HTN and CHF

HYPERTENSION AND CONGESTIVE HEART
FAILURE
Hypertension
• Hypertension is defined as an increase in arterial blood
pressure at several determinations that is associated
with increased cardiovascular morbidity and mortality
• no rigidly defined threshold reliably predicts who will
suffer ill effects.
• Nevertheless, sustained diastolic pressures greater
than 90 mmHg, or sustained systolic pressures in
excess of 140 mm Hg, are associated with an increased
risk of atherosclerosis and are therefore used as cutoffs
in diagnosing hypertension in clinical practice.
• Hypertension is a major health problem in the both developed
and developing world.
• Although it occasionally manifests in an acute aggressive form,
high blood pressure is much more often asymptomatic for many
years.
• Generally, hypertension increases the risk of
 stroke
 atherosclerotic coronary heart disease,
 cardiac hypertrophy and heart failure (hypertensive heart disease)
 aortic dissection
 multi-infarct dementia
 renal failure
• Hypertensive Emergency is when there is
acute impairment of an organ system (CNS,
CVS, Renal). In these conditions, the blood
pressure should be lowered aggressively over
minutes to hours.
• Hypertensive Urgency in which BP is high and
there is potential risk but has not yet caused
acute end-organ damage.
– These patients require BP control over days.
Epidemiology of Hypertension
• The prevalence of pathologic effects of high blood pressure
increases with age and is also higher in African Americans.
• A small percentage of hypertensive patients (approximately
5%) present with a rapidly rising blood pressure that, if
untreated, leads to death within 1 to 2 years
• Such malignant hypertension usually is severe (i.e., systolic
pressures over 200 mm Hg or diastolic pressures over 120
mmHg)
PATHOGENESIS
• Most cases (95%) are idiopathic (essential hypertension).
This form is compatible with long life unless a myocardial
infarction, stroke, or another complication supervenes.
• secondary hypertension are due to primary renal disease,
renal artery narrowing (renovascular hypertension), or
adrenal disorders
• Several relatively rare single-gene disorders cause
hypertension (and hypotension) by affecting renal sodium
resorption
• Although the specific triggers are unknown, it
appears that both altered renal sodium
handling and increased vascular resistance
contribute to essential hypertension.
MORPHOLOGY
• Hypertension not only accelerates atherogenesis
but also causes degenerative changes in the
walls of large and medium sized arteries that
can lead to aortic dissection and cerebrovascular
hemorrhage.
• Two forms of small blood vessel disease are
hypertension-related: hyaline arteriolosclerosis
and hyperplastic arteriolosclerosis
Diagnostic workup
• Laboratory investigations: Unless a secondary cause for hypertension is
suspected, only the following routine laboratory studies should be performed:
– CBC
– Urinalysis including microscopy , protein , blood and , glucose
– Fasting blood glucose
– Serum electrolytes :
– Lipid profile (total cholesterol, low-density lipoprotein [LDL] and high-density
lipoprotein [HDL], and triglycerides).
– Serum creatinine, uric acid,
ECG
• Imaging Studies:
– Echocardiography: to detect LVH
– CXR (if necessary)
Therapy of Hypertension
• non pharmacologic therapy
– Sodium (salt)restriction
– Lifestyle modifications
• Pharmacologic therapy – involves the use of one or more
of the following agents
– Diuretics
– β-adrenergic blocking agents
– Centrally acting agents
– Vasodilators
– ACE inhibitors
– Angiotensin receptor blockers
HEART FAILURE
HEART FAILURE
• Heart failure generally is referred to as
congestive heart failure (CHF).
• CHF is the common end point for many forms
of cardiac disease and typically is a progressive
condition that carries an extremely poor
prognosis
• Most cases of heart failure are due to systolic
dysfunction—inadequate myocardial
contractile function, characteristically a
consequence of ischemic heart disease or
• Alternatively, CHF also can result from
diastolic dysfunction—inability of the heart to
adequately relax and fill, such as in massive
left ventricular hypertrophy, myocardial
fibrosis, amyloid deposition, or constrictive
pericarditis.
• Finally, heart failure also can be caused by
valve dysfunction (e.g., due to endocarditis) or
can occur in normal hearts suddenly burdened
with an abnormal load (e.g., with fluid or
• CHF occurs when the heart cannot generate
sufficient output to meet the metabolic
demands of the tissues—or can only do so at
higher-than-normal filling pressures;
• In a minority of cases, heart failure can be a
consequence of greatly increased tissue
demands, as in hyperthyroidism,or poor
oxygen carrying capacity as in anemia (high-
output failure).
• CHF onset can be abrupt, as in the setting of a
large myocardial infarct or acute valve
dysfunction.
• In many cases, however, CHF develops
gradually and insidiously owing to the
cumulative effects of chronic work overload or
progressive loss of myocardium.
• Inadequate cardiac output—called forward
failure—is almost always accompanied by
increased congestion of the venous circulation
• The cardiovascular system attempts to
compensate for reduced myocardial
contractility or increased hemodynamic
burden through several homeostatic
mechanisms:
– The Frank-Starling mechanism

– Activation of neurohumoral systems(Release of
norepinephrine; Activation of the renin-
angiotensin-aldosterone system; Release of atrial
natriuretic peptide )
Left-Sided Heart Failure
• Heart failure can affect predominantly the left
or the right side of the heart or may involve
both sides.
• The most common causes of left-sided cardiac
failure are
Ischemic heart disease (IHD)
 systemic hypertension
mitral or aortic valve disease
 primary diseases of the myocardium(e.g.,
amyloidosis).
MORPHOLOGY
Heart –
 the left ventricle usually is hypertrophied and can be dilated,
sometimes massively with possible exceptions
 mitral insufficiency and left atrial enlargement, which is associated
with an increased incidence of atrial fibrillation.
Lungs.
congestion and edema as well as pleural effusion
lungs are heavy and boggy, and microscopically show perivascular
and interstitial transudates,
hemosiderin-laden alveolar macrophages—so-called heart failure
cells
Clinical Features
• Dyspnea (shortness of breath) on exertion;
cough, orthopnea, Paroxysmal nocturnal
dyspnea
• tachycardia, a third heart sound (S3), and fine
rales at the lung bases, caused by the opening
of edematous pulmonary alveoli; mitral
regurgitation and a systolic murmur; atrial
fibrillation; strokes and manifestations of
infarction in other organs
Complications
• AF – that could cause sudden death due to
worsening of impaired electrical activity; form
thrombi (particularly in the atrial appendage)
that can shed emboli and cause strokes and
manifestations of infarction in other
organs.
• Acute pulmonary edema
• Cardiogenic shock
• prerenal azotemia
Right-Sided Heart Failure
• Right heart failure usually is the consequence
of left-sided heart failure
• Isolated right-sided heart failure also can
occur in a few diseases. The most common of
these is severe pulmonary hypertension,
resulting in right-sided heart pathology
termed cor pulmonale. Other causes include
 primary pulmonic or tricuspid valve disease
 congenital heart disease, such as with left-to-right
shunts causing chronic volume and pressure
• The major morphologic and clinical effects of pure rightsided heart
failure differ from those of left-sided heart failure in that
 engorgement of the systemic and portal venous systems typically is
pronounced and
 pulmonary congestion is minimal.
MORPHOLOGY
 congestive hepatomegaly that can later become cardiac cirrhosis
 portal hypertension with congestive splenomegaly
 Chronic passive congestion of the bowel wall with edema.
transudates (effusions) in the pleural and pericardial spaces
Peripheral edema of dependent portions of the body, especially ankle
(pedal) and pretibial edema – In particularly severe cases - (anasarca)
Clinical Features
• Hepatic and splenic enlargement, peripheral
edema, pleural effusion, and ascites.
• Of note, in most cases of chronic cardiac
decompensation, patients present with
biventricular CHF, encompassing the clinical
syndromes of both right-sided and left-sided
heart failure.
Diagnosis.
• Echocardiography is the test-of-choice to
confirm the diagnosis of HF and to classify the
type (systolic vs. diastolic).
• With the echocardiogram, the clinician is able
to determine ejection fraction and identify
valvular heart disease as well as other cardiac
anomalies (dilated ventricle, thickened
ventricle, etc.).
• Chest x-rays are also used to aid in the
diagnosis of heart failure. They may show
cardiomegaly, vascular redistribution, Kerley B-
lines, and interstitial edema.
• Electrocardiogram(ECG) is used to identify
ventricular hypertrophy and/or the presence
of ischemic heart disease, arrhythmias, or
conduction delays which may cause or
precipitate HF.
• Laboratory Tests include CBC, Serum
electolyte, U/A, LFT, RFT, Blood sugar, Lipid
Profiles...
• Principles of management of heart failure
include
 treat congestive state with diuretics
 treat precipitating factors
 manage underlying cause
 supportive care

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HYPERTENSION AND CONGESTIVE HEART

– The Frank-Starling mechanism

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