Patho Exam 3

Describe the normal process of blood flow through the heart

blood enters the heart through the inferior and superior vena cava and it empties oxygenated blood into the right atrium. blood flows from the right atrium into the right ventricle passing through the tricuspid valve. Once the ventricle is full the tricuspid valve shuts to prevent blood from flowing backwards. The ventricle contracts and oxygenated blood leaves the heart through the pulmonary valves and enters the pulmonary artery. The pulmonary valve empties oxygenated blood into the left atria, passes through the bicuspid valve, into the left ventricle. Blood leaves the heart through the aortic valve and up the aorta.

What does tissue perfusion mean?

blood continuously flowing through the capillaries

what are the five stages that link the evolution of an atherosclerotic plaque to myocardial infarction?

damaged endothelium

fatty streak (yellow)

fibrous plaque (white)

complicated lesion

plaque rupture

what is damaged endotheloium?

excess LDL particles accumulate in the artery wall and become chemically modified

modified LDLS stimulate endothelial cells to display adhesion molecules which latch onto monocytes and t cells (fuel inflammation)

monocytes mature into active macrophages and display scavenger receptors

what is the role of scavenger receptors?

helps macrophages ingest modified LDLS

what can cause a damaged endothelium?

smoking

hypertension

diabetes

turbulent blood flow 

bacteria

viruses

homeocysteine 

what is the fatty streak?

growth factors produced stimulating smooth muscle growth 

lipid laden macrophages bind to endothelium 

LDL become oxidized 

vascular lesion can be reversible with diet modification 

what is the fibrous plaque?

smooth muscle proliferates in lesion and deposit collagen which creates a more firm and rigid mass

what is the result of a complicated lesion?

years of progressive and relentless events with deposition of calcium

lesion can produce ulceration/rupture of endothelium 

endothelial lesions can initiate thrombus (blood clot) formation and can instantly occlude the lumen 

what can a plaque rupture cause?

if clot is big enough, this halts the flow of blood to the heart which can produce a heart attack

how does atherosclerosis affect the normal physiology of a coronary artery to eventually cause an increased workload on the heart?

deposition of fat and fibrin in the arterial walls which tends to harden overtime 

decrease compliance of vessels

occludes arterial lumens 

reduces blood flow to tissues-ischemia 

increases resistance to blood flow 

increases workload on heart 

what are the non-modifiable risk factors for atherosclerosis?

age

gender

family history

race

what are the modifiable risk factors for atherosclerosis?

LDL

HDL

hypertension

smoking

C reactive Protein (CRP) 

what are the biomarkers for C-reactive protein and how does this serve as an index for the relative risk of a future heart attack? IDK if this is right

CRP is released from the liver in response to acute inflammation

high cholesterol and high CRP=higher risk factor for a heart attack

what endocrine disorders can be a causative factor of secondary hypertension?

cortisol

TH

aldosterone

adrenaline

what is a normal blood pressure?

less than 120 and 80 

what is an elevated blood pressure?

120-129

less than 80

what is the value of a stage 1 hypertension bp?

130-139

80-89

what is the value of stage 2 hypertension bp?

greater or equal to 140 and 90 

what is the value of hypertensive crisis bp?

greater than or equal to 180

greater than 120

what is the mechanism of diuretics?

reduce blood volume by increasing urine output by the kidneys

what is the mechanism of beta blockers?

decrease heart rate and contractility by preventing adrenergic receptors from contracting 

what are calcium channel blockers?

block entry of calcium ions in the heart and vascular smooth muscles which inhibits contraction and promotes vasodilation

how do ACE inhibitors act to decrease the workload of the heart?

ACE inhibitors bind to angiotensin II receptors on the arterioles which prevents smooth muscle from contracting and lowers BP 

what is the normal process of angiotensinogen?

renin converts angiotensinogen to angiotensin I

ACE- angiotensin converting enzyme converts angiotensin I to angiotensin II

what happens when angiotensin II binds to angiotensin II receptors?

vasoconstriction to increase BP

what are the pathophysiological consequences the myocardium may suffer with chronic untreated hypertension?

Increased workload combined with diminished blood flow through coronary arteries can cause left ventricular hypertrophy, myocardial ischemia, heart failure

what are the risk factors with the development of coronary artery disease?

hyperlipidemia/dyslipidemia

hypertension

smoking

diabetes

obesity

genetic predisposition

sedentary lifestyle

loss of estrogen

alcohol

gender

personality

what is the difference between myocardial ischemia and myocardial infarction? 

myocardial ischemia is caused by less blood flow and oxygen to the myocardium vs myocardial infarction has no blood flow and cells die 

is a myocardial ischemia reversible/transient or permanent tissue damage?

transient/reversible

is a myocardial infarction reversible/transient or permanent tissue damage?

permanent tissue damage

what is the pathophysiology associated with myocardial ischemia for changes in the myocardial cellular function?

increased anaerobic metabolism which causes less contraction and cells become weaker 

lactic acid is produced 

what happens to the ventricular function in myocardial ischemia?

impaired ventricular function due to hypoxia and lactic acid

what happens to stroke volume in myocardial ischemia?

decreased stroke volume due to less blood being pumped out and more blood remains in chamber and blood accumulates which makes it harder to breathe

what happens to end diastolic volume in myocardial ischemia?

increased EDV

what is EDV?

volume of blood in each ventricle at the end of diastole (relaxation)

what is stroke volume?

amount of blood pumped out

what is the normal range for stroke volume?

70 ml

what is the normal range for end diastolic volume?

120 ml

how do you calculate ejection fraction?

SV/EDV

usually 55-70%

does ejection fraction increase or decrease during myocardial ischemia?

decreases due to a decrease in contractility due to less blood being pumped out (SV) and less blood filling the ventricles at rest (EDV)

what is stable angina?

occurs during exertion due to buildup of lactic acid or abnormal stretching of the ischemic myocardium

what is unstable angina?

occurs frequently at rest 

what is used to relieve the pain of stable angina?

rest

nitroglycerin

how does nitroglycerin work?

decreases preload by decreasing tension and afterload which decrease oxygen demands

nitroglycerin is absorbed into the circulatory system and nitric oxide is a potent vasodilator which lowers blood pressure and the heart doesn’t have much resistance and have to work as hard=removes pain 

what is preload?

amount of tension before contraction

what is afterload?

pressure the heart must work against to eject blood

what is a subendocardial ischemia?

portion of width of wall of myocardium is experiencing ischemia 

consists of ST segment depression and T wave inversion

what is a transmural ischemia?

entire width of wall of myocardium is experiencing ischemia 

ST segment elevation

how does coronary artery bypass graft (CABG) work to treat coronary artery disease and myocardial ischemia?

most invasive

take left internal thoracic artery and surgically suture into coronary artery downstream which allows for clean blood flow into coronary artery past the lesion

what veins can you use for CABG?

Saphenous vein 

left internal thoracic artery 

radial artery 

how does balloon angioplasty work in the treatment of coronary artery disease and myocardial ischemia?

reopen the narrow coronary artery by placing a balloon catheter so more blood can flow through

how does stents work in the treatment of coronary artery disease and myocardial ischemia?

can place these into reopened artery to keep it open

what are the characteristics of a myocardial infarction?

end point of coronary artery disease

prolonged ischemia (20 mins)

hypoxic injury——cell death=tissue necrosis

what are the changes in cardiac function in myocardial infarction?

Decreased cardiac contractility, stroke volume, ejection fraction

altered left ventricular compliance

increased end-diastolic pressure

possible sino-atrial node malfunction

what is the characteristics of transmural myocardial infarction? 

ST segment elevation

 STEMI: if they have ST elevation and elevated troponin

what is the characteristics of a subendocardial myocardial infarction? 

ST segement depression

T wave inversion without ST elevation (aka non-STEMI)

How does the myocardium respond after 24 hours following a myocardial infarction?

leukocyte infiltration into blood stream due to cells dying

proteolytic enzymes degrade necrotic tissue

catecholamines released which increases blood sugar and can cause hyperglycemia

How does the myocardium respond after 2 weeks following a myocardial infarction?

weak collagen matrix formed

increased insulin release

How does the myocardium respond after 6 weeks following a myocardial infarction?

strong scar tissue develops

scar tissue is non-contractile/non-conductive

What are the symptoms associated with myocardial infarction?

sudden/severe chest pain

initial drop in blood pressure

sympathetic nervous system activation

abnormal heart sounds,

release of iso-enzymes from damaged myocardial cells

can pain be relieved through the use of nitrates in myocardial infarctions?

no

what does the activation of the sympathetic nervous system cause in myocardial infarctions?

profuse sweating

cool and clammy skin

reflexive increase in blood pressure and heart rate 

What causes the release of cardiac iso-enzymes?

released from dead blood cells

no physiological need

what other myocardial-specific proteins are present in the plasma during a myocardial infarction?

myoglobin

troponin T

troponin I

myeloperoxidase

how is creatine Kinase affected in myocardial infarctions?

CK-MB2 higher than CK-MB1 post MI

rises within 6-8 hours

peaks at 24 hours

returns to normal 36-48 hours

how is lactate dehydrogenase (LDH) affected in myocardial infarction? 

LDH-1 higher than LDH-2 post MI

peaks at 3 days 

normal within 14 days 

what is the significance of cold spots in a myocardial perfusion scan using thallium-201?

a cold spot is a region of dead tissue and infarction so it does not take up an radiation. This shows the location of the myocardial infarction  

Referring to a person that has (or is having) severe chest pain along with elevated cardiac proteins in their blood, describe the significance of an elevated ST segment and/or a very large Q wave appearing on their electrocardiogram. 

an elevated ST segment and large Q wave indicates a transmural infarction. If there is an elevation of troponin levels and ST elevation, they also have STEMI. A large Q wave cannot revert back to normal

what is the purpose of giving blood thinners such as aspirin or heparin to a person following a myocardial infarction?

can prevent the blood from clotting 

what is the purpose of giving tissue plasminogen activator to a person following a myocardial infarction?

activates plasmin which breaks up blood clots (fibrin)

What are the complications associated with myocardial infarctions?

dysrhythmias (altered rythm)

left ventricular failure=cause death from heart attack

rupture of heart structures

systemic thromboembolism

sudden death

which heart structures are ruptured in myocardial infarctions?

chordae tendinae

papillary muscles

ventricular wall rupture

What is cardiac tamponade?

fluid rapidly accumulates in the pericardial sac, compressing the heart and restricting ventricular filling 

what are the signs of cardiac tamponade?

right side heart failure first 

causes PEA (pulseless electrical activity)

how much fluid can be held in gradual accumulation of fluid in the pericardial sac?

up to 1000 cc of fluid

how much fluid can be held in rapid accumulation of fluid in the pericardial sac?

50-200 cc 

what does rapid accumulation of fluid in the heart cause?

creates hydrostatic pressure, connective tissue is resistant to stretch so it ends up compressing the heart

what are the two procedures that can rapidly eliminate accumulated fluid in the pericardial space?

thoracotomy

pericardialcentesis

what is the goal of a thoracotomy and pericardialcentesis?

to relieve pressure on heart by removing excess fluid

restore normal ventricular filling

improve cardiac function

what is the pathophysiology of dilated cardiomyopathy?

enlarged heart which weakens the heart

decreases muscle cells and contraction

what does decreased contractility cause in dilated cardiomyopathy?

more blood remains in the chamber, which increases volume and pressure

what are the treatment options for dilated cardiomyopathy? how do they work?

ACE inhibitors

beta blockers

these help reduce workload and improve cardiac output

what is the pathophysiology for hypertrophic cardiomyopathy?

hypertrophy of interventricular septum (increases size of myocardium)

causes muscle cells to become bigger and noncompliant 

decrease volume in chamber, decrease CO

what are the potential treatments for a person suffering from hypertrophic cardiomyopathy?

need to decrease cardiac output so muscle isn’t contracting to full extent 

beta blockers, calcium channel blockers 

remove tissue surgically 

use chemical substances such as 100% ethanol to debulk tissue and increase BV

what are the 3 diseases associated with restrictive cardiomyopathy?

amyloid

hemochromatosis

glycogen storage disease 

what is the amyloid protein disease in restrictive cardiomyopathy?

keeps expressing immunoglobulin proteins (amyloid protein) that circulates at high levels and can infiltrate the heart which leads to inflammation and collagen buildup

is the amyloid protein disease reversible in restrictive cardiomyopathy?

no

what is hemochromatosis in restrictive cardiomyopathy?

too much iron gets deposited in heart tissue which causes the heart to become fibrotic and stiff 

what is glycogen storage disease in restrictive cardiomyopathy?

excess glycogen triggers inflammation and activates cytokines

what do the 3 infiltrative diseases cause?

triggers inflammation

collagen scar tissue builds up and infiltrates heart which causes the heart to become fibrotic so heart cannot contract/relax

What is valvular stenosis?

valves do not open fully (stiff and rigid)

outflow is obstructed

chamber behind valve has increased workload 

what valve is mostly affected in valvular stenosis?

left side 

what is valvular incompetence?

valves do not close fully (become stretchy)

causes regurgitation (flow backwards-retrograde)

what is the pathophysiology of aortic valvular stenosis?

aortic valves become narrowed

increasing left ventricular pressure during systole 

left ventricle generates greater force to eject blood= left ventricular hypertrophy\

decreae SV, CO

narrowed pulse pressure 

how does aortic valvular stenosis lead to heart failure?

decreased tissue perfusion (o2 going to tissues) so left ventricle needs to work harder to compensate (undergoes compensatory hypertrophy) and myocardial cells eventually die

what happens to the left ventricle when it undergoes LV hypertrophy?

increased pressure from LV hypertrophy causes an elevated LA and pulmonary vein pressures, which causes fluid to travel into the pulmonary alveoli and results in pulmonary congestion and trouble breathing

what is the equation for pulse pressure?

systolic-diastolic

why does the systolic pressure decrease in aortic valvular stenosis?

the left ventricle has difficulty ejecting blood through the narrowed aortic valve which reduces SV

why does the diastolic pressure increase in aortic valvular stenosis?

due to prolonged ejection time and decreased arterial compliance (less blood in arterial sys)