyspnoea.
Induces venodilatation, mild arterial dilatation, and reduce
heart rate.
3 mg iv (repeated if required)
Anticoagulant
Heparin showed no clinical improvement, but reduce venous
thrombosis.
Treatment of AHF – Vasodilators
First line therapy, if hypoperfusion is associated with an adequate blood
pressure and signs of congestion with low diuresis (to open peripheral
circulation and to lower preload).
Nitrates
Low dose venodilatation
High doses venodilatation + arteries dilatation (coronary).
Balanced doses reduce left ventricular preload and afterload, without
impairing tissue perfusion.
U-shaped curve effect; low dose: limited effect in preventing AHF
recurrences; high dose: less effectiveness.
Nitrates iv have rapid development of tolerance: 16-24 h.
Initially N. may be given orally but i.v.N. are also well tolerated in AMI.
N. i.v. dose tritation to the highest haemodynamically tolerable + low dose
furosemide is superior than high dose of diuretic treatment alone.
Tritating the dose against blood pressure decrease.
The dose should be reduced if systolic blood pressure < 90-100 mmHg.
Indications and dosing of vasodilators in AHF
Vasolidator
Indication
Dosing
Main side
effects
Other
AHF when blood
pressure is
adeguate
Start 20µg/min,
increase up to
200 µg/min
Hypotension,
headache
Tolerance
on
continuous
use
Isosorbide
Dinitrate
AHF when blood
pressure is
adeguate
Start 1mg/h
increase up to
10 mg/h
Hypotension,
headache
Tolerance
on
continuous
use
Nitroprusside
Hypertensive crisis,
mitral regurgitation,
cardiogenic shock
combined with
inotropes
0.3 – 5 µg/Kg/min
Hypotension,
isocyanate
toxicity
Drug is light
sensitive
5-monotritate
Treatment of AHF
Calcium antagonist should be considered contraindicated.
ACE-inhibitors are not indicated in the early stabilisation of
patients with AHF.
B-Blocking agents should be used cautiously in patients with
overt AHF and more than basal pulmonary rales. Among such
patients where ongoing ischaemia and tachycardia are
present, iv metoprololo ca be considered.
Treatment of AHF - Diuretics
Decrease in plasma and extracellular fluid volume, total body water and
sodium, reduction in right and left ventricular filling pressures and a
decrease in peripheral congestion and pulmonary oedema.
IV loop D. exerts a vasodilating effect (5-30 min) with decrease of right atrial
and pulmonary wedge pressure as well as pulmonary resistances.
With high bolus doses (> 1 mg/Kg) there is a risk of reflex vasoconstriction.
In acute coronary syndromes D should be used in low doses and
preference given to vasodilator therapy.
Dose should be tritated according to the diuretic response and relief of
congestive symptoms.
Administration of a loading dose followed by continued infusion of
furosemide or torasemide is more effective than bolus alone.
Combinations with thiazides and spironolattone or with dobutamine,
dopamine, and nitrates are more effective than increasing doses of D.
Diuretic dosing administration
Severity of fluid
retention
Diuretic
Dose (mg)
Moderate
Furosemide, or
20 - 40
Torameside, or
10 – 20
Oral or iv according to symptoms
Tritate dose according to clinical
response
Monitor Na+, K+, creatinine,
blood pressure
Furosemide, or
Furosemide infusion
40 - 100
5 - 40 mg/h
i.v.
Better then very high bolus doses
Torameside
20 – 100
Orally
Refractory to loop
Diuretics
Add HCTZ, or
Metolazone, or
Spironolactone
25 - 50 twice daily
2.5 - 5 once daily
25 - 50 once daily
Combination with loop diuretic
better than very high dose of loop
diuretics alone.
Metolazone more potent if
creatinine clearance <30mL/min
Spironolactone best choice if
patient not in renal failure and
normal or low serum K+
In case of alkalosis
Refractory to loop
diuretic and thiazides
Acetazolamide
Add dopamine for
renal vasodilatation,
or dobutamine as an
inotropic agent
Severe
Comments
i.v.
Consider ultrafiltration or
haemodialysis if co-existing renal
failure
Treatment of AHF
Diuretic resistance
Causes:
- intravascular volume depletion,
- renal failure (NSAIDs),
- decreased renal perfusion (low output),
- impaired gut absorption of an oral diuretic,
- neurohormonal activation (angiotensin - aldosterone system, sympathetic
nervous system).
Associated with poor prognosis.
More frequent in patient with severe, chronic HF on long-term
diuretic therapy.
Treatment of AHF - Inotropic agents
Indicated in the presence of peripheral hypoperfusion (hypotension, decreased
renal function) with or without congestion or pulmonary oedema refractory to
volume replacement diuretics and vasodilators at optimal doses.
Their use is potentially harmful as they increase oxygen demand.
NO BOLUS
If no response is seen, the therapy should be terminated.
Dopamine in AHF with hypotension and low urine output:
< 2 ug/Kg/min i.v. (dopaminergic) improved renal blood flow
and diuresis and lowers peripheral resistance.
2 - 3 ug/Kg/min i.v. (B-adrenergic) increase myocardial
contractility and cardiac output.
5 ug/Kg/min i.v. (A-adrenergic) increase peripheral
resistance (useful only in patients with hypotension).
Treatment of AHF
Dobutamine is used to increase the cardiac output.
2-3 ug/Kg/min i.v. increased to 20 ug/Kg/min
because haemodinamic actions are proportional to its dosage.
The elimination is rapid after cessation of infusion.
Prolonged infusion (>24-48 h) is associated with tolerance and
partial loss of haemodinamic effects.
Risk of arrhythmia.
Weaning may be difficult because of recurrence of
hypotension, congestion, or renal insufficiency. Progressive
decrease in dosage by step of 2-3 ug/Kg/min/day.
Treatment of AHF
Cardiac glycosides produces a small increase in cardiac
output and a reduction of filling pressures.
Indication: tachycardia-induced AHF (atrial fibrillation)
No in AHF after myocardial infarction, bradycardia, AV block,
SSS, hypoK, hyperCa.
Efficacious in reducing the re-occurrence of AHF;
predictors:
- 3° heart sound
- extensive LV dilatation
- distended jugular veins.
Treatment of AHF - Underlying diseases and comorbidities
Coronary artery disease (ICU)
Most frequent cause. History an typical ECG signs.
Inotropic agents may be deleterious.
AHF and hypertension (no ICU)
“Flash pulmonary oedema” because of its rapid onset. Systolic function is
often preserved, while diastolic abnormalities is often present.
Treatment should be started immediately (systolic o diastolic pressure < 30
mmHg in 2 min; after progressive decrease to the values measured before
the hypertensive crisis in several hours):
- oxygen therapy, CPAP, NIPPV
- furosemide i.v. (if CHF and fluid overload)
- nitroglicerina i.v. (to decrease venous preload and arterial afterload and
increase coronary blood flow)
- nicardipina (diastolic disfunction with an increased afterload; but may
cause adrenergic activation – tachycardia, intrapulmonary shunt hypoxaemia)
- NO B-blocker.
Treatment of AHF
Renal failure
Concomitant renal failure requires the treatment of alectrolyte
abnormalities, metabolic acidosis.
Serum Cr > 2.5 – 3 mg/dl is necessary increase the dose of loop diuretics
an add a diuretic with different mechanism of action (metolazone).
Pulmonary diseases and bronchoconstriction
When bronchoconstriction due to astma, chronic obstructive bronchitis, lung
infection) is present bronchodilators should be used.
They may improve cardiac function, but should not be used instead of
relevant AHF treatment.
Salbutamol nebulization over 20 min., repeated hourly during the first few
hours.
Arrhythmias (Atrial Fibrillation - AF)
Verapamil and diltiazem should be avoided in acute AF as they may worsen
HF and cause a III AV block.
Amiodarone and B-blocking agents have been successfully used in AF for
rate control and prevention of recurrrence. Rapid digitalization should be
considered especially when AF is secondary to AHF.
Treatment of AHF
Infections:
in elderly patients with CHF, infections as pneumonia may be a cause for
worsening HF and dyspnoea.
An increase in CRP and a decrease in general condition may be the only
signs of infection.
Diabetes:
AHF is associated with impaired metabolic control; hypoglycemic drugs
should be stopped and shift to insulin.
Catabolic state
Renal failure:
Both may cause, aggravate, and influence, the outcome of the other.