3.3.2. Cardiac Pathology Part 1: Ischemic, CHF, Congenital Defects Flashcards
Ischemic heart disease is usually due to what?
Atherosclerosis of coronary arteries
What is stable angina?
Get angina with stress or activity
Why in stable angina do we not always have pain?
It’s mild decreased blood flow in the coronary artery, but when we exercise and need more blood to the heart tissue, we can’t get it, it gets a little ischemic, and we feel pain
In Stable Angina, it is due to atherosclerosis of coronary arteries with ____ ____.
> 70% stenosis
What type of injury is stable angina?
It is reversible!
in Stable Angina, the cells don’t die, hence it being reversible. However, they do do this…
Get bigger
Presentation of Stable Angina
- CP < 20 minutes that radiates to left arm or jaw
- Diaphoresis
- SOB
What EKG finding do we get with Stable Angina? Why?
ST Depression due to subendocardial ischemia
Why is the damage caused by Stable Angina subendocardial?
Coronary arteries feed epicardium to endocardium, so if there is a blockage, the most affected portion will be the latest, which typically happens just below the endocardium, or, subendocardial.
Treatment for Stable Angina?
Rest or NTG
What is unstable angina?
Pain even at rest due to a rupture of an artherosclerotic plaque with thrombosis and incomplete occlusion of the coronary artery.
How is reversibility different between stable and unstable angina?
It’s not both irreversible
What is an important note about the occlusion in unstable angina?
It is incomplete occlusion
EKG and treatment for unstable angina
NTG, EKG shows ST depression
For unstable angina we have a high risk for ____.
MI
Prinzmetal angina is what?
Vasospasm of the coronary artery
What is different about prinzmetal angina from stable and unstable angina?
Prinzmetal is complete and random occlusion, so the chest pain is still episodic, but it is completely unrelated to exertion
EKG for prinzmetal angina? Why?
ST elevation because the early part of the coronary artery is clamped in the epicardium, so the blood is lost through the entire vessel whih leads to ST elevation.
Treatment for Prinzmetal Angina
NTG and Ca Channel blockers
What is a myocardial Infarction?
Necrosis of cardiomyocytes due to a rupture of the atherosclerotic plaque leading to a thrombosis and complete occlusion of the coronary artery
How long does it take for the cardiac tissue to turn necrotic?
> 20 minutes
How can vasculitis cause an MI?
Inflammed interior wall, coag pathway, thrombus, complete occlusion results.
Presentation for MI
- Severe crushing chest pain > 20 minutes
- Diaphoresis
- Dyspnea
Effect of NG on an MI
None.
Infarction usually involves the _____
Left Ventricle.
Most common ischemic location on the heart
On the left ventricle anteriorly running down the anterior descending artery causing infarct to the anterior heart and IV septum
If we see infarction on the posterior wall of the Left ventricle and the posterior aspect of the IV septum, what artery is affected?
Right coronary artery
Lateral LV infarction indicates what artery being affected?
Left circumflex artery
During the initial phase of MI, what damage do we see? EKG?
Subendocardial at first with ST depression and accounting for only about 50% of damage
How does the MI progress?
With time, we see full thickness necrosis (transmural) so we’ll see ST elevation
Lab tests for MI
- Troponin I
- CKMB
Best marker for MI and what does it show?
Troponin I is the most sensitive and specific marker
Occurs 2-4 hours after an infarction and peaks at 24 hours. Returns to normal by 7 - 10 days
Besides Troponin I, what can we use? How does it work?
CKMB
- Rises 4 - 6 hours after infarction
- Peaks at 24 hours
- Returns to normal by 72 hours
Best treatment for MI and why
- ASA and Heparin to eliminate additional thrombosis
Besides ASA and Heparin what else can we treat MIs with?
Oxygen due to ischemia
Nitrates to vasodilate arteries and veins, veins in particular in order to decrease preload on the heart
Beta blockers to slow HR and decrease demand for oxygen and possibility of arrhythmia
ACE inhibitor to decrease left ventricular dilation.
ACE inhibitors are good for MIs. What do they do and why is it so great
ACE blocks angiotensin I to Angiotensin II.
Angio II constricts arterioles and also causes fluid retention after stimulating the adrenal glands to make aldosterone
More definitive treatments for MI
- Fibrinolysis
2. Angioplasty
Action of fibrinolysis
Destroy the thrombus
When blood is restored, it hits now dead heart tissue in MI. What complications does this cause?
- Contraction Band Necrosis - Calcium returns to dead cell and causes creation of band lines as it causes portions of it to contract.
- Reperfusion injury - returning oxygen to dead tissue can cause the creation of free radicals which can further injure the myocardium
You help your patient who suffered from a MI but noticed that his enzymes were still present beyond the normal time. What happened?
Reperfusion injury!
When and what microscopic changes occur after an MI?
<4 hours = nothing
4 - 24 hours = Coagulative Necrosis
1 - 3 days = Neutrophils
4 - 7 days = Macrophages
1 - 3 weeks = Granulation tissue with plump fibroblasts, collagen and blood vessels
Months - Fibrosis
When do we see a yellow pallor on the heart?
1 - 7 days s/p an MI
When do we see a Dark discoloration on the heart?
4 - 24 hours s/p MI
When do we see a white scar on the heart?
Months s/p MI
When, s/p and MI, do we see a red border emerge as granulation tissue enters the edge of an infarct?
1 - 3 weeks s/p MI
When do MI affected cells lose their nuclei?
4 - 24 hours, during coag necrosis
Complications within the first four hours of an MI (3)
Cardiogenic shock (massive infarction) where the heart fails and lack of blood flow to major organs.
You can also get CHF due to a decrease ejection fraction
arrhythmia
Complication in the coagulative necrosis stage?
4 - 24 hours
Arrhythmias
When the neutrophils arrive s/p an MI, what complications do we face? Why?
Fibrinous pericarditis - presents as chest pain with friction rub.
During these first few days when we are inflamming with neutrophils, some of that inflammation goes to the pericardium and causes pericarditis.
When the macrophages arrive s/p an MI, what complications do we face?
Ruptures due to marcophages eating all that bad stuff
- Rupture of ventricular free wall (could lead to cardiac tamponade)
- Rupture of IV septum causing shock as blood gets shunted from LV to RV
- Rupture of papillary muscle, causing the valves to become messed up, causing systolic backflow into the atria
If we have papillary muscle issues, what do we know about the MI?
It was caused by a blockage to the right coronary artery (which feeds the papillary muscles)
Why does a red border form during granulation?
Blood vessels come from the outside in to heal
When the scar formation occurs s/p an MI, what complications are we worried about?
Aneurysm due to a weakened wall
Also a mural thrombus due to a weakened wall.
Dressler Syndrome also possible. MI can cause the pericardium to release antibodies and your immune system to attack the pericardium causing pericarditis 6-8 weeks s/p MI.
Moving on to heart failure, what can cause left sided heart failure?
Ischemia HTN Dilated cardiomyopathy MI Restrictive cardiomyopathy
Clinical signs of left sided heart failure will be indicated by what?
Pulmonary congestion - Can’t pump the blood forward, its gonna pump back towards the lung
Symptoms of left sided heart failure
- Pulmonary edema with dyspnea
- PND
- Orthopnea
- Crackles
- Heart failure cells
What are heart failure cells?
Hemosiderin laiden macrophages
Decreased forward perfusion caused by left sided heart failure leads to what?
Activation of Renin angiotensin system
Most common cause of right sided heart failure?
Left sided failure.
Other important causes of right sided heart failure besides left sided heart failure
Left to right shunt and chronic lung disease
Cor Polmonale
When your heart fails due to chronic lung disease
Clinical features of right cardiac failure
Due to congestion
- JVD
- Painful Hepato Splenomegaly that may lead to cardiac cirrhosis
- Dependent pitting edema
Ventricular Septal Defect
Defect in the septum dividing the ventricles
VSD associated with what?
Fetal Alcohol syndrome
What is the most common congenital heart defect?
VSD
Key problem in VSD? Explain timeline.
Blood chooses lower pressure and will go from LV to RV leading into Left Right shunt.
This leads to lung back up as more fluid is coming from the Right side. Eventually the pulmonic pathway will have the highest pressure, and the RV willchoose the lower pressure pathway, the LV, which will send deoxygenated blood back around systemically
This leads to Cyanosis
Small vs. large defects from VSD
Small - Asymptomatic
Large - Eisenmenger - RV hypertrophy due to larger pressure gradients, clubbing, etc
ASD?
Defect in atrial septa
Most common type of ASD?
Ostium secundum
What is ostium primum type associated with?
Down Syndrome
Heart sound associated with ASD? How?
Split S2
Blood in LA travels to RA, causing it to have more blood, leading to a delay in pulmonic valve closure
Paradoxical Embolus
Normally emboli from DVT goes into the RA then RV and into the lungs to cause a Pulmonary Embolus but inASD, it can go from the RA to LA to LV and then anywhere in the body, even the brain.
What is Patent Ductus Arteriosus? What is it associated with?
Failure of Ductus Arteriosus to close.This is associated with congenital Rubella
Problem with Ductus Arteriosus being active in an adult?
Blood will go from the Aorta back to the pulmonary artery and cause pulmonary HTN, increasing pressure and causing blood to go from the RV to the pulomary artery and then straight to the Aorta which is now a lower pressure.
This will cause deoxygenated blood to circulate, causing cyanosis in the LE only (the DA occurs after the upper extremity pathways, so those are unaffected)
Results of Left to Right Shunt between aorta and PA?
- Asymptomatic t birth
- Eisenmerger Syndrome results in lower extremity cyanosis
Treatment of Patent DA?
Indomethacin which decreases PGE, which results in PDA closure
Problems with Tetralogy of Fallot
- Stenosis of RV outflow tract
- Right ventricular hypertrophy
- VSD
- Aorta that overrides the VSD
Explain what is happening with Tetralogy of Fallot
Stenosis of RV outflow and an enlarged Right Ventricle cause the ventricle to be less efficient. Since these patients also have a VAD with the Aorta taking over, the blood from the RV will go through the Aorta immediately and cause cyanosis
Patients learn to ____ in response to cyanotic changes caused by Tetralogy of Fallot
Squat
Film study for Tetralogy of Fallot
CXR with heart looking like a boot
In transposition of great vessels what happens?
Aorta and Pulmonary Artery switch, but not their end goals, so they just feed their own sided chmbers
Ex. Blood to RA to RV to aorta back to RA
How do we treat transposition of great vessels?
Keep the Ductus Arteriosus open with PGE and make a shunt
___ ___ is associated with Transposition of Great vessels
Maternal diabetes
Presentation of transposition of great vessels
Early cyanosis due to no oxygenated blood in circulation
What is happening with Truncus Arteriosus?
Single large vessel arising from both ventricles due to the trunk failing to divide
How does Truncus Arteriosus also show signs of early cyanosis?
Deox and ox blood are mixed together and then sent through Aorta or pulmonary.
Tricuspid Atresia
Tricuspid valve orifice fails to develop, so blood cannot enter the RV.
- Causes opening to occur between atria (ASD) and causes the right ventricle to become hypoplastic
Sign of Tricuspid Atresia?
Early cyanosis
What is Coarctation of the Aorta?
Narrowing of the Aorta
Child Coarctation of the Aorta
Associated with PDA. Narrowing occurs between the aortic arches and the DA. Blood will flow from the RA to the RV to the pulmonary, through DA and through the rest of the body, giving you LE cyanosis since the DA is after the arches.
Infantile Coarctation is associated with ____ ____.
Turner syndrome
Adult Coarctation
Not associated with a PDA
Get coarctation after the aortic arch. Causes buildup of blood (HTN) in the upper extremities with lower blood pressure in the LE since the blood cannot get to the LE.
Presentation of adult coarctation
HTN in UE and hypotension in LE with weak pulses in LE
Adult coarctation associated with ___ ___ ___.
Bicuspid Aortic valve
____ ____ develops across intercostal arteries due to Adult coarctation
Collateral circulation
Chest x ray of someone with adult coarctation
Engorged arteries cause notching of ribs in xray due to collateral circulation
