Cardiology Deck 3 Flashcards
Hypertension is the leading risk factor for
Cardiovascular disease
The young with hypertension are more likely to be
obese
Determinants of BP
are cardiac output (i.e., HR × SV) and systemic vascular resistance
In hypertension, what is sustained?
arterial systemic vasoconstriction
In hypertension, the cardiovascular system dysfunction includes
SNS overreactivity resulting in an increased heart rate and vasoconstriction
The SNS overreactivity in hypertension is due to
catecholamine increases and/or catecholamine receptor sensitivity.
what happens with RAAS in hypertension
also overreactive. This overreactivity and a decreased renal perfusion from the SNS effects -> renin release. -> angiotensin II production, which is a powerful vasoconstrictor. -> Na+ and water are reabsorbed ->Aldosterone is released -> Na+ and water retention -> blood volume increases. ->The increased volume stimulates the release of natriuretic hormones that normally act to reduce Na+ retention and promote water excretion while causing vasodilation. These natriuretic hormones, however, are dysfunctional in hypertension, leading to worsening of vasoconstriction. The RAAS dysfunction also causes vascular changes.
Risk factors for HTN
Age: Vessel compliance decreases with aging.
Race: prevalent in Blacks
Family history: Genetic factors.
Overweight or obesity: Increased RAAS and SNS activity, inflammation, insulin resistance, endothelial dysfunction, and vascular remodeling. Adipokines (cytokines released by adipose tissue) are changed with obesity and may cause vascular dysfunction.
Physical inactivity: Increases heart rate, which increases cardiac workload; increased insulin resistance; and possible vascular and endothelial dysfunction.
Tobacco use: Nicotine immediately raises blood pressure temporarily, and the chemicals in tobacco can cause vascular dysfunction.
High-sodium diet: Too much sodium causes fluid retention, which increases blood pressure. Some patients are salt sensitive while for others salt intake does not have as much of an influence on blood pressure. There are no practical tests to determine who falls into which category.
Low -potassium, -calcium, and -magnesium diet: These elements help balance the amount of sodium in cells; without enough, too much sodium accumulates in the blood.
High vitamin D intake: This factor has an uncertain effect, though vitamin D may affect the RAAS.
Excessive alcohol consumption: Over time, heavy drinking—that is, more than two to three drinks in one sitting—can cause hypertension via several mechanisms such as SNS and RAAS dysfunction.
Stress: High levels of stress can lead to a temporary, but dramatic, increase in blood pressure.
Clinical manifestations of hypertension
fatigue, headache, malaise, and dizziness
nocturnal hypertension
Normally, the blood pressure dips by 10% at night, and the patient is diagnosed with nocturnal hypertension if dipping does not occur. Cardiovascular risk may be higher with nocturnal hypertension than in those whose pressure dips at night.
Hypertensive urgency,
blood pressure systolic ≥ 180 and/or diastolic ≥120 mmHg in a patient who is relatively asymptomatic (e.g., mild headache) and there is no evidence of acute target end-organ damage (e.g., ischemia).
A hypertensive emergency (i.e., malignant hypertension)
is defined as the same blood pressure as an urgency but the patient is symptomatic and/or with evidence of acute/ongoing target organ damage.
Diagnostic testing for those newly diagnosed with HTN
an EKG and laboratory tests (e.g., urinalysis, CBC, lipid panel, and chemistry panel for glucose, calcium, creatinine, potassium, and thyroid profile). Other exams are dependent on presence or suspicion of other disorders such as an albumin creatinine ratio for chronic kidney disease or an echocardiogram for heart failure. In primary hypertension, these results may all be normal.
DASH diet
Limiting saturated fat, cholesterol, total fat, and salt
Focusing on fruits, vegetables, and fat-free or low-fat dairy products
Increasing whole grains, fish, poultry, beans, seeds, and nuts
Minimizing sweets, added sugar and sugary beverages, and red meats
Stage I hypertension
a child’s BP is greater than the 95th percentile but less than or equal to the 99th percentile plus 5 mm Hg.
Stage II hypertension
child’s BP is greater than the 99th percentile plus 5 mm Hg
prehypertension
BP is between 90th to 95th percentile.
Factors that affect cardiac output
aroreceptors
Extracellular volume
Effective circulating volume - Atrial natriuretic hormones, mineralocorticoids, angiotensin
Sympathetic nervous syndrome
Factors that affect vascular resistance
Pressors - Angiotensin II, calcium (intracellular), catecholamines, sympathetic nervous system, vasopressin
Depressors - Atrial natriuretic hormones, endothelial relaxing factors, kinins, prostaglandin E2, prostaglandin I2
Under normal conditions, the amount of sodium excreted in the urine
matches the amount ingested, resulting in near constancy of extracellular volume. Retention of sodium results in increased extracellular volume, which is associated with an elevation of BP. By means of various physical and hormonal mechanisms, this elevation triggers changes in both the glomerular filtration rate (GFR) and the tubular reabsorption of sodium, resulting in excretion of excess sodium and restoration of sodium balance.
A rise in the intracellular calcium concentration, due to changes in plasma calcium concentration,
increases vascular contractility. In addition, calcium stimulates release of renin, synthesis of epinephrine, and sympathetic nervous system activity. Increased potassium intake suppresses production and release of renin and induces natriuresis, decreasing BP.
In a child who is obese, hyperinsulinemia may
elevate BP by increasing sodium reabsorption and sympathetic tone.
In general, the younger the child and the higher the blood pressure (BP), the greater the likelihood that hypertension is
secondary to an identifiable cause
Prior to puberty hypertension is usually primary (essential) or secondary?
Secondary
