Ischemic Heart Disease Flashcards
Define IHD
Condition in which there is an inadequate supply of blood and oxygen to a portion of the myocardium
IHD typically occurs when
there is an imbalance between myocardial oxygen supply and demand
Most common cause of IHD is
atherosclerotic disease of an epicardial coronary artery or arteries sufficient enough to cause a decrease in blood flow and perfusion
Symptoms of IHD
may not appear until someone exerts themselves
What RF are associated with the emergence of IHD
Genetics
High fat and energy-rich diet
Smoking
Sedentary lifestyle
Obesity
Insulin resistance
T2DM
Myocardial oxygen demand =
Oxygen delivery
Oxygen problems
No oxygen = ischemia
Anemia = less oxygen carrying capacity
Define Hypoxia
Lack of oxygen
Exacerbates effects of atherosclerosis
Example of Hypoxia
Anemia
Cyanotic heart disease (abnormal connection between left and right heart –> lack of blood)
Advanced lung disease (problems with oxygenating the blood)
MVO2 Demaind
Heart rate Myocardial contractility Myocardial wall tension (stress) BP Inotropic status
Satisfactory level of oxygen-carrying capacity determined by:
Inspired level of oxygen
Pulmonary function
Hgb concentration and function
Coronary Blood Flow & 3 arteries where 75% of total resistance occurs
Blood flows through the coronary arteries, majority during diastole
- Large epicardial arteries (R1)
- Prearteriolar vessels (R2)
- Arteriolar and intramyocardial capillary vessels (R3)
Major determinants of coronary resistance is
Prearteriolar vessels (R2) Arteriolar and intramyocardial capillary vessels (R3)
Metabolic regulation
Exercise
Emotional stress (coronary vascular resistance)
Muscles –> aerobic –> lactic acid –> decrease pH –> affects size of blood vessels
Auto regulation
Coronary blood flow is maintained on the same level, independently on physiologic alterations in BP
Protective mechanisms
Where would the most myocardium be affected?
Left coronary artery atherosclerosis
Rupture of atherosclerotic plug
Fibrosis cap breaks which leads to tissue factor that is normally separate from the blood to be exposed
TF initiates coagulation leadign to a thrombus which leads to narrowing of blood vessels, complete occlusion, or resolve
Spasm of a atherosclerotic plug
Sudden contraction of the coronary arteries –> Prinzmetal’s angina
Define Emboli
Blockage of the blood vessels and related to a thrombosis
Where does coronary atherosclerosis occur?
Sites of increased turbulence in coronary flow
Branch points in the epicardial arteries
Coronary atherosclerosis RF
High LDL Low HDL Smoking HTN DM
50% Stenosis
Limited ability to increase blood flow in the response to an increased demand
80% stenosis
Blood flow at rest may be reduced
Stenosis that are hazardous?
Left main coronary artery or proximal left anterior descending coronary artery
Cause of ischemia
Mechanical, biochemical and electrical disturbances –> decreased myocardial oxygen tension –> inadequate perfusion
Effects of ischemia
Regional disturbance of ventricular contractility Segmental hypokinesia Segmental akinesia Segmental dyskinesia Reduced myocardial pump function
So the heart cannot function properly:
Dramatic decreased BP
Hyperperfusion in the brain (loss of consciousness)
Transient left ventricle failure
Heart is pumping blood to the aorta but the blood is coming back to the atrium –> Left sided heart failure –> see problems in the pulmonary circulation
Transient ischemia leads to
Angina pectoris
Prolong ischemia leads to
Acute MI (necrosis; irreversible damage)
What is happening when you have ischemia?
Less energy production
Lactic acid production
Time: If the ischemia si very short, you might not have a MI but it is last 2-4 hours you will have cell death and MI
More time = more damage
EKG in ischemia
Helps to determine if it is ischemia or MI
Acute vs chronic
Extent (entire thickness or partial)
Location
Partial Ischemia
Probelms with repolarization
ST depression
Entire thickness ischemia
ST elevation
Ischemia Arrhythmias
Electrical instability which may lead to isolated ventricular premature beats or even ventricular tachycardia or fibrillation
Sudden death from IHD caused by
Ischemia-induced ventricular tachyarrhythmias
Asymptomatic
No clinical manifestations despite exercise induced EKG changes, coronary artery plaques and scars secondary to MI
Symptoms
Chest discomfort due to angina pectoris or acute MI
Progressive IHD
Symptoms are currently more often or occur after exercise so they decrease their exercise but the symptoms keep coming
Acute Coronary Syndromes (ACS)
Acute MI with STEMI and Q wave Unstable angina, non-ST elevation NSTEMI, no Q wave Sudden cardiac death Prinzmetal's Variant Angina
P wave
Reflects the initial stimulation of impulses from atria to ventricle
QRS =
Depolarization of ventricles
ST
Depression = ischemia Elevation = IHD, MI or angina
Q wave
Represents the normal left to right depolarization
IHD + Atherosclerosis
Narrowing of the lumen, decreased blood flow –> ischemia is prevalent
IHD + Plug
Starts with platelet aggregation (adhere to endothelial)
Clot can lead to fully developed thrombus
Thrombus healing can lead to more narrowing or thrombus continues to grow and occludes the vessel –> MI
Partial occlusion represents
Unstable angina pectoris or NSTEMI
Thormbus healing represents
Chronic coronary artery disease or stable angina pectoris
Complete occlusion =
STEMI
Partial occlusion =
NSTEMI or unstable angina
Stable Angina Pectoris
Male over 50 Women over 60
Chest discomfort
Typically places a hand over the sternum
Crescendo (loud and fast)-decrescendo (2-5 min)
Can radiate to either shoulder and to both arms
Stable Angina Pectoris Clinical Manifestations
Arises in the back, root of the neck, jaw, teeth, epigastrium
Typically caused by exertion or emotions
Symptoms are relieved by rest or sublingual nitroglycerin
Symptoms of MI other than angina
Dyspnea
Nausea
Fatigue
Faintness
Indication of UA
Angina occuring with less exertion than in the past
Occuring at rest
Awakening the patient from sleep
Intermittent claudication
Stroke
TIA
- things to ask
FH of premature IHD
DM, hyperlipidemia, HTN
Smoking
RF for atherosclerosis
Physical Exam
Search for evidence of atherosclerotic disease at other sites
Xanthomas
Ophtalmologic examination of HTN
Anemia, thyroid disease (lipid abnormalities)
Cardiac enlargment
Systolic murmur
Carotid arterial bruits
Noise at the carotid artery bc of decreased flow
Lab Exams
Urine for DM Cholesterol A1c Creatinine Hct Thyroid Xray Protein C EKG Stress test
Define NSTEMI/UA
Angina pectoris or equivalent ischemic discomfort with at least one of three features
Features is NSTEMI/UA
Occurs at rest for 10 minutes or more
Sever and new onset
Occurs with a crescendo pattern
NSTEMI/UA Pathophysiology
Athersclertic plaque rupture or erosin with a nonocclusive thrombus
Progressive mechanical obstruction
Secondary to increased myocardial oxygen demand or decreased supply
NSTEMI/UA Manifestations
Severe chest pain
Dyspnea and epigastric discomfort
Pale cool skin, sinus tachycardia, third or fourth hear sound, hypotension
NSTEMI/UA Biomarkers
CKMB and troponin: elevation = NSTEMI
Troponin elevation = CHF, myocarditits, PE or false positives
Why are CKMB and troponin increases seen?
Myocardial destruction releases them
STEMI
Myocardial cell death due to prolong and severe ischemia
- Complete occlusion by thrombus
STEMI Pathophysiology
Thrombotic occlusion previously affected by atherosclerosis
Thrombus develops rapidly
Plaque ruptures
Plaques prone to disruption:
Rick lipid core and thin fibrous cap
Increased amount of inflammatory cells
Extent of damage
Territory supplied by affected vessel
Extent of occlusion
Duration of occlusion
Quantity of blood supplied to affected tissue
Demand for oxygen of the myocardium whose blood supply is limited
Endogenous factors that can produce early spontaneous lysis of the occlusive thrombus
STEMI RF
Multiple coronary RF
UA
Hypercoagulability
Collagen vascular disease (autoimmune disorder)
Cocaine abuse
Intracardiac thrombi (sluggish blood flow)
Coronary emboli
STEMI Clinical manifestations
Pain is deep and visceral (heavy, squeezing, crushing)
Occurs at rest, more sever and last longer that AP
Anxiety, N/V
Make sure its not something else
STEMI Physical Findings
Substernal chest pain >30 minutes + diaphoresis Tachycardia/HTN (anterior MI) Bradycardia/HypOTN (inferior MI) Pericardial friction rub Fever Systolic pressure decline
STEMI EKG
ST elevation
Q wave present
STEMI Biomarkers
Troponin
Troponin-1
CK
CKMB
MI is
the most common form of IHD
Deaht of cardiac muscle due to prolong severe ischemia
STEMI =
Transmural infarction
Entire thickness
ST elevation
NSTEMI =
Subendocardial infarction
Partial thickness
ST depression
If a patient dies within 24 hours…
It is hard to determine if there is tissue necrosis or not because all that occurs is a change in the myocyte shape but not a loss of nuclei
Day 3-4 after MI
Inflammatory changes are prominent
Lack of nuclei can be seen
Day 7-10 after MI
Macrophages are coming into the damaged tissue and removing necrotic tissue
new blood vessels are being formed
Elevated fibroblast can be see
Tissue is called Granulation tissue
Day 10-weeks after MI
Repair process leads to scar tissue made of collagen
Reperfusion
Restore circulation to the tissue
- Not always a good thing!
Reperfusion can lead to:
Arrhythmias, hemorrhage, prolong ischemic function
Preconditioning is
preparing the tissue for repetitive ischemia to occur
If ischemia is longer and reperfusion occurs after 2-4 hours,
the tissue will be nectrotic but some of it can be healthy after time
Complications of MI + mortality
30% mortality rate now down to 7% mortality rate if patient receiving therapy timely
Arrhythmias are the:
Most common cause of pre-hospital death
Papillary muscle dysfunction leads to
Mitral regurgitation
Cardiac tamponade
Accumulation of blood in the pericardium
Cerebrovascular Disease
Dealing with changes in the nervous tissue in the brain due to vascular changes such as thrombosis, embolism, hemorrhage
Thrombosis, embolism, hemorrhage are all related to
atherosclerosis and HTN
Thrombosis and embolism
Decreased blood supply to the CNS leading to ischemia (infarction), hypoxia and tissue damage
Hemorrhage
Rupture of blood vessel walls
Global cerebral ischemia
Affects the entire brain
Leads to systemic issues
Can cause: cardiac arrest, shock, sever hypotension
Focal cerebral ischemia
One area of the brain
Caused by: embolic occlusion, thrombotic occlusion, vasculitis, atherosclerosis
Mild cases of ischemia
Post-ischemic confusional state followed by complete recovery
Sever cases of ischemia
Death or vegetative state
Hemorrhagic:
Emboli
Nonhemorrhagic:
Thrombosis
