Transcript Cardiac Pathophysiology

Cardiac Pathophysiology
1
Pericarditis


Often local manifestation of another
disease
May present as:
– Acute pericarditis
– Pericardial effusion
– Constrictive pericarditis
2
Acute Pericarditis



Acute inflammation of the pericardium
Cause often unknown, but commonly
caused by infection, uremia,
neoplasm, myocardial infarction,
surgery or trauma.
Membranes become inflamed and
roughened, and exudate may develop
4
Symptoms:




Sudden onset of severe chest pain that
becomes worse with respiratory movements
and with lying down.
Generally felt in the anterior chest, but pain
may radiate to the back.
May be confused initially with acute myocardial
infarction
Also report dysphagia (difficulties swallowing),
restlessness, irritability, anxiety, weakness and
malaise
5
Signs



Often present with low grade fever and
sinus tachycardia
Friction rub (sandpaper sound) may be
heard at cardiac apex and left sternal
border and is diagnostic for pericarditis
(but may be intermittent)
ECG changes reflect inflammatory process
through PR segment depression and ST
segment elevation.
6
7




Treatment
Treat symptoms
Look for underlying cause
If pericardial effusion develops, aspirate
excess fluid
Acute pericarditis is usually self-limiting,
but can progress to chronic constrictive
pericarditis
8
Pericardial effusion

Accumulation of fluid in the pericardial
cavity
– May be transudate
– May be exudate
– May be blood


Not clinically significant other than to
indicate underlying disorder, unless:
Pressure becomes sufficient to cause
cardiac compression – cardiac
tamponade
9
Outcome depends on how fast
fluid accumulates.



If development is slow, pericardium
can stretch
If develops quickly, even 50 -100 ml
of fluid can cause problems
When pressure in pericardium =
diastolic pressure, get ↓ filling of
right atrium,
↓ filling of
ventricles, ↓ cardiac output →
circulatory collapse.
11
Clinical manifestations





Pulsus paradoxus – B.P. higher
during expiration than inspiration by
10 mm Hg
Distant or muffled heart sounds
Dyspnea on exertion
Dull chest pain
Observable by x-ray or ultrasound
12
Treatment



Pericardiocentesis
Treat pain
Surgery if cause is aneurysm or
trauma
13
Constrictive (chronic)
pericarditis


Years ago, synonymous with T.B.
Today, usually idiopathic, or associated
with radiation exposures, rheumatoid
arthritis, uremia, or coronary bypass
graft
14
Pathophysiology:





Fibrous scarring with occasional
calcification of pericardium
Causes parietal and visceral layers to
adhere
Pericardium becomes rigid, compressing
the heart →↓ C.O.
Stenosis of veins entering atria
Always develops gradually
15
Symptoms and Signs




Exercise intolerance
Dsypnea on exertion
Fatigue
Anorexia
16
Clinical manifestations






Weight loss
Edema and ascites
Distention of jugular vein (Kussmaul
sign)
Enlargement of the liver and/or spleen
ECG shows inverted T wave and atrial
fibrillation
Can be seen on imaging
17
Treatment


Drugs and diet
– Digitalis
– Diuretics
– Sodium restriction
Surgery to remove restrictive
pericardium
18
Cardiomyopathies




Disorders of the heart muscle
Most cases idiopathic
Many due to ischemic heart disease and
hypertension.
Three categories:
– Dilated ( formerly, congestive)
– Hypertrophic
– Restrictive

Heart loses effectiveness as a pump
19
Dilated cardiomyopathy
AKA: congestive, ↓ C.O.; ↑ thrombi formation, slow
blood flow ; ↓ contractility, and mitral valve
incompetence, arrhythmias
20
Treatment: relieve symptoms of heart
failure, decrease workload, and
anticoagulants; transplants
Hypertrophic Cardiomyopathy
Often inherited,
C.O. is normal,↑ inflow resistance,
and mitral valve incompetence,
arrhythmais and sudden death.
22



Chest pain
Dizziness
Fainting, especially during exercise

major cause of death in young
athletes who seem completely healthy
but die during heavy exercise

The goal of treatment is to control
symptoms and prevent complications
Restrictive cardiomyopathy
Reduced diastolic compliance of the
ventricle. C.O. is normal or↓; ↑ formation
of thrombi, dilation of left atrium, and
mitral valve incompetence.
26
Disorders of the Endocardium:
Valvular dysfunction


Endocardial disorders damage heart
valves
Changes can lead to :
– Valvular Stenosis = too narrow
– Valvular Regurgitation = too
leaky
(or insufficiency or incompetence)
27
28


Valves that are most often affected are the
mitral and aortic valves, but in I.V. drug
users and in athletes that inject
performance enhancing drugs, > 50 %
involve only the tricuspid valve.
Heart Murmur – sound caused by turbulent
blood flow through damaged valves.
29
Both types of valve disorders:




Cause increased cardiac work, and increased
volumes and pressures in the chambers.
This leads to chamber dilation and
hypertrophy.
Chamber dilation and myocardial hypertrophy
are compensatory mechanisms to increase the
pumping capability of the heart.
Eventually, the heart fails from overwork
30
Aortic Stenosis

Three common causes:
– Rheumatic heart disease -Streptococcus
infection – damage by bacteria and autoimmune response
– Congenital malformation
– Degeneration resulting from calcification
31
Aortic Stenosis


Blood flow obstructed from LV into aorta during
systole
Causes increased work of LV
→ LV dilation & hypertrophy as
compensation
→ prolonged contractions as compensation
Finally heart overwhelmed
→ increased pressures in LA, then lungs, then
right heart
32
Clinical manifestations








Develops gradually
Decreased stroke volume
Reduced systolic blood pressure
Narrowed pulse pressure
Heart rate often slow and pulse faint
Crescendo-decrescendo heart murmur
Angina, dizziness, syncope, fatigue
Can lead to dysrhythmias, myocardial
infarction, and left heart failure
33
Mitral Stenosis





Most common of all valve disorders
Usually the result of rheumatic fever or
bacterial endocarditis
During healing the orifice narrows, the
valves become fibrous and fused, and
chordae tendineae become shortened
Get decreased flow from LA to LV during
filling
Results in hypertrophy of LA
34







By causing LA to become pump:
Get increased pulmonary vascular
pressures; pressures increase through LA
into lung
→pulmonary congestion
→lung tissue changes to accommodate
increased pressures
→increased pressure in pulmonary artery
→increased pressure in right heart
→right heart failure
35
Clinical Manifestations





Atrial enlargement can be seen on x-ray
Rumbling decrescendo diastolic
murmur, and accentuated first heart
sound
Dyspnea
Tachycardia and risk of atrial fibrillation
Other signs and symptoms are of
pulmonary congestion and right heart
failure
36
Aortic Regurgitation

Caused by acute or chronic lesion of
rheumatic fever, bacterial
endocarditits, syphilis, hypertension,
connective tissue disorder (e.g.Marfan
syndrome) or atherosclerosis
37




Reflux of blood from aorta to LV during
ventricular relaxation.
Causes LV to pump more blood w/ each
contraction
→ LV hypertrophy
– LV takes on “globular shape”
→ increased pressures in LA, lung, right
heart
38
Clinical manifestations







Widened pulse pressure
Prominent carotid pulsations and
throbbing peripheral pulses
Palpitations
Fatigue
Dyspnea
Angina
High-pitched or blowing heart sound
during diastole
39
Mitral Regurgitation



Causes: mitral valve prolapse, rheumatic
heart disease, infective endocarditis,
connective tissue disorders, and
cardiomyopathy
Permits backflow of blood from the LV
into the LA during ventricular systole
Loud pansystolic murmur that radiates
into the back and axilla
40
See the animated


Causes blood to flow simultaneously to
aorta and back to LA.
Both LV and LA pump harder to move
same blood twice
– →LV hypertrophy and dilation as
compensation
– Compensation works awhile, then see ↓C.O.
– → heart failure
– Also →LA hypertrophy


→ increased pressures through lungs →
↑ pressures in right heart →right heart failure
Can see edema, shock
42
Clinical Manifestations



Weakness and fatigue
Dyspnea
Palpitations
43
Mitral Valve Prolapse






Cusps of valve billow upward into the LA
during ventricular systole
Mitral regurgitation can occur
Most common valve disorder in U.S.
Studies suggest an autosomal dominant
inheritance pattern
Many cases completely asymptomatic
Regurgitant murmur or midsystolic click
44
Clinical manifestations






Palpitations
Tachycardia
Light-headedness, syncope, fatigue,
weakness
Chest tightness, hyperventilation
Anxiety, depression, panic attacks
Atypical chest pain
46
Management






Echocardiography for diagnosis
Related to degree of regurgitation
Antibiotics before invasive procedures
Beta blockers to relieve syncope,
severe chest pain, or palpitations
Avoid hypovolemia
Surgical repair
47
General Treatment for Valve
disorders





Antibiotics for Strep
Anti-inflammatories for autoimmune
disorder
Analgesics for pain
Restrict physical activity
Valve replacement surgery
48
Heart failure


Definition – When heart as a pump is
insufficient to meet the metabolic
requirements of tissues.
Acute heart failure
– 65% survival rate

Chronic heart failure
– Most common cause is ischemic heart
disease
49
Right heart failure

Systemic symptoms
– Edema, ascites
– Enlarged liver, spleen
– Swollen feet, ankles
– Nausea
– Swollen internal jugular veins
Left hear failure

Fluid accumulation in lungs
– Shortness of breath
– Orthopnea
– Coughing, foaming sometimes
– Tiredness
– weakness
Ischemic Heart Disease

Coronary Artery Disease (CAD),
myocardial ischemia and myocardial
infarction are progression of conditions
that impair the pumping ability of the
heart by depriving it of oxygen and
nutrients.
52
Coronary Artery Disease


Any vascular disorder that narrows or
occludes the coronary arteries.
Most common cause is atherosclerosis
53




The arteries that supply the heart are the first
branches off the aorta
Coronary artery disease decreases the blood flow
to the cardiac muscle.
Persistent ischemia or complete occlusion leads to
hypoxia.
Hypoxia can cause tissue death or infarction,
which is a “heart attack,” which accounts for
about one third of all deaths in U.S.
54
Risk Factors









Hyperlipidemia
Hypertension
Diabetes mellitus
Genetic predisposition
Cigarette smoking
Obesity
Sedentary life-style
Heavy alcohol consumption
Higher risk for males than
premenopausal women
55
Myocardial Ischemia


Myocardial cell metabolic demands not met
Time frame of coronary blockage:
10 seconds following coronary block
– Decreased strength of contractions
– Abnormal hemodynamics
 See a shift in metabolism, so within minutes:
– Anaerobic metabolism takes over
– Get build-up of lactic acid, which is toxic within
the cell
– Electrolyte imbalances
– Loss of contractibility

56
 20
minutes after blockage
–Myocytes are still viable, so
–If blood flow is restored, and increased
aerobic metabolism, and cell repair,
– →Increased contractility
 About 30-45 minutes after blockage, if no
relief
–Cardiac infarct & cell death
57
Clinical Manifestations


May hear extra, rapid heart sounds
ECG changes:
– T wave inversion
– ST segment depression
58
Chest Pain







First symptom of those suffering
myocardial ischemia.
Called angina pectoris (angina – “pain”)
Feeling of heaviness, pressure
Moderate to severe
In substernal area
Often mistaken for indigestion
May radiate to neck, jaw, left arm/
shoulder
60

Due to :
– Accumulation of lactic acid in myocytes or
– Stretching of myocytes

Three types of angina pectoris:
– Stable, unstable and Prinzmetal
61
Stable angina pectoris





Caused by chronic coronary
obstruction
Recurrent predictable chest pain
Gradual narrowing and hardening of
vessels so that they cannot dilate in
response to increased demand of
physical exertion or emotional stress
Lasts approx. 3-5 minutes
Relieved by rest and nitrates
62
Prinzmetal angia pectoris
(Variant angina)




Caused by abnormal vasospasm of
normal vessels (15%) or near
atherosclerotic narrowing (85%)
Occurs unpredictably and almost
exclusively at rest.
Often occurs at night during REM sleep
May result from hyperactivity of
sympathetic nervous system, increased
calcium flux in muscle or impaired
production of prostaglandin
63
Unstable Angina pectoris


Lasts more than 20 minutes at rest, or
rapid worsening of a pre-existing
angina
May indicate a progression to M.I.
64
Silent Ischemia



Totally asymptomatic
May be due abnormality in innervation
Or due to lower level of inflammatory
cytokines
65
Treatment


Pharmacologically manipulate blood
pressure, heart rate, and contractility to
decrease oxygen demands
Nitrates dilate peripheral blood
vessels and
 Decrease
oxygen demand
 Increase oxygen supply
 Relieve coronary spasm
66



Beta blockers:
– Block sympathetic input, so
– Decrease heart rate, so
– Decrease oxygen demand
Digitalis
– Vagal effect
Calcium channel blockers
– Decrease force of contraction, decrease blood
pressure

Antiplatelet agents (aspirin, etc.)
67
Surgical treatment


Angioplasty – mechanical opening of
vessels
Revascularization – bypass
– Replace or shut around occluded
vessels
68
Myocardial infarction

Necrosis of cardiac myocytes
– Irreversible
– Commonly affects left ventricle
– Follows after more than 20 minutes of
ischemia
69
Structural, functional
changes






Decreased contractility
Decreased LV compliance
Decreased stroke volume
Dysrhythmias
Inflammatory response is severe
Scarring results –
– Strong, but stiff; can’t contract like healthy
cells
70
Clinical manifestations

Sudden, severe chest pain
– Similar to pain with ischemia, but stronger
– Not relieved by nitrates
– Radiates to neck, jaw, shoulder, left arm



Indigestion, nausea, vomiting
Fatigue, weakness, anxiety, restlessness
and feelings of impending doom.
Abnormal heart sounds possible (S3,S4)
71

Blood test show several markers:
– Leukocytosis
– Increased blood sugar
– Increased plasma enzymes
 Creatine kinase
 Lactic dehydrogenase
 Aspartate aminotransferase (AST or SGOT)
– Cardiac-specific troponin
72
ECG changes



Pronounced, persisting Q waves
ST elevation
T wave inversion
73
Treatment







First 24 hours crucial
Hospitalization, bed rest
ECG monitoring for arrhythmias
Pain relief (morphine, nitroglycerin)
Thrombolytics to break down clots
Administer oxygen
Revascularization interventions: bypass grafts, stents or balloon
angioplasty
74
Tetralogy of Fallot


Most common cause of blue baby
syndrome.
Tetralogy of Fallot has four key features.
– obstruction from the right ventricle to the lungs
(pulmonary stenosis) are the most important. A
– Also, the aorta lies directly over the ventricular
septal defect, overriding aorta B
– A ventricular septal defect (a hole between the
ventricles) -- C see next image
– and the right ventricle develops thickened
muscle, right ventricular hypertrophy D
Symptoms



high pressure from right ventricle
related to right hypertrophy A and D
Mixing of oxygenated and
deoxygenated blood (B and C)
Left to right shunt first (septal defect),
then right to left shunt when pressure
in the right is higher than left
Treatment

Surgery
– Palliative, not used common now
– Total repair