Advanced Cardiac Examination Techniques Quiz

ASD, or atrial septal defect, is characterized by a fixed splitting of the second heart sound due to the delayed closure of the pulmonic valve. This distinguishes it from paradoxical splitting (seen in conditions like aortic stenosis), wide splitting (seen in conditions like right bundle branch block), and incomplete splitting (seen in conditions like mitral valve prolapse).

In atrial septal defect (ASD), fixed splitting of S2 occurs due to delayed P2 component timing. This delay in P2 is influenced by the flow dynamics through the right sided chambers during expiration and inspiration, resulting in fixed splitting.

Patients with LBBB/RV pacing may present with paradoxical splitting of S2 due to altered ventricular depolarization patterns.

In LBBB/RV pacing, the delayed activation of the LV causes the paradoxical splitting phenomenon due to the delayed closure of the AV. This results in the P2 component of S2 occurring before A2, which is further accentuated during inspiration.

Paradoxical splitting of S2 in conditions such as aortic stenosis (AS), hypertrophic obstructive cardiomyopathy (HOCM), or severe left ventricular (LV) systolic failure is due to delayed left ventricular outflow. This delay disrupts the normal timing of aortic and pulmonary valve closures, resulting in the paradoxical splitting sound on auscultation.

A loud P2 is commonly associated with pulmonary hypertension due to increased pressure in the pulmonary artery, causing the closure of the pulmonic valve to be heard more prominently during auscultation.

When the PA systolic pressure exceeds 50 mmHg, physical exam findings include hearing the P2 component at the apex and possible persistent splitting of S2 due to delayed PV closure. Increased JVP with prominent V waves, pulmonary edema with crackles, and a systolic ejection murmur at the left sternal border are not direct consequences of elevated PA systolic pressure.

S3 is actually thought to originate from rapid filling of the LV followed by abrupt attenuation of flow in the LV, rather than being caused by aortic stenosis, a blockage in the pulmonary artery, or a congenital heart defect.

The S3 heart sound is often considered normal in children and young athletes due to their healthier hearts. However, in older populations, the presence of an S3 can indicate underlying heart conditions and is considered abnormal.

The 'sucker' concept in a young, healthy individual refers to the LV vigorously relaxing and drawing blood quickly from the LA with normal LA pressure. In contrast, the 'pusher' concept in heart failure patients involves elevated LA pressure pushing blood into the poorly functioning LV.

An S4 heart sound is typically associated with reduced ventricular compliance, which leads to a stiff ventricle. This stiffness causes the atrium to contract forcibly to push blood into the non-compliant ventricle, resulting in the S4 sound.

S4 heart sound is associated with decreased compliance of the left ventricle and is commonly heard in patients with conditions that cause left ventricular hypertrophy such as hypertension (HTN), aortic stenosis (AS), and hypertrophic cardiomyopathy (HCM). It is not typically heard in patients with atrial fibrillation, pediatric patients under the age of 5, or patients with a history of asthma.

The S4 heart sound is associated with atrial contraction, which is typically not heard in patients with atrial fibrillation where the atria are not contracting effectively. Therefore, it is not possible to hear an S4 in patients with a.fib.

The correct answer defines the difference between clicks and snaps based on when they are heard in the cardiac cycle.

The correct answer includes etiologies specifically related to systolic clicks, such as ejection clicks due to abnormal valves and MVP. The incorrect answers do not directly relate to the etiologies of systolic clicks.

The correct answer explains how the venous flow dynamics and timing of the pulmonary valve opening contribute to the change in intensity of the pulmonary ejection click during inspiration.

In patients with aortic stenosis (AS), the carotid pulsation is characterized by a parvus (slowed) and tardus (delayed) waveform with a delayed S2 sound. This is due to the obstruction of blood flow through the stenotic aortic valve, leading to delayed ejection of blood into the systemic circulation.

Parvus and tardus carotid pulsations may not be appreciated in elderly patients with AS due to decreased arterial compliance and increased arterial stiffness commonly seen in this population.

Carotid pulsation in severe aortic regurgitation is characterized by a rapid upstroke followed by a bisferiens pulse, percussion wave, tidal wave, and rapid runoff. This is due to the regurgitation of blood into the left ventricle during diastole, causing a characteristic waveform in the carotid arteries.

Carotid pulsation in HOCM is characterized by a 'spike and dome' pattern, which refers to a bifid quality with an initial percussion wave followed by a secondary wave.

Pulsus alternans is defined as a carotid pulsation that alternates between a strong and weak pulse, representing a regular rhythm. It is not associated with a normal heart rate pattern, low blood pressure, or a pulmonary embolism.

During valve opening, the right sided valves open earlier due to the lower pressure gradient in the right sided chambers, allowing for efficient blood flow through the heart.

In the human heart, the right sided valves close last during the cardiac cycle. The right sided valves include the pulmonary and tricuspid valves, while the left sided valves are the mitral and aortic valves.

The correct answer is based on the closure of the mitral and tricuspid valves, resulting in the first heart sound S1. The other options do not align with the generation of S1.

The closure of aortic and pulmonary valves corresponds to the second heart sound (S2), as the semilunar valves shut after the ventricles have emptied their blood into the aorta and pulmonary artery. This closure produces the 'dub' sound heard during diastole.

P2 occurs later than A2 because it is a right sided valve and therefore closes later.

Physiologic splitting of S2 occurs due to a delay in the closure of the pulmonic valve during inspiration, caused by increased venous return. This delay results in the perception of two distinct heart sounds instead of a single sound.

Abnormal splitting of the 2nd heart sound can be caused by various conditions listed in the correct answer, such as persistent splitting, RBBB, pulmonary HTN, fixed splitting, ASD, paradoxical splitting, LBBB, RV pacing, LV systolic failure, AS, and HOCM. VSD, Aortic stenosis, and Bradycardia are not typically associated with abnormal splitting of the 2nd heart sound.

In a patient with Right Bundle Branch Block (RBBB), the common exam finding is persistent splitting due to the delay in the right ventricular activation, which results in the aortic valve closing before the pulmonic valve.

Persistent splitting in RBBB is specifically due to the delay in the activation of the right ventricle. This delay causes the pulmonary component of the second heart sound to be delayed, resulting in the persistent splitting sound.