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50 Cards in this Set

  • Front
  • Back
Reduced blood flow through one of the coronary arteries causes _______ then ________ then ________
ischemia
cell injury
infarct
WHAT HAPPENS TO Cardiac TISSUE during infarct: (MI)
Reduced contractility and abnormal wall motion
Altered Lf vent compliance w/ decreased SV and ejection fraction
Elevated Lf vent end diastolic pressure or Lf vent systolic dysfunction
With MI: Ischemia = __________________ = _________________
Inflammation

Scar Tissue
With MI: Cell injury trigger ____________________
inflammatory response
With MI Scar tissue inhibits __________________ – this triggers
contractility

compensatory mechanism
what are the compensatory mechanism related to ischemia due to MI
1. Vascular constriction
2. increased heart rate
3. renal retention of Na and H2o in order to maintain cardiac output
Signs and symptoms of MI
1. crushing chest pain, referred pain down the L arm, jaw, neck and nausea
2. Fatigue and SOB
3. Nausea and vomiting-biggest reason for misdiagnosis
4. Anxiety, feelings of doom, restlessness, perspiration
What is the biggest reason of misdiagnosis in MI
nausea and vomiting
Treatment of MI
Oxygen, Vasodilators, Thrombolytic agents
If arrhythmia then antiarrhythmic agents
IV morphine(important vasodilator)
Beta 1 blockers help reduce re-infarction but…monitor for heart failure
3 Mitral Valve Disorders
Mital Stenosis
Mitral Regurgitation
Mitral Prolaspe
cor pulmonae
Rt sided heart failure
What is affected with Mitral Stenosis
left artia to left ventricle, narrowed valve, obstructed
Mirtal stenosis is characterized by (pressure gradient)
abnormal left atrial-ventricular pressure gradient during diastole
Mitral stenosis results in
chronic pulmonary HTN,
Rt vent. Hypertropy
Rt sided heart failure
mitral reguration
backflow from lf vent into rt atrium due to valve not closing all the way
mitral regurgitation pressure
pressure gradient during vent systole
mitral regurgitation results in
chronic pulmonary HTN
Rt vent. Hypertropy
Lt sided heart failure.
s/sx mitral stenosis:
increased HR, a-fib due to excessive atrial volume, atrial clots leading to systemic embolization and stroke. Secondary sumptoms to pulmonary congestion orthopnea, cough, dyspnea on exertion, abnormal breath sounds, poor arterial oxygenation
Lf vent stroke volume: fatigue, poor activity tolerance, and weakness
s/sx mitral regurgitation:
chronic weakness and fatigue
s/sx Aortic Stenosis:
angina (due to thickening of ventricle), syncope, fatigue, low systolic BP, faint pulse
s/sx Atrial regurgitation:
bounding peripheral pulsation, pounding heart
Atrial Stenosis (Aortic):
Lt ventricle to aorta impaired: obstruction
Atrial Stenosis: Pressure gradient:
Lt ventricular/aorta during systole
Lt Ventricular pressure higher
Atrial Stenosis Patho
: chronic pulmonary HTN, Lt vent. failure
s/sx atrial stenosis
angina (due to thickening of ventricle), syncope, fatigue, low systolic BP, faint pulse
Atrial Regurgitation
Circulation: Lt ventricle to aorta impaired: leaking
Atrial Regurgitation pressure
Pressure gradient: Lt ventricular/aorta diastole
Lt Ventricular pressure higher
Atrial Regurgitation Patho:
Lt vent. Hypertrophy and dilatation. Lt sided heart failure
s/sx: Atrial regurgitation:
bounding peripheral pulsation, pounding heart
Endocardium: Rheumatic Heart Disease Pathogen:
group A β-hemolytic streptococcus
Endocardium: Rheumatic Heart Disease Pathology:
1. Proteins on cardiac myosin, valves, skin, joints, brain resemble bacterial epitomes.
2. Results in endocardial inflammation with valve destruction.
Endocardium: Rheumatic Heart Disease Clinical Manifestations:
1. Joint inflammation
2. Sydenham chorea-TICS OR NOISES,
3. truncal rash-AROUND BACK AND AB.
Dx: Endocardium: Rheumatic Heart Disease
1. LABS: Elevated antibody titer: antistreptolysin O, anti-Dnase B
Tx: Endocardium: Rheumatic Heart Disease
Prophylactic antibiotics for life- DURING DENTAL, SMALL SIGNS OF INFECTIONS, OR FULL TIME
Endocardium: Infective Heart Disease, Pathogen:
Several microbes
Infective heart disease: Pathology:
Antigen antibody recognition with resulting cascade. Results in endocardial inflammation with valve destruction- ANY OF THE 4 VALVUES.
Infective heart disease: Clinical Manifestations:
Acute and subacute presentations.
EVALUATE VALVE infective heart disease BY:
12 LEAD ECG, NUCLEAR STUDIES, XRAY
positive blood culture of infective agent, pathogen
Tx: infective heart disease
Surgical replacement of valves. Match the drug to the bug.
Prophylactic antibiotics for life
symptoms of subacute infective heart disease
subacute: low grade fever, wt. loss, nonspecific fatigue, flulike symptoms
symptoms of acute infective heart disease
fever, chills, malaise, frequently a heart murmur
Myocarditis
Inflammatory disorder due to virus
Acute and stormy clinical picture
Histology: necrosis
Myocarditis prognosis
recovery or death
s/sx Myocarditis
Pain, fast breathing
Cardiomyopathy
Non-inflammatory disorder
Evolves insidiously over years
Histology: hypertrophy or atrophied
Pathogen:Cardiomyopathy
virus, genes, autoimmune
Cardiomyopathy prognosis
Heart failure
Pericardial Effusion
Fluid in the pericardial sac exceeding 50 ml.
Need 15-20 ml in pericardial sac, book says normal is 30-50 ml
Cardiac Tamponade-
Accumulation of pericardial fluid resulting in tamponade which refers to external compression of heart chambers such that filling is impaired.
Pericarditis
Inflammation of the pericardium by viral or post MI