This document discusses the pharmacologic management of hypertension and congestive heart failure. It begins by defining cardiac output and its relationship to heart rate and stroke volume. It then discusses factors that affect blood pressure such as total peripheral resistance, cardiac output, and blood volume. The document reviews treatment for both chronic hypertension through lifestyle modifications and medication, as well as treatment for hypertensive emergencies and urgencies through rapid-acting parenteral and oral antihypertensive agents. The goal of therapy is to reduce blood pressure by no more than 25% over 1-2 hours to prevent target organ damage.
This Slideshare includes the introduction of congestive heart failure, signs and symptoms, pathogenesis, epidemiology, etiology, pathophysiology, classification of drugs which is used to manage CHF, and recent drugs used to manage CHF.
This presentation deals with the use of various drugs in the treatment of heart failure such as Digoxin, ace inhibitors, beta bloockers, calcium channel blockers
This Slideshare includes the introduction of congestive heart failure, signs and symptoms, pathogenesis, epidemiology, etiology, pathophysiology, classification of drugs which is used to manage CHF, and recent drugs used to manage CHF.
This presentation deals with the use of various drugs in the treatment of heart failure such as Digoxin, ace inhibitors, beta bloockers, calcium channel blockers
A Global Problem
HIGHLY LETHAL 5 yr Survival rate “50%”
More M.I. cases now survive More Incidence of CHF due to damaged myocardium
Better options than before now available to treat CHF
Congestive heart failure (CHF) is a chronic progressive condition that affects the pumping power of your heart muscles. While often referred to simply as “heart failure,” CHF specifically refers to the stage in which fluid builds up around the heart and causes it to pump inefficiently. You have four heart chambers.
A Global Problem
HIGHLY LETHAL 5 yr Survival rate “50%”
More M.I. cases now survive More Incidence of CHF due to damaged myocardium
Better options than before now available to treat CHF
Congestive heart failure (CHF) is a chronic progressive condition that affects the pumping power of your heart muscles. While often referred to simply as “heart failure,” CHF specifically refers to the stage in which fluid builds up around the heart and causes it to pump inefficiently. You have four heart chambers.
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3. Cardiac Output
CO= HR x SVR
Cardiac output: The quantity of blood pumped into the
aorta each minute by the heart
Also the quantity of blood that flows through the circulation
Perhaps the most important factor to consider in relation to
circulation
4. Normal Values for Cardiac
Output
Varies widely with the level of activity
The following factors directly affect CO
Basic level of body metabolism
Whether the person is exercising
Age
Size of the body
Young healthy men resting CO about 5.6L/min
For women, about 4.9L/min
5. Cardiac Index
CI = CO/BSA
The CO per square meter of body surface area
The normal range of cardiac index in rest is 2.6 - 4.2
L/min per square meter
6. Control of Heart Rate (HR)
The SA node of the heart is innervated by both sympathetic
and parasympathetic nerves
Parasympathetic fibers release acetylcholine
Decrease HR
Sympathetic release norepinephrine and release of
epinephrine from the adrenal medulla.
Increase HR
7. Control of Stroke Volume (SV)
The ventricles of the heart empty only about 50% of their
volume during systole.
During periods of exercise, the heart fills up with more blood
and the heart contracts more strongly.
Stroke volume is increased by 2 mechanisms:
increase in end-diastolic volume
increase in sympathetic system activity
8. Control of Cardiac Output by
Venous Return
This means it is NOT the heart itself that is the primary
controller of CO
Peripheral factors usually more important in controlling CO
Heart will pump regardless the amount of blood flowing into
the right atrium
Frank-Starling law
As a result of increased quantities of volume the heart will stretch
and eject blood with increased force
Stretch of the right atrium with stretch the sinus node and
increase heart rate (remember for Afib)
9. End-diastolic Volume
End- diastolic Volume: Volume of blood in the ventricles
at the end of diastole
Larger end-diastolic volume will stretch the heart
Stretching the muscles of the heart optimizes the
length-strength relationship of cardiac fibers, resulting
in stronger contractility and greater stroke volume
12. Regulation of Blood Volume by
the Kidneys
Regulation of water excretion directly affects blood volume
Regulated by the kidneys, controlled by anitdiuretic
hormone (ADH)
ADH
Produced by the hypothalamus and secreted by the posterior
pituitary
Regulated by hypothalamus based on plasma osmolality
13. Regulation of Blood Flow
Blood flow = Pressure / Resistance
If pressure in a vessel increases flow will increase
However if resistance in vessel increases flow will decrease
Resistance in the vessels effected by:
Length of the vessel (the longer the vessel the greater the
resistance
Viscosity of the blood (greater the viscosity the greater
the resistance
Radius of the vessel (smaller the radius the greater the
resistance
14. Regulation of Blood Flow
Extrinsic regulation
Sympathetic control of arteriolar radius
Norepinephrine causes vasoconstriction
Vasodilation accomplished by decreased sympathetic
stimulation
Endocrine control of arteriolar radius
Epinephrine secreted by adrenals in response to sympathetic
response
Intrinsic regulation
Some organs regulate their own blood flow regardless of
what is happening elsewhere
15.
16. Effect of Peripheral Resistance
on the Long-Term CO
CO= Arterial Pressure/Total Peripheral Resistance
Under most normal conditions the long term cardiac output
level varies reciprocally with changes in total peripheral
resistance
As resistance increase the CO decreases and vice versa
17.
18. Mean Arterial Pressure
Average blood pressure in an individual
3 most important variables effecting MAP
Total peripheral resistance
Cardiac output
Blood volume
MAP= (COxSVR) + CVP
MAP= ((2x DP) + SP)/3
19. Total Peripheral Resistance
(TPA)
TPA refers to the sum of total vascular resistance to
flow of blood in the systemic circulation
Arterioles given their small radii provide the greatest
resistance
If resistance increases then pressure increases
20. Cardiac Output/Blood Volume
CO is a measure of blood flow and directly proportional
to pressure.
Therefore an increase in CO will cause an increase in
pressure (MAP)
Blood volume is directly related to blood pressure
As stroke volume goes up -> CO goes up -> BP rises
22. Baroreceptor Reflexes
Regulation of MAP
Is controlled on a minute-to-minute basis by
baroreceptor reflexes
Specialized stretch receptors located in the carotid
sinus and aorta
Communicate with the brain stem to normalize BP
24. EPIDEMIOLOGY
HTN AFFECTS ABOUT 58 MILLION AMERICANS
33.5% non-Hispanic blacks
28.9% non-Hispanic whites
20% in Mexican Americans
PREVALENCE OF HTN INCREASING AS THE POPULATION AGES
ESTIMATED ABOUT 1% OF HYPERTENSIVE PATIENTS WILL DEVELOP A HYPERTENSIVE EMERGENCY
UNABLE TO KNOW FOR SURE THE PERCENTAGE OF OCCURANCE OF HYPERTENSIVE URGENCY
ED PRESENTATION- 2-3% OF VISITS ANNUALLY
70% URGENCY, 3% EMERGENCY
BOTH ENVIRONMENTAL AND GENETIC FACTORS MAY CONTRIBUTE TO REGIONAL AND RACIAL VARIATIONS
26. Objectives
Describe drug therapy options for chronic and acute
hypertension
Explain the clinical pharmacology of commonly used
antihypertensive drugs
27. Chronic Hypertension
Primary or “essential”
No identifiable cause
Also know as essential HTN
Accounts for ~90% of cases
Secondary
Identifiable cause
CRI, Cushing’s, pheochromocytoma, oral
contraceptives, etc.
29. Risk Factors
Age > 60 years
Male gender
Smoking
Diabetes
Family history
Heart failure
PVD
Hyperlipidemia
Renal Disease
30. Mechanism of Hypertension
Intravascular Volume
Autonomic Nervous System
Renin-Angiotensin-Aldosterone
Vascular Mechanisms
31. Intravascular Volume
• BP = CO x Peripheral Vascular Resistance
• Autoregulation: (ie. Kidneys and Brain)
If constant blood flow is to be maintained in the face of
increased arterial pressure, resistance within that bed must
increase
– Initial in BP is in response to vascular volume due
to increased CO; however reverts back to normal over
time (peripheral resistance remains elevated likely to due
to epithelial damage)
32. Intravascular Volume
“Pressure- Natriuresis”
Increased urinary excretions of sodium along with water to
maintain normal BP
Involves subtle increase in GFR
Decreased absorbing capacity in renal tubules
Hormonal factor (atrial natriuretic factor/peptide)
39. Hypertension
Target Organ Damage
Independent predisposing factor for heart
failure, coronary artery disease, stroke, renal
disease, and peripheral artery disease
40. Hypertension
Heart
Heart disease is most common cause of death in
hypertensive patients
Structural Damage
LVH
Diastolic dysfunction
CHF
CAD
Arrhythmias
41. Hypertension
Brain
Important risk factor for infarction and hemorrhage
Incidence of stroke increases with increase in BP
Treatment decreases incidence of both ischemic and
hemorrhagic stroke
Associated with impaired cognition in aging
population
May cause hypertensive encephalopathy
Can lead to stupor, coma, seizures, death
42. Hypertension
Kidney
Risk factor for renal injury and ESRD
The atherosclerotic, HTN-related vascular lesions
Resulting in glomerular ischemia and atrophy
Macro (urine albumin/creatinine ratio >300 mg/g) and
microalbuminuria (30-300 mg/g)
44. Lifestyle Modifications
Diet
DASH diet rich in fruit, vegetables and low-fat dairy foods
Reduce sodium intake to 2.4 grams/day
Limit alcohol consumption
Exercise
Aerobic and weight-bearing activity
Stop smoking!
45. Drug Dosing
“Start low and go slow!”
No need to drop BP immediately unless in an
emergency
46. Hypertensive Emergencies and Urgencies
“Emergencies” (>180/120)
Require immediate BP reduction to limit target organ
damage (TOD)
Encephalopathy, ICH, AMI, pulmonary edema, aortic
aneurysm, eclampsia, etc.
“Urgencies” (>180/120)
Reduce BP over 1-2 days to prevent TOD
47. Goals of Therapy
Reduce MAP by no more than 25% (within 2 minutes
to 2 hours)
Achieve BP of 160/90 within 6 hours (drastic drops in
BP may induce ischemia)
Elevated BP alone without target organ damage or
symptoms rarely requires emergency therapy
48. Management
Use parental drugs for HTN emergency:
Enalaprilat
Esmolol
Fenoldopam
Labetalol
Nicardipine
Nitroglycerin
Nitroprusside
Phentolamine
Use fast-acting, oral agents for HTN urgency:
Loop diuretics
BBs and CCBs
ACE-Is
Alpha-2 agonists (clonidine)
Editor's Notes
Of all of the factors that effect blood flow, the radius of the blood vessel is the most potent. Blood flow is proportional to the 4th power of vessel radius. This means that if the radius of a blood vessel doubles (by vasodilation) then the flow will increase 16 fold (2 to the 4th power is 16). On the other hand, if the radius of a vessel is reduce in half (by vasoconstriction), then the blood flow will be reduced 16 fold
HYPERTENSION IS EXTREMELY COMMONEd PRESENTATIONS 2-3 % OF ALL VISITS ANNUALLY, 70% URGENCY, 30 % EMERGENCY