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coronary heart disease (CHD)
characterized by insufficient delivery of oxygenated blood to the myocardium (ischemia) because of atherosclerotic coronary arteries (coronary arteries become narrowed or blocked)
also called coronary artery disease
main cause of CHD
atherosclerosis of coronary arteries
atherosclerosis
the buildup of fatty deposits, cholesterol and inflammatory material (plaque) inside arteries
causes progressive narrowing of the arterial lumen and predisposes to a # of processes that can precipitate myocardial ischemia including thrombus formation, coronary vasospasm, endothelial cell dysfunction
clinical syndrome
a group of signs and symptoms associated with a particular disease: for CHD
*critical narrowing of the coronary lumen overtime or sudden rupture of a plaque followed by thrombus formation and…
angina
acute coronary syndrome
chronic ischemic cardiomyopathy
sudden cardiac arrest
angina
chest pains or discomfort that occurs when the heart muscle temporarily does not receive oxygen rich blood
types:
stable
unstable
vasospastic
stable angina pectoris
predictable, exercise induced angina pain
most common
improves with rest or prescribed nitroglycerin
signs and symptoms: chest pressure, tightness, squeezing, pain that may spread to arm, neck, jaw, or back
characterized by stenotic atherosclerotic coronary vessels
acute coronary syndrome
refers to conditions where blood flow to the heart suddenly is reduced or blocked (group of conditions that make sudden decrease in blood flow to heart)
three types (this may present as)…
unstable angina
non ST elevation myocardial infarction
ST elevation myocardial infarction
patient may be asymptomatic
ECG and biomarkers used for diagnosis
unstable angina
when heart suddenly receives insufficient blood flow, often b/c a coronary plaque becomes disrupted (sudden reduction in blood flow)
chest pain may occur at rest
pain may be new, worsening, or more frequent
no heart death
troponin lvls normal, partial blood flow reduction
occlusion is partial - artery is partially blocked = heart doesn’t receive enough oxygen = myocardial ischemia
non ST elevation MI
type of heart attack in which heart muscle damage occurs without persistent ST segment elevation on ECG
blood flow to heart is significantly reduced, incomplete coronary artery occlusion (partial blockage)
ECG does not show persistent ST (segment elevation) but still heart muscle death
elevated troponin levels without persistent ST elevation
ST elevation MI
heart attack caused by sudden, severe blockage of a coronary artery
blood flow to heart is critically reduced - complex coronary artery occlusion (complete blockage)
ECG shows characteristics of ST elevation
heart muscle death
elevated troponin levels with persistent ST elevation
chronic ischemic cardiomyopathy
long term ischemic damage, coronary artery disease / previous heart attacks damage heart muscle, weakening its ability to pump blood (reduced blood supply) which leads to heart failure
long term weakening of heart muscle due to reduced blood supply
sudden cardiac arrest
abrupt loss of heart function, heart stops pumping effectively, immediate CPR is needed
primary cause = lethal dysrhythmia
(ventricular fibrillation, VF), pulseless ventricular tachycardia (VT)
vasospastic angina (VSA)
unpredictable type of chest pain that occurs when a coronary artery suddenly tightens or spasms reducing blood flow and oxygen to the heart muscle (sudden coronary artery spasm)
occurs at rest, at night when patient is resting, or early mornings
when spasm relaxes, blood flow can improve = chest pain disappears
rare chest pain - can be severe
caused by sudden artery tightening, can be relieved by nitroglycerin or Ca+ blockers
valvular heart disease
occurs when one or more of the heart’s valves become damaged and cannot open or close properly
most common disease affects the aortic or mitral valves
causes of VHD
inflammation
scarring'
calcification
congenital malformation
types of valve disorders
stenosis
regurgitation
prolapse
murmurs
stenosis
failure of a valve to open completely; significant hemodynamics consequences generally begin to occur when the valve opening is reduced to half its normal diameter
results in extra pressure work for the heart b/c blood must be forced through the high resistance of a narrow valve opening
progresses slowly over years = time for affected heart chambers to compensate through myocardial cell hypertrophy (increased resistance = thicker heart muscle to compensate)
regurgitation
valves do not close completely; develop suddenly from valvular infection or rupture of a supporting papillary muscle so valve does not close completely (volume overload)
blood leaks backward through the valve, so heart must pump extra blood to maintain adequate forward circulation
prolapse
valve bulges backward into the chamber behind it when the valve closes
murmurs
turbulent blood flow, extra sound caused by turbulent blood flow through the heart
mitral stenosis
when the mitral valve becomes narrow and cannot open completely
blood flow from left atrium to left ventricle is difficult
BP increases in LA
main symptom is expertional dyspnea (SOB from physical activity)
mitral regurgitation
mitral valve does not close tightly, so back flow of blood from LV to LA during systole
blood has to pump more blood to compensate
mitral valve prolapse
mitral valve leaflets bulge backward into the LA during ventricular contraction
can lead to regurgitation if valve isn’t sealed properly
aortic stenosis
aortic valve becomes narrowed and cannot open completely; the aortic cusps (the flaps that make up the valve become stiff due to calcium deposits, LV to aorta flow difficulty
symptoms - angina, syncope (fainting), dyspnea (SOB) = classic triad
aortic regurgitation
aortic valve does not close completely, blood leaks backward from aorta to LV during diastole
Infective endocarditis
infection of the hearts inner lining & valves (endocardium)
bacteria or other microorganisms enter the bloodstream, attach to the heart valves and begin multiplying
can be acute or chronic
Process
bacteria enter bloodstream
bacteria reach heart
bacteria attach to the heart valve (damaged usually)
multiply and form masses called vegetations
vegetations can damage the valve or break off and travel through bloodstream
acute endocarditis
sudden rapid progression
high fever
chronic subacute
developing slowing, overtime
low grade fever and mild symptoms
pericardium
protective, durable layered sac surrounding heart
pericardial effusion
means an abnormal build up of fluid inside the pericardial sac surrounding the heart
caused by: inflammation, infection, cancer, kidney failure
cardiac tamponade
life threatening condition in which fluid accumulates around the heart and creates enough pressure to compress the heart chambers (prevents heart from filling properly with blood)
3 processes of atherosclerosis
thrombus formation
coronary vasospasm
endothelial cell dysfunction - vessel wall becomes damaged
three processes that are caused by atherosclerosis that can then lead to myocardial ischemia
nitroglycerin
causes vasodilation and lightens prelaod; sublingual taken PRN
up to 3 doses, 5 mins apart
myocardial infarction
heart attack, complete occlusion
artery is completely blocked = heart muscles become deprived = muscle death
cardio biomarkers
records troponin lvls
ECG
records whether there is ST (segment elevation)
chronic ischemic cardiomyopathy symptoms
Chest pain or pressure
Pain spreading to arms, neck, or jaw
Shortness of breath, Sweating, Nausea
Women may have different symptoms
CHD treatment options
Medications to dissolve clots
Catheter procedures to open blockages - catheter gets removed after procedure
Stents to keep arteries open - stent stays in place
Emergency surgery if needed
Implications for cardiac function
when valves do not function properly, heart must work harder
valve damages
stenosis or regurgitation develops
increased pressure or volume overload
heart muscle thickens or chambers enlarge
heart may eventually weaken
heart failure may develop
rheumatic heart disease
caused by complication of rheumatic fever
immune attack that chronically attacks heart valves
common in children
risk factors for infective endocarditis
IV drug use
previous endocarditis
prosthetic heart valve
HAI
renal failure
diseases of the endocardium
rheumatic heart disease
infective endocarditis
myocardial diseases
myocarditis
cardiomyopathy
myocarditis
inflammation of heart muscle; necrosis and degeneration of heart muscle
cardiomyopathy
dilated cardiomyopathy
hypertrophic cardiomyopathy
restrictive cardiomyopathy
dilated cardiomyopathy
Dilation of one or both ventricular chambers (cardiac failure)
Hypertrophic cardiomyopathy
Thickened, hyperkinetic ventricular muscle mass
Left ventricle most affected
Restrictive cardiomyopathy
Stiff, fibrotic ventricle - resist diastolic filling
heart can’t fill properly due to restriction
pericardial diseases
pericardial effusion - cardiac tamponade
pericarditis
pericardial effusion
accumulation of fluid in pericardial sac
can be blood or serous fluid
pericardial effusion cm and treatment
Reduced stroke volume - amount of blood pumped out of one ventricle with each heartbeat (not enough blood = less blood pumped out)
Compensatory increases in heart rate - tachycardia b/c body tries to maintain CO by increasing HR
Pulsus paradoxus - abnormally large decrease in systolic BP during inspiration
Hypotension, distended neck veins and muffled heart sounds―called Beck’s triad
treatment: pericardiocentesis
pericardiocentesis
insertion of needle or catheter into pericardial space to remove excess fluid
pericarditis
inflammation of the pericardium
acute or chronic
acute pericarditis
Assumed to be viral: viral infection may trigger inflammation
Uncomplicated acute pericarditis resolves spontaneously within 2 weeks
causes sticking and rubbing of visceral pericardium layers = pericardial friction rub sound may be heard
symptoms: back pain, chest pain that worsens when deep breathing or lying flat, can be reduced by sitting up or leaning forward
chronic pericarditis
Adhesion - surrounding mediastinal structures (scar tissue can form around heart)
destruction of pericardial sac
Constrictive pericarditis
fibrous, scarred pericardium
secondary to tuberculosis
impair cardiac contractions
management
Lifestyle: diet, exercise, smoking cessation
Medications: angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, diuretics, anticoagulants
Surgical: valve repair, Coronary Artery Bypass Graft (CABG), pacemaker, transplant
treatment
aims to resture funcitons, relieve symptoms, and prevent progression
becks triad
Hypotension
distended neck veins
muffled heart sounds
clinical manifestations for pericardial effusion
classic triad
angina,
syncope (fainting),
dyspnea (SOB)
clinical manifestations for aortic stenosis