Transcript Cardiogenic shock

HEART FAILURE
Heart 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.
HEART FAILURE
• 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 Gender
United States: 1988-94
10
8
Percent of
Population
Males
Females
6
4
2
0
20-24 25-34 35-44 45-54 55-64 65-74
Source: NHANES III (1988-94), CDC/NCHS and the American Heart Association
75+
Diagnosis of heart failure
Typical symptoms and signs of
HF
Less typical signs and
symptoms of HF
Cardiac Output
• Cardiac output is the amount of blood that
the ventricle ejects per minute
Cardiac Output = HR x SV
Determinants of Ventricular Function
Contractility
Afterload
Preload
Stroke
Volume
• Synergistic LV Contraction
• Wall Integrity
• Valvular Competence
Heart Rate
Cardiac Output
Left Ventricular Dysfunction
Volume
Overload
Pressure
Overload
Loss of
Myocardium
Impaired
Contractility
LV Dysfunction
EF < 40%
 End Systolic Volume
 Cardiac
Output
Hypoperfusion
 End Diastolic Volume
Pulmonary Congestion
Hemodynamic Basis for
Heart Failure Symptoms
LVEDP 
Left Atrial Pressure 
Pulmonary Capillary Pressure 
Pulmonary Congestion
Hemodynamic Basis for
Heart Failure Symptoms
Compensatory Mechanisms
• Frank-Starling Mechanism
• Neurohormonal Activation
• Ventricular Remodeling
Compensatory Mechanisms
Frank-Starling Mechanism
a. At rest, no HF
b. HF due to LV systolic
dysfunction
c. Advanced HF
Compensatory Mechanisms
Neurohormonal Activation
• Sympathetic nervous system (SNS)
• Renin-angiotensin-aldosterone system
(RAAS)
• Vasopressin (a.k.a. antidiuretic hormone,
ADH)
Compensatory Mechanisms:
Sympathetic Nervous System
Decreased MAP
Sympathetic Nervous System
 Contractility
Tachycardia
Vasoconstriction
MAP = SV x HR
x TPR
Compensatory Mechanisms:
Renin-Angiotensin-Aldosterone (RAAS)
Angiotensinogen
Renin
Angiotensin I
Angiotensin
Converting
Enzyme
Angiotensin II
AT I receptor
Vasoconstriction
Oxidative Stress
Cell Growth
Vascular remodeling
LV remodeling
Proteinuria
Compensatory Mechanisms:
Renin-Angiotensin-Aldosterone (RAAS)
Renin-Angiotensin-Aldosterone
( renal perfusion)
Salt-water retention
Thirst
Sympathetic
augmentation
Vasoconstriction
MAP = SV x HR x
TPR
Compensatory Mechanisms:
Vasopressin
Decreased systemic blood pressure
Central baroreceptors
-
Increased systemic blood pressure
Vasoconstriction
Stimulation of hypothalamus, which produces
vasopressin for release by pituitary gland
Release of vasopressin by pituitary gland
Concentric remodelation
Excentric remodelation
Other 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 Vasoactive
Substances
Endothelium-derived relaxing factors (EDRF) –
Vasodilators:
• Nitric Oxide (NO)
• Bradykinin
• Prostacyclin
Endothelium-derived constricting factors (EDCF) –
Vasoconstrictors:
• Endothelin I
Cytokines
• Negative inotropes
• Elevated levels associated with worse
clinical outcomes
• Examples:
– Tumor necrosis factor (TNF)-alpha
– Interleukin 1-alpha
– Interleukin-2
– Interleukin-6
– Interferon-alpha
Neurohormonal Responses to Impaired
Cardiac Performance
Initially Adaptive, Deleterious if Sustained
Response
Short-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
Jaski, B, MD: Basics of Heart Failure: A Problem Solving Approach
Sympathetic Activation in Heart
Failure
 CNS sympathetic outflow
 Cardiac sympathetic
activity
1receptors
2receptors
 Sympathetic
activity to kidneys
+ peripheral vasculature
1receptors
Myocardial toxicity
Increased arrhythmias
1-
Activation
of RAS
Vasoconstriction
Sodium retention
Disease progression
Packer. Progr Cardiovasc Dis. 1998;39(suppl I):39-52.
1-
Vicious Cycle of Heart Failure
LV Dysfunction
Increased cardiac workload
(increased preload and afterload)
Increased cardiac output (via increased
contractility and heart rate)
Increased blood pressure (via vasoconstriction
and increased blood volume)
Decreased cardiac output
and
Decreased blood pressure
Frank-Starling Mechanism
Remodeling
Neurohormonal activation
CHRONIC HEART FAILURE
etiology
• Decreased contractility – IHD, DCMP,
infection, toxic agents…
• Pressure overload – hypertension, aortic
stenosis…
• Volume overload – aortic or mitral
regurgitation…
CHRONIC HEART FAILURE
symptoms
• Dyspnoe – on exertion, paroxysmal
nocturnal, at rest
• Fatigue, muscular weakness, oliguria,
cardiac cachexia
New York Heart Association
Functional 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
prognosis
Mortality
• NYHA II
• NYHA III
• NYHA IV
5-15%
20-25%
30-70%
CHRONIC HEART FAILURE
initial 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
General Measures
LifestyleModifications:
• Weight reduction
• Discontinue smoking
• Avoid alcohol and other cardiotoxic
substances
• Exercise
CHRONIC HEART FAILURE
General Measures
Medical Considerations:
• Treat HTN, hyperlipidemia, diabetes, arrhythmias
• Coronary revascularization
• Anticoagulation
• Immunization
• Sodium restriction
• Daily weights
• Close outpatient monitoring
CHRONIC HEART FAILURE
Pharmacologic 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
Pharmacologic 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
Heart Failure Management
Chronic HF
Diurese &
Home
Hospitalization
IV Lasix
or Admit
Emergency
Room
SOB
 Weight
MD’s Office
PO Lasix
CHRONIC HEART FAILURE
Pharmacologic 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
Pharmacologic 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
Pharmacologic 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
Pharmacologic 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
Pharmacologic Management
Inotropic agents
• Digoxin
• Catecholamines (dopamin - Tensamin,
noradrenalin, dobutamin - Dobuject, adrenalin)
• Phosphodiesterase inhibitors (amrinonWincoram, milrinon - Corotrop)
• Ca-sensitizers (levosimendan - Simdax)
– improve symptoms, decrease mortality?
CHRONIC HEART FAILURE
Pharmacologic 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
Pharmacologic 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
Non-pharmacologic management
Cardiac 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 Atrial
Lead
Right Ventricular
Lead
Left Ventricular
Lead
CHRONIC HEART FAILURE
Non-pharmacologic management
Cardiac 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
Non-pharmacologic management
• Left-ventricle assisst devices (LVAD)
• Implantable cardioverter-defibrilator (ICD)
• Cellular therapy??
• Heart transplantation
CHRONIC HEART FAILURE
Non-pharmacologic management – 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
CHRONIC HEART FAILURE
Modes of Death
NYHA II
NYHA III
CHF
CHF
12%
Other
26%
59%
Sudden
Death
24%
64%
Other
15%
n = 103
Sudden
Death
n = 103
NYHA IV
CHF
Other
33%
56%
11%
Sudden
Death
n = 27
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). LANCET. 1999;353:2001-07.
ACUTE HEART FAILURE
definition, 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 FAILURE
• Asthma cardiale
• Pulmonary oedema
– Intersticial (> 25 mmHg)
– Alveolar (> 35 mmHg)
• Cardiogenic shock
ACUTE HEART FAILURE
pulmonary oedema
symptoms, 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
pulmonary 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 FAILURE
causes
• Pressure overload
– Precapillar pulmonary hypertension (PH) –
Primary right HF
– Postcapillar PH
• Volume overload (L-R shunt)
• Decreased contractility
RIGHT HEART FAILURE
cor pulmonale
hypertrophy and dilatation of right
ventricle, caused by pre-capillar PH in
diseases of lungs, pleura, thoracic wall or
pulmunary vasculature
RIGHT HEART FAILURE
forms
• Hypoxic (COPD)
• Restrictive (pulmonary fibrosis,
pneumoconiosis, resection of lungs)
• Vascular (pulmonary embolism, primary
pulmonary hypertension, ARDS)
RIGHT HEART FAILURE
symptoms, 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
hypoxic 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
restrictive form
• Vital capacity 80-50%  latent PH
• Vital capacity below 50%  rest PH
• Therapy – management of primary disease
PRIMARY RIGHT HEART FAILURE
vascular form
• Pulmonary embolism
– Dg.: history, physical exam., ECG, angioCT,
ventilatory-perfusion scan, pulmonary
angiography, ECHO
– Therapy: anticoagulation, thrombolysis
PRIMARY RIGHT HEART FAILURE
vascular form
• Primary PH
– Rare disease, mid-age women
– Therapy:
•
•
•
•
Ca-antagonists
Prostacyklin
Bosentan (antagonist ET-1 R)
Sildenafil
SHOCK
SHOCK
definition
• acute circulatory failure with inadequate
perfusion of vital tissues systemically,
leading to generalized tissue hypoxia.
SHOCK
basic signs
•
•
•
•
•
•
Hypotension
Increased heart rate
Decreased diuresis
Pale, cool skin
Metabolic acidosis
Cerebral dysfunction
SHOCK
classification
• 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 shock
• Sympathetic stimulation (catecholamines)
• Neuroendocrine stimulation (cortisol)
• Inflammatory mediators (cytokines,
complement, arachidonic acid
metabolites, lysosomal enzymes,
vasoactive mediators)
• Toxic agents
SHOCK
therapeutic 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 monitoring
Swan-Ganz catheter
Hemodynamic 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)
SHOCK
therapy
• Aim: restoration of tissue oxygen supply
with simultaneous effort to eliminate cause
of shock
• Intravenous administration of drugs !!!
(intramuscular medication should be
avoided)
SHOCK
therapy - 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
SHOCK
therapy - circulatory support
• Positive inotropic drugs
– catecholamines (dopamin, noradrenalinnorepinephrin, dobutamin, adrenalin-epinephrin)
– phosphodiesterase inhibitors (amrinon, milrinon)
– digoxin
– Ca-sensitizers (levosimendan) ?
• Non-pharmacological circulatory support
– IABP – intraaortic baloon counterpulsation
– LVAD, Impella
SHOCK
therapy - other methods
•
•
•
•
•
Surgery (abscess drainage, stop bleeding)
Catheterization, endoscopy
Antibiotics
Hemodialysis
Correction of mineral and acidobasis
dysbalances
• Ventilatory support
– Intubation
– Artefitial pulmonary ventilation
Cardiogenic shock
Pulmonary 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
Hypovolemic shock
• Hemorrhage, burns, trauma to major
vessels
•  CVP,  PCWP,  MAP,  HR,
 SVR
• Therapy
– Prevention of volume loss progression
– Volume replacement
Distribuive shock
septic 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 shock
• Myocardial (acute myocardial infarction,
myocarditis, cardiomyopathy)
• Mechanical (acute valvular dysfunction)
• Arrhythmogenic
• Obstructive (pulmonary embolism,
cardiac tamponade)
Cardiogenic shock
pathogenesis
• 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 shock
monitoring
• 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 shock
Acute 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 shock
Acute myocardial infarction
•  MAP,  CO (CI),  PCWP
• Diagnosis
– History
– Physical examination
– ECG, ECHO
Cardiogenic shock
AMI - 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 shock
AMI - therapy
Cardiogenic shock
AMI - therapy
• Positive inotropic drugs
– catecholamines (dopamin, dobutamin,
noradrenalin, adrenalin)
– (phosphodiesterase inhibitors)
– (levosimendan)
• Mechanical circulatory support
– IABP, LVAD, Impella
Cardiogenic shock
AMI - 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
(IABP)
Impella
Impella
Impella
TandemHeart
• Inflow Oxygenated blood
from the left atrium
– transseptal
cannulation.
• Pump –
Magnetically
driven, six-bladed
impeller
• Outflow - One or
both femoral
arteries via arterial
•cannulas.
Extra-Corporeal Membrane Oxygenator
Cardiogenic shock
Arrhythmogenic
• Causal therapy (AMI, poisoning)
• Symptomatic therapy
– Antiarrhythmic drugs
– DC cardioversion
– Temporary pacemaker
Cardiogenic shock
Cardiac tamponade
• Diagnosis: history, physical examination,
ECG, ECHO
• Therapy
– Pericardiocentesis
– Surgical drainage
– Causal therapy