Myocardial Infarction and Myocardial Ischemia
What are the definitions of myocardial ischemia and myocardial infarction?
myocardial ischemia: temporary blockage of arterial blood supply to the heart, is reversible.
myocardial infarction: permanent blockage of arterial blood supply to the heart, death of myocardial cells and is irreversible.
What is ACS?
plaque ruptures leading to thrombosis and sudden blockage of blood supply to the heart
What is heart failure?
inability of the heart to maintain adequate cardiac output to support body functions, heart fails as a pump
What is pericarditis?
swelling and inflammation of the pericardium
results after an MI or other trauma
CMs: pleuric chest pain, worse with deep inspiration, coughing, swallowing, or supine, pericardial friction rub (sounds like sandpaper)
Splinter Hemorrhages
mico-emboli in nail beds
Types of angina
stable: predictable, frequency, intensity, duration, rest relieves pain in 5 mins
variant: vessel spasm, unpredictable, can occur at rest
silent: asymptomatic, can occur with stable angina, high risk for MI and sudden death
unstable: plaque ruptures and forms a thrombus, sudden, intense, can occur during rest, emergency
What is NSTE-ACS?
Non-ST-segment elevation acute coronary syndrome... can progress to actual MI
happens when atherosclerotic plaque ruptures --> coronary artery vasoconstriction --> myocardial oxygen demand and supply imbalance
risk factors: cigarette smoking
What are the compensatory mechanisms that are actually not helpful?
1. ventricular hypertrophy- heart enlarges to increase CO
2. SNS (sympathetic nervous system) stimulated- ^ HR, SV, and workload
3. ADH (anti-diuretic hormone) causes H2O retention by kidneys which ^ blood volume and workload
4. renin release- ^ angiotensin 2 --> ^ workload
What is the most severe complication of pericarditis
cardiac tamponade
compresses the heart and it cannot contract
Osler's Nodes
infected micro emboli
Classic and non-classic clinical manifestations of myocardial ischemia
classic: transient angina (3-20 mins), substernal pain, discomfort, heaviness, pressure, tightness, squeezing, aching, may radiate to neck, left arm, jaw, teeth, or back
non-classic: indigestion, upper back pain, jaw pain only, increasing fatigue
What is a STEMI?
ST-segment elevation MI
atherosclerotic plaque ruptures --> coronary artery vasoconstriction --> myocardial oxygen demand and supply imbalance
prevention of death: recognition, reperfusion treatment, management
LV Failure backward, forward and clinical manifestations
backward: decreased emptying of the LV --> increased volume in the LV --> ^ volume in LA --> ^ volume in pulmonary veins --> ^ volume in pulmonary capillary bed --> movement of fluid from capillaries to alveoli --> rapid filling of alveolar spaces --> pulmonary edema --> RVF
forward: dec CO --> dec perfusion of tissues of the body --> dec BP --> dec GFR --> dec UOP --> RAAS activation --> Na and H2O retention
CMs: hypotension, dyspnea, lung sounds (crackles), frothy sputum, fatigue, exercise intolerance
Dilated cardiomyopathy
enlarged heart due to degeneration of the heart fibers, heart balloons out leads to both RVF and LVF
Janeway Lesions
red spots from micro emboli
Classic and non-classical signs of myocardial infarction
classic: substernal pain, discomfort, heaviness, pressure, tightness, squeezing, aching, may radiate to neck, left arm, jaw, teeth, back, n/v, diaphoresis, cool, clammy skin, change in BP, HR, or rhythm, NTG usually does not relieve
non-classic: upper back pain, weakness/fatigue, dyspnea, no symptoms
Diagnosis of an MI/STEMI
Hx, PE, ^ CK-MB enzyme, ^ troponin, ^ WBC, ^ blood glucose, ECG
RV Failure backwards, forwards, and clinical manifestations
backward: dec emptying of RV --> ^ volume in RV --> ^ volume in RA --> ^ volume in vena cava --> ^ volume in systemic venous circulation --> ^ volume in distensible organs (hepatomegaly, splenomegaly) --> ^ capillary pressure --> peripheral, dependent edema
forward: dec volume from RV to the lungs --> dec return to LA and dec LV CO --> all forward effects of LVF
CMs: increased CVP, abdominal distention (hepatomegaly, splenomegaly), JVD, peripheral edema, wt gain, fatigue, exercise intolerance
Hypertrophic cardiomyopathy
ventricular septum hypertrophy and LV hypertrophy mostly LVF
Restrictive cardiomyopathy
myocardial fibers are infiltrated with toxins causing ventricular dysfunction, manifestations are RVF and LVF
How does CAD cause myocardial ischemia?
imbalance between supply and demand --> decrease in blood flow to the myocardium and myocardium needs O2 and nutrients --> myocardial cells become ischemic within 10 seconds --> anaerobic metabolism --> accumulation of lactic acid in area of ischemia --> angina
Post MI/STEMI, how long does the remodeling process take? How long does it take for the stronger scar to form?
10-14 days
6 weeks
diagnosis of HF
BNP
Steps in the pathophys of infective endocarditis
1. endocardium prepared for colonization
2. colonization (organisms adhere to the damaged endothelium)
3. infective vegetation forms: fibrin forms which protects the colonies from our host defenses
4. valve dysfunction and potential emboli
RA: 2-8
RV: 15-25/0-8
LA: 4-12
LV: 110-130/4-12
Left Ventricle