Hypertension (HTN)

Chapters:

Introduction0:00–0:10

Hypertension occurs when the force of the blood pushing against the artery walls is too high, causing damage to organs. Ok.
So as the heart pumps blood throughout the body, it creates pressure against the walls of the arteries, which is referred to as BP or BP.

Physiology0:10–3:42

BP is expressed as a fraction where the top number called the systolic pressure represents the pressure in the arteries.
When the heart is contracting and pumping blood. And the bottom number called the diastolic pressure represents the pressure in the arteries.
When the heart is relaxed and filling with blood, normal BP is less than 100 and 20 millimeters of mercury systolic and less than 80 millimeters of mercury diastolic factors that impact BP include cardiac output or co and systemic vascular resistance or SVR.
First, cardiac output is the quantity of blood pumped by the heart and is measured in liters per minute. The two components of cardiac output are stroke, volume or SV and heart rate or hr stroke volume is the amount of blood leaving the heart with each contraction and heart rate is the number of contractions in one minute.
The higher the stroke, volume and heart rate, the higher the cardiac output. Next, systemic vascular resistance is determined by the radius and elasticity of blood vessels.
If blood vessels are narrow or stiff, systemic vascular resistance increases, which then increases BP. Now, BP is regulated by short term and long term mechanisms.
Short term regulation is mainly controlled by the autonomic nervous system or A s. For example, when changing from a lying to a standing position, BP tends to drop when this happens barrow receptors which are pressure sensitive receptors located mostly in the aortic arch.
And carotid sinuses respond by sending signals to the vasomotor center. In the medulla.
The medulla activates the sympathetic nervous branch of the autonomic nervous system which increases heart rate, systemic vascular resistance and cardiac contractility.
Together these actions increase BP. On the other hand, long term regulation is mainly controlled by the renin angiotensin aldosterone system or ras which begins in special cells in the kidneys called juxtaglomerular cells.
When BP is low, these cells release an enzyme called renin into the circulation. Renin converts angiotensinogen an inactive protein made by the liver that's always floating around in the blood into angiotensin.
One which is then converted into angiotensin two by angiotensin converting enzyme primarily in the lungs. Angiotensin two then increases BP by causing vasoconstriction and increased systemic vascular resistance.
It also increases stroke volume by triggering the release of aldosterone which causes the kidneys to retain sodium and water.
And lastly, it acts on the hypothalamus, stimulating thirst and production of anti diuretic hormone which increases water reabsorption by the kidneys.
Finally, the ras is a negative feedback system. So, once BP is normalized, the kidneys stop releasing renin and ras activity is essentially turned off.

Causes and Risk Factors3:42–4:30

Now, hypertension can be categorized as primary or secondary, primary hypertension has no clear identifiable cause. There are both modifiable and non modifiable risk factors for primary hypertension, modifiable risk factors include obesity, sedentary lifestyle, tobacco use and a diet high in sodium and saturated fats.
Non modifiable risk factors include increasing age and a genetic predisposition for hypertension. On the other hand, secondary hypertension is secondary to an underlying medical condition.
Risk factors for secondary hypertension depend on the underlying cause but can include conditions like renal disease or obstructive sleep apnea.
Ok. So primary hypertension is a consequence of complex changes to regulatory and metabolic mechanisms.

Pathophysiology4:30–6:47

So, as far as regulatory mechanisms go sympathetic nervous system or S NS dysfunction can lead to hypertension by stimulating cardiac activity, increasing heart rate and systemic vascular resistance.
Likewise, ras overactivity also leads to increased vasoconstriction and increased systemic vascular resistance along with increased sodium and water retention by the kidneys and increased stroke volume.
The resulting chronic hypertension causes vascular remodeling or a change in the vessel structure that decreases elasticity or stretch of the vessels.
This decreased elasticity contributes to sustained systemic vascular resistance and elevated BP there are also metabolic mechanisms that contribute to hypertension.
These can be brought about by obesity and dysfunction of adipocytes or fat cells and impaired secretion of adipokines. A type of cell signaling molecule made by these cells.
This can result in inflammation and insulin resistance. Both of which can decrease release of the vasodilator nitric oxide by endothelial cells that line the blood vessels leading to vasoconstriction and increased systemic vascular resistance.
Other effects of obesity include increased sympathetic nervous system and ras activity resulting in hypertension. Now sustained hypertension can cause end organ damage leading to severe complications.
The physical stress from hypertension over time accelerates the development of atherosclerosis and coronary artery disease, which can lead to myocardial infarction.
And the elevated systemic vascular resistance increases the workload of the heart leading to left ventricular hypertrophy and heart failure damage to the kidneys can lead to kidney failure.
While in the brain, it can cause stroke. Hypertension occurs when the systolic BP is consistently above 100 and 30 millimeters of mercury or the diastolic is consistently above 80 millimeters of mercury.

Clinical Manifestations6:47–7:13

However, because individuals with hypertension usually don't experience any symptoms. It's sometimes called the silent killer.
Since its effects are not evident until end organ damage has occurred. All right, it's a quick recap hypertension occurs when the force of the blood pushing against the artery walls is too high hypertension can be primary, which has no clear cause or secondary which is caused by an underlying medical condition, untreated hypertension can cause end organ damage that can lead to problems like myocardial infarction, heart failure, stroke and kidney failure.

Review7:13–7:39