Cardiac pathology part 1 Angina/MI/CHD Flashcards
Describe the pathophysiology of a stable angina
Chest pain lasting less than 20 minutes that’s triggered by emotional/physical stress
Signs:
- Chest pain radiating to the left arm or jaw
- Diaphoresis
- Shortness of breath
- Depressed ST segments
Rx with rest or nitroglycerin
A 45 yr old man with a BMI of 30 took up running for his new years resolution. He suddenly collapsed complaining of chest pain radiating down his left arm.
Upon arrival to the hospital patient has diaphoresis & shortness of breath but he exclaimed he felt “fine now & wanted to go home”. What’s the next best step in treatment? What did the patient likely suffer?
Next best step would be to do an ECG to assess whether this patient had an MI or angina
If results show ST depression = Stable angina
If results show ST elevation & significant Q waves = MI
Because the Chest pain was short acting it’s likely the patient has a stable angina
Describe the pathophysiology of an unstable angina
Chest pain that presents at rest. It usually happens because of an atherosclerotic plaque rupture with thrombosis
Signs:
ST Depression
Chest pain at rest
Rx with nitroglycerin
What is a major concern when treating a patient experiencing an unstable angina?
There’s a high risk of it progressing to an MI which is irreversible (necrosis)
Describe the pathophysiology of a prinzemetal angina
Episodic chest pain that happens when platelets release more thromboxane A2 which cause vasospasm in the coronary arteries
Signs:
ST Elevation
Episodic chest pain
Rx Nitroglycerin or Calcium channel blockers
What are the causes of an MI?
- Most common
- Other
MC = Rupture of atherosclerotic plaques
Other:
- Vasospasms (prinzmetal angina, cocaine, emboli, vasculitides i.e Kawasaki’s)
Signs of an MI
- Severe & crushing chest pain that lasts longer than 20 minutes (radiates to left arm &/or jaw)
- Diaphoresis
- Dyspnea
(symptoms won’t be relieved with nitroglycerin)
60 yr old woman is brought the ER complaining of crushing chest pain that radiates to her jaw. The team administers nitroglycerin but to no effect. What is the next course of action?
No relief of symptoms means this is likely an MI, administer:
- Aspirin/heparin
- Supplemental O2
- Nitrates
- B-blockers
- ACE inhibitors
Team should prep for fibrolysis or angioplasty while confirming the diagnosis with an ECG via ST elevation and significant Q waves
Crushing/severe chest pain radiating to the left arm or jaw that lasts longer than 20 minutes (don’t wait to find out though!)
Diaphoresis
Dyspnea
(symptoms won’t be relieved with nitroglycerin)
signs of an MI
What part of the heart is typically affected in an MI & what are the arteries involved?
1. LAD (most common, infarcts the anterior wall of the LV)
Typically, it’s the left ventricle.
MI’s can involve complete occlusion of the LAD, RCA & Circumflex artery (most common in that order) what areas of the LV are infarcted in each of these cases?
1. LAD (most common, infarcts the anterior wall of the LV)
How does an MI present as initially (ECG) then what are the changes as it progresses?
Initially MIs have subendocardial necrosis involving less than half of the heart wall & ST Depression
If the ischemic damage progresses to transmural necrosis (all the heart wall) there will be ST Elevation
MI Timeline:
What would you expect to see 2-4hrs post MI? What are the potential complications?
Elevated troponin
Comps:
- Cardiogenic shock
- Congestive heart failure
- Arrythmia
MI Timeline:
What would you expect to see 7-10 days post MI? What are the potential complications?
Normalized troponin levels
Granulation tissue (macrophages, fibroblasts, collagen, & blood vessels)
MI Timeline:
What would you expect to see 4-6hrs post MI? What are the potential complications?
Elevated CK-MB
Dark discoloration
Coagulative necrosis
Comps:
- Arrythmia
MI Timeline:
What would you expect to see 4-24hrs post MI? What are the potential complications?
Dark discoloration
Coagulative necrosis
Comp:
Arrythmia
MI Timeline:
What would you expect to see 1-3 days post MI? What are the potential complications?
Lots of neutrophils **
Yellow pallor
Comp:
Fibrous pericarditis (chest pain + friction rub)
MI Timeline:
What would you expect to see 4-7 days post MI? What are the potential complications?
Lots of macrophages
Yellow pallor
Comp:
- Cardiac tamponade (rupture)
- Shunt (ruptured IV septum)
- Mitral insufficiency (ruptured papillary muscles)
How old is the MI?
1-2 hrs old the wavy fibers are necrotic myocytes
How old is the MI?
18-24 hrs
Coagulative necrosis
Eosinophilia
Contraction band necrosis (reperfusion injury)
How old is the MI?
1-3 days (24-72hrs)
Complete coagulative necrosis with neutrophil infiltration and fragmentation
How old is the MI?
4-7 days
Macrophages with granulation tissue at the edges of the infarct
No more neutrophils & the walls are weakened at this point
How old is the MI?
4-7 days old you can see the central pallor & hyperemic border
MI Timeline:
What would you expect to see 1-3 weeks post MI? What are the potential complications?
A red border with granulation tissue (fibroblasts, collagen, & blood vessels)
MI Timeline:
What would you expect to see Months post MI? What are the potential complications?
White scar tissue & fibrosis
Comps:
- Aneurysm
- Mural thrombosis
- Dressler’s syndrome
What treatment(s) option for an MI would reduce the risk of thrombosis?
Aspirin & Heparin
What treatment(s) option for an MI would minimalize ischemic damage?
Supplemental oxygen
What treatment(s) option for an MI would help dilate veins & the coronary artery to reduce BP?
Nitrates
What treatment(s) option for an MI would reduce heart rate & oxygen demand by the heart?
Beta blockers
What treatment(s) option for an MI would reduce LV dilation?
ACE inhibitors
What treatment(s) option for an MI are useful for opening up blockages & what is the major drawback?
Fibrinolysis & angioplasty both help open up the occluded blood vessel but have significant risk of a reperfusion injury
A young patient with Downs syndrome dies suddenly, the physician suspects a cardiomyopathy… why?
Down syndrome is associated with ostium primum defect (whole between the atria) meaning an embolus may have formed & passed into systemic circulation i.e the brain
What is sudden cardiac death and what causes it? (most common & other)
When death follows within an hour of symptoms onset (chest pain etc)
Common:
- Ventricular arrythmia (Ischemia due to atherosclerosis is a risk)
Other:
- MVP
- Cocaine
- Cardiomyopathy
Describe the pathophysiology of Left-sided CHF
The heart can’t pump blood into systemic circulation well, so there’s backflow into the pulmonary circulation. Overall there’s not enough blood in systemic & too much in pulmonary. This means pulmonary experiences congestion while systemic organs are at risk of ischemia
What are the causes of Left-sided CHF?
Ischemic damage to the heart
Hypertension
Dilated cardiomyopathy
MI
Restrictive cardiomyopathy
What are the clinical symptoms of someone with left-sided CHF?
Pulmonary edema:
- dyspnea
- paroxysmal nocturnal
dyspnea
-Orthopnea
- Cracking lungs
Reduced blood flow to kidneys
- Activated RAAS = high BP
What medication is used to treat left-sided CHF?
ACE inhibitors to lower BP
Describe the pathophysiology of right-sided CHF? What causes it?
It’s usually caused by left-sided CHF, which causes congestion in the systemic circulation
It can also be caused by
- Left-to-right shunts
- Chronic lung disease (cor pulmonale)
What are the clinical signs of Right-sided CHF?
Increased JVD
Painful hepatosplenomegaly
aka Nutmeg liver
Pitting edema (lots of hydrostatic pressure)
- Chest pain that radiates to the L.arm or jaw (lasting less than 20min)
- Triggered by exertion or emotional stress
- Diaphoresis
- SOB
Stable angina
What is the classical presentation of a Stable angina?
- Chest pain that radiates to the L.arm or jaw (lasting less than 20min)
- Triggered by exertion or emotional stress
- Diaphoresis
- SOB
What would you expect on an EKG reading for a stable angina? Why?
ST depression, because subendocardial ischemia reduces conductivity in the heart)
A 60yr old man presents with chest pain that radiates to his jaw. He said he was gardening in the hot sun. He’s sweating & is short of breath, he states after sitting down he feels better. He recounts he’s experienced brief episodes like this before & that they never last long.
- What is the likely diagnosis?
- What would his EKG show?
- What would you administer to relieve his symptoms?
- Which artery is affected & what is the major cause of this condition?
- Stable angina
- ST depression
- Nitroglycerin
- Narrowing of the Coronary artery likely caused by atherosclerosis
What are the signs of an unstable angina?
- Chest pain at rest that radiates to the L.arm or jaw (<20min)
- Diaphoresis
- SOB
What would you expect on an EKG reading for a stable angina? Why?
ST depression (subendocardial ischemia)
What condition is likely to cause an unstable angina ?
Atherosclerosis with thrombosis causing incomplete occlusion of the coronary artery
What is a major concern regarding the sequelae of an unstable angina?
It has a high risk of progressing to an MI
How would you treat an unstable angina?
Give nitroglycerin (a vasodilator) to reduce preload/work the heart has to do
What is the clinical presentation of a prinzmetal angina?
- Episodic chest pain that radiates to the L.arm/jaw (<20min)
- Diaphoresis
- SOB
What would you expect to see on an EKG in a person with Prinzmetal angina?
ST elevation because it has transmural ischemia (all layers of the heart)
How would you treat a prinzmetal angina?
Give nitroglycerin (reduce preload) & Ca2+ channel blockers
What causes a prinzmetal angina?
Vasospasms of the coronary artery
What are the key signs of an MI?
- Crushing/severe chest pain radiating to the L.arm & jaw lasting longer than 20min
- Diaphoresis
- SOB
What is the most common cause of an MI?
Rupture of an atherosclerotic plaque causing complete occlusion of the coronary artery
Which part of the heart does an MI typically impact?
The left ventricle (other parts are usually spared because the coronary artery feeds the LV most)
What are the less common causes of MI’s?
MVP
Cardiomyopathies
Cocaine abuse
Vasospasms
How do you treat an MI?
Aspirin/heparin
ACE inhbitors
B-blockers
Nitrates
Supplemental O2
(Nitroglycerin won’t help)
Describe the features of the initial phase of an MI
It starts with subendocardial necrosis of less than 50% of the myocardial thickness & the EKG shows ST depression
Explain what a ventricular septal defect (VSD) is & what is it associated with?
A defect in the intraventricular septum that is associated with FAS.
It causes a right-left shunt between the ventricles that’s usually asymptomatic at birth (except when it’s large)
What’s the congenital heart defect?
VSD
What is the most common congenital heart defect?
VSD
Explain what an Atrial Septal Defect is & what is it associated with?
A defect in the atrial septum that present in two ways:
90% of cases = ostium secundum
Down syndrome = ostium primum
Both result in left-to-right shunting & and S2 split (more blood in the right atrial delays the pulmonary artery from closing)
What is a major complication of an ASD?
A paradoxical embolism
What is the congenital heart defect? & what are the findings?
ASD
Left-to-right shunting & S2 split
Explain what an Patent Ductus Arteriosus (PDA) is & what is it associated with?
It’s when the arteriosus didn’t close during development resulting in a left-to-right shunt between the aorta & pulmonary artery
It’s associated with congenital rubella
How does PDA clinically present?
At birth it is usually asymptomatic with a machine-like murmur that can lead to Eisenmenger syndrome
How do you treat/fix PDA?
Administer Indomethacin to decrease PGE (to decrease the patency of PDA) & close the PDA opening
What’s the congenital heart defect? What condition is it associated with?
PDA (machine murmur) & it’s associated with congenital rubella
Explain what a Tetralogy of Fallot is & what is it associated with?
It’s a combination of many structural defects including:
- R. ventricular stenosis & hypertrophy
- VSD
- Aorta that overrides the VSD
It results in Right-to-left shunting & early cyanosis (depending on the degree of stenosis)
What is the congenital heart defect?
Tetralogy of Fallot
Explain what a Truncus Arteriosus is?
The truncus didn’t divide so there’s ONE large vessel acting as the aorta & pulmonary artery, this means O2 rich & poor blood mix before reaching systemic or pulmonary circulation (mixer)
Shows early cyanosis
What’s the congenital heart defect?
Truncus arteriosus
Explain what a Tricuspid Atresia is & what is it associated with?
It’s when the tricuspid valve orifice doesn’t develop & the right ventricle is hypoplastic,
resulting in a right-to-left shunt.
It’s associated with ASD
A warning sign is early cyanosis
What is the congenital heart defect? What is it associated with
A Tricuspid Atresia & it’s typically associated with an ASD
Explain what a Coarctation of the aorta is?
It’s narrowing of the aorta, it presents in two forms:
Infantile= It’s associated with a PDA & the coarctation is after the aortic arch but before a PDA
Adult= It may be associated with a bicuspid aortic valve& the coarctation sits after the aortic arch
What are the symptoms of an infantile coarctation of the aorta? What conditions is it associated with?
Cyanosis in the lower extremities & it’s associated with PDA & Turners syndrome
What are the symptoms of an adult coarctation of the aorta? What condition is it associated with?
- Hypertension in the upper extremities
- Hypotension & weak pulse in the lower extremities
- Collateral circulation in the intercostal arteries
- Engorged arteries
Associated with a bicuspid aortic valve
What’s the congenital heart defect? What is particularly unique about it?
Coarctation of the aorta & it has an adult and infantile form!
Acute Rheumatic fever is diagnosed by the Jones criteria split into major & minor symptoms. What are the major criteria needed for a diagnosis?
- The presence of elevated ASO or Anti-DNase B Titres
- Migratory polyarthritis (joint swelling that moves aroud)
- Pan carditis
- Endocarditis of mitral valve vegetation + regurgitation
- Myocarditis with Aschoff bodies
- Pericarditis with friction rub & chest pain - Subcutaneous nodules
- Erythema marginatum (rash on trunk/limbs)
- Sydenham chorea (invol movements)
- The presence of elevated ASO or Anti-DNase B Titres
- Migratory polyarthritis (joint swelling that moves around)
- Pan carditis
- Endocarditis of mitral valve vegetation + regurgitation
- Myocarditis with Aschoff bodies
- Pericarditis with friction rub & chest pain - Subcutaneous nodules
- Erythema marginatum (rash on trunk/limbs)
- Sydenham chorea (invol movements)
Are all signs of which cardiac-related condition?
Acute rheumatic fever
What happens to the heart if the Aortic valve is scarred by CRHD?
The commissures end up fusing together
What are the signs of Aortic regurgitation?
- An early-blowing diastolic murmur
- Hyperdynamic Circulation:
- Different pulse pressures between systolic (higher because increased stroke vol) & diastolic (lower because of regurgitation)
- Bounding pulse “Water-hammer pulse”
- Quincke pulse (pulsing nail-beds)
- Head bobbing
Patient presents with an early blowing diastolic murmur
What is the condition?
Aortic regurgitation
Explain what mitral regurgitation is?
When the mitral valve leaks blood back into the L. atrium during systole, resulting in volume overload
What causes Mitral regurgitation?
Common
Other
Common: A complication of MVP
Other:
Infective endocarditis
Acute rheumatic heart disease
Papillary muscle rupture post MI
Patient has an opening snap followed by a diastolic rumble
Mitral stenosis
