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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
0
2
4
6
8
10
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
LVEDP
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
Compensatory MechanismsCompensatory Mechanisms
Frank-Starling Mechanism
a. At rest, no HF
b. HF due to LV systolic dysfunction
c. Advanced HF
Compensatory MechanismsCompensatory Mechanisms
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
11--
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)…
CHRONIC HEART FAILURE CHRONIC HEART FAILURE Pharmacologic ManagementPharmacologic Management
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
CHRONIC HEART FAILURE CHRONIC HEART FAILURE Pharmacologic ManagementPharmacologic Management
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)
CHRONIC HEART FAILURE CHRONIC HEART FAILURE Pharmacologic ManagementPharmacologic Management
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
CHRONIC HEART FAILURE CHRONIC HEART FAILURE Pharmacologic ManagementPharmacologic Management
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
CHRONIC HEART FAILURE CHRONIC HEART FAILURE Pharmacologic ManagementPharmacologic Management
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
CHRONIC HEART FAILURE CHRONIC HEART FAILURE Pharmacologic ManagementPharmacologic Management
Inotropic agents
• Digoxin
• Catecholamines (dopamin - Tensamin, noradrenalin, dobutamin - Dobuject, adrenalin)
• Phosphodiesterase inhibitors (amrinon- Wincoram, milrinon - Corotrop)
• Ca-sensitizers (levosimendan - Simdax)
– improve symptoms, decrease mortality?
CHRONIC HEART FAILURE CHRONIC HEART FAILURE Pharmacologic ManagementPharmacologic Management
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
CHRONIC HEART FAILURE CHRONIC HEART FAILURE Pharmacologic ManagementPharmacologic Management
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
CHRONIC HEART FAILURE CHRONIC HEART FAILURE Non-pNon-pharmacologic harmacologic mmanagementanagement
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
CHRONIC HEART FAILURE CHRONIC HEART FAILURE Non-pNon-pharmacologic harmacologic mmanagementanagement
• 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
SuddenSuddenDeathDeath
n = 103n = 103
NYHA IIINYHA III
56%56%
11%11%
33%33%
CHFCHF
OtherOther
SuddenSuddenDeathDeath
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)
Cardiogenic shockCardiogenic shockAAMI - therapyMI - therapy
Cardiogenic shockCardiogenic shockAAMI - therapyMI - therapy
• Positive inotropic drugs– catecholamines (dopamin, dobutamin,
noradrenalin, adrenalin)– (phosphodiesterase inhibitors)– (levosimendan)
• Mechanical circulatory support– IABP, LVAD, Impella
Cardiogenic shockCardiogenic shockAAMI - therapyMI - therapy
• 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
ImpellaImpella
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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