Patho/CP
Compare and contrast the development of HFpEF and HFrEF. [300pts] (SO2:LO4)
HFpEF (Preserved EF): The primary mechanical defect is impaired ventricular relaxation and filling due to severe myocardial stiffness and non-compliance. The ventricle undergoes concentric hypertrophy, characterized by thickened walls and a normal or severely restricted (shrunken) cavity volume (decreased internal radius).
HFrEF (Reduced EF): The primary mechanical defect is impaired myocardial contraction and emptying due to a weakened, stretched muscle. The ventricle undergoes eccentric hypertrophy and dilation, where the muscle walls become thinned, stretched out, and weak, and the left ventricular chamber becomes abnormally enlarged (increased internal radius).
What is the inheritance pattern of hypertrophic cardiomyopathy? [300 pts] (LO2:SO1)
Autosomal dominant - each child of an affected biological parent has a 50% chance of inheriting the genetic mutation.
Explain the purpose of urine toxicology in HCM. [300 pts] (LO3:SO3)
Urine toxicology rules out substance-induced arrhythmias. Recreational sympathomimetics like cocaine or amphetamines can trigger severe coronary vasospasm, acute myocardial ischemia, and electrical instability. Identifying or excluding these toxic triggers is clinically essential in sudden cardiovascular collapse.
What is the mechanism of Epinephrine during cardiac arrest, and how does it make subsequent defibrillation shocks more successful? [500 pts] (LO1:SO2)
Epinephrine, an alpha-1 adrenergic agonist, causes intense peripheral vasoconstriction, increasing systemic vascular resistance and aortic diastolic pressure. Since coronary arteries fill during diastole, this raises coronary perfusion pressure during chest compressions, delivering oxygen and ATP to starving myocytes. This restores mechanical contractility, making them highly responsive to depolarization from subsequent defibrillation.
What is the difference between arteriosclerosis, atherosclerosis, and arteriolosclerosis? [400 pts]
Arteriosclerosis: This is a broad umbrella term for the thickening, hardening, and loss of elasticity of arterial walls ("hardening of the arteries"). It encompasses both atherosclerosis and arteriolosclerosis, as well as non-inflammatory degenerative conditions like Monckeberg medial calcific sclerosis.
Atherosclerosis: This is the most common and clinically prominent form of arteriosclerosis. It selectively affects large and medium-sized elastic and muscular arteries (e.g., the aorta, coronary, carotid, and renal arteries). It is characterized by the formation of lipid-rich plaques (atheromas) within the intima of the vessel. Over time, these plaques develop a necrotic core composed of cholesterol and cellular debris, capped by a fibrous layer of smooth muscle cells and collagen.
Arteriolosclerosis: This condition selectively affects small arteries and arterioles (typically associated with chronic systemic diseases like hypertension and diabetes mellitus).
Which cardiac conditions produce a harsh crescendo-decrescendo systolic murmur after S1? [300 pts] (SO2:LO2)
Aortic stenosis: Narrowing of the aortic valve, which blocks blood flow from the left ventricle to the body.
Pulmonary stenosis: Narrowing of the pulmonary valve, which blocks blood flow from the right ventricle to the lungs.
Hypertrophic cardiomyopathy: Genetic disease where the heart muscle thickens, sometimes blocking blood flow out of the lower left chamber (obstructive type)
What are the main genes that are mutated in patients with HCM? [500 pts] (LO2:SO1)
β-myosin heavy chain 7 (MYH7) and myosin-binding protein C3 (MYBPC3)—are the most common, accounting for about 75% of all known mutation-positive cases.
They encode essential structural proteins that form the sarcomere—the basic contractile unit inside cardiac muscle cells
Altered proteins cause structural changes (myocardial stiffness, abnormal calcium handling, and replacement fibrosis/scarring), preventing normal relaxation during filling (diastolic dysfunction) and creating an unstable electrical environment predisposing to malignant ventricular arrhythmias.
Justify why a Cardiac MRI (CMR) is the preferred diagnostic gold standard when evaluating suspected apical HCM. [400 pts] (LO3:SO2)
Per AHA guidelines, a Cardiac MRI is indicated when TTE is inconclusive or suboptimal. It is preferred for definitively diagnosing apical HCM because its superior spatial resolution and complete left ventricular apex coverage ensure localized distal thickening is not missed.
Why is a permanent AICD preferred over long-term antiarrhythmic medication alone to prevent sudden cardiac death in a patient diagnosed with apical HCM? [400 pts] (LO3:SO4)
Antiarrhythmic medications reduce premature beats or slow rapid rhythms but cannot alter structural myofiber disarray and scarring. These permanent scarred zones act as unstable triggers for re-entry loops that can degenerate into VF. Since medications cannot reliably prevent these loops, an AICD is necessary as a continuous internal safeguard to immediately shock the heart back to a normal rhythm and prevent sudden death.
Differentiate the main EKG findings between the AV Conduction blocks. [400 pts]
First-Degree - PR interval is prolonged (> 200 ms / > 5 small boxes) and remains constant from beat to beat.
Second-Degree, Mobitz Type 1 - Progressive prolongation of the PR interval with each consecutive beat until a P wave is completely blocked and fails to conduct, resulting in a dropped QRS.
Second-Degree, Mobitz Type 2 - PR intervals remain constant and fixed (may be normal or prolonged) before a P wave is suddenly and unpredictably blocked, dropping a QRS complex.
Third-Degree - Complete AV dissociation. P-P intervals are regular and R-R intervals are regular, but they are beating completely independently.
What is LaPlace’s law and use it to explain how changes in the structure of the heart lead to the development of HFPEF in relation to MRI. [400 pts] (SO2:LO3)
The core formula is Wall Stress = (Pressure × Radius) / (2 × Wall Thickness)
To counter high internal cavity pressures (p) and normalize myocardial wall stress (T), the heart undergoes compensatory hypertrophy, increasing wall thickness (h). According to LaPlace's Law, this initially manages wall stress. However, the thickening wall reduces the internal radius (r) and stiffens the tissue. Consequently, filling pressure (p) must rise exponentially to fill this restricted chamber, resulting in decompensated diastolic heart failure.
List at least 3 risk factors for HCM. [300 pts] (LO2:SO1)
Prior cardiac arrest (the ultimate secondary risk factor).
Family history of sudden cardiac death in a first-degree relative.
Recent, unexplained episodes of syncope (especially if exertional).
Massive left ventricular hypertrophy (wall thickness (greater than or equal to 30 mm)
Frequent or prolonged episodes of non-sustained ventricular tachycardia (NSVT) on ambulatory monitoring.
Extensive scarring
The presence of an apical LV aneurysm.
An abnormal blood pressure response during exercise.
Interpret expected ECG findings of left ventricular hypertrophy. [400 pts] (LO3:SO1)
High QRS voltage criteria due to increased heart muscle mass.
Dagger-Like Q Waves: Deep, narrow (non-infarct) Q waves in lateral (I, aVL, V5–V6) and inferior (II, III, aVF) leads caused by septal thickening.
ST-Segment and T-Wave Abnormalities: Deep or giant T-wave inversions, especially in the lateral or precordial leads, and ST-segment depression.
Atrial Enlargement: Signs of left atrial enlargement, such as wide or notched P waves, reflecting increased filling pressures.
Associated Patterns: Occasional presence of pre-excitation patterns like Wolff-Parkinson-White (WPW) syndrome.
What is the antiarrhythmic class of Amiodarone, and how does it affect the heart? [400 pts] (LO1:SO2)
Amiodarone, a Class III antiarrhythmic agent, primarily blocks potassium channels to inhibit potassium outflow during repolarization, prolonging action potential duration and the heart tissue's effective refractory period.
What are the histological findings seen in a patient with myocarditis? What are some common organisms that cause it (name at least 3)? [400 pts]
myocardial interstitial inflammatory infiltrates (e.g. lymphocytes, eosinophils) that can be seen directly adjacent to areas of myocyte necrosis, degeneration, or focal cell death
Organisms: Coxsackievirus B, Adenovirus, T. cruzi, Influenza virus
Why is no arachnodactyly important in the differential diagnosis of a young athlete presenting with sudden cardiac collapse? [500 pts] (SO2:LO2)
Disproportionately long extremities and arachnodactyly are classic skeletal signs of Marfan syndrome, a genetic connective tissue disorder carrying a high risk of sudden cardiac death from exercise-induced aortic dissection or rupture.
What age is HCM more commonly seen in? [300 pts] (LO2:SO1)
Hypertrophic cardiomyopathy (HCM) can manifest at any age from infancy to late adulthood, most commonly presenting clinically in a person's 20s. However, because many patients remain asymptomatic for years, the majority do not receive an official diagnosis until middle age.
Dominick’s calculated end-diastolic volume and end-systolic volume are 103 mL and 47 mL, respectively, revealing an ejection fraction of 54%. What is the formula for ejection fraction? [300 pts]
EF = (EDV-ESV)/EDV x 100
Detail the ACLS algorithm for cardiac arrest. [500 pts] (LO1:SO1)
Deliver Shock #1 (defibrillation) and immediately resume CPR for 2 minutes.
Establish IV or intraosseous (IO) access.
Assess rhythm at the end of the 2-minute cycle. If VF/pVT persists, Deliver Shock #2 and resume CPR.
Administer Epinephrine (1 mg IV/IO) during CPR; repeat every 3 to 5 minutes.
Assess rhythm at the end of the 2-minute cycle. If VF/pVT persists, Deliver Shock #3 and resume CPR.
Administer Amiodarone (300 mg bolus IV/IO) or Lidocaine during CPR to stabilize the excitable myocardium.
Repeat rhythm assessments, shocks, and drug deliveries in 2-minute cycles until Return of Spontaneous Circulation (ROSC) is established.
Website:https://cpr.heart.org/-/media/CPR-Files/CPR-Guidelines-Files/Algorithms/AlgorithmACLS_CA_200402.pdf
Why is dabigatran given to a patient who has atrial fibrillation? [400 pts]
Dabigatran is a Direct Oral Anticoagulant (DOAC) prescribed to patients with atrial fibrillation (AFib) to prevent ischemic stroke.
During AFib, the atria quiver chaotically instead of contracting in a coordinated, synchronized manner. This loss of mechanical contraction leads to stasis of blood, particularly within the pocket-like structure of the left atrial appendage (LAA). Stagnant blood is highly prone to forming a thrombus (clot).
What do inspiratory rales signify? [400 pts] (SO2:LO2)
A stiffened left ventricle impairs diastolic relaxation, causing blood to back up into the left atrium and pulmonary veins. The resulting pulmonary venous hypertension increases pressure in the pulmonary capillaries, forcing fluid into the alveoli.
Explain why sudden cardiac death (SCD) is triggered and witnessed in athletes. [500 pts] (LO2:SO1)
Intense physical exertion raises cardiac oxygen demand. Narrowed intramural arterioles and a restricted coronary flow reserve create a severe myocardial supply-demand mismatch in hypertrophied muscle. This acute local ischemia triggers rapid ventricular tachycardia, quickly degenerating into ventricular fibrillation.
What test is recommended as the primary, non-invasive screening and diagnostic tool for suspected HCM? [400 pts] (LO3:SO2)
A transthoracic echocardiogram (TTE) uses ultrasound to create moving pictures of the heart. This non-invasive test allows doctors to check heart size, shape, and pumping strength, evaluate valve function, and investigate symptoms like chest pain or shortness of breath.
How does ACLS restore normal cardiac cycle? [400 pts] (LO1:SO2)
High-quality chest compressions compress the heart between the sternum and spine to force blood into systemic circulation (mimicking systole). Full recoil creates negative pressure to draw blood back into the chambers (mimicking diastole), manually sustaining minimal oxygenation to the brain and myocardium until a perfusing rhythm returns.
A defibrillation shock delivers a high-voltage current that simultaneously depolarizes all cardiac muscle cells, silencing chaotic re-entry loops via a brief refractory period. This temporary electrical silence allows the Sinoatrial (SA) node to regain control and resume intrinsic pacing.
How does alcoholic dilated cardiomyopathy change the pressure volume loop? [400 pts]
Rightward Shift of the Entire Loop: Chronic remodeling, myocyte loss, and progressive ventricular stretching from alcohol toxicity increase chamber volume. This raises both End-Diastolic Volume (EDV) and End-Systolic Volume (ESV), shifting the entire loop rightward along the volume axis.
Flattening of the End-Systolic Pressure-Volume Relationship (ESPVR) Slope: Dilated cardiomyopathy severely depresses myocardial contractility. This causes the ESPVR line to rotate downward/flatten on the PV loop, showing the weakened heart cannot generate high systolic pressures at any given volume.