The document discusses congestive heart failure (CHF) and hypertension. It defines CHF as diminished cardiac output that is insufficient to meet metabolic needs. Common causes include congenital heart disease, ischemic heart disease, and hypertensive heart disease. Types of heart failure include high output, low output, forward, and backward failure. Symptoms include dyspnea, fatigue, edema, and signs include cardiomegaly, gallops, and rales. The document also discusses hypertension causes, pathogenesis, complications like hypertensive heart disease, and related conditions like congestive heart failure and coronary artery disease.

1. Cardiovascular
System
Al-Quds University
Faculty of Medicine
Pathology Department
1
Lecture I: CHF and Hypertension

2. Congestive Heart Failure (CHF)
• Definition: diminished
functional capacity of the
heart which is unable to
maintain an output sufficient
for metabolic needs.
• Can involve the heart's left side,
right side, or both sides
• Called congestive because of
pulmonary congestion and
peripheral edema
2

3. CHF: Causes
• Congenital heart disease (valvular problems)
• Ischemic heart disease
• Rheumatic heart disease and other immune disease :
– E.g., SLE, RA, Scleroderma
• Hypertensive heart disease
• Inflammatory disease of the heart
• Nutritional, endocrine, and metabolic diseases including:
– Thyrotoxicosis
– Myxedema
– Beriberi
– Carcinoid syndrome
– Storage disease
– Amyloidosis
• Cardiomyopathy
3

4. Types of heart failure
• High output failure: inability of the heart to meet the
increased demand for blood by tissues
– Thyrotoxicosis, anemias, arteriovenous shunts
• Low output failure: cardiac output is insufficient at rest or at
exertion:
– MI, cardiomyopathy, valvular disease
• Forward failure: Decreased left ventricular output
– Cardiac tamponade, aortic stenosis
• Backward failure: increased congestion of the venous
circulation, because the failing ventricle is unable to eject
the normal volume of venous blood delivered to it during
diastole 4

5. • Compensated heart failure: If the dilated ventricle
is able to maintain cardiac output at a level that
meets the needs of the body
• Decompensated heart failure: With time, the
failing myocardium is no longer able to propel
sufficient blood to meet the needs of the body, even
at rest.
• Right-sided cardiac failure
• Left-sided cardiac failure
Types of heart failure
5

6. • Systolic heart failure: is the result of impaired
contractile function
– E.g., MI, Dilated cardiomyopathy
• Diastolic heart failure: reduced ventricular
compliance in the setting of normal or near normal
systolic function
– E.g., HTN, aortic stenosis
Types of heart failure
6

7. CHF: Symptoms
• Dyspnea on ordinary exertion
• Exercise intolerance
• Fatigue
• Nocturia
• Cough (nonproductive)
• Orthopnea
• Paroxysmal nocturnal dyspnea
7

8. CHF: Signs
• Acute pulmonary edema
• Cardiomegaly
• Laterally displaced apical impulse
• Increased central venous pressure
• Hepatojugular reflux
• Hepatomegaly
• Lower extremity edema
• Neck vein distention
• Pleural effusion
• Rales (abnormal lung sounds).
• S3 gallop (third heart sound, aka “ventricular gallop)
• Tachycardia
• Unexplained weight gain 8

9. The most common causes:
• Left sided heart failure (the most common cause)
• Intrinsic diseases of the lung: (in the absence of LHF)
– pulmonary HTN (cor pulmonale)
– COPD
– Pulmonary fibrosis
• Pulmonic or tricuspid valve disease
• Congenital heart diseases (left-to-right shunt)
Right-sided cardiac failure
9

10. Clinical Features: Right heart failure
Systemic venous congestion:
• distended neck veins
• passive congestion of the liver
• generalized venous congestion including jugular veins
• enlarged, sometimes tender liver
• increased frequency of deep venous thrombi & pulmonary
embolism
Edema:
• subcutaneous edema
• weight gain
• ascites, pleural effusions
• dependent edema (the feet and lower legs)
10

11. Left-sided cardiac failure
The most common causes:
• systemic hypertension
• mitral or aortic valve disease
• ischemic heart disease
• primary diseases of the myocardium.
11

12. • Dyspnea due to pulmonary congestion and edema:
– Exertional dyspnea: during physical activity
– Orthopnea: when the person is lying down
– Paroxysmal nocturnal dyspnea: sudden, severe
dyspnea, with coughing, choking sensation, & wheezing
• muscle fatigue
• Enlarged heart, Tachycardia
• Third heart sound (S3)
• Rales at the lung bases
• Mitral regurgitation with systolic murmur
• Atrial fibrillation: "irregularly irregular" heartbeat due to
chronic dilation of the left atrium
Clinical Features: Left heart failure
12

13. Compensated heart failure:
adaptive responses
• Neurohumoral reactions: release of catecholamines in
response to reduced cardiac output, this leads to:
– Increased force of contraction (inotropic effect)
– Increased heart rate (Tachycardia)
• Hypertrophy: 1) Concentric, 2) Eccentric
• Dilatation
• Activation of the renin-angiotensin system 13

14. Cardiac hypertrophy:
• Concentric hypertrophy: the
thickness of the ventricular wall
increases without increase in the size
of the chamber
• Pure pressure load
• increase the diameter of individual
muscle fibers
• e.g., HTN, valvular stenosis
Compensated heart failure:
adaptive responses
14

15. Cardiac hypertrophy:
• Eccentric hypertrophy:
• an increase in heart size as well as an increase in
ventricular wall thickness
• pure volume load
• increase in cardiac fiber length
• E.g., valvular regurgitation, abnormal shunts
Compensated heart failure:
adaptive responses
15

16. 16
Hypertension (HTN) - Introduction
 “Sustained increase in blood pressure”
 Silent Killer– asymptomatic until late
 Symptoms: dizziness, headache, and visual difficulties
 Risk factor for – MI, DM, Stroke, heart & renal failure
 25% of population, <35% aware
 Chronic, end organ & vascular damage
 Complications: ATH, IHD, Renal damage, Stroke
 95% of HTN is idiopathic, 5% is secondary HTN

17. 17

18. 18
Malignant (Accelerated) Hypertension
 Occurs in 5% of hypertensive persons
 Rapidly rising blood pressure that if untreated leads
to death within 1 or 2 years.
 May complicate any type of HTN.
 Severe hypertension (diastolic > 120 mm Hg)
 Characterized by:
• renal failure
• retinal hemorrhages and exudates, with or
without papilledema

19. 19
Causes of Hypertension
Essential Hypertension (90%-95% of cases)
Secondary Hypertension (5%-10%)
Renal:
 Acute glomerulonephritis
 Chronic renal disease
 Polycystic disease
 Renal artery stenosis
 Renal vasculitis
 Renin-producing tumors

20. 20
Renal Causes:
 Polycystic Disease

21. 21
Endocrine:
 Adrenocortical hyperfunction (Cushing syndrome, primary
aldosteronism, congenital adrenal hyperplasia)
 Exogenous hormones (glucocorticoids, estrogen [including
pregnancy-induced and oral contraceptives], sympathomimetics
and tyramine-containing foods, monoamine oxidase inhibitors)
 Pheochromocytoma
 Acromegaly
 Hypothyroidism (myxedema)
 Hyperthyroidism (thyrotoxicosis)
 Pregnancy-induced
Causes of Hypertension

22. 22
Cardiovascular:
 Coarctation of aorta
 Polyarteritis nodosa
 Increased intravascular volume
 Increased cardiac output
 Rigidity of the aorta
Neurologic:
 Psychogenic
 Increased intracranial pressure
 Sleep apnea
 Acute stress, including surgery
Causes of Hypertension

23. 23
Regulation of BP:

24. 24
Pathogenesis of HTN
 both increased blood volume and increased peripheral
resistance contribute to the increased pressure
 Cardiac output is influenced by blood volume, which is
greatly dependent on body sodium
 Total peripheral resistance is determined at the
level of arterioles, and depends on the effects of the
neural and hormonal influences
 Normal vascular tone depends on the competition
between vasoconstricting influences and vasodilators

25. 25
 Through renin angiotensin system, the kidney influences
both peripheral resistance and sodium homeostasis
 Natriuretic factor is believed to be a neurohormone that is
secreted by atria and left ventricle in response to volume
expansion. It inhibits Na reabsorption in distal tubules and
cause vasodilation
 Mutations in proteins that affect sodium reabsorption,
for example mutations in an epithelial sodium channel
protein lead to increased distal tubular reabsorption of Na
induced by aldosterone, and decreased renal Na excretion.
This results in a moderate to severe form of salt
sensitive hypertension called Liddle’s syndrome

26. 26
Pathogenesis of Renovascular HTN
GFR
Renin by JGA
Angiotensin II
Vasoconstriction
 Peripheral Vascular
 Resestance
Sodium Retention
Blood Volume
Aldosterone
Hypertension

27. 27
Pathogenesis of Essential Hypertension
Essential hypertension is a complex multifactorial disorder
 Genetic factors:
• Polygenic mutations are more likely
• Gene defects in some enzymes like:
• Aldosterone synthase, 11 hydroxylase, 17 hydroxylase
• Lead to increase in secretion of aldosterone with the
result of increased Na and water reabsorption, plasma
volume expansion, and HTN
 Environmental factors
• Stress
• Obesity
• Physical inactivity
• Heavy consumption of salt

28. 28
Complications of HTN
 Large Blood Vessels – Macroangiopathy
• Atherosclerosis and its complications
 Small Blood Vessels – Microangiopathy
• hyaline and hyperplastic arteriolosclerosis
 Heart:
• LVH
 Kidney:
• Benign nephrosclerosis
 Eyes:
• Hypertensive retinopathy
 Brain:
• Hemorrhage, infarction

29. 29
Benign
Nephrosclerosis
Leathery Granularity
due to minute scarring

30. 30
LV Hypertrophy secondary to HTN

31. 31
Retinopathy secondary to HTN
Normal retina

32. Hypertensive Heart Disease
• Left ventricular hypertrophy with a history of hypertension
• other causes of ventricular hypertrophy have been excluded.
– (e.g., aortic stenosis or primary hypertrophic
cardiomyopathy)
• Cause: sustained pressure load on LV
• with increasing degrees of hypertrophy, the metabolic
requirements continue to increase but the ability of the heart
to meet these demands decreases.
• hypertrophy decreases diastolic filling and stroke volume
• Complication: CHF, MI, arrhythmias. 32

33. Morphology
• LV concentric hypertrophy
• Heart weight > 450 g.
• wall thicknesses > 2.0 cm.
• When LV fails, RV undergoes hypertrophy, and dilation
may also develop
• Histology: cardiac myocytes enlarge, and contain
hyperchromatic , rectangular box-car shaped nuclei
33

34. LV hypertrophy: Clinical features:
• Initially: no symptoms
• Later: LV may decompensate (fail)
• Diagnosis: CXR, echo, ECG
• Complications:
– heart failure is a poor prognosis
– progressive renal damage
– cerebrovascular accidents
– sudden cardiac death 34

35. Cor Pulmonale (Pulmonary Heart Disease)
• Describe disease of right side chambers of the heart.
• This results from pulmonary hypertension, occurred from
pulmonary parenchymal or vascular disease
• Characterized by hypertrophy and/or dilation
Morphology:
• In acute cor pulmonale: RV is usually dilated.
• In chronic cor pulmonale:
– RV & right atrium hypertrophy.
– Thickness of the RV may exceed that of the LV
– Later: RV failure with RV & right atrium dilation 35

36. DISORDERS THAT PREDISPOSE TO COR PULMONALE
Diseases of the Lungs:
 Chronic obstructive lung disease (the most common chronic cause)
 Diffuse pulmonary interstitial fibrosis
 Extensive, persistent atelectasis
 Cystic fibrosis
Diseases of Pulmonary Vessels:
 Pulmonary embolism (the most common acute cause)
 Primary pulmonary vascular sclerosis
 Pulmonary arteritis (e.g., Wegener granulomatosis)
 Drug-, toxin-, or radiation-induced vascular sclerosis
Disorders Affecting Chest Movement:
 Kyphoscoliosis
 Marked obesity
 Neuromuscular diseases
Disorders Inducing Pulmonary Arteriolar Constriction:
 Metabolic acidosis
 Hypoxemia
36