- 1 What is Hypertension (HTN) ?
- 2 Pathophysiology of hypertension
- 3 Pathophysiology of Pregnancy Induced Hypertension
- 4 Pathophysiology of Pulmonary Hypertension
- 5 Pathophysiology of Portal Hypertension
- 6 Pathophysiology of Essential Hypertension
What is Hypertension (HTN) ?
Hypertension is a chronic condition in which there is high blood pressure. Depending on the specific type, there are some variations in its pathophysiology.
Pathophysiology of hypertension
To understand the pathophysiology of hypertension, the basic physiology of blood pressure must be discussed. The determinants of blood pressure (BP) are cardiac output (CO) and total peripheral resistance (TPR).
BP = CO x TPR
Cardiac output is amount of blood in the heart that is pumped out in 1 minute. It is in turn affected by stroke volume (SV) and heart rate (HR).
CO = SV x HR
Stroke volume is the amount of blood delivered in each contraction. Its determinants are inotropism and cardiac preload (venous return).
Total peripheral resistance on the other hand is called the cardiac afterload. It refers to the resistance of blood to flow. It is affected by the tone of the arterioles.
To summarize BP = [SV x HR] x TPR.
Since the three determinants are directly proportional to blood pressure any increase in each of them will result to high blood pressure or hypertension. An increased SV is brought about by any venoconstriction and high fluid volume. Arteriolar constriction on the other hand increases total peripheral resistance. Arteriolar and venoconstriction may occur in the presence of angiotensin II. Angiontensin II also enhances the effect of norepinephrine that increases heart rate and stimulates the synthesis of aldosterone that increases fluid volume.
Pathophysiology of Pregnancy Induced Hypertension
The exact process of the occurrence of pregnancy induced hypertension (PIH) remains unknown but there are suggested theories to explain it.
Changes in prostaglandin metabolism play a major role in the hypertension and coagulopathy of PIH. It is believed that the following happens:
1. There is increased thromboxane A2 production.
2. Thromboxane A2 stimulates platelet aggregation and vasoconstriction.
3. Thrombosis, platelet hyperactivity and vasoconstriction results.
Dilated and constricted arterial segments occur in turn that interrupts the blood circulation. The lack of blood supply in constricted segments will cause damage to the blood vessel. The blood flow is also forced on those segments where dilation is occurring. The injury of the endothelium that these situations caused allows blood products like platelet and fibrinogen to empty into the interendothelium.
The fluid found in the intravascular space transfers to the intracellular space. Elevated hematocrit and hemoglobin is expected.
PIH is further categorized as preeclampsia and eclampsia. A more detailed turns of events happens in each category.
Pathophysiology of Pulmonary Hypertension
In pulmonary hypertension the capillaries and arteries of the lungs are obstructed, damaged or constricted. The blood has difficulty to flow in and out of the lungs raising the artery pressure. To compensate for the high pulmonary pressure the heart works more forcefully to be able to deliver blood to the lungs. Continuous increased pumping will result to heart failure.
Pathophysiology of Portal Hypertension
Elevated vascular resistance, inefficient decompression through the venous collaterals and continuous high inflow of splanchnic are all contributing factors to the pathogenesis of portal hypertension. Since the arteries and veins of the liver together with the portal veins plays a vital role in the regulation of blood flow to the liver, any damage to the liver or these vessels will contribute to portal hypertension.
Portal hypertension starts with a portal pressure above 25 mmHg. The venous channels receive decreased blood supply and thus collaterals are formed. Organs connected to the portal system such as the spleen endure the effects of congestion.
Pathophysiology of Essential Hypertension
Hypertension where there is no underlying medical cause is termed primary or essential hypertension. What basically happens in essential hypertension is that the arterioles render unusual resistance to blood flow. Patients may experience few or no symptoms of hypertension at the beginning of the condition as there are still no major changes in the blood vessels or different organs.
Hypertension can start with the abnormal changes of the small and large vessels. The large vessels are involved in the following episodes:
1. Large vessels become twisty and sclerosed
2. The lumen narrows down
3. The extremities, brain and heart receives decreased blood supply
4. Large vessels eventually get obstructed or rupture resulting to hemorrhage
The small vessels on the other hand experience the following:
1. Diastolic blood pressure elevates
2. The inner most layer of the vessel (intima) are damaged
3. Fibrin gathers in the vessel
4. Local edema manifests
5. Clotting may follow
These processes results to diminished supply of blood and eventually loss of function of the retina, brain, kidneys and the heart.
When hypertensive cardiovascular disease develops, the arterioles are constricted. The heart then needs to increase its contractility to compensate to the increased afterload and preserve the cardiac output at normal levels. The prolonged increased contractility will soon result to hypertrophy of the cardiac muscle which in turn may result to myocardial infarction or coronary insufficiency. If the heart cannot maintain the needed cardiac output the following takes place:
1. Left ventricle will collapse and congestion follows.
2. Elevated diastolic pressure will bring forth congestion up to the lungs.
3. Pulmonary congestion will lead to right ventricular failure.
4. Systemic venous pressure may raise leading to congestion.
5. Venous congestion results to decreased kidney perfusion.
6. Kidney failure.