Cardiovascular Assessment and Clinical Findings Quiz

The factors noted when taking a patient's pulse include pulse rate and rhythm, character (slow rising pulse – aortic stenosis, collapsing pulse – aortic regurgitation), and regularity or irregularity.

The ideal angle for examining the internal jugular vein is 45 degrees, and it reflects the pressure changes within the right atrium.

In right-sided heart failure, the venous column is seen above the right sternoclavicular joint at a 45-degree incline, indicating an increase in venous pressure.

The key areas to auscultate are the aortic, pulmonic, tricuspid, and mitral areas. In each area, one should listen for heart sounds, added sounds, and murmurs.

The manoeuvres to accentuate murmurs during auscultation include using the bell at the apex in expiration in the left lateral position, at the left axilla with the diaphragm, and over the carotids with the diaphragm in held inspiration.

The learning outcomes of the Cardiovascular Examination are: to demonstrate an understanding of the fundamentals of the Cardiovascular Examination, to identify physical signs of cardiovascular disease, to relate clinical signs to underlying pathology, and to recognize the importance of using history & examination findings to help reach a diagnosis.

The components of the Traditional Medical Model are: History, Examination, Investigation, Diagnosis, Treatment, and Follow-up.

The steps involved in the INTRODUCTION phase of the Cardiovascular Examination are: ensuring adequate hygiene of hands and stethoscope, introducing yourself, confirming the patient’s name and date of birth, asking if the patient is in any discomfort, explaining the procedure, seeking permission to examine, and positioning the patient at 45 degrees with the chest adequately exposed.

The purpose of the GENERAL and CLOSE INSPECTION in the Cardiovascular Examination is to observe the patient for any signs of illness, breathlessness, discomfort, or pain.

Applying scientific knowledge in the Cardiovascular Examination is significant because the Cardiovascular System does not exist in isolation from other systems, and using scientific knowledge can help direct and focus the clinical examination.

Malar flush, a high color over the cheekbones, can indicate mitral valve disease but may not always be present in individuals with heart disease.

Butterfly rash, a characteristic skin lesion of systemic lupus erythematosus (SLE), appears in a butterfly distribution on the face and may precede SLE by weeks or months.

Koilonychia, spoon-shaped nails, is primarily recognized as a manifestation of chronic iron deficiency.

Clubbing, changes in the area around the nails, can occur with heart and lung diseases that reduce oxygen in the blood and may develop quickly, often within weeks.

Infective endocarditis is characterized by fever, heart murmurs, petechiae, subungual hemorrhages, Osler nodes, Janeway lesions, and Roth spots.

DSCAM, COL6A2, and TBX1 genes are associated with the problems in Down syndrome and 22q11.2 deletion syndrome (DiGeorge Syndrome).

The common cardiac abnormalities associated with 22q11.2 deletion syndrome (DiGeorge Syndrome) include interrupted aortic arch, tetralogy of Fallot, and ventricular septal defect.

Mutations in genes such as SCN5A are associated with Long QT syndrome which has an autosomal dominant mode of inheritance.

Identifying mutations in genetic diseases is important for understanding the underlying causes, predicting disease progression, and developing targeted treatment strategies.

The characteristic defects in Down syndrome related to cardiology include atrioventricular septal defect, ventricular septal defect, atrial septal defect, and patent ductus arteriosus.

Deletions arise in 22q11.2 deletion syndrome (DiGeorge Syndrome) due to mutations in the TBX1 gene, which is a transcription factor with dose-dependent phenotype.

DiGeorge syndrome without deletion is associated with mutations in the TBX1 gene, leading to defects in the 4th pharyngeal arch arteries.

Familial Hypercholesterolemia can result from mutations in genes such as ApoB - Arg3500Gln, LDL receptor associated protein - null mutations, and PCSK9 - Asp374Tyr. These mutations can lead to impaired synthesis, transport, binding, internalization, or recycling of LDL cholesterol.

According to the Simon Broome criteria, definite Familial Hypercholesterolemia is diagnosed when there is a cholesterol level >6.7mM (LDL>4mM) in children under 16 OR >7.5mM (LDL>4.9mM) in adults, along with either tendon xanthoma in the patient or 1st/2nd degree relative, or a family history of myocardial infarction. Possible FH is diagnosed when the cholesterol levels and other criteria are met.

Inclisirin treatment harnesses a natural process to reduce LDL cholesterol levels. It acts by targeting the PCSK9 pathway, which normally leads to the degradation of LDL receptors. By inhibiting PCSK9, more LDL receptors are available on the cell surface, leading to increased clearance of LDL cholesterol from the bloodstream.

Gene dosage effects in Familial Hypercholesterolemia refer to the impact of having one or two copies of the mutated gene. In an autosomal dominant condition like FH, having one copy of the mutated gene is sufficient to cause the disorder, while having two copies can lead to more severe manifestations.

Cascade testing involves identifying and testing relatives of an affected individual to determine if they have inherited the genetic mutation. Population screening, on the other hand, involves testing a broader population regardless of family history to identify individuals with the condition.

Compound heterozygosity in Familial Hypercholesterolemia refers to having two different mutated alleles of the same gene. This can result in a more severe form of the disorder due to the combined effects of the two mutations.

Penetrance refers to the proportion of individuals carrying a specific genetic mutation who exhibit clinical symptoms of the associated disorder. In the case of Familial Hypercholesterolemia, high penetrance would mean that a large proportion of individuals with the mutation develop the characteristic high LDL cholesterol levels and related symptoms.

Locus heterogeneity refers to the existence of different genetic loci (locations) that can give rise to the same disorder, while allelic heterogeneity refers to the presence of different mutations within the same gene that can cause the disorder. Understanding these concepts is important for comprehensively characterizing the genetic basis of Familial Hypercholesterolemia.

Causes of ischemic heart disease include atherosclerosis with plaque rupture or erosion, obesity, diabetes, hypertension, hypercholesterolemia, blood clot formation due to atherosclerosis, coronary artery spasm, Takotsubo cardiomyopathy, and alcohol withdrawal.

Microscopic features of an atheroma include lipid-laden macrophages, smooth muscle cells, lymphocytes, and a fibrous cap.

Clinical features of an acute MI include chest pain, shortness of breath, nausea, vomiting, and diaphoresis. Investigatory features include ECG changes, cardiac biomarker elevation, and sometimes imaging studies such as echocardiography or coronary angiography.

Complications of an acute MI include arrhythmias, heart failure, cardiogenic shock, and mechanical complications such as ventricular septal rupture or papillary muscle dysfunction.

Unstable angina is chest pain at rest with no pathological ECG changes or biomarker changes (troponin). It is classified as an acute coronary syndrome and warrants admission into the hospital.

STEMI occurs when a major artery of the heart becomes completely blocked, diagnosed based on ECG findings only. NSTEMI occurs when a major artery of the heart becomes severely narrowed or transiently blocked, diagnosed based on ECG findings and cardiac biomarkers.

Arrhythmia refers to an abnormal heart rhythm, which can manifest as a heartbeat that is too fast, too slow, or irregular.

The sino-atrial node is a group of cells located in the right atrium of the heart that serves as the natural pacemaker. It generates electrical impulses to initiate the heartbeat and propagate them through the atria, leading to atrial depolarization.

Arrhythmias are categorized based on rate (fast vs slow), size of complexes (narrow vs broad), and origin (atrial, AV, ventricular, ectopic, re-entrant/short circuit). Examples include sinus tachycardia, atrial fibrillation, ventricular tachycardia, and atrio-ventricular heart block.

Atrial fibrillation is characterized by the absence of discernible P waves, irregularly irregular rhythm, and may have a fast or slow ventricular response. Atrial flutter typically exhibits a sawtooth pattern on ECG and has a heart rate roughly divisible by 300. Treatment may focus on converting to normal rhythm or controlling the ventricular rate.

WPW syndrome is a type of supraventricular tachycardia (SVT) that is congenital and results from an accessory pathway causing a short circuit. It is characterized by a delta wave and T wave opposite QRS concordance. Treatment may involve cardiac ablation.

VT/VF presents with a broad complex and fast rate, and pulseless VT is treated as cardiac arrest. Long QTc and Torsades de pointes can complicate the condition and may be related to certain medications or electrolyte imbalance. Treatment may involve administering magnesium IV.

Atrio-ventricular heart block includes 1st degree (long PR interval), 2nd Degree Mobitz Type 1 (progressive prolongation, dropped beat then reset), 2nd Degree Mobitz Type 2 (fixed ratio), and 3rd Degree/Complete heart block. Complete heart block might need pacing as definitive treatment.

SVT is a broad definition based on origin, usually with narrow complexes and typically above the bundle of His. Ventricular tachycardia presents with a broad complex and may result in pulseless VT, requiring immediate medical intervention.

PEA is a life-threatening condition that requires immediate action, including starting CPR. It can present as pulseless VT, VF, or asystole, and prompt recognition and intervention are crucial for patient survival.