Increase in central, peripheral and pulmonary venous pressure

Significance of Hypertension

Hypertension is a risk factor (more precisely, a syndrome) that contributes to the development of a relatively large number of diseases. Two types of the significance of hypertension as a factor can be distinguished:

Significant factor

A significant factor is one of several factors that contribute to the development of a disease. For example, hypertension contributes to the development of atherosclerosis, but atherosclerosis may also be caused by many other factors, such as hypercholesterolemia, obesity, inflammation, etc.

Decisive factor

A decisive factor is one of the main determining factors that directly cause a disease. For example, hypertension is a major decisive factor in the development of stroke (cerebrovascular accident).

Acute Consequences

1. Development of Ischemic Heart Disease

Hypertension contributes to the formation of atherosclerotic plaques and may also cause their rupture and embolization, particularly in the coronary arteries, leading to the development of ischemic heart disease.

2. Development of Stroke

Elevated blood pressure increases the risk of mechanical disruption of cerebral circulation, with the possibility of arterial hemorrhage, which is particularly dangerous for cerebral vessels (especially in the presence of aneurysms). Hemorrhage most commonly occurs in the basal ganglia.

3. Aortic Dissection

In hypertension, a tear in the endothelium may occur, allowing blood to enter the vessel wall and create a false lumen. This condition most frequently affects the aorta. Dissections of the ascending aorta are usually fatal, while the prognosis of descending aortic dissections depends on the degree of stabilization.

Chronic Consequences

1. Atherosclerosis

Hypertension causes endothelial damage, promoting the formation of atherosclerotic plaques, which may subsequently rupture due to elevated pressure, leading to peripheral embolization and ischemic heart disease.

2. Left Ventricular Hypertrophy

Elevated systolic and diastolic blood pressure increases afterload (the resistance against which blood is ejected from the heart), leading to increased myocardial workload and concentric left ventricular hypertrophy (characterized by wall thickening without chamber dilation). Although hypertrophy initially improves contractility, it is associated with impaired coronary perfusion, resulting in increased susceptibility to ischemia. Additionally, increased myocardial workload leads to higher myocardial oxygen consumption.

3. Chronic Renal Failure

Sustained hypertension initially causes glomerular hyperfiltration, followed by fibrosis, leading to a decrease in glomerular filtration rate. This damage may manifest as proteinuria and erythrocyturia and can ultimately progress to renal failure.

4. Hypertensive Retinopathy

Characteristic vascular changes occur in the fundus of the eye. With prolonged hypertension, exudation of fluid, hemorrhages, ischemic changes, and deposition of lipid substances may develop. In the macular region, these deposits can form a stellate (star-shaped) pattern.

WHO Classification of Hypertensive Complications

1. Hypertension without Target Organ Damage

In newly diagnosed hypertension, no anatomical or functional changes are initially present.

2. Hypertension with Target Organ Damage (Structural Changes)

After prolonged exposure to hypertension, anatomical changes develop, but without functional impairment:

Heart – left ventricular hypertrophy

Kidneys – benign nephrosclerosis

Eyes – vascular changes (angiopathia retinae, angiosclerosis retinae)

3. Hypertension with Functional Impairment

Functional disorders develop as a consequence of structural changes:

Heart – heart failure, left ventricular dilation, manifestation of ischemic heart disease, myocardial infarction

Kidneys – progression from benign nephrosclerosis to malignant nephrosclerosis with renal failure

Eyes – retinopathy, neuroretinopathy

Brain – hypertensive encephalopathy (status lacunaris), stroke

Increase in Central Venous Pressure

CVP (central venous pressure) is the pressure in the large veins at the entry into the right atrium. Its fluctuations during the cardiac cycle are depicted by the phlebogram. Normal values range from 0 to 8 mmHg.

Elevated CVP is observed in:

• hypervolemia
• right-sided heart failure
• pulmonary embolism
• coughing and impaired expiration
• increased intrathoracic pressure
• tension pneumothorax
• mechanical ventilation
• valvular heart disease

Increase in Peripheral Venous Pressure

Similar mechanisms as in elevated CVP, primarily due to right-sided venous congestion. Peripheral venous pressure may also be increased due to thrombophlebitis, as well as lower limb venous valve insufficiency, venous thrombosis, or other causes leading to venous obstruction.

Increase in Pulmonary Venous Pressure

Elevated in postcapillary pulmonary hypertension, which develops secondary to left-sided heart failure (e.g. uncontrolled systemic hypertension, mitral and/or aortic valve disease), and in mitral valve disorders.

Pulmonary Hypertension

A condition characterized by an increase in arterial blood pressure in the pulmonary circulation. The diagnostic criteria for pulmonary hypertension include:

• systolic pulmonary arterial pressure > 35 mmHg
• mean pulmonary arterial pressure > 25 mmHg
• diastolic pulmonary arterial pressure > 12 mmHg

Compared to the systemic circulation, the pulmonary circulation is a low-pressure system (normal values approximately 25/10 mmHg, mean 15 mmHg), with a lower blood volume, but the same blood flow.

The lower pressure values determine specific features of pulmonary hypertension development:

• pulmonary hypertension may develop acutely (e.g. during massive pulmonary embolism)
• increased pressure in the pulmonary veins (and consequently in the left heart) may significantly contribute to its development

The general principle of development is the same as in systemic hypertension – an altered relationship between blood flow and total pulmonary vascular resistance.

Classification

Two basic mechanisms of development are distinguished:

Primary pulmonary hypertension – without an identifiable cause,

Secondary pulmonary hypertension – resulting from another condition (precapillary, postcapillary, hyperkinetic).

Primary Pulmonary Hypertension

Also referred to as obliterative or obstructive pulmonary hypertension. Chracterized by progressive reduction of the total vascular cross-sectional area and an increase in peripheral resistance, the underlying cause is likely dysregulation of pulmonary arteriolar structure, with proliferation of the vascular wall, associated with a disturbed BMP cytokine signaling pathway due to receptor mutation.

The disease has a progressive course, with worsening dyspnea and development of right-sided heart failure, manifested by:

• peripheral cyanosis
• peripheral edema
• increased jugular venous distension

Treatment options may include lung transplantation.

Secondary Pulmonary Hypertension

Precapillary (reactive) pulmonary hypertension. Pulmonary capillary wedge pressure is normal. Increased pressure is caused by vasoconstriction as a response to alveolar hypoxia (hypoxic pulmonary vasoconstriction), caused by diseases leading to chronic alveolar hypoventilation, such as:

• chronic bronchitis
• emphysema
• neuromuscular disorders
• severe obesity

A similar mechanism may occur during exposure to high altitude (usually above 3000 m above sea level).

Postcapillary pulmonary hypertension

caused by elevated pressure in the left atrium, occurs in:

• left-sided heart failure
• cardiomyopathies
• mitral stenosis
• constrictive pericarditis

Hyperkinetic pulmonary hypertension

develops in left-to-right cardiac shunts, such as:

• patent ductus arteriosus,
• atrial septal defect,
• ventricular septal defect,

Increased pulmonary blood flow must be reduced to prevent blood accumulation in the left heart, therefore, peripheral resistance increases. Pulmonary vessels respond by arteriolar remodeling, with hypertrophy of the muscular layer. These changes become irreversible, leading to fixation of pulmonary hypertension. Surgical correction is required before this fixation occurs.

Other causes

pulmonary fibrosis and other conditions reducing pulmonary parenchyma (including lung resections) – reduction of total vascular cross-section leading to hypertension,

chronic thromboembolic pulmonary hypertension – repeated embolic events lead to organization and fibrosis rather than adequate recanalization, narrowing the lumen and increasing resistance,

acute massive pulmonary embolism – obstruction of large pulmonary vessels leads to:

• increased pulmonary vascular resistance
• increased right ventricular pressure
• the non-hypertrophied right ventricle has limited ability to generate pressure
• resulting in right heart dilation and acute right-sided heart failure
• with a concomitant reduction of blood volume in the left heart

Symptoms

• exertional dyspnea
• easy fatigability
• chest pain
• syncope
• hemoptysis
• lower limb edema and other signs of right-sided heart failure

Diagnostics and Investigations

ECG – signs of right ventricular hypertrophy:

• peaked P waves in leads II and III
• vertical electrical axis
• tall R wave in lead V1
• inverted T waves in leads V1–V3
• prolonged right ventricular activation time

Chest X-ray – enlargement of right heart chambers, dilatation of the pulmonary artery.

Echocardiography – detection of right ventricular hypertrophy; Doppler measurement of the pressure gradient across the tricuspid valve allows estimation of systolic pulmonary artery pressure; assessment of pulmonary or tricuspid valve regurgitation.

High-resolution CT (HRCT) of the chest – detailed imaging of cardiac chambers; typically shows right ventricular enlargement and hypertrophy compared to the left ventricle (which is compressed and assumes a D-shaped configuration).

Pulmonary function tests:

Spirometry – detects functional pulmonary impairment

Whole-body plethysmography

Ventilation–perfusion scintigraphy – reveals ventilation–perfusion mismatch

Right heart catheterization – definitive diagnostic method, measuring:

• mean pulmonary arterial pressure (> 25 mmHg),
• pulmonary capillary wedge pressure (> 12 mmHg).

Six-minute walk test – simple functional assessment measuring walking distance in 6 minutes (normal ≈ 650 m; pulmonary hypertension ≈ 250 m); correlates with disease severity and prognosis.

Pulmonary biopsy

Laboratory tests – markers of heart failure (natriuretic peptides, cardiac troponins).

Consequences

Right ventricular hypertrophy (cor pulmonale chronicum) and development of right-sided heart failure.

In massive pulmonary embolism: acute dilation of right heart chambers (cor pulmonale acutum) with rapid onset of right-sided heart failure.

Capillary remodeling and increased hydrostatic pressure in the pulmonary circulation leading to pulmonary edema, prolonged diffusion distance, and respiratory failure,

Altered blood flow resulting in ventilation–perfusion mismatch.

Literature

• Incomplete citation of publication. NEČAS, Emanuel. Obecná patologická fyziologie. Karolinum, 2000. ISBN 80-246-0051-X.