CHAPTER 7 VALVULAR HEART DISEASE

AORTIC STENOSIS
MCC elderly calcification of leaflets; 2nd bicuspid AV; 3rd developed rheumatic fever
RF: pharyngeal infection 0> beta-hemolytic strep (MV>AV>TV)
JONES Criteria: Joint (migratory polyarthiritis), carditis, Nodules in skin, erythema marginatum, Sydenham chorea

1. Resistance to flow causes LV hypertrophy: increased voltages in ECG (esp. noticeable is deep S in V2 and tall R in V5); sustained (but not
displaced) PMI on palpation, harsh crescendo-decrescendo systolic murmur that might radiate to apical region

2. Stenosed valve the A2 (sound of closure) decreased and A2 takes longer than P2 to close causing either a single S2 sound or paradoxical splitting

3. S4 gallop (stiff heart from AS or restrictive cardiomyopathy)

3. Ventricle can’t eject blood quickly: carotid pulses w/ low amplitude (pulsus parvus*) and delay in reaching peak (et tardus)

TTE is gold standard for Dx. Mortality of asymptomatic AVS low (<1% per year), but once symptomatic the survival rate is abysmal
*may be absent on older patients

AORTIC REGURGITATION
If acute infectious endocarditis and aortic dissection MCC
IE: MV>AV>TV acute: staph; subacute: viridians streptococci; Drugs: staph, pseudomonas, candida
Very bad if Acute: cardiogenic shock -> tachy/hypotension; fulminant pulmonary edema due to markedly increased filling pressure
-Respiratory failure from pulm edema
-tachypnea and tachycardia impede recognition of diastolic descresendo murmur because of shortening of diastole
-chest CT can show a normal size hart w/ pulmonary edema -> very suspicious; but TTE/TEE is key
If chronic, leaflet abnormalities, aortic root disease, or a combination of the two
Much better tolerated if chronic (months to years) due to LV remodelling; symptoms of dyspnea and fatigue

1. laterally displaced and diffuse PMI and cardiomegaly on radiography

2. low diastolic pressure = large pulse pressure
3. S3 gallop even without heart failure
4. Classic diastolic decrescendo murmur heard is left OR right sternal border (but stick to left), hearing improved if ask patient to lean forward at
end-expiration
5. large stroke volumes -> peripheral findings like systolic plethora (opposite of pallor) and diastolic blanching with pressure; head bobbing;
bounding full carotid pulse w/ rapid downstroke
6. Hill’s Sign: Opposite of Ankle-Brachial Index for PAD, here the leg pressure may be 20+ mmHG higher than arm pressure
7. carotid arterial pulse: may be bisferiens (two systolic peaks) esp. if AR is concomitant with AS

PULOMONARY STENOSIS
Caused predominant by congenital heart disease (esp. Noonan’s Syndrome) and identified in childhood. Rare acquired causes: carcinoid tumor and
rheumatic heart disease but in those cases other valves also involved.
- Pulmonary Regurgitation MCC previous mechanical treatment of pulmonary stenosis

DIABETES DRUGS
Criteria: fasting glucose 126+, 2hr glucose of 200+ during 75g oral glucose tolerance test, random glucose of 200+ with symptoms of hyperglycemia,
HbA1c of 6.5%+ (Drug Goals: fasting 120, GTT 140, HbA1c 7%); Other diabetic goals: 135/85 bp, LDL under 100, and immunize pneumococcal
vaccine and annual inflluenza vaccine

Type 1 diabetes primarily use insulin: combo short acting prior to meals + intermediate/long basal insulin (or insulin pump )
-Rapid: Lispro, Aspart, Glulisine Peak: half hour to 1.5 hours, lasts 4 hours
-Short: Regular Insulin Peak: 1-2 hours, lasts 5-8 hours
-Intermediate: NPH Insulin Peak: 12 hours, lasts 75% to the full day
- Long: Detemir, Glargine Peak: lasts 24 hours (full day)

Type 2 start with biguanides (metformin): decrease glucose output during gluconeogenesis, often lowers HbA1c 1.5-2%
+ reduce in CV events, all-cause mortality, no hypoglycemia, reduced insulin levels, minor weight loss, reduced TG and LDL
- nausea and diarrhea (reduced by giving with meals); more dangerous: lactic acidosis which is increased in renal insufficiency
(contraindicated in if creatinine more than 1.5 in men or 1.4 in women). Also CI’d in hepatic insufficiency or CHF (FA: also B12 def)
-Second line is sulfonylurea or insulin add-ons

1. Sulfonylureas (-ride, -mide, -zide): simulate beta cells to secrete insulin

+ 2% reduction in HbA1c, 1x or 2x day dosing, low cost
 - risk of hypoglycemia (increase in renal insufficiency), weight gain, decreases efficiency over time (FA: first generation also have a
disulfiram-like effect)
2. Thiazolidinediones (Glitazones) improves insulin sensitivity in muscle and adipose tissue
+ decreases TG and HDL; metabolized in liver (CAN BE USED IN RENAIL IMPAIRED), not an insulin secretalogue so no hypoglycemia
- slower onset of actionslight increase LDL, weight gain, cause water retention/edema -> CI’d in CHF (FA: also increase risk of fractures)
3. Meglitindes (-glinides): also stimulate beta cells to secrete insulin, but more short-acting (RAPID onset and short duration of action – take 1 hr
before meal)
+ great if blood sugar vary at mealtime but are controlled when fasting
- risk of hypoglycemia (not to be used in hepatic dysfx.); expensive
4. alpha-Glucosidase (acarbose, miglitol) delay carbohydrate absorption by inhibiting alpha-glucosidase enzyme in small intestine
+ specifically decreases postprandial hyperglycemia – good for patients with erratic eating habits b/c hypoglycemia won’t occur in meals
skipped)
- GI upset (flatulence); not if kidney function or renal isufficiency
5. Pramlitinide - amylin mimicking agent – inhibits inappropriately high glucagon during hyperglycemia – e.g. after a meal – but w/o impairing
normal glucagon response to hypoglycemia)
+ subcutaneous injection, NO requirements for renal/hepatic impairment
- hypoglycemia if you mistime your prandial insulin, nausea/diarrhea
6. GLP-1 agonist (-tides; exenatide, liraglutide) – mimics GLP-1, an incretin, that stimulates insulin release
+ hypoglycemia when added to sulgonylurea (but not when added to metformin!) (FA: also weight loss & satiety)
- nausea/vomiting/diarrhea, pancreatitis
7. DDP-4 Inhibitors (-gliptins, sitagliptin) inhibtits the DDP4 enzyme that inactivates GLP-1 and GIP, both stimulate insulin release & GLP-1 also
decreases glucagon release leading to decrease hepatic glucose production
- respiratory symptoms and sometimes severe hypersensitivity (analphylaxis/angioedema)
8. SGLT2 inhibitors (-gliflozins) block reabsorption of glucose in PCT
- glucosuria -> UTI, vaginal yeast infection
- hyperkalemia, dehydration, NOT recommended if kidney impaired (low GFR)
- dehydration -> orthostatic hypotension
+ weight loss