Hypertension, Heart Failure, and Hyperlipidemia: Pathophysiology, Risk
Stratification, Hemodynamics, Neurohormonal Activation, Preload, Afterload,
Contractility, Cardiac Output, Ejection Fraction, Systolic Dysfunction, Diastolic
Dysfunction, LV Remodeling, RAAS Activation, Sympathetic Nervous System,
End-Organ Damage, Secondary Hypertension, Renal Artery Stenosis,
Pheochromocytoma, Hyperaldosteronism, Lifestyle Modification, Thiazide
Diuretics, ACE Inhibitors, ARBs, Beta-Blockers, Calcium Channel Blockers, SGLT2
Inhibitors, Natriuretic Peptides, BNP, Dyslipidemia, Statin Therapy, PCSK9
Inhibitors, DASH Diet, Cardiovascular Risk Assessment Exam Questions Verified
and Provided with Complete A+ Graded Rationales Latest Updated 2026
Hypertension: risk factors
Obesity
Metabolic Syndrome
Higher dietary intake of fat
Excess sodium intake
Physical inactivity
Excess alcohol intake
HTN: pathophys
Hemodynamic factors:
BP is the product of CO and total peripheral resistance (BP = CO x TPR)
CO is the product of stroke volume and heart rate (CO = SV x HR)
Stroke volume is determined by: venous return to the heart (preload) and resistance the left ventricle
must overcome to eject blood in the aorta (afterload)
stroke volume
,volume of blood ejected from the ventricle during systole (end diastolic volume minus end systolic
volume)
Cardiac output
SV x HR: volume of blood ejected from the ventricle per minute
Ejection fraction (EF)
fraction of end diastolic volume ejected from the ventricle during each systolic contraction (normal 55-
75%)
At least 4 systems are responsible for regulation of blood pressure
Heart: which supplies pumping pressure
Blood vessel tone: which largely determines systemic resistance
Kidney: which regulates intravascular volume
Hormones: which modulate the function of the other 3 systems
Primary (essential) HTN
Cause is unknown
Almost 95% of those with HTN are diagnosed with essential HTN
It likely results from multiple defects of BP regulation that interact with environmental stressors
Hypothesized links to primary HTN:
1. hereditary appears to play an important role but exact genetic markers have not be linked - there is a
higher degree of HTN among first degree relatives and even higher among identical twins compared to
dizygotic twins
2. sympathetic nervous system: people under psychologically stressful conditions (such as fever, anger
or anxiety) develop excessive increases in heart rate which ultimately increases BP - evidence suggests
,that chronic stress may lead to HTN due to increase in HR caused by catecholamines and excessive
sympathetic response
Secondary HTN
HTN attributed to a definable cause
It is important to differentiate since secondary HTN may have amendable cures
Renal influences primary htn
Kidneys can induce volume based on HTN by retaining excessive sodium and water this is a result of:
Failure to regulate renal blood flow appropriately
Ion channel defects (NaK-AtPase) which directly cause sodium retention
Inappropriate hormonal regulation
Renin
1.Renin is an enzyme produced and released by the juxtaglomerular apparatus of the kidney in response
to low fluid state, sympathetic nervous system stimulation and/ or catecholamine release, and
hypokalemia.
2.Once released, renin acts on ANGIOTENSION to create ANGIOTENSION I which is ultimately converted
to ANGIOTENSION II ( a potent vasoconstrictor).
3. With prolonged production, overtime this process causes arterial stiffening and hypertrophy.
4. Angiotension II causes aldosterone stimulation which enhances sodium and water reabsorption from
the renal tubules and increases circulating volume.
5. This process should provide feedback to maintain hoemostasis; however, thisprocess may not work
properly in some individuals leading to higher levels of renin and thus higher BP.
HTN primary other causes
, 1)Insulin resistance: elevated insulin levels may contribute to HTN by increasing sympathetic activation
or by stimulation of vascular smooth muscle cell hypertrophy which increases vascular resistance.
2)Obesity: accounts for high percentage of HTN in both men & women.
3)Metabolic Syndrome
Secondary HTN
Accounts for approximately 5% (3 million people) or population with HTN
Renal artery stenosis
Phenochromocytoma
Hyperaldosteronism
Coarctation of the aorta
Cushing's syndrome
Sleep apnea
ETOH
Use of contraceptives
Steroids
Thyroid disease
Renal artery stenosis
results when there is 70-80% blockage of renal artery, this often results in activation of renin-
angiotension system.
In younger people (<30) it is result fibrodysplasia or fibromuscular dysplasia which causes a tight fibrous
band that alternates with thin or normal tissue along the renal artery or.
Affects more women than men
After age 50 most likely result of atherosclerosis within the renal artery or in the aorta at the origin of
the renal artery.
Elevated BP from RAS results from reduced renal blood flow to the affected kidney which responds to
the decrease perfusion pressure by releasing renin which ultimately leads to sodium retention and
vasoconstriction.
Stratification, Hemodynamics, Neurohormonal Activation, Preload, Afterload,
Contractility, Cardiac Output, Ejection Fraction, Systolic Dysfunction, Diastolic
Dysfunction, LV Remodeling, RAAS Activation, Sympathetic Nervous System,
End-Organ Damage, Secondary Hypertension, Renal Artery Stenosis,
Pheochromocytoma, Hyperaldosteronism, Lifestyle Modification, Thiazide
Diuretics, ACE Inhibitors, ARBs, Beta-Blockers, Calcium Channel Blockers, SGLT2
Inhibitors, Natriuretic Peptides, BNP, Dyslipidemia, Statin Therapy, PCSK9
Inhibitors, DASH Diet, Cardiovascular Risk Assessment Exam Questions Verified
and Provided with Complete A+ Graded Rationales Latest Updated 2026
Hypertension: risk factors
Obesity
Metabolic Syndrome
Higher dietary intake of fat
Excess sodium intake
Physical inactivity
Excess alcohol intake
HTN: pathophys
Hemodynamic factors:
BP is the product of CO and total peripheral resistance (BP = CO x TPR)
CO is the product of stroke volume and heart rate (CO = SV x HR)
Stroke volume is determined by: venous return to the heart (preload) and resistance the left ventricle
must overcome to eject blood in the aorta (afterload)
stroke volume
,volume of blood ejected from the ventricle during systole (end diastolic volume minus end systolic
volume)
Cardiac output
SV x HR: volume of blood ejected from the ventricle per minute
Ejection fraction (EF)
fraction of end diastolic volume ejected from the ventricle during each systolic contraction (normal 55-
75%)
At least 4 systems are responsible for regulation of blood pressure
Heart: which supplies pumping pressure
Blood vessel tone: which largely determines systemic resistance
Kidney: which regulates intravascular volume
Hormones: which modulate the function of the other 3 systems
Primary (essential) HTN
Cause is unknown
Almost 95% of those with HTN are diagnosed with essential HTN
It likely results from multiple defects of BP regulation that interact with environmental stressors
Hypothesized links to primary HTN:
1. hereditary appears to play an important role but exact genetic markers have not be linked - there is a
higher degree of HTN among first degree relatives and even higher among identical twins compared to
dizygotic twins
2. sympathetic nervous system: people under psychologically stressful conditions (such as fever, anger
or anxiety) develop excessive increases in heart rate which ultimately increases BP - evidence suggests
,that chronic stress may lead to HTN due to increase in HR caused by catecholamines and excessive
sympathetic response
Secondary HTN
HTN attributed to a definable cause
It is important to differentiate since secondary HTN may have amendable cures
Renal influences primary htn
Kidneys can induce volume based on HTN by retaining excessive sodium and water this is a result of:
Failure to regulate renal blood flow appropriately
Ion channel defects (NaK-AtPase) which directly cause sodium retention
Inappropriate hormonal regulation
Renin
1.Renin is an enzyme produced and released by the juxtaglomerular apparatus of the kidney in response
to low fluid state, sympathetic nervous system stimulation and/ or catecholamine release, and
hypokalemia.
2.Once released, renin acts on ANGIOTENSION to create ANGIOTENSION I which is ultimately converted
to ANGIOTENSION II ( a potent vasoconstrictor).
3. With prolonged production, overtime this process causes arterial stiffening and hypertrophy.
4. Angiotension II causes aldosterone stimulation which enhances sodium and water reabsorption from
the renal tubules and increases circulating volume.
5. This process should provide feedback to maintain hoemostasis; however, thisprocess may not work
properly in some individuals leading to higher levels of renin and thus higher BP.
HTN primary other causes
, 1)Insulin resistance: elevated insulin levels may contribute to HTN by increasing sympathetic activation
or by stimulation of vascular smooth muscle cell hypertrophy which increases vascular resistance.
2)Obesity: accounts for high percentage of HTN in both men & women.
3)Metabolic Syndrome
Secondary HTN
Accounts for approximately 5% (3 million people) or population with HTN
Renal artery stenosis
Phenochromocytoma
Hyperaldosteronism
Coarctation of the aorta
Cushing's syndrome
Sleep apnea
ETOH
Use of contraceptives
Steroids
Thyroid disease
Renal artery stenosis
results when there is 70-80% blockage of renal artery, this often results in activation of renin-
angiotension system.
In younger people (<30) it is result fibrodysplasia or fibromuscular dysplasia which causes a tight fibrous
band that alternates with thin or normal tissue along the renal artery or.
Affects more women than men
After age 50 most likely result of atherosclerosis within the renal artery or in the aorta at the origin of
the renal artery.
Elevated BP from RAS results from reduced renal blood flow to the affected kidney which responds to
the decrease perfusion pressure by releasing renin which ultimately leads to sodium retention and
vasoconstriction.
