Pericarditis
Inflammation of the pericardium causes:
Pain (sharp and abrupt)
Exudate
Serous -pericardial effusion
Fibrous - friction rub; adhesions
ECG changes
*most common cause: virus
Pericardial effusion
Serous EXUDATE filling the pericardial cavity, it can increase intracardiac pressure, compress the heart and interfere with venous return to the heart
common cause: cardiac surgery, trauma, cancers
Cardiac Tamponade
Rapid compression of the heart, resulting from excess FLUID in the pericardial sac, most common cause= Trauma*
Constrictive pericarditis
Fibrous scar tissue making the pericardium stick to the heart
What is the immediate treatment for severe cardiac tamponade?
a. Oxygen
b. Cardiac drugs
c. Surgery
d. Pericardiocentesis (removal of fluid from the sac with a needle)
d. Pericardiocentesis (removal of fluid from the sac with a needle)
In severe cardiac tamponade, there is so much fluid in the pericardial sac compressing the heart that its function declines rapidly. The fluid must be removed quickly by inserting a needl
Coronary Artery Disease
Atherosclerosis blocks coronary arteries
Ishemia
Angina
Heart attack
Cardiac arrhythmias
Conduction deficits
Heart failure
Sudden death
Are ALL causes of what?
Ischemia
Coronary arteries
feed the heart itself!
Cardiac Catherization
insert dye into blood vessels to see where clot is, on which artery of heart
Chronic Ischemic Heart Disease
-stable angina
-variant angina
-silent myocardial ischemia
Acute coronary syndrome
-No ST-segment elevation--> unstable angina, Non-STEMI elevation AMI
-ST-segment elevation--> Q-wave AMI
Chronic Ischemic Heart Disease
Imbalance in blood supply and the heart's demands for oxygen
-Less blood (b/c blockage)
-Atherosclerosis
-Vasospasm
-Thrombosis
Higher oxygen demand
-Stress
-Exercise
-Cold
Angina
-chest pain
-more women experience chest pain in areas other than the chest ex. jaw, shoulder, left arm
-
people can experience angina in areas other than the chest
Risk Factors of Angina
-smoking, overweight,
Chronic Stable angina
-Pain when heart's oxygen demand increases
-chest pain on and off
-chronic but stable, goes away with rest
Variant angina
-Pain when coronary arteries spasm
-temporary, goes away
Silent myocardial ischemia
-Myocardial ischemia WITHOUT pain
-no pain, FULL BLOCKAGE*
Acute Coronary Syndromes
-ECG changes**
-Serum cardiac markers (Biomarkers)
Proteins released from necrotic heart cells
Myoglobin, creatine kinase, troponin**
Biomarkers
blood work, can help determine if theres damage to the heart, troponin
ECG/EKG
how we recognize acute coronary syndromes
Unstable Angina
NO BIOMARKERS*
Pain
Persistent and severe- occurs at rest
Low, intermittent or high risk for MI
Non-ST elevation Myocardial Infarction(NSTEMI)
BIOMARKERS*
Pain
Persistent and severe- occurs at rest
Low, intermittent or high risk for MI
- no ECG changes?
Acute Angina
Unstable- no biomarkers
Mild MI- biomarkers
NSTEMI- troponin levels rise, biomarkers
ST Elevation Myocardial Infarction (STEMI)
HEART ATTACK!!*
-Ischemic death of myocardial tissue
-Abrupt onset
-Severe and crushing chest pain
-Prolonged and not relieved with rest
-GI complaints
-Nausea/vomiting
-Sudden death- occurs within 1 hours of symptoms
Troponin
biomarker, high specifity of cardiac muscle
Acute Unstable Angina
NOT a full blown heart attack
true or false:
Chronic ischemic heart disease is more likely to result in stable angina than acute coronary syndromes.
True!
Ischemic heart disease is characterized by stable angina, which is associated with plaques that are fixed obstructions.
-Unstable angina is characterized by plaques with platelets stuck to them (these are likely to form a thrombus); they cause a ran
Acute Myocardial Infarction
-Chest pain
-Severe, crushing, constrictive OR like heartburn
-Sympathetic nervous system response
-GI distress, nausea, vomiting (decreased blood flow)
-Tachycardia and vasoconstriction
-Anxiety, restlessness (decreased blood to brain)
-Hypotension and s
True or False:
An Acute MI leaves behind an area of yellow necrosis?
True
Goals of Treatment
-Repurfusion
-Fibrinolytic agents (prevent further clot formation)
-Percutaneous coronary intervention
-Stent implantation
-Coronary bypass grafting (CABG)
Percutaneous coronary intervention
-Stent implatation
-Angioplasty (stent)
Complications of AMI (acute myocardial infarction)
Heart failure
Cardiogenic shock
Pericarditis
Thromboemboli
Rupture of the heart
Ventricular aneurysms
Cardiomyopathies
-
NONFUNCTIONAL HEART MUSCLE
-
affects VENTRICLES
Hypertrophic Cardiomyopathy-HCM
Ventricles are unusually THICK so there is not a normal amount of room for blood inside them
Restrictive Cardiomyopathy
Ventricles are too STIFF (rigid) to stretch
Dilated Cardiomyopathy
Ventricles are too WEAK to pump out the blood that is in them
Which type of cardiomyopathy is characterized by weakened ventricles?
a.) Dilated cardiomyopathy
b.) Hypertrophic c.)cardiomyopathy
d.) Restrictive cardiomyopathy
Peripartum cardiomyopathy
a.) Dilated cardiomyopathy
Ineffective Endocarditis*
-
Life threatening infection of the inner surface of the heart (most commonly caused by bacteria- Staphylococci leading causative agent)
**
Rheumatic Heart Disease*
-
Rheumatic fever- an immune-mediated multisystem inflammatory disease- occurs after a streptococcal pharyngitis (sore throat)
**
Atrioventricular Valves
Left Side- Mitral (bicuspid)
Right side- Tricuspid
Semilunar Valves
Pulmonary Valve
Aortic Valve
Stenosis
: valve will NOT OPEN all the way; it is harder to force blood through it
Regurgitation
: valve will NOT CLOSE all the way; it leaks when it should be closed
true or false:
Mitral valve regurgitation results in a diminished stroke volume.
True
If the mitral valve does not close as it should, a portion of the stroke volume (amount of blood ejected by the ventricle/beat) leaks back into the left atrium, decreasing the amount of blood that is ejected during that beat (SV).
Stroke Volume
-amount of blood ejected with each beat
BP Formula
BP= CO (SVxHR) X PR
Heart Murmurs
can be detected in a way we hear a valve problem