Beruflich Dokumente
Kultur Dokumente
Manuel B. Zacarias, MD
02.19.08
Definition of Terms
v Cardiac output Quantity of blood pumped by the LV into the
aorta each minute (NV = 5L/min)
v Cardiac index CO/m2 (NV = 3.4L/min/m2; range of 2.8-4.2)
v Stroke volume End diastolic volume End systolic
volume
v Ejection fraction (SV/EDV) * 100 (NV = 60-75%)
Regulatory factors of myocardial contraction
v Preload
Load before ventricular contraction
Physiologically, the venous returne
The LVEDP
Wall stress at the end of diastole
v Afterload
The force resisting shortening of the myofibrils
v Contractility
Inotropic state
Accounts for alteration of performance induced by
hormonal and biochemical change
Increased when there is enhanced interaction between
calcium and contractile protein
Age
45-54
55-64
65-74
75-84
85-94
Men
2
4
9
18
39
Women
1
2
6
12
31
Cardiovascular Diagnosis
v Etiologic
v Anatomic
v Physiologic
v Functional Capacity (I-IV)
v Objective Assessment
No objective evidence of CVD
Objective evidence of minimal CVD
Objective evidence of moderately severe CVD
Objective evidence of severe CVD
Stages
Stage A
Stage B
Stage C
Stage D
Examples
v Stage A
Systemic HPN
CAD
DM
Cardiotoxic drug therapy or alcohol abuse
Personal history of rheumatic fever
Family history of cardiomyopathy
v Stage B
LVH or fibrosis
LV dilatation or hypocontractility
Asymptomatic valvular heart disease
Previous myocardial infarction
v Stage C
Dyspnea or fatigue due to LV systolic dysfunction
Asymptomatic patients who are undergoing
treatment for prior symptoms of HF
v Stage D
End stage disease who requires specialized
treatment strategies such as mechanical circulatory
support, continuous inotropic infusions, cardiac
transplantation, or hospice care
Lala 3C-Med-09
Acute MI
v 20-25% LV mass infarcted = LV dysfunction
v >40% LV mass infracted = cardiogenic shock
Systolic HF
v Impaired contractility leads to reduction in cardiac output.
This leads to fall in tissue perfusion, the activation of the
rennin-angiotensin and sympathetic nervous systems,
and eventually sodium and water retention
Heart failure
v Acute heart failure acute dyspnea with signs of pulmonary
congestion including pulmonary edema
v Cardiogenic shock low arterial pressure, oliguria, and cool
extremities
v Chronic HF punctuated by exacerbations
v Right HF syndromes presenting predominantly with
congestion of the systemic circulation
v Left HF syndromes presenting predominantly with
congestion of the pulmonary circulation
v Principal hallmark of HF
Systolic dysfunction: depressed LV EF (<40%)
Diastolic dysfunction: normal EF with impairment of one
ore more indices of ventricular filling
v Etiologies
Ischemic
Nonischemic
Unspecified
Specified
Idiopathic
Valvular
Hypertensive
Ethanol
Vital
Postpartum
Amyloidosis
Others
Frank-Starlings Law
v Intrinsic ability of the heart to adapt itself to changing
loads of inflowing blood
v Within physiologic limits, the heart pumps all the blood
that comes to it without allowing excessive damming of
blood in the veins
v Heterometric autoregulation
Cardiovascular continuum
Index Event
Acute MI
Gene mutation
Acute
inflammation
Onset of HPN
Valvular Heart
Disease
Others
Structural remodeling
and progression of
disease
Myocyte hypertrophy
Fibrosis, chamber
dilatation
Collagen shunt
dissolution
Cell drop out
(apoptosis)
Cell necrosis
Neuroendocrine
activation
Cytokine release
Increased wall
stretching
Chamber dysfunction
Clinical syndrome of
HF
Salt and water
retention
Congestion, edema
Low cardiac output
Diastolic dysfunction
Increasing
symptoms
HF as a progressive disorder
v LV dysfunction begins with some injury to the
myocardium and is usually a progressive process, even
in the absence of a new identifiable insult to the
myocardium
v The principal manifestation of such progression is a
process known as remodeling, which occurs in
association with homeostatic attempts to decrease wall
stress through increases in wall thickness, which
ultimately results in a change in the geometry of the LV
such that the chamber dilates, hypertrophies, and
becomes more spherical
v Cardiac remodeling
Generally precedes the development of symptoms,
occasionally by months or even years
Continues after the appearance of symptoms
May contribute importantly to worsening of
symptoms despite treatment
v Factors that contribute to LV remodeling
Neurohormones and cytokines
Increased LV volume and pressure
Myocardial cell elongation
Replacement and reactive collaged deposition (ie.
Increased collagen turnover)
Myocyte slippage secondary to dissolution of
collagen struts
Apoptosis
Necrosis
Myocardial infarct expansion
Dilation and reshaping of the LV
Ischemic cascade
v Coronary artery occlusion
v Diastolic abnormalities
v Systolic abnormalities
v Perfusion defects
v Hemodynamic abnormalities
v ECG changes
v Angina
Lala 3C-Med-09
Vascular Pathophysiology of HF
Pathophysiology
Terminal events in HF
v Systemic organ failure
v Pulmonary/ cerebral embolus
v Lethal arrhythmias
Neuroendocrine factors known to be increased in HF
Endothelin
Norepinephrine
Beta-endorphins
Epinephrine
Calcitonin gene-related peptide
Renin activity
Growth hormone
Angiotensin II
Cortisol
Aldosterone
TNF alpha
Arginine vasopressin
Neurokinin A
Neuropeptide Y
Substance P
VIP
Adrenomedullin
Prostaglandins
Brain natriuretic peptide
Atrial natriuretic factor
Assessment of patients with HF
v History and PE
v Diagnostic Studies
Laboratory tests
Electrocardiography
CXR
Exercise testing
ECG
Radionucleotide imaging
Cardiac catheterization
Endomyocardial biopsy
Lala 3C-Med-09
Dependent edema
Facial edema
Ascites
Hypoalbuminemia
Proteinuria
Cardiac
Severe
Absent
Hepatic
Moderate
Absent
Absent/
mild
Absent
Severe
Moderate/
Mild
Absent/
trace
Absent/
trace
Severe
Severe
Minor
Extremity edema
Night cough
Dyspnea on exertion
Hepatomegaly
Pleural effusion
Reduced vital capacity
Tachycardia (>120/min)
Urinalysis
Finding
Anemia
Serum creatinine
Proteinuria
RBCs or cellular
casts
Elevated failure
Serum albumin
Decreased
Abnormal T4 or TSH
PE findings
v CAP assessment
Normal: brisk, tapping
Sustained: plateau, dome-shaped, rising movement
v Sustained AB
LV outflow obstruction
Systemic HPN
Depressed systolic function
v Hepatojugular/ abdominojugular refex
Firm, sustained upper abdominal pressure
Patient breathing quietly
Normal transient 1cm JVP increase
HF: sustained elevation of JVP
v Cardiovascular edema
History of HPN/ heart disease
Primarily complaining of SOB
Peripheral
Renal
Mild
Severe/
moderate
Absent/ mild
Suspected
HF due to or
aggravated by
decreased O2carrying capacity
Nephritic syndrome
Glomerulonephritis
Volume overload
due to renal
dysfunction
Increased
extravascular
volume due to
hypoalbuminemia
HF due to or
aggravated by hypo/
hyperthyroidism
Myocardial ischemia
Thyroid disease or
HF due to rapid
ventricular rate
HF due to low heart
rate
HF due to reduced
contractile tissue
Pericardial effusion
Diastolic dysfunction
Chest X-ray
v Cardiomegaly
v Hilar vascular congestion
v Bronchial cuffing
v Cephalization of vessels
v Kinsley lines
Echocardiography
v Advantages
Permits concomitant assessment of valvular
disease, LVH, and LA size
Less expensive than radionucleotide
ventriculography in most areas
Able to detect pericardial effusion and ventricular
thrombus
More generally available
Lala 3C-Med-09
v Pharmacologic Therapy
Improvement of symptoms
v Disadvantages
Difficult to perform in patients with lung disease
Usually only semiquantitative estimate of ejection
fraction provided
Technically inadequate in up to 18% of patients under
optimal circumstances
Digoxin
Diuretics
Beta blockers
ACEI
ARB
Radionucleotide ventriculogram
v Advantages
More precise and reliable measurement of EF
Better assessment of right ventricular function
v Disadvantages
Requires venipuncture and radiation exposure
Limited assessment of valvular heart disease and LVH
Vascular Pathophysiology
v Vasoconstricting systems
Atrial Natriuretic Peptide (ANP)
Released from the atria (sometimes the ventricle) in
response to volume expansion (stretch)
ANP ANP receptor guanylate cyclase cGMP
Inhibit RAS and inhibit sympathetic activity
vasodilator
Promotes sodium excretion natriuresis and
diuresis
Brain Natriuretic Peptide (BNP)
Released from the brain (and ventricle) in response to
volume expansion (stretch)
Diagnosis of HF
Screening for diastolic HF
Predictor of HF
Prognosis of HF
Guide to therapy of HF
Prognosis in ACS
BNP > 100pg/mL = HF
Sensitivity 90%
Specificity - 76%
Predictive accuracy of 83%
General Principles of Treatment
v General Principles of Treatment
Correction of systemic factors
Lifestyle modification
Review drugs that my contribute to HF
Treatment of the cause of HF
Pharmacologic therapy
ACEI
ARB
Beta blockers
Spirinolactone/ eplerenone
Relief of symptoms
Slow progression
Improve survival
v Lifestyle modification
Stop smoking
Limit alcohol intake
Decrease salt intake : 2 to 3g sodium/day
Restrict water intake
Daily weight monitoring
Cardiac rehab, program for stable patients
Lala 3C-Med-09
v ARBs
Summary of Management
v Stage A High risk for developing HF but has no
structural disorder of the heart
Treat HPN
Smoking cessation
Treat dyslipidemia
Discourage alcohol and illicit drug use
ACEI in appropriate patients
v Stage B Structural disorder of the heart but who has
never developed symptoms of HF
All measures under stage A
ACEI in appropriate patients
Beta blockers in appropriate patients
v Stage C Past or current symptoms of HF associated
with underlying structural heart disease
All measures under stage A
Drugs for routine use: diuretics, ACEI, beta
blockers, digitalis
Salt restriction
v Stage D End stage disease who requires specialized
treatment strategies
All measures under stages A, B, C
Mechanical assist device
Heart transplant
Continuous IV inotropic infusion
Hospice care
HR < 60
Systolic arterial pressure <100 mmHg
PR interval > 0.24 sec
Second or third degree AV block
Severe COPD
History of asthma
Severe peripheral vascular disease
v
v
v
v
IV vasodilators
Nitroprusside
Nitroglycerine
Hemodynamic monitoring
Pacemakers
Hemofiltration
Mechanical circulatory support
Criteria for LV assist device implantation
v Surgery
v Cardiac Transplantation
Treatment of Associated Conditions
v Supraventricular arrhythmias
Rate control
Restoration of sinus rhythm
v Ventricular arrhythmias
v Anticoagulation
v Anemia
Methods
Venodilators, Diuretics, Morphine,
Tourniquet, Salt Restriction
Cardioversion of AF, Atrial antiarrhythmics,
Avoid atrial distension
Anti-HPN therapy
Anti-HPN therapy
Exercise limitation, beta blocker,
cardioversion of AF, rate control of AF
Anti-HPN therapy, Control HR, Beta
blocker, CACB, nitrates, revascularization
CACB? Beta blocker? ACEI?
Prognosis
v Less than 50% of patients will survive for 5 years after
the onset of heart failure
v Sudden cardiac death is responsible for approximately
1/3 of deaths in patients with heart failure
Lala 3C-Med-09