PCL Week 1: Atrial Fibrillation

PCL 1: FRANK’S OUT OF RHYTHM

PATIENT HX

Name: Frank Gan
Age: 66 years old
Sex: Male
Occupation: Semi-retired. Owner of an orchid and garden business.
Marital Status: Married to Hwi Bee.
Chief Complaint: Heart palpitations.
HPI:
When: A few weeks from previous visit to Dr. Tan.
Where: Heart.
Quality: Persisted overnight.
Quantity:
Associated Symptoms: Feeling dizzy.
Alleviating and Aggravating Factors:
Notes:

· Pulse deficit present – Comparing the radial pulse rate and the precordial (apex beat) rate.

· ECG results:

o RR intervals irregular

o No P waves seen

o QRS complexes were narrow

· Jugular venous pulse – ‘a’ wave not present

· BP – 98/60

· Pulse – 140 beats per min.

Past Medical Hx:

Past Medical Diseases or Illnesses: Episodes of palpitation
Past Surgical Hx:
Past Hospitalisation Hx:
Notes:

· Has put on weight over the years

· Previous examination of CVS normal

· BP rising at 145/90

Family Hx:
Drugs Hx: Statin tablets and low dose aspirins.
Alcohol Hx:
Allergy Hx:
Social Hx: Has a few sons. Does less physically demanding work now that he is semi-retired. Does not like doctors and hates taking medications.

KEY ISSUES:

· Predisposing factors for CVS diseases: Weight/Obesity , active/sedentary lifestyle and High BP.

· Compliance for treatment and medication. How to deal with difficult patients.

· Different techniques of examination and history taking for CVS patients.

· The availability of better resources and services available at hospitals compared to clinics.

Terminology:

· Apex beat – the beat felt over the apex of the heart, normally in or near the fifth intercostals space

· Stenosis – abnormal narrowing of the blood vessels

· Statins – Drug that reduces the level of plama LDL-C. The rate-limiting enzyme in cholesterol synthesis is HMG-CoA reductase, which catalyses the conversion of HMG-CoA to mevalonic acid .

o Simvastatin, lovastatin and pravastatin are specific, reversible, competitive HMG-CoA reductase inhibitors l.Atorvastatin and rosuvastatin are long-lasting inhibitors.

o Decreased hepatic cholesterol synthesis up-regulates LDL receptor synthesis, increasing LDL-C clearance from plasma into liver cells. The main biochemical effect of statins is therefore to reduce plasma LDL-C. There is also some reduction in plasma triglyceride and increase in HDL-C

· Low Density Lipoproteins (LDL) - LDL-C provides the source of cholesterol for incorporation into cell membranes and for synthesis of steroids but is also key in atherogenesis, as described above. Cells take up LDL-C by endocytosis via LDL receptors that recognise LDL apolipoproteins. Some drugs (notably statins) reduce circulating LDL-C by inhibiting endogenous cholesterol synthesis and stimulating the synthesis of hepatic LDL receptors.