heart failure. heart failure (hf) definition a complex clinical syndrome in which the heart is...

HEART FAILUREHEART FAILURE

Heart Failure (HF) DefinitionHeart Failure (HF) Definition

A complex clinical syndrome in which the heart is incapable of maintaining a cardiac output adequate to accommodate metabolic requirements and the venous return.

HHEART EART FFAILUREAILURE

• Prevalence 1-2%• Incidence 1-3 new cases annually per

1000 inhabitants• Causes

– IHD 70%– Other myocardial diseases incl.

cardiomyopathy 10-15%– Valvular heart disease 10%– Hypertension 6-10%

Prevalence of HF by Age and GenderPrevalence of HF by Age and Gender

United States: 1988-94

Percent of Population

20-24 25-34 35-44 45-54 55-64 65-74 75+

MalesFemales

Source: NHANES III (1988-94), CDC/NCHS and the American Heart AssociationSource: NHANES III (1988-94), CDC/NCHS and the American Heart Association

Diagnosis of heart failure

Typical symptoms and signs of HF

Less typical signs and symptoms of HF

Cardiac OutputCardiac Output

• Cardiac output is the amount of blood that the ventricle ejects per minute

Cardiac Output = HR x SV

StrokeStrokeVolumeVolume

PreloadPreload AfterloadAfterload

ContractilityContractility

Cardiac OutputCardiac Output

Heart RateHeart Rate• Synergistic LV ContractionSynergistic LV Contraction• Wall IntegrityWall Integrity• Valvular CompetenceValvular Competence

Determinants of Ventricular FunctionDeterminants of Ventricular Function

Volume Volume OverloadOverload

Pressure Pressure OverloadOverload

Loss of Loss of MyocardiumMyocardium

Impaired Impaired ContractilityContractility

LV DysfunctionLV DysfunctionEF < 40%EF < 40%

Cardiac Cardiac OutputOutput

Hypoperfusion Hypoperfusion

End Systolic Volume End Systolic Volume

End Diastolic Volume End Diastolic Volume

Pulmonary Congestion Pulmonary Congestion

Left Ventricular DysfunctionLeft Ventricular Dysfunction

Hemodynamic Basis forHemodynamic Basis forHeart Failure SymptomsHeart Failure Symptoms

Left Atrial Pressure

Pulmonary Capillary Pressure

Pulmonary Congestion

Hemodynamic Basis for Hemodynamic Basis for Heart Failure SymptomsHeart Failure Symptoms

Compensatory MechanismsCompensatory Mechanisms

• Frank-Starling Mechanism

• Neurohormonal Activation

• Ventricular Remodeling

Frank-Starling Mechanism

a. At rest, no HF

b. HF due to LV systolic dysfunction

c. Advanced HF

Neurohormonal Activation

• Sympathetic nervous system (SNS)

• Renin-angiotensin-aldosterone system (RAAS)

• Vasopressin (a.k.a. antidiuretic hormone, ADH)

MAP = MAP = SV x SV x HRHR x x TPRTPR

Sympathetic Nervous SystemSympathetic Nervous System

ContractilityContractility TachycardiaTachycardia VasoconstrictionVasoconstriction

Compensatory Mechanisms: Compensatory Mechanisms: Sympathetic Nervous SystemSympathetic Nervous System

Decreased MAPDecreased MAP

VasoconstrictionVasoconstriction

Oxidative StressOxidative Stress

Cell GrowthCell Growth ProteinuriaProteinuria

LV remodelingLV remodeling

Vascular remodelingVascular remodeling

AngiotensinogenAngiotensinogen

Angiotensin IAngiotensin I

Angiotensin IIAngiotensin II

AT I receptorAT I receptor

ReninRenin

AngiotensinAngiotensinConvertingConverting

EnzymeEnzyme

Compensatory Mechanisms: Compensatory Mechanisms: Renin-Angiotensin-Aldosterone Renin-Angiotensin-Aldosterone

(RAAS)(RAAS)

MAP = MAP = SV x SV x HR x HR x TPRTPR

Renin-Angiotensin-AldosteroneRenin-Angiotensin-Aldosterone(( renal perfusion) renal perfusion)

Salt-water retentionSalt-water retentionThirstThirst

SympatheticSympatheticaugmentationaugmentation VasoconstrictionVasoconstriction

Compensatory Mechanisms: Compensatory Mechanisms: Renin-Angiotensin-Aldosterone Renin-Angiotensin-Aldosterone

(RAAS)(RAAS)

Decreased systemic blood pressureDecreased systemic blood pressure

Central baroreceptorsCentral baroreceptors

Stimulation of hypothalamus, which producesStimulation of hypothalamus, which producesvasopressin for release by pituitary glandvasopressin for release by pituitary gland

Release of vasopressin by pituitary glandRelease of vasopressin by pituitary glandVasoconstrictionVasoconstriction

Increased systemic blood pressureIncreased systemic blood pressure

Compensatory Mechanisms: Compensatory Mechanisms: VasopressinVasopressin

Concentric remodelationConcentric remodelation

Excentric remodelationExcentric remodelation

Other NeurohormonesOther Neurohormones

• Natriuretic Peptides– Atrial Natriuretic Peptide (ANP)

• Predominantly found in the atria• Diuretic and vasodilatory properties

– Brain Natriuretic Peptide (hBNP) • Predominantly found in the cardiac ventricles • Diuretic and vasodilatory properties

Endothelium-derived relaxing factors (EDRF) – Vasodilators:

• Nitric Oxide (NO)• Bradykinin• Prostacyclin

Endothelium-derived constricting factors (EDCF) – Vasoconstrictors:

• Endothelin I

Endothelium-Derived Vasoactive Endothelium-Derived Vasoactive SubstancesSubstances

CytokinesCytokines

• Negative inotropes

• Elevated levels associated with worse clinical outcomes

• Examples:– Tumor necrosis factor (TNF)-alpha– Interleukin 1-alpha– Interleukin-2– Interleukin-6– Interferon-alpha

Initially Adaptive, Deleterious if SustainedInitially Adaptive, Deleterious if Sustained

ResponseShort-Term Effects

Long-Term Effects

Salt and Water Retention Augments Preload Pulmonary Congestion, Anasarca

Vasoconstriction Maintains BP for perfusion of vital organs

Exacerbates pump dysfunction (excessive afterload), increases cardiac energy expenditure

Sympathetic Stimulation Increases HR and ejection

Increases energy expenditure

Neurohormonal Responses to ImpairedNeurohormonal Responses to ImpairedCardiac PerformanceCardiac Performance

Jaski, B, MD: Jaski, B, MD: Basics of Heart Failure: A Problem Solving ApproachBasics of Heart Failure: A Problem Solving Approach

Packer. Progr Cardiovasc Dis. 1998;39(suppl I):39-52.Packer. Progr Cardiovasc Dis. 1998;39(suppl I):39-52.

CNS sympathetic outflowCNS sympathetic outflow

Disease progressionDisease progression

Cardiac sympatheticCardiac sympatheticactivityactivity

receptorsreceptors22--

receptorsreceptors11--

receptorsreceptors

VasoconstrictionVasoconstrictionSodium retentionSodium retention

Myocardial toxicityMyocardial toxicityIncreased arrhythmiasIncreased arrhythmias

SympatheticSympatheticactivity to kidneysactivity to kidneys

+ peripheral vasculature+ peripheral vasculature

ActivationActivationof RASof RAS

11-- 11--

Sympathetic Activation in Heart Sympathetic Activation in Heart FailureFailure

LV DysfunctionLV Dysfunction

Decreased cardiac outputDecreased cardiac outputand and

Decreased blood pressureDecreased blood pressure

Frank-Starling MechanismFrank-Starling MechanismRemodelingRemodeling

Neurohormonal activationNeurohormonal activation

Increased cardiac output (via increasedIncreased cardiac output (via increasedcontractility and heart rate)contractility and heart rate)

Increased blood pressure (via vasoconstrictionIncreased blood pressure (via vasoconstriction and increased blood volume) and increased blood volume)

Increased cardiac workloadIncreased cardiac workload(increased preload and afterload)(increased preload and afterload)

Vicious Cycle of Heart FailureVicious Cycle of Heart Failure

CHRONIC HEART FAILURECHRONIC HEART FAILUREetiologyetiology

• Decreased contractility – IHD, DCMP, infection, toxic agents…

• Pressure overload – hypertension, aortic stenosis…

• Volume overload – aortic or mitral regurgitation…

CHRONIC HEART FAILURE CHRONIC HEART FAILURE symptomssymptoms

• Dyspnoe – on exertion, paroxysmal nocturnal, at rest

• Fatigue, muscular weakness, oliguria, cardiac cachexia

New York Heart Association New York Heart Association Functional ClassificationFunctional Classification

Class I: No symptoms with ordinary activity

Class II: Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, dyspnea, or angina

Class III: Marked limitation of physical activity. Comfortable at rest, but less than ordinary physical activity

results in fatigue, palpitation, dyspnea, or anginal pain

Class IV: Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency may be present even at rest

CHRONIC HEART FAILURE CHRONIC HEART FAILURE prognosisprognosis

Mortality

• NYHA II 5-15%

• NYHA III 20-25%

• NYHA IV 30-70%

CHRONIC HEART FAILURE CHRONIC HEART FAILURE initial work-upinitial work-up

• Patient history

• Physical examination

• BP, ECG, chest X-ray, ECHO, SpO2

• minerals, creatinin, BNP, blood count

• (Coronary angiography, stress test...)

CHRONIC HEART FAILURE CHRONIC HEART FAILURE General MeasuresGeneral Measures

LifestyleModifications:

• Weight reduction

• Discontinue smoking

• Avoid alcohol and other cardiotoxic substances

• Exercise

CHRONIC HEART FAILURE CHRONIC HEART FAILURE General MeasuresGeneral Measures

Medical Considerations:

• Treat HTN, hyperlipidemia, diabetes, arrhythmias

• Coronary revascularization

• Anticoagulation

• Immunization

• Sodium restriction

• Daily weights

• Close outpatient monitoring

CHRONIC HEART FAILURE CHRONIC HEART FAILURE Pharmacologic ManagementPharmacologic Management

ACE Inhibitors

• Blocks the conversion of angiotensin I to angiotensin II; prevents functional deterioration

• Recommended for all heart failure patients

• Relieves symptoms and improves exercise tolerance

• Reduces risk of death and decreases disease progression

• Captopril (Capoten), enalapril (Enap), perindopril (Prestarium), ramipril (Tritace), trandolapril (Gopten)…

Diuretics

• Used to relieve fluid retention

• Improve exercise tolerance

• Patients can be taught to adjust their diuretic dose based on changes in body weight

• Electrolyte depletion a frequent complication

The Vicious Cycle of The Vicious Cycle of Heart Failure ManagementHeart Failure Management

Chronic HFChronic HF

MD’s OfficeMD’s Office

Emergency Emergency RoomRoom

HospitalizationHospitalization

SOBSOB

WeightWeight

PO LasixPO LasixIV Lasix IV Lasix or Admitor Admit

Diurese & Diurese & HomeHome

Beta-Blockers

• Cardioprotective effects due to blockade of excessive SNS stimulation

• In the short-term, beta blocker decreases myocardial contractility; increase in EF after 1-3 months of use

• Reduce the combined risk of morbidity and mortality, or disease progression

• Metoprolol SR (Betaloc ZOK), bisoprolol (Concor COR), carvedilol (Dilatrend)

Digoxin

• Slightly enhances inotropy of cardiac muscle

• Reduces activation of SNS and RAAS

• Reduces symptoms, Increases exercise tolerance

• Reduces hospitalization rates for decompensated HF

• Does not improve survival

Aldosterone Antagonists

• Shown to reduce heart failure-related morbidity and mortality

• Generally reserved for patients with NYHA Class III-IV HF

• Side effects include hyperkalemia and gynecomastia. Potassium and creatinine levels should be closely monitored

• spironolacton (Verospiron), eplerenon

Angiotensin Receptor Blockers (ARBs)

• Block AT1 receptors, which bind circulating angiotensin II

• In clinical practice, ARBs should be used to treat patients who are ACE intolerant due to intractable cough or who develop angioedema

• valsartan, telmisartan, candesartan, losartan

Inotropic agents

• Digoxin

• Catecholamines (dopamin - Tensamin, noradrenalin, dobutamin - Dobuject, adrenalin)

• Phosphodiesterase inhibitors (amrinon- Wincoram, milrinon - Corotrop)

• Ca-sensitizers (levosimendan - Simdax)

– improve symptoms, decrease mortality?

Other drugs

• Statins

• Antiarrhythmics

• Drugs under clinical investigation– neutral endopeptidase inhibitors

– natriuretic peptides agonists

– endothelin receptor inhibitors

– vasopressin antagonists (tolvaptan)

– renin inhibitors (aliskiren)

– cytokin modulators

Therapeutic strategy• Asympt. LV dysfunction non-ischemic etiol.

– ACEI

• Asympt. LV dysfunction ischem. etiol.

– ACEI, BB, ASA

• NYHA II-III, EF 20-40%

– ACEI, BB, diuretics, (ASA, digoxin, AC)

• NYHA II-III, EF < 20%

– ACEI, BB, diuretics, digoxin, spironolacton, (ASA, AC)

• NYHA IV

– ACEI, BB, diuretics, digoxin, spironolacton, (ASA, AK, nitrates, inotrops?)

CHRONIC HEART FAILURE CHRONIC HEART FAILURE Non-pNon-pharmacologic harmacologic mmanagementanagement

Cardiac resynchronization therapyCardiac resynchronization therapy

– Standard pacing lead in RA and RV– Specially designed left heart lead placed in a left

ventricular cardiac vein via the coronary sinus

Right AtrialRight AtrialLeadLead

Right VentricularRight VentricularLeadLead

Left VentricularLeft VentricularLeadLead

Cardiac resynchronization therapyCardiac resynchronization therapy

• Abnormal interventricular septal wall motion1

• Reduced dP/dt3,4

• Reduced pulse pressure4

• Reduced EF and CO4

• Reduced diastolic filling time1,2,4

• Prolonged MR duration1,2,4

• Left-ventricle assisst devices (LVAD)

• Implantable cardioverter-defibrilator (ICD)

• Cellular therapy??

• Heart transplantation

CHRONIC HEART FAILURE CHRONIC HEART FAILURE Non-pNon-pharmacologic harmacologic mmanagementanagement – cell Tx – cell Tx

Ideally, „stem cell therapy“ should:• enhance the number of functional (cardio)myocytes• enhance systolic and diastolic function of the heart• reduce LV dilatation and remodeling• be safely administered

First clinical experiences are, however, rather unconvincing

MERIT-HF Study Group. Effect of Metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL randomized MERIT-HF Study Group. Effect of Metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL randomized intervention trial in congestive heart failure (MERIT-HF). intervention trial in congestive heart failure (MERIT-HF). LANCET. LANCET. 1999;353:2001-07.1999;353:2001-07.

CHRONIC HEART FAILURE CHRONIC HEART FAILURE Modes of DeathModes of Death

12%12%

24%24%

64%64%

CHFCHF

OtherOther

SuddenSuddenDeathDeath

n = 103n = 103

NYHA IINYHA II

26%26%

15%15%

59%59%

CHFCHF

OtherOther

n = 103n = 103

NYHA IIINYHA III

56%56%

11%11%

33%33%

CHFCHF

OtherOther

n = 27n = 27

NYHA IVNYHA IV

ACUTE HEART FAILUREACUTE HEART FAILUREdefinition, causesdefinition, causes

• Definition: rapid onset of symptoms and signs, caused by abnormal cardiac performance

• New onset: acute MI, mechanical complication of AMI, acute valvular regurgitation, acute arrhythmias, acute myocarditis, hypertensive crisis, severe aortic stenosis, cardiac tamponade, aortic dissection

• Decompensation of chronic HF

ACUTE HEART FAILUREACUTE HEART FAILURE

• Asthma cardiale

• Pulmonary oedema– Intersticial (> 25 mmHg)– Alveolar (> 35 mmHg)

• Cardiogenic shock

ACUTE HEART FAILURE ACUTE HEART FAILURE pulmonary oedemapulmonary oedema

symptoms, signs, testsymptoms, signs, test

• Dyspnoe, ortopnoe, cough, anxiety, paleness, sweating

• Physical examination: pulmonary crackles, whistles, tachycardia, gallop

• BP, ECG, chest X-ray, ECHO, SpO2

• CRP, electrolytes, creatinin, BNP, blood count, troponin, blood gases

ACUTE HEART FAILURE ACUTE HEART FAILURE pulmonary oedema - therapypulmonary oedema - therapy

• Oxygen – mask, CPAP, non-invasive ventilation support, ventilation support

• Diuretics – i.v. furosemide• Vasodilatation – i.v. nitrates, nitroprusside,

(nesiritid)• Levosimendan• Causal therapy of acute HF

• Morphin, syntophyllin, antiarrhythmics, pacing, cardioversion…

RIGHT HEART FAILURERIGHT HEART FAILUREcausescauses

• Pressure overload– Precapillar pulmonary hypertension (PH) –

Primary right HF– Postcapillar PH

• Volume overload (L-R shunt)

• Decreased contractility

RIGHT HEART FAILURERIGHT HEART FAILURE cor pulmonalecor pulmonale

hypertrophy and dilatation of right ventricle, caused by pre-capillar PH in diseases of lungs, pleura, thoracic wall or pulmunary vasculature

RIGHT HEART FAILURERIGHT HEART FAILURE formsforms

• Hypoxic (COPD)

• Restrictive (pulmonary fibrosis, pneumoconiosis, resection of lungs)

• Vascular (pulmonary embolism, primary pulmonary hypertension, ARDS)

RIGHT HEART FAILURERIGHT HEART FAILUREsymptoms, signssymptoms, signs

• Dyspnoe

• Systemic venous congestion– Increased jugular vein filling– Hepato-jugular reflux– Hepatomegaly– Cardiac swelling (according to the highest

hydrostatic pressure)– Anasarca

PRIMARY RIGHT HEART FAILURE PRIMARY RIGHT HEART FAILURE hypoxic form - COPDhypoxic form - COPD

• Chronic bronchitis (with obstruction), emphysema

• Respiratory insuficiency hypoxia PH right HF (cor pulmonale chronicum)

• Therapy– therapy of COPD– oxygen therapy

PRIMARY RIGHT HEART FAILURE PRIMARY RIGHT HEART FAILURE restrictive formrestrictive form

• Vital capacity 80-50% latent PH

• Vital capacity below 50% rest PH

• Therapy – management of primary disease

PRIMARY RIGHT HEART FAILURE PRIMARY RIGHT HEART FAILURE vascular formvascular form

• Pulmonary embolism– Dg.: history, physical exam., ECG, angioCT,

ventilatory-perfusion scan, pulmonary angiography, ECHO

– Therapy: anticoagulation, thrombolysis

PRIMARY RIGHT HEART FAILURE PRIMARY RIGHT HEART FAILURE vascular formvascular form

• Primary PH– Rare disease, mid-age women– Therapy:

• Ca-antagonists• Prostacyklin• Bosentan (antagonist ET-1 R)• Sildenafil

SHOCKSHOCK

SHOCKSHOCKdefinitiondefinition

• acute circulatory failure with inadequate perfusion of vital tissues systemically, leading to generalized tissue hypoxia.

SHOCKSHOCKbasic signsbasic signs

• Hypotension

• Increased heart rate

• Decreased diuresis

• Pale, cool skin

• Metabolic acidosis

• Cerebral dysfunction

SHOCKSHOCKclassificationclassification

• Cardiogenic shock• Complication of acute myocardial infarction

• Obstructive shock• Pulmonary embolism• Cardiac tamponade

• Hypovolemic shock• Blood loss (hemorrhage, burns)

• Distributive shock• Septic shock

Modulators of shockModulators of shock

• Sympathetic stimulation (catecholamines)

• Neuroendocrine stimulation (cortisol)

• Inflammatory mediators (cytokines, complement, arachidonic acid metabolites, lysosomal enzymes, vasoactive mediators)

• Toxic agents

SHOCKSHOCKtherapeutic targetstherapeutic targets

• (i) basic life function support

• (ii) assessment and therapy of the cause of shock

• (iii) prevention of damage extension– Multiple organ dysfunction syndrome

Hemodynamic monitoringHemodynamic monitoringSwan-Ganz catheterSwan-Ganz catheter

HemodynamiHemodynamic parametersc parameters• CVP (central venous pressure) 0-7 mmHg

• PCWP (pulmonary capillary wedge pressure) 6-12 mmHg

• CO (cardiac output, SVxHR) 4-8 L/min

• CI (cardiac index, CO/body surface) 2.5-4.2 L/min/m2

• MAP (mean arterial pressure) optimum at least 75-80 mmHg

• SVR (systemic vascular resistance)

• PVR (pulmonary vascular resistance)

SHOCKSHOCKtherapytherapy

• Aim: restoration of tissue oxygen supply with simultaneous effort to eliminate cause of shock

• Intravenous administration of drugs !!! (intramuscular medication should be avoided)

SHOCKSHOCKtherapy - circulatory supporttherapy - circulatory support

• Optimum - MAP 75-80 mmHg

• Volume replacement– Blood (red blood cells, plasma)– Crystaloides (saline, solution Ringer)– Colloides (HAES - hydroxy aethyl starch),

polygelatines (Haemaccel), dextranes (Rheodextran), human albumin

SHOCKSHOCKtherapy - circulatory supporttherapy - circulatory support

• Positive inotropic drugs– catecholamines (dopamin, noradrenalin-norepinephrin,

dobutamin, adrenalin-epinephrin)– phosphodiesterase inhibitors (amrinon, milrinon)– digoxin– Ca-sensitizers (levosimendan) ?

• Non-pharmacological circulatory support – IABP – intraaortic baloon counterpulsation– LVAD, Impella

SHOCKSHOCKtherapy - other methodstherapy - other methods

• Surgery (abscess drainage, stop bleeding)• Catheterization, endoscopy• Antibiotics• Hemodialysis• Correction of mineral and acidobasis

dysbalances• Ventilatory support

– Intubation– Artefitial pulmonary ventilation

Cardiogenic shockCardiogenic shockPPulmonary embolismulmonary embolism

PAP, CVP, PCWP• Diagnosis: history, physical examination,

ECG, ECHO, laboratory investigation (CT angio, pulmonary angiography, perfusion scan)

• Therapy – Thrombolysis– Catheterization or surgical intervention– Anticoagulation

HypovolemicHypovolemic shock shock

• Hemorrhage, burns, trauma to major vessels

CVP, PCWP, MAP, HR, SVR

• Therapy– Prevention of volume loss progression– Volume replacement

DistribuDistribuive shockive shocksepticseptic shock shock

• SIRS, sepsis, inflammation mediated damage SVR, HR, CO (CI)• Mikrobiological examination (blood, sputum, urine,

skin, abscess, etc.)• Therapy

– Antibiotics, therapy of the source of infection– Increase of SVR (catecholamines - noradrenalin, volume

replacement)– Hemodialysis

Cardiogenic shockCardiogenic shock

• Myocardial (acute myocardial infarction, myocarditis, cardiomyopathy)

• Mechanical (acute valvular dysfunction)

• Arrhythmogenic

• Obstructive (pulmonary embolism, cardiac tamponade)

Cardiogenic shock Cardiogenic shock pathogenesispathogenesis

• Stage I– Vasoconstriction (skin)– Preserve perfusion of vital organs

• Stage II– Decreased organ perfusion– Marked deterioration of tissue metabolism– Organ failure

• Stage III– Irreversible microcirculation failure– Severe tissue hypoxia, acidosis– Cell death

Cardiogenic shockCardiogenic shockmonitormonitoringing

• Clinical monitoring (mental functions, pulse, BP, respiration, diuresis, fluid balance, skin perfusion)

• ECG

• Arterial catheter (invasive BP measurement, blood gases)

• Swan-Ganz catheter

• Chest X-rays

• Biochemical and haematological tests

Cardiogenic shockCardiogenic shockAAcute myocardial infarction (AMI)cute myocardial infarction (AMI)

• 5-8% of patients with AMI

• Damage > 40% of left ventricle

• Mortality 50-90%

• Myocardial

• Arrhythmogenic

• „Mechanical complications“ of AMI (acute mitral regurgitation, free-wall rupture of LV, interventricular septal defect)

Cardiogenic shockCardiogenic shockAAcute myocardial infarctioncute myocardial infarction

MAP, CO (CI), PCWP

• Diagnosis– History– Physical examination– ECG, ECHO

Cardiogenic shockCardiogenic shockAAMI - therapyMI - therapy

• SHOCK trial

early invasive x early conservative management

early invasive approach superior

• Percutaneous coronary intervention– Open closed coronary artery (coronary

angioplasty/stent implantation)

• Positive inotropic drugs– catecholamines (dopamin, dobutamin,

noradrenalin, adrenalin)– (phosphodiesterase inhibitors)– (levosimendan)

• Mechanical circulatory support– IABP, LVAD, Impella

• Surgical intervention of mechanical complications– Valvuloplasty or valve replacement (mitral

regurgitation caused by papillary muscle rupture)

– Resection and/or patch of LV (LV rupture, septal defect)

Intra-Aortic Balloon Pulsation Intra-Aortic Balloon Pulsation (IABP)(IABP)

ImpellaImpella

TandemHeartTandemHeart

• Inflow - Oxygenated bloodfrom the left atrium – transseptal cannulation.• Pump – Magnetically driven, six-bladed impeller• Outflow - One or both femoral arteries via arterial•cannulas.

Extra-Corporeal Membrane OxygenatorExtra-Corporeal Membrane Oxygenator

Cardiogenic shockCardiogenic shockArArrhythmogenicrhythmogenic

• Causal therapy (AMI, poisoning)

• Symptomatic therapy– Antiarrhythmic drugs– DC cardioversion– Temporary pacemaker

Cardiogenic shockCardiogenic shockCardiac tamponadeCardiac tamponade

• Diagnosis: history, physical examination, ECG, ECHO

• Therapy – Pericardiocentesis– Surgical drainage– Causal therapy

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