I.

Systemic hypertension: Hypternsion is when the SBP measures 140/90 mmHg or higher at least 2
occasions a minimum of 1-2 weeks apart. PreHTN is SBP of 120-139 or dbp of 80-89. Higher incidence in
black menand increases with age. Risk factor for ischemic heart disease and a major cause of CHF
a. Pathophysiology: systemic hypertension is characterized as essential or primary hypertension when
a cause for the increased BP is unknown. Secondary HTN when an identifiable cause is present.
b. Essential hypertension: accounts for 95% of all cases of HTN.
i. Essential risk factors: increased Sympathetic nervous system acitivity in response to stress,
1. Over production of sodium retaining hormones and vasoconstrictors,
2. High sodium intake
3. Inadequate dietary intake of potassium and calcium
4. Increased renein secretion,
5. Deficiencies of endogenous vasodialators such as prostaglandins and NO
6. Presence of medical diseases such as DM
7. Obesity
8. Salt and water retention
9. Alcohol and tobacco
10. A history of ischemic heart disease, angina, left ventricular hypertrophy, CHF, CVD,
stroke, peripheral vascular disease, or renal insufficiency suggest end-organ disease
due to chronic poorly controlled HTN.
11. Diagnostic testing is done to document target organ damage includes BUN and
creatineine assays to quantify renal function.
12. Low K=primary hyperaldosteronism.
13. Fasting BGL
ii. TREATMENT OF ESSENTIAL HTN:
1. Patients will be seen every 1-4 weeks to titrate antihypertensive drug dose and then
every 3-4 moths once the desired degree of blood pressure control has been
achieved.
2. Thiazide diuretics are best for uncomplicated HTN. And can increase the efficacy of
multidrug regimens
3. Goal is to decrease SBP to less than 140/90. In presence of DM less than 130/80.
4. Decreasing by life style modification and pharmacologic therapy is intended to
decrease morbidity and mortality.
5. Tx resulting in normalization of BP
6. Patients with risk factors and target organ damage will most likely benefit from
pharmacologic antihypertensive therapy.
iii. LIFESTYLE MODIFICATION:
1. Weight reduction or prevention of weight gain,
2. Moderate etoh
3. Increase physical activity
4. Adhere for dietary calcium and potassium intake, and moderation in dietary salt
intake. STOP smoking
5. 10 kg weight loss decreases the Systolic and diastolic pressures by an average of 6
and 4.6.
6. too much ETOH will decrease overall cardiovascular risk in the population.
7. Sodium restriction can minimize diuretic-induced hypokalemia and may enhance the
control of blood pressure with diuretic therapy.
c. Secondary HTN: accounds for less than 5%. Renal artery stenosis leading to renovascular HTN is the
most common cause of secondary HTN
i. Common causes of 2ndary HTN:
1. Renovascular disease
2. Hyperaldosteronism
3. Aortic coarctation
4. Pheochromocytoma
5. Cushings syndrome
6. Renal parenchymal disease
7. Pregnancy-induced hypertension
d. Treatment of Secondary hypertention: is often surgical pharmacologic therapy is for those who cant
have surgery.
i. SURGICAL THERAPY: is used to treat identifiable causes of secondary HTN.
1. Sx includes correction of renal arteruy stenosis via angioplasty or direct repair for
renovascular hypertension, and adrenalectomy for adrenal adenoma or
pheochromocytoma.

ii. PHARMACOLOGIC THERAPY: for patients whom renal artery repair is not possible, BP control
may be complished by ACE inhibitors alone or in combination with diuretics. Renal function
and seium K conc. Must be carefully monitored with ACE inhibitor therapy when initiated in
these patients.
iii. Hyperaldosteronism is tx with spironolactone an aldosterone antagonist. And use amiloride
in men due to gynecomastia that spirno causes.
e. Hypertensive crisis: typically present with a BP of more that 180/120 and is either a hypertensive
urgency or a hypertensive emergency, based on the presence or absensce of impending or
progressive target organ damage. Patients with chronic systemic hypertension can tolerate a higher
systemic blood pressure than previously normotensive individuals and are more likely to experience
urgencies rather than emergencies.
i. Hypertnsive EMERGENCY (HE): Patients with evidence of acute or on going target organ
damage (encephalopathy, intracerebral hemorrhage, acute left ventricular failure with PE,
ujnstable agina, dissecting aortic aneurysm, acute MI) require prompt pharmacologic
intervention to lower the systemic blood pressure.
1. Encephalopathy rarely develops in patients with chornic HTN until DBP is greather
than 150.
2. Pregnancy induced HTN may develop encephlopahty with DBP of less than 100. And
even in the absence of symptoms a DBOP of greater than 100 is an emergency and
needs to be treated immideatly.
a. Tx: drop DBP promptly but gradually. MAP is decreased by 20%within the 1st hr
and then more gradually over the next 2 to 6 hours to a target BP of 160/110.
ii. HYPERTENSIVE URGENCY: are situations in which the BP is severely elevated, but the patient
is not enxhibiting evidence of target organ damage. Thse patients have a HA, nose bleeds or
ansxiety at presentation.
1. Caused due to non adherence to medications unavailability of prescribed medications
2. PHARMACOLOGIC THERAPY: Insert A lineto continuously monitor SBP is recommended
during treatment with potent vasoactive drugs.
a. GOAL decrease BP below 20% to 25% to avoid organ hypoperfusion.
b. Na nitroprusside 0.5 to 10mcg/kg/min IV is drug of choice for HE.
i. Use can become complicated because it can cause cyanide toxicity
and lactic acidosis.
c. Fenoldopam for renal insufficiency patients returns blood flow to kid and
inhibits sodium reabsorption.
f. Management of anesthesia in patients with essential hypertension
i. Most drugs that effectively control SBP need to be continued to ensure optimum BP control.
ii. PREOPERATIVE EVALUATION:
1. Determine adequacy of BP control
2. Review pharmacology of drugs being administered to control BP
3. Evaluate for evidence of end-organ damage
4. Continue drugs used for control of BP
a. Preop: Intraoperative hypotension may be particularly problematic.
b. CRITERION FOR POSTPONEMENT DBP 100 to 115.
c. End organ damage should be evaluated preoperatively.
d. Patients with essential HTN should be presumed to have ischcemic heart
disease until proven otherwise.
e. Patient should remain on antihypertensive therapy throughout the
perioperative period to avoid the risk of rebound hypertension
f. ACE inhibitors are not associated with rebound HTN
g. ACE INHIBITORS:
i. There is a risk of hemodynamic instability and hypotension during
anesthesia in patients received ACE inhibitors.
ii. Only one system is remianig to support BP and its the vasopressin
system so BP is volume dependent. Sympathethetic NS (General
anesthesia) and RAAS is blunted by ACE
iii. Surgical procedures involving major fluid shifts have been associated
with hypotension in patients treated with ACE inhibitors but will
respond to fluid infusion and administration of sympathomimetic drugs.
iv. Recommended to discontinue ACE 24 to 48 hrs can cause
h. ARBS
i. Blockade of RAAS increases the potential for hypotension during
anesthesia.

ii. Discontinue before surgery because if ARBS is continued patient will

require vasoconstrictor treatment during sx.

II.

iii. InDUCTION AND MAINTENANCE OF ANESTHESIa:

1. Anticipate exaggerated BP response to anesthetic drugs
2. Induction of anesthesia with rapidly acting IV drugs may produce significant
hypotension due to peripheral vasodilation in the presense of a decreased
intravascular fluid volume.
3. Limit duration of DL to less than 15 seconds.
4. Administer a balanced anesthetic to blunt hypertensive responses
5. Consider placement of invasive hemodynamic monitors
6. Monitor for Myocardial ischemia
iv. MAINTENANCE OF ANESTHESIA: hemodynamic goalfor hypertensive patients during
maintenance of anesthesia is to minimize wide fluctuations in blood pressure.
1. INTRAOPERATIVE HYPERTENSION:
a. Volatile anesthetics produce a dose-dependent decrease in BP, which reflects
a decrease in SVR and or myocardial depression.
b. Nitrous oxide-opiod technique can be used for aintenace of anestheis,
although it is likely that a volatile agent will be needed at times to control
hypertension, especially during periods of abrupt change in surgical
stimulation.
2. INTRAOPERATIVE HYPOTENSION:
a. Hypotension during mainteneca of anesthesia may be treated by decreasing
the depth of anesthesia and/or by increasing the intravascular colume.
b. Ephedrine or phenylephrine may be necessary to restore vital organ perfusion
pressures until the underlying cause of hypotension can be ascertained and
corrected.
3. MONITORING:
a.
v. POSTOPERATIVE MANAGEMENT: postoperative hypertension is common in patients with
essential hypertension. Requires prompt assessment and treatment to decrease the risk of
myocardial ischemi, CHF stroke, or dysrhythmias.
1. Anticipate periods of systemic HTN
2. Maintain monitoring of end-organ function.
Pulmonary arterial hypertension: patients with PAH succumb to progressive right ventricular failure.
Patients with PAC are at risk of perioperative RV failure, hypoxemia, and coronary ischemia.
a. Definition: is defined hemodynamically as a mean Pulmonary aretery pressure of more than 25
mmHg at rest with a PCWP, LAP, or LVEDP of 15 mmHg or less, and a pulmonary vascular resistance
of more than 3 wood units.
i. IPAH refers to sporadic cases of PAH with no familial context and no identifiable risk factor.
Most patients with heritable PAH have mutations in bone morphogenetic protein receptor
type 2
b. Clinical presentation and evaluation
i. PAH often presents with vague symptoms including
1. Breathlessness
2. Weakness
3. Fatigue
4. Abdominal distention
5. Syncope and angina pectoris are indicative of severe limitations in CO and possible
myocardial ischemia.
ii. On physical examiniation, the patient may exhibit a parasternal lift, murmurs of pulmonic
insufficiency and/or tricuspid regurgitation, a pronounced pulmonic component of S2 and S3
gallop, JVD with a large a wave in the jugular venous pulsation, peripheral edema,
hepatomegaly, and ascites. Left RLN can become paralyzed because of compression by a
dilated pul monary artery (ortners syndrome). Right sided catheterization provides a
definitive means to determine disease severity and to ascertain which patients can respond
to vasodilator therapy.
1. Administration of a vasodilator such as prostacyclin, NO, adenosine, or prostaglandin
E1 will result positive if PVR and mean pulmonary arterial pressure both decrease by
20% or more.
c. Physiology and pathophysiology

i. Normal pulmonary circulation can accommodate flow rates ranging from 6 to25L/min with
minimal changes in pulmonary artery pressure. PAH develops as a result of pulmonary
vasoconstriction, vascular wall remodeling, and thrombosis in situ.
ii. Pulmonary HTN there is an increase in endotheline and arteries in lung become narrow. This
causes BP in lungs to become high and RV enlargement
iii. PAH are at risk of hypoxemia because of 3 mechanisms:
1. As right sided pressures increase, right to left shunding can occur thorugh a patent
foramen ovale
2. In the presence of the relatively fiex CO, the increased oxygen extraction associated
with exertion produces hypoxemia;
3. Ventilation/perfusion mismatch can reslt in perfusion of poorly ventilated alveoli. If
hypoxeic pulmonary vasocosntricion occurs, overall pulmonary hypertension will be
worsened.
d. Treatment: CCB and warfarin.
i. Oxygen, anticoagulation and diuretics:
1. Oxygen therapy can be helpful in reducing hhypoxic pulmonary vasoconstriction.
2. Anticoagulation to prevent thrombus and thromboembolism resulting form sluggish
pulmonary BF, dilation of right side of heart and venous statis and limitaions in
physical activity imposed by this disease.
3. Diuretics can be used to decrease preload in patients with right-sided heart failure,
espiecially when hepatic congestion, ascites, and severe peripheral edema are
present.
ii. CCB improve 5 year survival
iii. Phophodiesterase inhibitors: produce pulmonary vasodilation and improve CO. Viagra
iv. NO diffuses into vascular SM where it activates Gyanylate cyclase; increasing cGMP which
reduces the intracellular calcium concentration and results in SM relaxation.
1. Increases ventilation/perfusion matching and improves oxygenation and lowers PAP.
v. Prostacyclins are systemic and pulmonary vasodilators that have antiplatelet activity.
1. Reduce PVR and improve CO and exercise tolerance.
2. Can cause rebound pulmonary HTN.
3. Epoprostenol, treprostinil and ilprost
vi. Endothelin receptor antagonists: endothelin interacts with 2 receptors: endothelin A
receptors and endothelin B receptors
1. A cause pulmonary vasoconstriction and smooth muscle proliferation
2. B produce vasodialation via enhanced endothelin clearance and increased production
of NO and prostacyclin.
a. ER antagontninsts have shown to lower PAP and PVR; to improve RV fuicntion,
exercise tolerance , quality of life, and to reduce mortality.
3. Only ER antagonist: bosetan
vii. Sx Treatment:
1. Ballon atrial septostomy is an investigational procedure that creast an atrial septal
defect and allows right to left shunting of blood to decompress the right side fo the
heart at the expense of an expected and generally well-tolerated decrease in arterial
oxygen saturation.
2. Lung transplant only cureative option with PAH.
e. Management of anesthesia: risk of right-sided heart failure is significantly increased during the
perioperative period in patients with PAH.
i. Pulmonary vasodialators need to be maintained at their usual dosage to prevent rebound
PHTN.
ii.
f. Perioperative preparation and induction
i. Patients newly diagnosed need Viagra.
ii. Sedatives used with caution because respiratory acidosis may increase PVR.
iii. Avoid ketamine and etomidate because it suppresses some mechanisms of pulmonary
vasorelxation.
iv. PAY CLOSE ATTENTION TO SVR
g. Monitoring:
i. Central venous catheterization is recommened but with precaution
h. Maintenance:
i. Inhalation anesthetics, neuromuscular blockers and opiods.
ii. Hypotension can be corrected with norepi, phenylephrine or fluids.

i.

j.

iii. Pulmonary vasodialators such as milrinone, nitroglycerine, NO, or prostacyclin for PHTN
POSTEOPERATIVE PERIOD:
i. Patients with PAH are at risk of sudden death in the early post op because of wroseinig PAH,
pulmonary thromboembolism, dysrhythmias, and fluid shifts.
ii. Need to be monitored intensively in the opstop period to help maintain hemodynamic
parametesr and oxygenation at acceptable levels.
OBGYN POP: use forceps to aid delivery and prevent pt effort. Nitor should be available immediately
at the time of the uterine involution, because the return of uterine blood to the central circulation
may be poorly tolerated in pt with parturient with PAH.

Heart Fialure and Cardiomyopathies:

I.
Heart Failure: is the inability of the heart to fill with or eject blood at a rate appropriate to meet tissue
requirements.
a. Signs and sumptoms:
i. Dyspnea
ii. Fatigue
iii. Signs of circulatory congestion
iv. Hypoperfusion
II.
EPIDEMIOLOGY AND COSTS:
a. Systolic heart failure more common in middle aged men due to association with CAD
b. Distolic HF seen in elderly women because of association with hypertension, obesity, and diabetes
after monepause.
III.
ETIOLOGY:
a. The principal pathophysiologic feature of HF is the inability of the heart to fill or empty the
ventricles.
i. HF is the most often a result of impaired myocardial contractility cause by ischemic heart
disease or cardiomyopathy
ii. Cardiac valve abnormalities,
iii. Systemic HTN
iv. Disease of the pericadirum,
v. Pulmonary HTN
vi. Most common cause of RVF is LVF
IV.
FORMS OF VENTRICULAR DYSFUNCTION: can be described in several ways systolic or diasolic, acute or
chronic, lef or right sided, high output or low output.
a. All horms of HF are characterized by high ventricular end diastolic pressure because of altered
ventricular function and neurohormonal regulation.
V.
Systolic and diastolic heart failure: decreased venbtricular systolic wall motion reflexts systolilc
dysfunction, wheras diastolic dysfunction is charcacterized by abnmormal ventricular relxation and
reduced compliance.
a. SYSTOLIC HF: causes include LOW EF ASSOC with MI
i. CAD
ii. Dilated cardiomhyopathy
iii. Chronic pressure overload (aortic stenosis chronic HTN)
iv. Chronic volume overload ( regurgitant valvular lesions and high-output cardiac failure)
v. Hallmark of systolic dysfunction is decreased Ejection franction.
b. Diastolic HF: is age dependent and has 4 stages affects women more than men. Caused by
essential HTN
i. classI: is characterized by an abnormal LV relaxation pattern with normal left atrial pressure.
ii. Classes II,III,IV: are characterized by abnormal relaxation as well as reduced LV compliance
resulting in an increase in LV end-diastolic pressure (LVEDP).
iii. LV is thicker EJ is normal.
VI.
ACUTE AND CHRONIC HEART FAILURE:
a. acute HF is defined as a change in the sings and symptoms of heart failure requiring emergency
therapy.
i. Due to a sudden decrease in CO, systemic hypotension is typically present with out signs of
peripheral edema.
ii. Presents with 3 clinical entities:
1. Worsening CHF
2. New-onset hf (caused by cardiac valve rupture, large MI, severe hypertensive crisis.)
3. Terminal heart failure that is refractory to therapy
b. CHR is present in patients with longs standing cardiac disease.

VII.

VIII.

IX.

X.

XI.
XII.

XIII.

XIV.

i. Is accompanied by venous congestions BP is good

LEFT SIDED AND RIGHT SIDED HF
a. Signs and symptoms of hf:
i. Increased ventricular pressures
ii. Subsequent fluid accumulation upstream from the affected ventricle
b. Left sided HF:
i. High LVEDP promotes pulmonary venous congestion
ii. Dyspnea
iii. Orthopnea: dry non productive cough that develops in the supine position and is relieved by
sitting up.
iv. Paroxysmal nocturnal dyspnea:SOB that awakens a patient from sleep.
v. Turns into pulmonary edema
c. Right sided HF: causes systemic congestion
i. Pheripheral edema congestive hepatomegaly
ii. Can be caused by PHTN or right ventricular myocardial infarction but most common cause is
left sided HF.
LOW OUTPUT AND HIGH OUTPUT HEART FAILURE:
a. Normal CI varies between 2.2 and 3.5 L /min.
b. With low output you cannot distinguinsh
c. Causes of high output HF are anemia, pregnancy arteriouvenous fistulas, severe hyperthyroidism,
beriberi and pagets disease.
PATHOPHYSIOLOGY OF HEART FAILURE
a. The mechanisms of heart failure are caused due to
i. Pressure overload (aortic stenosis, essential hypertension)
ii. Volume overload (mitral or aortic regurgitation)
iii. MI, myocardial inflammatory disease,
iv. And restricted diastolic filling (constrictive pericarditis, restrictive myocarditis)
b. In the failing ventricle, carious adatptive mechanism are intiataed to help maitian a normal cardiac
output.these infludde:
i. Increases in SV according to the frank-starling relationship
ii. Activation of the sympathetic nervous system
iii. Alterations in the inotropic state , heart rate, and afterload,
iv. Humorally mediated responses.
FRANKSTARLING MECHANISM: if you have a greater amount of blood in the ventricles this causes an
increase in the contractile strength in the ventrilces and will therefore increase SV (the amount of blood
ejected)
a. When in heart failure myocardial contractility is decreased and there will be less SV regardless of
preload or LVEDP.
ACTIVATION OF SYMPATHETIC NERVOUS SYSTEM:
a. High NE are cardiotoxic and promote myocute necrosis and cell death, which lead to ventricular
remodeling.
ALTERATIONS IN THE INOTROPIC STATE, HEART RATE AND AFTERLOAD.
a. Inotropic state describes myocardial contractility as reflexted by the velocity of contraction
developed by cardiac muscle.
b. Vmax is the maximum velocity of contraction
c. When inotropic state increases v max increases.
d. Vmax is decreased when myocardial contractility is impaired as in HF.
e. SHF and low CO, SV is fixed and any increase in CO depends on an increase in HR.
f. DHF can present with tachycardia and produces a decrese in CO resulting form inadequate
ventricular relaxation and filling time. HR control is important tx goal of DHF
HUMORALLY MEDIATED RESPONSES AND BIOCHEMICAL PATHWAYS:
a. Vasoconstriction is initiatied via increase in activity of the SNS and the RAAS, parasympathetic
withdrawal , high levels of circulating vasopressin, and release of inflammatory mediators.
b. ANP is released in response to increases in atrial pressure such as produced by tachucardia or
hypervolemia
c. BNP is secredted by both the atria and ventricular myocardium. In the failitng heart, the ventricle
becomes the principa site of BNP production.
MYOCARDIAL REMODELING:
a. Myocardial remodeling is the result of the various endogenous mechanisms that the boyd uses to
maintain CO. its the process by which mechanical, neurhormonal, genetic factors change LV size,
shape and function.
i. Process includes: myocardial hypertrophy

XV.

XVI.

1. Myocardial lilation and wall thinning

2. Increased instereitial collagen deposition, myocardial fibrosis, and scar formation
resulting from myocite death.
PHYSICAL EXAMINATION FINDINGS:
a. LV Failures: physical findings are tachypnea and moist rales and will be confined to the lung bases
in patients with mild heart failure, or they may be diffuse in those with pulmonary edema. Resting
tachycardia and S3 heart soiund
b. Peripheral vasoconstriction, with cool pale extremities.
c. Lip and nailbed cyanosis may be present.
d. Narrow pulse and high DP reflects a decreased sv
e. Marked weight loss aka cardiac cachexia, a sign of severe chronic HF.
f. Right sided hf:
i. JVD
ii. Hepatomegaly
iii. Jaundice
iv. Pleural effusions
v. Bilateral pitting edema
Diagnosis of HF:
a. Laboratory tests:
i. BNP can ID cause of dyspnea.
ii. Plasma BNP below 100 indicate that HF is unlikely
1. 100-500 intermediate probability of HF
2. >500 dx hf