HF=cardiovascular problem No - uniba.sk · Normal heart HF Muscle weakness Organ hypoperfusion Pump failure Definition (pat.-physiol.) HF is the state, when the heart is not able

Heart failure

Chronic heart failure

25.3.2020

HF=cardiovascular problem No.1

Relatively very common (> 70 yr. 10%

prevalence)

Poor prognosis -

malignant disease: 5 yr mortality= 50%

HF NYHA IV : 1 yr mortality= 50%

Prognosis

...is worse than supposed.

Only 50% live longer than 5 yrs.after onset of

symptoms.

There are no data how they are dyeing:

40% dye suddenly (are in stabilised state),

60% primarily for progressive HF

HF - progressive state with ↑ mortality

↑frequency of acute events with progression of disease → need of frequent

hospitalisations and ↑ risk of death

myocardial damage with acute episodes HF → progression LV dysfunction

Chronic worsening

Mortality

Acute episodes

Disease progression

Function

LV

QoL

Gheorghiade et al.Am J Cardiol 2005;96:11G–17G; Gheorghiade & Pang. J Am Coll Cardiol 2009;53:557–73

Epidemiology

USA: 2-3 millions of patients

SK: cca 40 000

if 2000 pract.physicians, each has cca 20 pac.

Incidence:

In the last 40 yrs is increasing

- populations are elderly

- therapy is improving

HF history

1628 The heart is pump (W Harvey)

1761 Overload leads to heart´s enlargement(GB Morgagni)

1785 Digitalis (W Withering)

1806 Pericardial and valvular description (JN Corvisart)

1819 Stethoscope (R Laennec)

1912 Arterial hypertrophy leads to heart pathol.

(JB Herrick)

1954 US in cardiology (I Edler/H Herz)

Nonpharmacologic approaches...

1785 W Withering

– effets on kidneys

– effect on heart beats

Beginning of pharmacotherapy of HF

Milestones in the time

1920 - mercury diuretics

1958 - thiaside diuretics

1967 – heart transplant (C Barnard)

1975 - blockers (F Waagstein)

1987 - benefit of ACEI (ARB) (K Swedberg)

2015 – dual blockade of RAAS (McMurray)

Increased incidence and prevalence

1) improvement in survival after acute MI2) aging population3) improvement of diagnosis4) improvement of therapy

Congestive heart failure

represents complex clinical syndrome,

characterisied of abnormal LV function and

neurohumoral regulation, connected with effort

intolerance and fluid retention and decreased

chance of longevity.

CHF

Is syndrome based from LV dysfunction for:

a)mechanic overload

b)damaged myocardium (cell loss)

c)combination of both

Congestive heart failure

It is not a disease, but „symptomatic syndrome“,

Cardiac output is unadeqate to metabolic needs of organism

(heart,kidneys,lung,liver,muscles,vessels,brain...)

HF definitions

Is complex of symptoms of fatigue, dyspnea and congescion,

connected with tissue hypoperfusion during exercise and

often with fluid retention.

Primary cause is deterioration of the heart to fill in, or to empty

the LV.

Dysfunction

Systolic dysfunction

disturbed ability of myofibriles to shorten against the load

(i.e. generate the pressure and to empty)

Diastolic dysfunction

Ventricle is unable to accept the blood in the low pressure setting

(i.e. to relax and to fill in)

Filling is slow, uncomplete if compensation increase of pressure in

left atrium occurs

Different mechanical stresses induce dilatation and concentric hypertrophy.

Arnold M. Katz, and Ellis L. Rolett Eur Heart J 2016;37:449-

454

HF– abnormalities of structure and function

Normal heart HF

Muscle weakness

Organ hypoperfusion

Pump failure

Definition (pat.-physiol.)

HF is the state, when the heart is not able to secure

adeqate tissue perfusion

and despite

normal or increased filling pressure

HF

Systolic – Diastolic

LV failure - RV failure

Acute HF – Chronic HF

Pump function of the heart is regulated:

- preload

- contractility

- afterload

- heart rate

-synergism of the heart parts

Preload

load to the left ventricle before beginning of

formation contraction action of systole

Tension in the ventricle wall at the end

of diastole

Frank - Starling mechanism:

...power of contraction during

systole is the greater, the greater

is source lenght of muscle fibers

Contractility

factor, influencing contract ability independently

from diastolic muscle fiber lenght,

but dependently from positive or negative

inotropic effects

Regards of increasing of number of created

actine-myosin connections per unit time,

regards of enhancement of their creation

Afterload

Tension in the wall during systole

Determinants:

– aortic stiffness

- peripheral arteriolar resistance

- blood volume in arterial bed

Frequency increases minute volumewith more frequent emptying of ventricles

-frequency effect

-up to critical value of contractions frequency

-disadvantageous with aortal and mitral sten.

Synergism of actions

- atrias and ventricles

- right and left ventricle

- base, middle and apex

Hemodynamic (edema) model of HF

Disturbance of pump function ventricul.pressure

forward failure backward failure

reduction of renal perfusion venous pressure

fluid elimination disturbed ven.return from kidneys

edema edema

Compensation mechanisms

1) Frank-Starling mechanism

2) Neurohumoral activation (SNS,RAAS)

Hemodynamic overload /Loss of cardiomyocytes

stroke volumeProliferative effect

EpinephrineNorepinephrine

Ang IIEndotellin

Arg.vasopressinAldosterone

RetentionNa+, H2O

Tension of LV wall

Endotelial dysfunction,

atherosclerosis

O2 demands O2 supply

myocardial ischemia,LV remodellation, LV dysfunction

Myocardial hypertrophy/fibrosis

frequency

contractility

Definition - guidelines

1) Symptoms of HF (at rest, or during exersice) +

2) Objective evidence od heart dysfunction

(systolic diastolic) (at rest)

3) Response to the therapy – (improvement)

HF= Symptomatic syndrome

Syndrome of LV dysfunction:

mechanical overload

myocardial abnormalities (cell loss)

combination of both

Sequences

Exact reasons for these organ changes are not known yet, but decreased cardiac output (as a result of inability of the heart to create contraction and relaxation) makes the genesis of HF.

At the beginning several adaptation mechanisms are activated, plasmatic neurohumoral characteristics are changing and to circulation various peptides are releasing (to keep heart´s performance and blood pressure).

Prolonged exposition several organs to alterated „circulatory situation“ leads to organ remodellation and dysfunction.

Sequency of progression

Dysfunctiion LV → activation of RAAS

Growth factors(AgII,ALDO)modul.accumul.collagen

around the cardiomyocytes

accumul.interstitial.collagene ↓density of capillaries

↑diffuse oxygen distance →hypoxia of myocytes

Hypoxia→apoptosis of viable cardiomyocytes.

Chronic HF

progressive disease, during development deteriorates, despite

no clinical events are found (i.e MI, worsened CHD)

Apoptosis (programmed cell death)

with HF development loss of cardiomyocytes

„reactive interstitial fibrosis“ contributes

chronic hypoxia triggers apoptosis

HF causes

(2/3 patients) ischemic

(1/3 patient) nonischemic

hypertension

valvular

cardiomyopathies

anemias

endocrinopathies (thyroid gland)

congenital diseases

Processes, leading to HF

Heart: CHD,HY,CMP,specific myocardial diseases.

Valvular,or endocardial diseases- endocardial fibrosis

Pericardial: constrictive pericarditis

Arrhythmias: brady/tachy manifestations as HF

↑ MV: anemias, thyreotoxicosis, hypovitaminoses B1

Iatrogenic: CAA, AA, NSA

Main symptoms

1. Decreased exercise tolerance

2. Dyspnoe:

exercise d.

ortopnoe

paroxysmal noctirnal d.

3. Fatigue

4. Oedema

Classification

Functional classes NYHA

HF Classification Killip classes

Class I no lung rales and 3rd heart sound

Class II lung rales <50% and/or 3rd sound

Class III lung rales >50% / pulmonary edema

Class IV cardiogenic shock

Laboratory diagnostics

NOR

PRA

Arginine vasopressin

BNP/ANP (NT-proBNP)

Diagnosis

EKG

X-ray

ECHOCG

Exercise tests (6min.walking test)

Natriuretic peptides

States masking and worsening HF,

recommended investigations:

1. Lung diseases:

X-ray,lung functional tests, blood picture (sec.polycytemias)

2. Anemias: blood picture

3. Renal and hepatal diseases:

biochemic exams, urine

4. Reversible myocardial ischemia:

exercise myocardial depicting methods

Guidelines classes

Class I recommended/is indicated

Class II a should be considered

II b may be considered

Class III not recommended

Levels of evidence

Level A from more RCT/metaanalyses

Level B from 1 RCT/more non RCT

Level C consensus/small retrospective

trials/registers

Positive inotropes

Na+/K+-ATP-inhibitors

Vasodilators

Nitrates

Hydralasine

Neurohumoral.blockade

ACE-inhibitors

ARB

Aldosteroneantagonists

blockers

-adrenergic agonists

Diuretics

Loop diuretics

Thiasides

Farmacotherapy

Therapy

ivabradine,NEPI,SGLT2

Positive inotropes

Digitalis

Spironolactone

blockers

Diuretics

ACE-Inhibitors

In HF patients, if increased vagotonus =

better prognosis

ACEI and BB significantly increase vagotonus

and decrease sudden cardiac death.

Farmacotherapy of HF (systolic HF) progresses

decreased mortality

improved functional state

Application of the Health Belief Model in Promotion of Self-

Care in Heart Failure Patients

180 patients with HF

38% do not know, what HF means

40% has no information of weight control meaning

43% has no information of salt restriction in meals

Persistence to the therapy

3 months 6 months 12 months

ACEI 83,6 % 75,3 % 64,5 %

ARB 84,8 % 77,5 % 66,3 %

BB 86,3 % 80,0 % 70,4 %

spironolaktone 76,3 % 65,3 % 50,7 %

Goals of therapy

1. Prevention

a) prevent.of diseases leading to LV dysfunction

b) prevention of progression to HF if dysf.LV pres

2. Morbidity

quality of life

3. Mortality

prolonged survival

Management of HF

Estimation of diagnosis

Diagnosis of present signs: pulmonary edema, dyspnoe, exercise fatigue, peripheral edemas.

Etiology of HF

Comorbidities

Estimation of symptome severity (NYHA)

Estimation of prognosis

Evaluation of possible complications

Education of patient and family

Selection of the appropriate therapy

Monitoring of progression and followed therapy

Goals

If possible estimate and adjust underlying cause

Factors worsening of disease: (hypertension,

arrhythmia, severe anemia...)

Adjust salt overload and water overload in body

Adjust main symptoms: (dyspnea,fatigue)

Improve prognosis

HF with EF – 30 yrs – results from RCT trials: 1986–2001.

John J.J.V. McMurray Eur Heart J 2015;36:3467-3470

HF with EF – 30 yrs – negative results from RCT trials: 1986–2001.


HF with EF – 30 yrs – positive results from RCT trials: 1986–2001.


Non-farmacologic

Patient with severe edema:

rest at bed:

Position with head supported

Aspiration of massive pulmonary exsudate

Fluid restriction (<1 l)

Salt restriction

Out-patient:

Non-salt diet

Regular walks

Farmacologic

Farmakologic treatment

Diuretics

RAAS inhibition (ACEI/ARB)

BB

Aldosterone antagonists

Digoxine

Dopaminergic agents

Antiarrythmics

Oxygen

If inhibition

Dual RAAS inhibition RAAS (ARB+NEPI)

Diuretics

In HF patients there is some Na+H₂0 retention,

therefore: NaCl restriction + diuretics (also none).

Mild forms: thiazides

Severe forms: loop diuretics

Doses such, to normalize.jugulular venous pressure

<8mmHg

In single dose, or doubled (cave ↓K,Mg)

ACEI/ARB

major advance in HF therapy

↓mortality with mild/moderate HF (SOLVD)

with severe HF (CONSENSUS,CHARM)

NYHA IV (yearly mortality from 57% to 26%)

NYHA II (yearly mortality from 40% to 35%)

improves functional status NYHA(40-50% patients of 0,5-1 NYHA)

EBM - ACEI

Captopril (SAVE)

Enalapril (CONSENSUS, SOLVD)

Lisinopril (ATLAS)

Ramipril (AIRE)

Trandolapril (TRACE)

Starting doses - targets (mg)

ACEI

captopril 6,25 (3xd) 50 (3xd)

enalapril 2,5 (2xd) 10-20 (2xd)

lisinopril 2,5-5 (1xd) 20-35 (1xd)

ramipril 2,5 (2xd) 5 (2xd)

trandolapril 0,5 (1xd) 4 (1xd)

Start low – go slow!

ACEI class level

Lowering of hospitalization risk and premature HF mortality

in pat. with EF ≤ 40%, (pats. should be on BB and MRA).

I. A

For lowering of hospitalization risk in HF pat. with EF ≤

40%, and persistent symptoms (NYHA II.-IV.) despite th.

BB, not tolerating MRA.

I. A

ACEI – symptomatic HF( NYHA II.-IV.)

ESC Guidelines for nthe diagnossis et treatment of acute and chronic heart failure 2012 European Heart Journal 2012. 1787-1847

Starting doses – targets (mg)

ARB

candesartan 4-8 (1xd) 32 (1xd)

valsartan 40 (2xd) 160 (2xd)

losartan 50 (1xd) 150 (1xd)

ARB class level

Lowering of hospitalization risk and premature HF mortality

in pat. with EF ≤ 40%, not tolerating ACEI (cough)

(pat should be on BB and MRA).

I. A

For lowering of hospitalization risk in HF pat. with EF ≤

40%, and persistent symptoms (NYHA II.-IV.) despite th.

ACEI and BB, not tolerating MRA.

I. A

ARBs – symptomatic HF( NYHA II.-IV.)


EBM - BB

Carvedilol (COPERNICUS,US-CARVEDIL)

Bisoprolol (CIBIS II)

Metoprolol (MERIT-HF)

Nebivolol (SENIORS)

(COMET): metoprolol, carvedilol

Starting doses - targets(mg)

BB

bisoprolol 1,25 (1xd) 10 (1xd)

carvedilol 3,125 (2xd) 25-50 (2xd)

metoprolol succinate 12,5-25 (1xd) 200 (1xd)

nebivolol 1,25 (1xd) 10 (1xd)

EBM - MRA

Spironolactone (RALES)

Eplerenone (EPHESUS, EMPHASIS-HF)

Starting doses – targets (mg)

MRA

eplerenone 25 (1xd) 50 (1xd)

spironolactone 25 (1xd) 25-50 (1xd)

MRA class level

For all pat.with persistent symptomsNYHA II-IV

and EF ≤ 35% despite therapy with ACEI (ARB)

and BB for lowering of HF hospitalization

and premature mortality risk.

I. A.

MRA - symptomatic (HF) (NYHA II.-IV.)


class level

ACEi I A

ARB I A

BB I A

MRA I A

Pharmacological treatment for

symptomatic systolic HF (NYHA II.-IV.)

ESC Guidelines for the diagnossis et treatment of acute and chronic heart failure 2012 European Heart Journal 2012. 1787-1847

Digoxin

HF with atrial fibrillation with rapid ventricular response

Improves performance and eases straits (quality of life)

Doesn´t improve survival.

Usually in severe forms of HF.

Carefully, event.: discontinuation of therapy.

Renal.insuff,arrhythmias with conduction abnormalities,

hypokalemia!

Therapeutic serum concentrations: digoxinemia: 0,9-1,9 μM/l

(in HF 0,7-1,5)

Digoxin in NYHA II.-IV with systolic HF.


Digoxin class level

For lowering of hospitalization risk HF in pat. with EF ≤ 45% and

AF, not tolerating BB (in pat. with HR ≥ 70/min = alternative is

ivabradín).

Pat. Should be on ACEI (or ARB) and MRA.

II.b B

For lowering of hospitalization risk HF pat. with EF ≤ 45%

and persistent symptoms (NYHA II.-IV.), despite therapy of BB,

ACEI (or ARB) and MRA.

II.b. B.

Ivabradin

lowers hospitalization risk for HF in pat. on sinus rhythm and EF ≤

35% where HR ≥ 70/min and symptoms (NYHA II.-IV.) despite

BB, ACEI (or ARB) and MRA.

II.a. B

May be to lower hospitalization risk for HF in patients on sinus

rhythm and EF ≤ 35% with HR ≥ 70/min, in BB intoleration.

Patients should be on ACEI(or ARB) and MRA.

II.b. B

Ivabradine NYHA II.-IV with systolic HF.


Other drugs (NYHA II.-IV.) systolic HF.

Hydralazin and Izosorbiddinitrate (H-ISDN) class level

As alternative for ACEI or ARB, if not netolerated, for

lowering of hospitalization risk of HF and lowering of

premature mortality risk in patients with EF ≤ 45% and LV

dilatation (or EF ≤ 35%). Patients should be on both BB

and MRA.

II. B

For lowering of hospitalization risk and premature mortality

of HF SZ with EF ≤ 45% and LV dilatation (or EF ≤ 35%)

with persistent symptoms (NYHA II.-IV.) despite BB, ACEI

(or ARB) and MRA.

II. B.


Farmakologic principles in HF:

SNS

RAAS

VazoconstrictionBlood pressurek

SympaticusAldosteroneHypertrophy

Fibrosis

Ang II AT1R

SYMPTOMS and

PROGRESSION HF

INACTÍVE

FRAGMENTs

NP system

VazodilatationBlood pressureSympaticusNatriuresis/diuresisVasopressineAldosteroneFibrosisHypertrophy

NPRs NPs

Epinephrin

Norepinephrineα1, β1, β2

receptors

VasoconstrictionRAAS activityVasopressine

Heart rate Contractility

Neprilysine

inhibítors

RAAS inhibitors

(ACEI, ARB, MRA)

β-blockers

A

Heart is an endocrinne organ, releasing natriuretic peptides as the

reaction to mechanic stress, with partially counteracts RAAS

Atrial natriuretic peptide (ANP)

Expression from atrias

Measured in plasma

NH2

COOH-

Vazodilatation

↑ Diuresis/natriuresis

↓ Proliferation

↓ Hypertrophy

↓ Aldosterone

↓ SNS

↓ CO preload

↑ Venous capacity

C-type natriuretic peptide (CNP)

Expressed in vascular endothelial

cells and central nervous system

Not detectable in plasma – primarily

synthesized in vasculature, acting

locally in tissues

NH2

COOH-

Vasodilatation

greater dilatation of veins, than ANP+

BNP

↓ Proliferation

Regulation of bome growthi

B-type natriuretic peptide (BNP)

Expression from atrias and

ventricles

Meased in plasma

NH2

COOH-

Vasodilatation

↑ Diuresis/natriuresis

↓ Aldosterone

↓ SNS

Vasodilatation

BP

SNS

Aldosterone

Fibrosis

Hypertrophy

Natriuresis/diuresis

Inactive

fragments

ANP, CNP, +other

vasoactive peptids

AT1 Receptor

Vasoconstriction

Blood pressure

Sympathetic tone

Aldosterone

Fibrosis

Hypertrophy

Angiotensinogen

(secrétion in

liver)

Ang I

Ang II

RAAS

Dual RAAS inhibition (ARB+NEPI)

Entresto

Sacubitril pro-drug

Inhibiting

zvýšenie

(NEP inhibitor)

OH

OHN

O

HO

O

Valsartan

N

NHN

N

N

O

OH

O

Entresto - first drug angiotensine receptor

neprilysine inhibitors (ARNI)

Entresto new treatment modality

simultanneous neprilysine inhibition

+ AT1 receptor blockade

Complex of two components:

– sacubitril – a pro-drug; metabolized to

neprilysine inhibítor and

– valsartan – AT1 receptor blocker

Ratio: 1:1 L

Symptoms Survival

Diuretics +++ -

ACEI/ARB ++ ++

BB + +

Digoxin + -

Antag.aldosterone ++ +

Amiodarone +- +-

Ivabradine + +

ARB+NEPI ++ ++

Oxygen + -

NEPI(Entresto) + +

SGLT2 inhibitors + +

Therapy algorithm

diuretics (improve symptoms and signs of congestion)

+

ACEI (ARB if ACEI intolerance)

adding BB

adding MRA

adding ivabradine

dual RAAS inhibition (ARB+NEPI)

other therapy (RSCH,ICD)

vazodilatation (H+ISDN) + digitalis

Tx

Pharmacokinetics of drugs

absorbtion

central compartment peripheral compartment

metabolism excretion

Pharmacokinetics od HF drugs

gut dysfunction absorbtion decreased distribution volume

central compartment peripheral compartment

metabolism excretion

liver dysfunction renal dysfunction

Farmacokinetics of HF

distribution volume

clearence

plasmatic drug concentrations in HF , than among

healthy → lowering of loading and maintenance

doses, longer time is needed for steady-state

reaching → slower drug titration

HF and RI are present together, have

common underlying causes (age, hyper-

tension, DM, atherosclerosis, comorbidi-

ties…) and as for disease of one organ

may lead to the dysfunction of other.

RI in HF is common.

Cave: limits effective drug doses usage.

Excessive diuresis - very common cause of RI in HF

For good control of edemas accept worsening of RI.

Clinical approach

chronic HF

+

cardiac cachexia

change in pfarmacokinetics of CV drugs

reevaluation of doses, but always in the context to clinical state

Chronic HF and cachexia

cachexia (3 from 5):

Weight loss at least decreased muscle strenght

5% of 12 months, fatigue, anorexia

or less index of free fat mass

(or BMI < 20kg/m²) abnormal biochemistry:

inflamm.marker.(CRP,IL-6)

anemia (Hb<12g/dl)

albuminemia(<3,2g/dl)

Evans: Cachexia-new definition. Clin Nutr.2008:27:793-799

Most common causes of HF worsening

Noncardial:

(noncompliance to therapy: salt, water, drugs)

Adverse effects of new prescribed drugs: (NSA,verapamil,AA)

Alcohol abuse

Renal dysfunction (excess of diuretics)

Infection

Pulmonary embolisation

Thyroid gland dysfunction (amiodarone)

Anemia (occult bleeding)

Cardial:

Atrial fibrillation

Other SV and V arrythmias

Bradycardia

Mitral/tricuspidal insufficiency (new, progressive, old)

Myocardial ischemia (often asymptomatic), incl. myocardial infarction

Excessive decrease of afterload (diuretics+ACEI)

Therapy of refractory HF

difficult, risky, cardiologist consider Tx

If volume overload:

FUR up to 480mg/d, direct salt restriction, iv, if N ren.ff spironolaktone carefully, during hospitalisation .iv dobutamine.

If exercise dyspnea:

+ hydralasine/nitrates, if lung congestion,↓BP nitrates

Hunt for states, worsening HF

+ revascularization

Surgery

Revascularisation and other cardiosurgery

Implantation of pacemaker/ICD

Ultrafiltration and hemodialysis

Resynchronic therapy

Supportive systems

Heart transplant

Complications

Arrythmias (myocardial,valvular,pericardial dis.)

Deep vein thrombosis (vein sthasis)

Tromboembolias (intracardiac thrombosis)

Vital organ failure (hypoxia)

Sudden cardiac death (malignant ventricular

arythmias)

Acute HF

It is the clinical syndrome with low minute volume,

tissue hypoperfusion, increased pulmonary

pressure and stasis in the tissues.

Acute heart failure

Evaluation of clinical manifestation

suddenly developed at rest

Evidence of myocardial dysfunction

disturbance of the function of the heart at rest

Response to treatment (if dg is questionable)

Suspicion of ac.heart failure

↓

ECG, X-ray (heart and lung)

↙ ↘

BNP/NT-pro BNP EchoCG

↙ ↘ ↓

ECG normal+ ECG abnormal+

NT-proBNP˂300 pg/ml NT-proBNP≥ 300pg/ml

BNP˂100pg/ml BNP≥100pg/ml

(HF not proved) if confirmed,

find ethiology

Clinical fenotypes of AHF

A. Ak.dekomp.HF (new,superponed on CHF)

B. Hypertension crisis with HF

C. Pulmonary oedema

D. Cardiogenic shock

E. HF with↑cardiac output (A,tyreotox.,sepsis)

F. Right HF with ↓minute volume

Clinical classification (Killip)

A. Without heart failure and sthasis

B. Failure with 3 heart sound,lung rales (lower 1/2)

C. Severe failure, lung rales above all lungs

D. Cardiogenic shock with hypotension, periferal

vasoconstriction, oligo/anuria, cyanosis

Clinical classification (Forrester)

A. Dry and warm (without congescion, hypoperfus.)

B. Wet and warm (with congestion and a.perfusion)

C. Wet and cold (with congesc.and hypoperfusion)

D. Dry and cold (with hypoperf., without congesc.)

AHF

Conditions of successful therapy of AHF is the

reversibility of disturbed myocardial function.

Liver tests

acute HF chronic HF

ALT ++

AST ++

AP

GMT ?

Bi celk

Albumine

Prognosis of AHF

Hospital mortality de novo AHF = 12%

decompensated CHF = 10%

Management of AHF

A. Symptom releaf

B. Hypervolemia reduction

C. Improvement of hemodynamics

D. Retention of perfusion of vital organs

Management of AHF

Primary care before hospitalisation

A. Posture of the patient (sitting, running legs)

B. Loading of turnstiles on the limbs

C. Oxygen

D. NTG s.l.

E. Bolus of furosemide

F. Sedatives if needed

G. Digoxin (atrial tachyfibrillation)

Management AHF

Hospital care

congestion

no yes

no warm and dry warm and wet

hypoperfusion diuretics

yes cold and dry cold and wet vazoD

inotropes ultrafiltration

mechanic circulation support

Perspective drugs for AHF

urodilatine

omecantiv mecarbil

cinaciquat

serelaxine

Documents

HF=cardiovascular problem No - uniba.sk · Normal heart HF Muscle weakness Organ hypoperfusion Pump failure Definition (pat.-physiol.) HF is the state, when the heart is not able