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CARDIAC DISEASES
MORTALITY
STAGES OF HYPERTENSION
ARTERIOSCLEROSIS VS ATHEROSCLEROSIS
CLINICAL MANIFESTATION:
I. ANGINA
- Cardiac-related chest pain is due to ischemia.
- Ischemia is a temporary condition due to the imbalance
between the myocardial oxygen supply and demand.
- (+) Levine Sign
- Referred pain: jaw, neck, upper traps chest shoulder L arm
- Angina can spread anywhere between the belly button and
the jaw, including to the shoulder, arm or hand- usually on
TYPES OF ANGINA
the left side.
1. Chronic Stable angina
- “predictable angina"
- Physical Exertion
- Emotional stress
- Respond to rest and nitrates
- Sensation as an intensity less than 5/10, which improves to
0/10
2. Unstable Angina
- “Preinfarction Angina"
- “Progressive Angina"
- “Cresendo Angina"
- occurs at rest
- Warrants immediate medical intervention
- Don't respond to nitrate
- C/I to exercise
3. Nocturnal Angina USUAL DISTRIBUTION OF PAIN WITH MYOCARDIAL
- Exertion caused by dreams LSCHEMIA
- Common among CHF
4. Prinzmetal Angina
- “Variant Angina”
- Common among: F>M
- Vasospasm of coronary arteries in the absence of occlusive
disease.
- Long term DOC: calcium blockers
ELECTROCARDIOGRAM
CARDIAC ENZYMES ASSOCIATED WITH MYOCARDIAL INJURY • Record of electrical events in the myocardium that can be
AND INFARCTION correlated with mechanical events
• P wave: depolarization of atrial myocardium.
Signals onset of atrial contraction
• QRS complex: ventricular depolarization (0.6-0.10
Signals onset of ventricular contraction..
• T wave: repolarization of ventricles
• PR interval or PQ interval: 0.16 sec (0.12-0.20s)
Extends from start of atrial depolarization to star of
ventricular depolarization (QRS complex) contract
and begin to relax
Can indicate damage to conducting pathway or ”-
AV node if greater than 0.20 sec (200 msec)
• Q-T interval: time required for ventricles to undergo a single
cycle of depolarization and repolarization
Can be lengthened by electrolyte disturbances,
conduction problems, coronary ischemia, myocardial
damage
ECG ABNORMALITIES
Absence of P-wave
C/I to exercise
PQ interval
< 0.12s — fast conduction
0.20s — slow conduction heart block)
HEART BLOCKS
FIRST DEGREE HEART BLOCK.
Prolonged P-R (or P-Q) Interval CLINICAL MANIFESTATIONS: MYOCARDIAL INFARCTION
increases to greater than 0.20 second Lasts for 20 mins
• Chest, upper extremity, mandibular or epigastric discomfort
(with exertion or at rest)
• dyspnea or fatigue
• the discomfort is diffuse not localized, nor positional, nor
SECOND DEGREE BLOCK.
affected by movement of the region
- HALLMARK: "dropped beats" of the ventricles
Recurrent Myocardial Infarction
• Mobitz Type 1 (Wenkebach)
• MI that occur 28 days following an incident of MI
Progressive lengthening of the PR interval and (+)
Reinfarction
dropped beats
• MI that occurs within 28 days of an incident or recurrent MI
• Mobitz Type 2 (Hay)
(N) PR interval and (+) dropped beats
CONGESTIVE HEART FAILURE
• “Cardiac decompensation
• A condition in which the heart is unable to maintain
adequate circulation of the blood to meet the metabolic
needs of the body
• Types of CHF
THIRD DEGREE HEART BLOCK 1. Left-sided (ventricular) Heart Failure
poor conduction in the A-V node or A-V bundle 2. Right-sided (ventricular) Heart Failure
becomes severe, complete block of the impulse from 3. Biventricular Heart Failure
the atria into the ventricles occurs
ECG ABNORMALITIES
QRS Complexes
Prolong (>0.10s): Bundle Branch Block (BBB)
Wide, bizzare, odd: Premature ventricular
contraction (PVC)
ST Segment
Prolonged: CHF
Elevated: Myocardial Infarction
Depressed: Myocardial Ischemia
T Wave
Inverted: Myocardial ischemia
MYOCARDIAL INFARCTION CLASSIFICATIONS OF HEART FAILURE
• “Coronary occlusion I. Dilated Cardiomyopathy
• Complete vessel occlusion • Most common cause > CAD
• Rupture of a vulnerable plaque w/ resultant formation of a • Other cause:
thrombus • Myocarditis
• Irreversible myocardial cell damage • Alcohol abuse
20 min-2 hr • LV failure and systolic dysfunction
• Complete necrosis
2-4 hr
• ST segment elevation + increased cardiac Enzymes
Dilated cardiomyopathy PATHOPHYSIOLOGY
PRESSURE-OVERLOAD HYPERTROPHY
• concentric increase in wall thickness
• new sarcomeres are predominantly assembled in parallel to
the long axes of cells, expanding the cross-sectional area of
myocytes
VOLUME-OVERLOAD HYPERTROPHY CAUSES OF CARDIAC MUSCLE DYSFUNCTION
• Ventricular dilation
• New sarcomeres assembled in response to volume overload
are largely positioned in series with existing sarcomeres.
3. Coarctation of Aorta
- Constriction of proximal and distal Aorta
- Inc BP especially on UE
4. Patent ductus Arteriosus
CLINICAL MANIFESTATION: MITRAL VALVE PROLAPSE
- Ductus arteriosus: connects the Pulmonary artery to aorta
- (+) ductus arteriosus after birth
- Blood shunt from (L) to (R)
5. Tetralogy of Fallot
- Pulmonary artery Stenosis
- Aorta Over-riding to the right
- Right ventricular Hypertrophy
- Interventricular septal defect
- Blood shunt from (R) to (L)
FUNCTIONAL CLASSIFICATIONS OF PATIENTS WITH DISEASES
OF THE HEART
Intravascular stents
• an endoprosthesis (pliable wire mesh) implanted post
angioplasty to prevent restenosis and occlusion in coronary
or peripheral arteries
• often coated in medication to prevent thrombosis
REVASCULARIZATION
Coronary Artery Bypass Graft (CABG)
• surgical circumvention of an obstruction in a coronary
artery using an anastomosing grañ
• Blood vessels:
Great saphenous vein
Internal mammary artery
Internal thoracic artery
MEDICAL MANAGEMENT Radial artery (non-dominant arm)
Revascularization
• PTCA
• CABG
Symptomatic CHF Class III/IV
• Heart transplant
• Left ventricular devices (LVAD)
• Myoplasty
• Pacemaker
PT MANAGEMENT: CARDIAC REHABILITATION
Four distinct phases:
• Acute inpatient care
• Home-based recuperation
• Outpatient program
• Independent self-care
EVIDENCE-BASED PT MANAGEMENT
Exercise-Based Cardiac Rehabilitation for Coronary Heart
Disease
This study confirms that exercise-based CR reduces
cardiovascular mortality and provides important
data showing reductions in hospital admissions and
improvements in quality of life. These benefits
appear to be consistent across patients and
intervention types and were independent of study
quality, setting, and publication date.