1

MINISTRY OF HEALTH OF UKRAINE

Vinnitsa national medical university of N.I.Pirogova

“Approved"
At methodical meeting of chair
Internal medicine №1
Head of the department

____________ prof. Stanislavchuk M. A.

«30» August 2021

METHODICAL RECOMMENDATIONS
For students

Subject matter Internal medicine

Module Emergencies in the clinic of internal medicine
Substantial module № 1 Emergencies in the clinic of internal medicine
Subject of the lesson Management of a patient with a hypertensive crisis, acute heart failure
Course 6
Faculty Medical # 1

Vinnytsya 2021
 2
1.Topicality: The cardiovascular risks associated with a given blood pressure (BP). A series of
randomized trials have demonstrated that antihypertensive therapy can reduce the incidence of stroke
and coronary heart disease. For every 20 mm Hg systolic or 10 mm Hg diastolic increase in blood
pressures above 115/75 mm Hg, the mortality rate from both ischemic heart disease and stroke doubles.
In the US, about 50 million people have hypertension. Only about 70% of these people are aware that
they have hypertension, only 59% are being treated, and only 34% have adequately controlled BP.
About 2⁄3 of people > 65 have AH, and people with a normal BP at age 55 have a 90% lifetime risk of
developing hypertension. The excess cardiac mortality and morbidity associated with hypertension is
largely due to a higher incidence of coronary artery disease.
Acute heart failure (AHF) is a life-threatening medical condition, where urgent diagnostic and treatment
methods are of key importance. However, there are few evidence-based treatment methods.
Interestingly, despite relatively similar ways of management of AHF throughout the globe, mid-term
outcome in East Asia, including South Korea is more favorable than in Europe. The cornerstone of AHF
management is identifying precipitating factors and specific phenotype. Multidisciplinary approach is
important in AHF, which can be caused or aggravated by both cardiac and non-cardiac causes. The
main pathophysiological mechanism in AHF is congestion, both systemic and inside the organs (lung,
kidney, or liver). Cardiac output is often preserved in AHF except in a few cases of advanced heart
failure.

2. Educational goal:

2.1. The student must know:

relatively complicated hypertensive crises:
• definition of hypertensive crisis;
• classification of hypertensive crises of the Ukrainian Association of Cardiology; a list of target
organ lesions in complicated hypertensive crises;
• diagnostic criteria for target organ damage;
• general principles of treatment;
• treatment features, drugs that are recommended, drugs that should be avoided with complicated
hypertensive crises:
• definition of AHF
• list of target organ lesions in AHF
• diagnostic criteria for target organ damage;
• general principles of treatment of AHF;
• treatment features, drugs that are recommended, drugs that should be avoided with AHF:
• etiology;
• pathogenesis;
• symptomatology of cardiac asthma and pulmonary edema;
• treatment of cardiac asthma and pulmonary edema:
- with normal blood pressure;
- with high blood pressure;
- with arterial hypotension.
• subsequent management of patients
- subsequent management of patients.
2.2. The student must be able:
• diagnose, treat, determine relative to the subsequent management of patients with
complicated hypertensive crises;
diagnose, treat, determine relative to the subsequent management of patients with AHF.

3. CONTENTS OF THE TRAINING MATERIALS:

Hypertensive crises
 3
- Hypertensive crises encompass a spectrum of clinical presentations where
uncontrolled BP lead to progressive or impending target organ dysfunction (TOD). The clinical
distinction between hypertensive emergencies and hypertensive urgencies depends on the presence of
acute TOD and not on the absolute level of the BP.

Common Causes of Hypertensive Crises

Antihypertensive drug withdrawal (e.g.,
clonidine)
Autonomic hyperactivity
Collagen-vascular diseases
Drugs (e.g., cocaine, amphetamines)
Glomerulonephritis (acute)
Head trauma
Neoplasias (e.g., pheochromocytoma)
Preeclampsia & eclampsia
Renovascular hypertension

- Hypertensive Emergency is defined as a clinical setting where BP must be reduced

effectively within minutes to <1hour, such as accelerated & malignant hypertension, hypertensive
encephalopathy, & severe diastolic hypertension (120-160 mmHg) that is associated with acute
pulmonary edema, ischemic chest pain, dissecting aortic aneurysm, or intracerebral hemorrhage,
papilledema (+/ ), evidence of renal function deterioration, or evidence of neurologic dysfunction,
etc. Hypertensive emergencies represent severe AH with acute impairment of an organ system (eg,
central nervous system, cardiovascular, renal). In these conditions, the BP should be lowered
aggressively over minutes to hours.
-
- Hypertensive Urgency is defined as a clinical setting of severe hypertension with minimal
or no symptoms, where severe elevation of BP (180 or higher for systolic pressure or 110 or higher
for diastolic pressure) are not causing immediate end-organ damage but should be effectively
lowered within 24 hours to reduce potential risk to the patient.
- Hypertensive urgency is defined as a severe elevation of BP, without evidence of
progressive TOD. These patients require BP control over several days to weeks
Accelerated hypertension and hypertensive urgency
Accelerated hypertension is defined as a recent significant increase over baseline blood
pressure that is associated with target organ damage. This is usually seen as vascular damage on
funduscopic examination, such as flame-shaped hemorrhages or soft exudates, but without
papilledema.
Hypertensive urgency must be distinguished from hypertensive emergency. Urgency is defined
as severely elevated blood pressure (ie, systolic >220 mm Hg or diastolic >120 mm Hg) with no
evidence of target organ damage.
Hypertensive emergencies require immediate therapy to decrease blood pressure within
minutes to hours. In contrast, no evidence suggests a benefit from rapidly reducing blood pressure in
patients with hypertensive urgency. In fact, such aggressive therapy may harm the patient, resulting
in cardiac, renal, or cerebral hypoperfusion. This article discusses hypertensive emergency, but
therapy for hypertensive urgency is discussed briefly.
Malignant hypertension
Malignant hypertension and accelerated hypertension are both hypertensive emergencies, with
similar outcomes and therapies. Malignant hypertension may or may not be associated with clinical
conditions present in hypertensive urgency. A patient with malignant hypertension always has retinal
papilledema (as seen in the image below), as well as flame-shaped hemorrhages and exudates. Other
clinical features of malignant hypertension may include encephalopathy, confusion, left ventricular
failure, intravascular coagulation, and impaired renal function, with hematuria and weight loss.
 4
The pathologic hallmark of malignant hypertension is fibrinoid necrosis of the arterioles, which
occurs systemically, but specifically in the kidneys. These patients develop fatal complications if
untreated, and more than 90% will not survive beyond 1-2 years.
-
- Papilledema. Note the swelling of the optic disc, with blurred margins
Up to 1% of patients with essential hypertension develop malignant hypertension, but the
reason some patients develop malignant hypertension whereas others do not is unknown. The
characteristic vascular lesion is fibrinoid necrosis of arterioles and small arteries, which causes the
clinical manifestations of end-organ damage. Red blood cells are damaged as they flow through
vessels obstructed by fibrin deposition, resulting in microangiopathic hemolytic anemia.
Another pathologic process is the dilatation of cerebral arteries following a breakthrough of the
normal autoregulation of cerebral blood flow. Under normal conditions, cerebral blood flow is kept
constant by cerebral vasoconstriction in response to increases in blood pressure. In patients without
hypertension, flow is kept constant over a mean pressure of 60-120 mm Hg. In patients with
hypertension, flow is constant over a mean pressure of 110-180 mm Hg because of arteriolar
thickening. When blood pressure is raised above the upper limit of autoregulation, arterioles dilate.
This results in hyperperfusion and cerebral edema, which cause the clinical manifestations
of hypertensive encephalopathy.
Other causes of malignant hypertension include any form of secondary hypertension;
complications of pregnancy; use of cocaine, monoamine oxidase inhibitors (MAOIs), or oral
contraceptives; and the withdrawal of alcohol, beta-blockers, or alpha-stimulants. Renal artery
stenosis, pheochromocytoma (most pheochromocytomas can be localized using computed
tomography (CT) scanning of the adrenals), aortic coarctation, and hyperaldosteronism are also
secondary causes of hypertension. In addition, both hyperthyroidism and hypothyroidism can cause
hypertension.
The following conditions should also be considered when making the diagnosis: stroke,
intracranial mass, head injury, epilepsy or postictal state, connective-tissue disease (especially lupus
with cerebral vasculitis), drug overdose or withdrawal, cocaine or amphetamine ingestion, acute
anxiety, and thrombotic thrombocytopenic purpura.[2]

Symptoms:
 Asymptomatic in some patients (ie. hypertensive urgency)
 Headache, Visual Changes, Papilledema
 Chest Pain (MI), Pain to Back (Dissection)
 Abdominal Pain - abdominal aneurysmal dissection
 Flank Pain - renal disease
 Mental Status Changes - stroke, leukoencephalopathy

There are a variety of hyperadrenergic states such as cocaine intoxication, thyroid storm,
autonomic hyperreflexia and pheochromocytoma that may resemble hypertensive emergency, but it
is the hyperadrenergic state that is the therapeutic target in these instances, not the hypertension. Do
not forget to actively cool patients hotter than 41°C (105°F).
Headache is not a hypertensive emergency, no matter how high the blood pressure. It is likely
the headache that is causing the hypertension, not the other way around. Treat the headache and the
pressure will come down. The same is true of epistaxis.
Lowering blood pressure quickly, for example with the infamous IV labetalol push, in a patient
who does not have a hypertensive emergency, subjects the patient to risk of harm without chance of
benefit. Many of these patients have been living with high blood pressure for a long time and quick
reductions can cause quick problems, like stroke. You can bring the blood pressure down with IV
meds, and this may make you feel powerful and may pacify the consultant/nurse/patient/family, but
as soon as you turn around the pressure will go right back up. Fixing the number is a great pacifier
but is bad for patients. The consultant/nurse/patient/family may not know better, but you are paid
 5
well to know better. It’s easier to write for 20 of IV labetalol than to explain to the
consultant/nurse/patient/family, but you are paid well to explain.

Hypertensive encephalopathy is not headache, patients with hypertensive encephalopathy

are encephalopathic and acutely ill. You are not going to diagnose hypertensive encephalopathy until
after you’ve ruled out intracranial hemorrhage, because when a patient presents altered and looking
bad with a very high blood pressure, it’s much more likely to be ICH, so that patient needs
management of ABC’s and then a quick CT scan. If the CT scan is negative, and the patient
continues to be altered and very hypertensive, start your nicardipine drip. If the patient’s mentation
improves with lowering of blood pressure, - that was hypertensive encephalopathy.
Acute ischemic stroke and spontaneous intracranial hemorrhage patients often have very
high blood pressure and medical science has not yet determined if patients with these conditions
benefit from blood pressure reduction. For ischemic stroke, If you’re using thrombolytics, keep
blood pressure under 180/105 using nicardipine or labetalol. Otherwise, the
latest recommendations are to lower blood pressure above 220/120 by 15% within 24 hours. The
AHA says it’s probably safe to lower systolic blood pressure to 140 in ICH patients. Otherwise they
suggest blood pressure management according to this table, which isn’t confusing at all.
In traumatic brain injury, leave hypertension alone; focus on preventing hypotension and teaching
your consultants that ketamine does not raise ICP and is an appropriate RSI agent in this context.

Common Antihypertensive Agents for Use in Hypertensive Crises

Nitroprusside 0.5-10 Labetalol 20 mg Diazoxide 25-150 mg IV

mcg/Kg/min bolus, 2 mg/min (max. over 5 min or infusion of 30
300 g/day) mg/min to effect
Nicardipine 5 mg/h, titrate to Trimethaphan l Nitroglycerin 5 mcg/min
effect by increasing 2.5 mg/h every mg-15 mg/min increase by 5 mcg- 10 mcg
5 min (max. 15 mg/h) every 3-5 min as needed)

- The emergency treatment of accelerated phase hypertension. In accelerated phase

hypertension it is unwise to lower blood pressure too quickly because this may compromise tissue
perfusion (due to altered autoregulation) and can cause cerebral damage, including occipital
blindness, and precipitate coronary or renal insufficiency. Even in the presence of cardiac failure or
hypertensive encephalopathy a controlled reduction, to a level of about 150/90, over a period of 24-
36 hours is ideal.
- Even in cases of hypertensive emergencies, the BP should not be lowered to normal levels.
- Rapid reduction in BP below the cerebral, renal, and/or coronary autoregulatory range
results in marked reduction in organ blood flow, possibly leading to ischemia and infarction.
- In most patients it is possible to avoid parenteral therapy and bring BP under control with
bed rest and oral drug therapy. Intravenous or intramuscular labetalol (2 mg/min to a maximum of
200 mg), intravenous glyceryl trinitrate (0.6-1.2 mg/hour), intramuscular hydralazine (5 or 10 mg,
repeated at half-hourly intervals), and intravenous sodium nitroprusside (0.3-1.0 mg/kg body weight
per minute) are all effective remedies but require careful supervision, preferably in an intensive care
unit.
The initial goal of treatment is to reduce the mean arterial pressure by no more than 25% to reach a
goal blood pressure of 160/100 mm Hg within 2 to 6 hours or to decrease diastolic blood pressure
10% to 15% or to approximately 110 mm Hg within 30 to 60 minutes.It is important that blood
pressure be lowered in a controlled manner to avoid risk for hypoperfusion of vital organs, which can
cause ischemia and infarction. To ensure controlled lowering of blood pressure, critical care nurses
should monitor blood pressure every 5 to 10 minutes until goals are reached.
 6
When choosing pharmacological therapy, fast-acting, intravenous, easily titratable antihypertensive
medications are generally used.

Intravenously administered nitroglycerin is a potent vasodilator, and when used in high doses,
arterial tone is affected. It reduces blood pressure by reducing both afterload and preload. These
effects are undesirable in patients with compromised renal and cerebral perfusion. It has an onset of
action of 1 to 5 minutes and a duration of action of 5 to 10 minutes after the continuous infusion is
discontinued. Although nitroglycerin has pharmacokinetic properties similar to those of sodium
nitroprusside, it is not considered a first-line agent for the treatment of hypertensive emergencies,
primarily because of its side effects of reflex tachycardia and tachyplylaxis. Nitroglycerine is not as
efficacious as sodium nitroprusside. However, it may be used as an adjunctive agent for hypertensive
emergencies associated with myocardial ischemia or pulmonary edema.
Historically, sodium nitroprusside was the drug of choice to treat hypertensive emergencies,
however, because of its toxicity, it has fallen out of favor as the first-line agent. This agent is a potent
arterial and venous vasodilator through the generation of cyclic guanine mono-phosphate. These
vasodilatory effects decrease both afterload and preload. Advantageous properties of this medication,
and benefit of its use, are its short duration of action of 1 to 2 minutes and its half-life of 3 to 4
minutes. This property also makes the drug easy to titrate. However, abrupt cessation of the infusion
results in a rapid increase in blood pressure. Because of its quick onset of action, arterial blood
pressure monitoring is recommended. Sodium nitroprusside increases intracranial pressure, which
would be disadvantageous in patients with hypertensive encephalopathy or cerebrovascular
accident. The use of sodium nitroprusside in patients with coronary artery disease may also result in
deleterious effects because of a reduction in regional blood flow, resulting in coronary steal in such
patients. Sodium nitroprusside may also lead to cyanide poisoning. It contains 44% cyanide by
weight that is released nonenzymatically from sodium nitroprusside, with the amount released
dependent on the dose. Infusions at rates of greater than 4 μg/kg per minute for 2 to 3 hours have led
to cyanide levels within the toxic range. This medication is recommended for use only in patients
who have normal renal and hepatic function and when other intravenous antihypertensive
medications are not available. If higher infusions of sodium nitroprusside are needed, an infusion of
thiosulfate should be used to prevent the accumulation of cyanide.
Labetalol, an intravenous nonselective β-blocker that also possesses α1-blocking effects, is an
agent that is commonly used to treat hypertensive emergencies. It produces its antihypertensive
effect by decreasing the heart rate and lowering SVR. This medication can be given as an
intravenous bolus or as a continuous infusion. The hypotensive effects of labetalol begin within 2 to
5 minutes after an intravenous bolus and peak at 5 to 15 minutes. The effects can last for 2 to 4
hours. Because this medication does not have pure β-blocking effects, the patient’s cardiac output is
maintained. Labetalol does reduce peripheral vascular resistance because of its α-blocking effects,
and it does not reduce peripheral blood flow. This medication is best used when the following
conditions are present: acute myocardial ischemia, aortic dissection, acute postoperative
hypertension, acute ischemic stroke, hypertensive encephalopathy, preeclampsia, and eclampsia.
Nicardipine is an intravenous dihydropyridine-derivative calcium channel blocker and produces its
antihypertensive effects by vasodilation of coronary vasculature and relaxation of smooth
muscle.7 This medication has high vascular selectivity and strong cerebral and coronary vasodilatory
activity. It has an onset of action of 5 to 15 minutes and duration of action of 4 to 6 hours. However,
because of nicardipine’s half-life of approximately 1 hour, titration of dosage is more difficult than
with other intravenous antihypertensive medications. The dosing of this medication is independent of
weight, which can be useful in most hypertensive emergencies, especially in high adrenergic states.
The newest intravenous antihypertensive agent approved for hypertensive emergencies is
clevidipine. This medication is a third-generation dihydropyridine calcium channel blocker that
inhibits L-type calcium channels in a voltage-dependent manner. The blood pressure lowering by this
medication is dose dependent and rapid, with a short half life of 1 to 2 minutes, a quick onset of
action of 2 to 4 minutes and a short duration of action of 5 to 15 minutes. These properties make this
medication easy to titrate.
 7
Fenoldopam is an unique agent among the intravenous antihypertensive medications. It is a
dopamine D1-receptor agonist that was approved in 1997 for hypertensive emergencies. This
medication causes peripheral vasodilation by acting upon peripheral dopamine type 1
receptors. Fenoldopam also activates dopaminergic receptors on the proximal and distal tubules of
the kidney, thereby inhibiting sodium reabsorption, resulting in diuresis and naturesis. It has an onset
of action of 5 minutes and a duration of effect of 30 to 60 minutes. This medication improves
creatinine clearance, urine flow rates, and sodium excretion in patients with and without normal
kidney function.
Urapidil is a peripheral postsynaptic alpha 1-adrenoceptor antagonist with central
agonistic action at serotonin 5-HT1A receptors. It reduces blood pressure by decreasing peripheral
vascular resistance. Oral urapidil decreases blood pressure in patients with mild to moderate essential
hypertension and associated risk factors such as hyperlipidaemia or type 2 (non-insulin-dependent)
diabetes mellitus with no effect on heart rate. Urapidil can be safely combined with other
antihypertensive agents such as hydrochlorothiazide and nifedipine and improves blood pressure
control in previous nonresponders to monotherapy. Intravenous urapidil reduces blood pressure in
patients with pre-eclampsia or hypertension in pregnancy and in patients with hypertensive crises or
peri- or postoperative hypertension. The decrease in blood pressure is similar to that observed after
nifedipine, enalaprilat, sodium nitroprusside and dihydralazine, greater than that of ketanserin
according to 1 larger study, and greater than that of sublingual nitroglycerin in 1 trial in patients with
nonsurgical hypertensive crises and pulmonary oedema.

Rapid BP reduction is indicated in the following circumstances:

 Acute myocardial ischemia
o Iv nitroglycerin Iv beta-blockers
 Heart Failure with pulmonary edema
o Iv nitroglycerin Iv furosemide (Lasix) Iv nitroprusside Iv ACE-inhibitors
 Acute aortic dissection: the SBP should be decreased as rapidly as possible to a goal of
100-110 mm Hg or lower.
o Iv labetalol. Alternative – Iv nitroprusside with Iv beta-blocker (eg, esmolol)
 Cerebral vascular accident: Evidence exists that patients who have acute strokes have
better outcomes with higher BPs. Antihypertensive therapy is not routinely recommended for
patients with acute stroke and AH.
o a patient with a recent ischemic stroke and a SBP higher than 220 mm Hg or a DBP
higher than 120-140 mm Hg can undergo reduction of BP by about 10-15% (with IV nitroprusside or
IV labetalol)
Guidelines for the Management of Spontaneous Intracerebral Hemorrhage
Table 6. Suggested Recommended Guidelines for Treating Elevated BP in Spontaneous
ICH
Note that these recommendations are Class C. SBP indicates systolic blood
pressure; MAP, mean arterial pressure.
1. If SBP is >200 mm Hg or MAP is >150 mm Hg, then consider aggressive
reduction of BP with continuous intravenous infusion, with frequent BP monitoring every
5 min.
2. If SBP is >180 mm Hg or MAP is >130 mm Hg and there is the possibility of
elevated ICP, then consider monitoring ICP and reducing BP using intermittent or
continuous intravenous medications while maintaining a cerebral perfusion pressure ≥60
mm Hg.
3. If SBP is >180 mm Hg or MAP is >130 mm Hg and there is not evidence of
elevated ICP, then consider a modest reduction of BP (eg, MAP of 110 mm Hg or target
BP of 160/90 mm Hg) using intermittent or continuous intravenous medications to
control BP and clinically reexamine the patient every 15 min.
 8

 Hypertensive encephalopathy: Do not exceed a 20% reduction in BP.

o Iv nitroprusside Iv labetalol
 Encephalopathy: Nitroprusside, Labetolol, Diazoxide
 Cerebral Infarction: no treatment (hemorrhage control), Nitroprusside, Labetolol
 Myocardial Ischemia, Infarction: Nitroglycerine, Labetolol, ß-adrenergic blockers
 Patients with active myocardial ischemia and hypertension should also be on a nitro
drip, titrated to relief of pain or untoward drop in blood pressure. Not patients with a positive
troponin who are legs crossed reading a newspaper, not patients with undifferentiated chest pain
waiting on their second enzyme, this applies to patients who are clutching their chest because their
heart wants more oxygen than their coronary arteries can deliver.
 Acute Pulmonary Edema: Nitroprusside (or Nitroglycerin) and Loop Diuretic
 Aortic Dissection: Nitroprusside and ß-adrenergic blockers, Labetolol
 Eclampsia: Hydralazine, Labetolol, Diazoxide
 Preeclampsia is an important hypertensive emergency that is easy to overlook,
especially postpartum–almost always within two weeks but possibly up to six weeks after delivery.
Hypertensive pregnant or postpartum patients with signs of preeclampsia should be treated with
high-dose magnesium (start with 6 g over 20 minutes). EMCREG recommends keeping blood
pressure under 160/110 in the antepartum and intrapartum period and less than 150/100 if postpartum
or if platelet count is < 100,000. Magnesium will have a salutary effect on blood pressure but if not
at target, labetalol is the recommended agent. Other beta blockers and ACE inhibitors should be
avoided in pregnancy. Delivery is the therapy of interest in most of these patients, they are therefore
usually best managed on L&D.
 Acute Renal Insufficiency: Nitroprusside, Labetolol, Ca antagonists
 Funduscopic changes: Nitroprusside, Labetolol, Ca antagonists
 Hemolytic Anemia, Microangiopathic: Nitroprusside, Labetolol, Ca antagonists
Adjuvant drug therapy of hypertension includes aspirin, statins.

Aortic dissection is the most common catastrophe of the aorta, 2-3 times more common than
rupture of the abdominal aorta. When left untreated, about 33% of patients die within the first 24
hours, and 50% die within 48 hours. The 2-week mortality rate approaches 75% in patients with
undiagnosed ascending aortic dissection.
Stanford classification
The Stanford classification divides dissections into 2 types, type A and type B. Type A
involves the ascending aorta (DeBakey types I and II); type B does not (DeBakey type III).
This system helps to delineate treatment. Usually, type A dissections require surgery, while
type B dissections may be managed medically under most conditions.
DeBakey classification
The DeBakey classification divides dissections into 3 types, as follows:
 Type I involves the ascending aorta, aortic arch, and descending aorta
 Type II is confined to the ascending aorta
 Type III is confined to the descending aorta distal to the left subclavian artery
Type III dissections are further divided into IIIa and IIIb. Type IIIa refers to dissections that
originate distal to the left subclavian artery but extend proximally and distally, mostly above the
diaphragm.
Type IIIb refers to dissections that originate distal to the left subclavian artery, extend only
distally, and may extend below the diaphragm.
Thoracic aortic dissections should be distinguished from aneurysms (ie, localized abnormal
dilation of the aorta) and transections, which are caused most commonly by high-energy trauma.
The mortality rate of patients with aortic dissection is 1-2% per hour for the first 24-48 hours.
Initial therapy should begin when the diagnosis is suspected. This includes 2 large-bore
 9
intravenous lines (IVs), oxygen, respiratory monitoring, and monitoring of cardiac rhythm,
blood pressure, and urine output.
The blood pressure isn’t the problem in aortic dissection, but we have good reason to believe
that elevated blood pressure (and heart rate) makes things worse. If strongly suspected or confirmed,
call a surgeon and aggressively dose opiates to abolish pain and anxiety as you bring heart rate down
to 60 using IV esmolol (or diltiazem/verapamil if beta blockers are contraindicated); this will also
reduce blood pressure. If at that point blood pressure isn’t as low as it could be, add a titratable
vasodilator like nicardipine and bring pressure as low as possible while maintaining organ perfusion.
Clinically, the patient must be assessed frequently for hemodynamic compromise, mental status
changes, neurologic or peripheral vascular changes, and development or progression of carotid,
brachial, and femoral bruits.
Aggressive management of heart rate and blood pressure should be initiated.
Beta blockers should be given initially to reduce the rate of change of blood pressure and
the shear forces on the aortic wall.
The target heart rate should be 60-80 beats per minute.
The target systolic blood pressure should be 100-120 mm Hg.
End organ perfusion should be evaluated. Balancing the risks of dP/dt on the aortic wall versus
the benefits of acceptable end organ perfusion may be a difficult clinical decision.
Retrograde cerebral perfusion may increase the protection of the central nervous system during
the arrest period.
The mortality rate from aortic arch dissections is about 10-15%, with significant neurologic
complications occurring in another 10% of patients. The mortality rate is influenced by the patient's
clinical condition.
Uncomplicated distal dissections may be treated medically to control blood pressure. Distal
dissections treated medically have a mortality rate that is the same as or lower than the mortality rate
in patients who are treated surgically.
Long-term medical therapy involves a beta-adrenergic blocker combined with other
antihypertensive medications. Avoid antihypertensives (eg, hydralazine, minoxidil) that produce a
hyperdynamic response that would increase dP/dt (ie, alter the duration of P or T waves).
Survivors of surgical therapy also should receive beta-adrenergic blockers.
A series of patients with type B dissections demonstrated that aggressive use of distal
perfusion, CSF drainage, and hypothermia with circulatory arrest improves early mortality and long-
term survival rates.
Endovascular stenting remains an option for treatment of some type B dissections. Some
studies recommend that patients with complicated acute type B dissections undergo endovascular
stenting with the goal of covering the primary intimal tear.
Definitive treatment involves segmental resection of the dissection, with interposition of a
synthetic graft.
Definition and Clinical Classification of AHF
ESC Guidelines on the diagnosis and treatment of acute heart failure
• Acute heart failure is defined as the rapid onset of symptoms and signs secondary to abnormal
cardiac function.
• AHF can present itself as acute de novo (new onset of acute HF in a patient without previously
known cardiac dysfunction) or acute decompensation of chronic HF:
• Hypertensive AHF - Signs and symptoms of HF are accompanied by high blood pressure and
relatively preserved LV function with a chest radiograph sings of acute pulmonary oedema.
• Pulmonary oedema (verified by chest x-ray) accompanied by severe respiratory distress, with
crackles over the lung and orthopnoea, with O2 saturation usually <90% on room air prior to treatment.
• Cardiogenic shock: evidence of tissue hypoperfusion induced by HF after correction of preload.
• High output failure is characterized by high cardiac output, usually with high heart rate (caused
by arrhythmias, thyrotoxicosis, anaemia)
 10

• Right HF is characterized by low output syndrome with increased jugular venous pressure,
increased liver size and hypotension

Nomenclature of AHF depends on the criteria used. Guidelines suggest that the most useful
classifications in practice are those that rely on clinical presentation. They help clinicians to identify the
patients at high risk and initiate the necessary treatment rapidly. Most AHF patients present with normal
or high blood pressure (BP) and symptoms/signs of congestion. Only 5–8% patients present with
hypotension, which is associated with poor prognosis, especially if accompanied with
hypoperfusion. Hypotension (systolic blood pressure [SBP] <90 mmHg or >90 mmHg maintained by
vasopressors) with the absence of hypovolemia and signs of hypoperfusion (cold sweated extremities,
oliguria, altered mental state, metabolic acidosis, etc.) is defined as CS. Although relatively rare, CS is
the most severe form of AHF, treated in the coronary care unit (CCU)/intensive care unit (ICU). With
delayed treatment, CS may initiate systemic inflammatory responses, leading to multiorgan failure and
death.
Another possible approach is classifying patients based on precipitating factors or causes leading
to decompensation, which have their specific treatments and need to be corrected urgently Moreover, 2
main mechanisms causing organ dysfunction in AHF are congestion, which is very frequent, and
hypoperfusion, which is rather rare. Classification based on bedside clinical examination evaluates the
symptoms or signs of congestion (“dry” vs. “wet”) and/or peripheral hypoperfusion (“warm” vs.
“cold”). This approach divides the patients into 4 groups, which helps guide the treatment in the initial
phase and also has prognostic value Classifications based on clinical presentation are intended to
provide personalized care for the AHF patient.

First hour management

Patients with AHF are at high risk of complications during the first hour of the onset of the
disease. Therefore, it is increasingly acknowledged that “time-to-treatment” approach, which is highly
established in ACS, should be considered in AHF to prevent adverse outcomes. Indeed, early
prehospital treatment is associated with lower mortality. Urgent treatment is also important to prevent
de novo AHF patients from developing chronic HF. Patients should be rapidly transferred to the
hospital, preferably to a center with a cardiology department and/or emergency department (ED) or
CCU/ICU with AHF expertise. Immediate and concomitant investigation, diagnostic tests,
pharmacologic and non-pharmacologic treatment should be initiated on the arrival
 11

Time-based management in AHF.

ACS = acute coronary syndrome; AHF = acute heart failure; ECG = electrocardiogram; HFOT =
heart failure oral therapy; NIV = non-invasive ventilation.

Initial clinical evaluation

In the earliest stages of diagnostic workup, emphasis should be given to determination of
cardiopulmonary stability based on dyspnea severity, hemodynamic status and heart rhythm.1)4) This
may be achieved by following assessments:
 Respiratory rate, orthopnea, accessory muscles use in respiration, visible cyanosis, pulse
oximetry as objective measurements of respiratory distress
 Audible rales as sign of pulmonary congestion
 SBP and diastolic blood pressure (DBP)
 Heart rate and rhythm
 Objective determination of body temperature and signs/symptoms of hypoperfusion3)
Patients with respiratory failure or hemodynamic compromise should be transferred to a location where
immediate respiratory and cardiovascular support is available. When AHF is caused by acute
myocardial infarction, patient must be referred to the closest clinical facility, where round-the-clock
cardiac catheterization service is available.4),15) If CS is present, patient should receive ventilation and
hemodynamic support and be transferred directly to CCU/ICU.16)
 12
Next, patient should be examined for signs of systemic congestion, such as peripheral edema, jugular
venous dilatation and others
Additional tests used in patients with suspected AHF include:

1) Electrocardiogram

Electrocardiogram (ECG) will exclude ST-segment elevation myocardial infarction (STEMI) and other
high risk changes. Additional ECG value is limited, since it is rarely normal in those with suspected
AHF and may reveal some chronic abnormality.

2) Imaging modalities

 Bedside thoracic ultrasound: With expertise, thoracic ultrasound can be a useful diagnostic tool
for visualizing directs signs of interstitial edema. Pulmonary congestion may be assessed by
analyzing comet-like vertical reverberation artefacts, called B-lines. The quantity and diffusion
of B-lines provides a semi-quantitative estimation of extravascular lung water (≤5, absent; 6–15,
mild degree; 16–30, moderate degree; >30, severe pulmonary edema). B-lines are useful in
differential diagnosis between AHF and non-cardiac causes of dyspnea.
 Chest X-ray: It is one of the most used modalities in AHF settings. Most specific signs of AHF
are pulmonary venous congestion, pleural effusion, interstitial or alveolar edema and
cardiomegaly.1) However, sensitivity of chest radiography is limited, since it may be completely
normal in almost 20% of the cases.20),21) If expertise is available, lung ultrasound may be more
sensitive and timesaving modality in detecting interstitial edema.3) Chest radiography can also
identify alternative etiology of dyspnea, such as pneumonia or other pulmonary infections.
 Echocardiography: Immediate cardiac ultrasound is mandatory in all patients with CS and when
acute life-threatening structural or functional cardiac abnormalities (mechanical complications,
aortic dissection, etc.) are suspected.1),3) In other cases, it may be performed later during
hospitalization, when expertise is available (preferably, during first 48 hours of admission).
Early echocardiography should be pursued in de novo AHF patients and those, whose cardiac
function is unknown.1)
 Chest computed tomography (CT): Though not particularly relevant in diagnosing AHF,
thoracic CT scan is essential, when pulmonary embolism (PE) is suspected as a precipitating
factor of AHF.

3) Laboratory tests

 NPs: Plasma NP level (B-type natriuretic peptide, N-terminal pro-B-type natriuretic peptide, or
mid-regional pro-atrial natriuretic peptide) should be measured at presentation to the ED or
CCU/ICU in all patients with acute dyspnea and suspected AHF. Due to their high sensitivity,
NPs are very important in ruling out AHF as an etiology of acute dyspnea, since detecting
normal levels makes AHF diagnosis improbable.3),23) However, there are numerous cardiac and
non-cardiac causes, which may be associated with elevated plasma NP level. Therefore, a higher
value of NP does not automatically confirm the diagnosis of AHF and interpretation of their
levels must be combined with clinical assessment and cardiac imaging. NPs have prognostic
value in AHF: higher concentrations mean more severe condition and increased risk for
readmission and mortality.
 Cardiac troponins: They are useful for detection of ACS as the precipitator of AHF.1) Elevated
troponin levels are also associated with poorer outcomes in AHF.25),26)
 The following laboratory assessments should be performed at admission in all patients with
AHF: blood urea nitrogen (BUN)/urea, creatinine, electrolytes (sodium, potassium), liver
function tests, glucose, and complete blood count. Abnormal liver function tests reflect different
 13
clinical profiles in AHF. ESC guidelines also recommend performing thyroid-stimulating
hormone (TSH), since both hypothyroidism and hyperthyroidism may precipitate AHF.
 Although not needed in most cases, arterial blood gas may be useful in severe cases of
hemodynamic instability and respiratory distress. Acid-base balance should be obtained on
admission, especially in patients with APE or previous history of chronic obstructive pulmonary
disease (COPD). If respiratory distress persists despite initial therapy with oxygen and/or non-
invasive ventilation (NIV), venous blood gas analysis is sufficient to detect respiratory or
metabolic acidosis.
 There are multiple novel biomarkers (sST2, Galectin-3, GDF-15, etc.) being investigated in
AHF, but they have yet to be introduced to routine clinical practice.

Initial therapy
1) Oxygen therapy and/or ventilatory support

Oxygen saturation (SpO2) should be monitored in all patients with dyspnea. Oxygen therapy should be
initiated when SpO2 is below 90% and fraction of inspired oxygen (FiO2) should be increased up to
100%, if necessary, according to SpO2 measurements. However, hyperoxia causes vasoconstriction and
may decrease coronary and cerebral blood flow and thus should be avoided.
NIV is indicated in patients with respiratory distress and should be initiated urgently, since it reduces
respiratory distress and rate of mechanical endotracheal intubation. NIV is contraindicated in patients
with respiratory arrest, decreased conscious state or significant hemodynamic instability,. Other
contraindications include lack of staff expertise or patient's cooperation, vomiting and possible
pneumothorax. Patients with these conditions and those unresponsive to NIV should be intubated.

2) Diuretics

Intravenous loop diuretics are a key of symptomatic treatment in AHF patients with signs of significant
fluid overload and congestion. They increase renal salt and water excretion, have vasodilator properties
and provide rapid decongestion and symptomatic relief.1) Intravenous furosemide is the first-line
diuretic in most of the cases. ACCF/AHA guidelines recommend administering diuretics immediately
upon presentation, as this approach may be associated with better outcomes. It is therefore
recommended to limit diuretic dose to the smallest amount needed to provide adequate symptomatic
relief and modify the dose according to renal function and prior dose of diuretics.

3) Vasodilators

Intravenous vasodilators, predominantly nitrates, provide additional symptomatic relief to diuretics and
are the second most used drugs in AHF. Nitrates have a dual mechanism of action as they act as both
venodilators and arteriodilators, reducing both preload and afterload and as a result increasing stroke
volume. Intravenous vasodilators are especially indicated in hypertensive AHF. Previous ESC
guidelines restricted vasodilators use in patients with SBP <110 mmHg;4 this has been changed — 2016
ESC guidelines recommends avoiding vasodilators when SBP is <90 mmHg or hypotension in
symptomatic.1) ESICM guidance recommends initiating vasodilators as soon as possible in patients with
normal to high BP;4) a delay of vasoactive drugs administration has been associated with higher
mortality.
Vasodilators are contraindicated in shock and should be used cautiously when significant mitral or
aortic valvular stenosis is suspected or in predominant right ventricular (RV) failure.4)

4) Other agents
 14
Even though they relieve dyspnea and anxiety, routine use of opiates is not recommended in AHF. In
the Acute Decompensated Heart Failure National Registry (ADHERE), morphine use was associated
with higher rates of mechanical ventilation, ICU admission and death.
As noted in the ESC guidelines, administration of vasopressor in AHF (excluding CS) should be
restricted to patients with hypotension and administration of sympathomimetic — to patients with signs
of low cardiac output.

First day management

After initial diagnostic tests and symptomatic treatment of the urgent symptoms, clinicians should seek
to rapidly identify the etiology or precipitating factor for AHF and initiate the specific treatment (Figure
1). This is extremely important to prevent worsening of AHF and avoid adverse outcomes and should be
achieved within the initial few hours of AHF management.1),2)

Precipitating factors and their specific treatment

 ACS: It is a frequent cause of both acutely decompensated HF and de novo AHF. Patients with
coexistent ACS (both non-ST elevation ACS and STEMI) and AHF are at a very-high risk group
and immediate revascularization is indicated, regardless of other findings.
 Severe arrhythmias/rhythm disturbances. Tachyarrhythmia, bradyarrythmia or conduction
disturbances may precipitate AHF. Several ESC guidelines address the management of severe
rhythm disturbances. Urgent electrical cardioversion is recommended if arrhythmia is related to
hemodynamic instability. In AHF patients with atrial fibrillation (AF) and rapid ventricular rate
(>110 bpm), intravenous boluses (0.25–0.5 mg intravenously, smaller doses of 0.0625–0.125 mg
in patients with moderate to severe renal dysfunction) of digoxin should be considered for rapid
control of the ventricular rate. In other patients with HF and AF, beta blockers are preferred to
control the ventricular rate.
 Acute mechanical causes: They include complications of ACS (e.g., free wall or ventricular
septal rupture, acute mitral insufficiency), chest trauma, cardiac intervention, endocarditis (acute
native or prosthetic valve lesion), aortic dissection and rarer causes of obstruction (e.g., cardiac
tumors). Immediate echocardiography is crucial to confirm the diagnosis when acute mechanical
cause is suspected and treatment comprises of urgent surgical or percutaneous repair.
 Acute PE: Pulmonary embolus should be considered as a precipitant of AHF since patients with
HF are more likely to be in a hypercoagulable state.2) Chest CT is a gold standard in the
diagnostic process. When acute PE is confirmed, immediate primary reperfusion is
recommended. This may be achieved by thrombolysis, catheter-based approach or surgical
embolectomy.
 Infection: Respiratory infections are frequent precipitants for HF. They cause hypoxia and are
associated with higher in-hospital and long-term mortality. Sepsis is associated with reversible
left ventricle hypokinesia.
 .

Pulmonary Edema
Pulmonary edema is acute, severe left ventricular failure with pulmonary venous hypertension and
alveolar flooding. It develops when imbalance in pump function causes an increase in lung fluid
secondary to leakage from pulmonary capillaries into the interstitium and alveoli of the lung.

Maintenance of plasma oncotic pressure (generally about 25 mm Hg) higher than pulmonary
capillary pressure (about 7-12 mm Hg), maintenance of connective tissue and cellular barriers relatively
 15
impermeable to plasma proteins and lymphatic drainage are the main mechanisms that keep the
interstitium and alveoli dry. Opposite, pulmonary capillary pressure and plasma oncotic pressure are
responsible for fluid transfer to the interstitium. Under normal circumstances, when fluid is transferred
into the lung interstitium with increased lymphatic flow, no increase in interstitial volume occurs.
If LV filling pressure increases suddenly, plasma fluid moves rapidly from pulmonary capillaries
into interstitial spaces and alveoli, causing pulmonary edema. When the capacity of lymphatic drainage
is exceeded, liquid accumulates in the interstitial spaces surrounding the bronchioles and lung
vasculature, thus creating interstitial pulmonary edema - cardiac asthma.
When increased fluid and pressure cause tracking into the interstitial space around the alveoli and
disruption of alveolar membrane junctions, fluid floods the alveoli and leads to alveolar pulmonary
edema.
About 1⁄2 of cases result from acute coronary ischemia; 1⁄4 from decompensation of significant
underlying HF, including diastolic dysfunction HF due to hypertension; and the rest from arrhythmia,
an acute valvular disorder, or acute volume overload often due to IV fluids. Drug or dietary
noncompliance is often involved.
Symptoms and Signs
- extreme dyspnea, restlessness, and anxiety
- a sense of suffocation
- Cough producing blood-tinged sputum - pink, frothy sputum, some patients froth at the
mouth
- pallor, cyanosis,
- marked diaphoresis
- The pulse is rapid and low volume
- BP is variable. Marked hypertension indicates significant cardiac reserve; hypotension
- Inspiratory fine crackles are widely dispersed anteriorly and posteriorly over both lung
fields.
- Marked wheezing (cardiac asthma) may occur. In pulmonary edema - bubble, boil
breathing
- Noisy respiratory efforts often make cardiac auscultation difficult; a summation gallop -
of 3rd (S3) and 4th (S4) heart sounds - may be present.
- Signs of RV failure (eg, neck vein distention, peripheral edema) may be present.
Diagnosis and Treatment
- A chest x-ray, done immediately, is usually diagnostic, showing marked interstitial edema.
- serum brain (B-type) natriuretic peptide (BNP) levels elevated in pulmonary edema;
- ECG

Marked pulmonary congestion suggests loss of LV contractile force (LV failure) as the cause.
Treatment depends on the cause. In some patients, determining the cause requires use of a pulmonary
artery catheter to measure intracardiac pressures. If pulmonary artery occlusion pressure is < 18 mm Hg,
decreased filling, usually due to hypovolemia, is likely; if pressure is > 18 mm Hg, LV failure is likely.

Killip Classification and Mortality Rate of Acute MI*

Class PAO2† Clinical Description Hospital
Mortality Rate
1 Normal No clinical evidence of left 3–5%
ventricular (LV) failure
2 Slightly reduced Mild to moderate LV failure 6–10%
3 Abnormal Severe LV failure, pulmonary 20–30%
edema
 16
4 Severely abnormal Cardiogenic shock: > 80%
hypotension, tachycardia, mental
obtundation, cool extremities,
oliguria, hypoxia
*Determined by repeated examination of the patient during the course of illness.
†Determined while the patient is breathing room air.
Modified from Killip T,.. The American Journal of Cardiology, 1967.

Prehospital Care:
- upright position - To reduce venous return, elevate the head of the bed. Patients may be most
comfortable in a sitting position with down legs, which allows for reduced venous return and
decreased preload.
- Alternating tourniquets have been used to decrease preload. Their use has been supplanted by
newer therapies such as intravenous nitroglycerin and nitroprusside.
- Administer supplemental oxygen, initially 100% nonrebreather facemask.
- Provide nitroglycerin sublingual or spray for active chest pain in the patient without severe
hypotension and IV furosemide.
Emergency Department Care:
- Administer oxygen O2, initially 100% by nonrebreather facemask.
- Obtain IV access.
- morphine 1 to 5 mg IV once or twice
- Therapy generally starts with nitrates and diuretics to decrease preload if patients are
hemodynamically stable - without arterial hypotension
- nitroglycerin and nitroprusside intravenous
- furosemide 0.4 mg sublingually q 5 min, followed by an IV drip at 10 to 20 mg/min,
- in arterial hypotension – dophamine 0,5% 5,0 ml or dobutamine
If hypoxia is significant, noninvasive ventilatory assistance with bilevel positive airway pressure
(BiPAP) is helpful, but if CO2 retention is present or the patient is obtunded, tracheal intubation and
assisted ventilation are required.
Specific additional treatment depends on etiology:
-thrombolysis or direct percutaneous coronary angioplasty with or without a stent for acute MI or
another acute coronary syndrome;
-a vasodilator for severe hypertension;
-direct-current cardioversion for supraventricular or ventricular tachycardia;
-an IV digoxin, or IV amiodarone to slow the ventricular rate for rapid atrial fibrillation
(cardioversion is preferred).
In patients with acute MI - [f BP falls or shock develops, IV dobutamine and an intra-aortic
balloon pump (counterpulsation) may be required;
levosimendan – calcium sensitizers - the most positive inotropic effect

4. Theoretical questions for the lesson:

1. Define AH.
2. Main causes of AH.
3. Classification of AH.
4. Clinical symptoms of AH.
5. Methods of long-term registration of BP
 17
6. Differential diagnosis of AH.
7. Treatment of AH

5. Literature:
А. Main:
1. Davidson’s Principles and Practice of Medicine, 22nd Edition, 2014, P. 542-551.
2. Harrison's Principles of Internal Medicine, 20e J. Larry Jameson, Anthony S. Fauci, Dennis L.
Kasper, Stephen L. Hauser, Dan L. Longo, Joseph Loscalzo) - sec 5-chapter 271.

B. Additional:
http://academic.oup.com/eurheartj/article/39/33/3021/5079119.
https://www.escardio.org/Guidelines/Clinical-Practice-Guidelines/Acute-and-Chronic-Heart-Failure
https://www.cardioaragon.com/wp-content/uploads/ejhf.1531.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5986746/

Tasks for control

Task № 1
A 52-year-old patient after the stressful situation had a strong pain in the hindhead, palpitations.
About 5 years she has the periodic increase of BP to 190/100 mm Hg She is not regularly treated.
Physical exam: general condition is moderate. The face is hyperemic. Pulse – 120/ 1 min,
rhythmical. BP 200/100 mm Hg. The S1on the apex is weak, accentuation of II tone on the aorta.
Vesicular breathing. The ECG - signs of left ventricular hypertrophy.
1. What is the diagnosis?
2. What is the therapeutic approach?

Situation task № 2
A 32-year-old female complains of dizziness, headache, palpitation, tremor. For the last several
months she has been under outpatient observation for the increased arterial pressure. Since recently
such attacks have become more frequent and severe. Objectively: skin is covered with clammy
sweat, tremor of the extremities is present. HR- 110/min, AP- 220/140 mm Hg. Heart sounds are
muffled. Blood test results: WBCs - 9,8x109/l, ESR - 22 mm/h. Blood glucose - 9,8 millimole/l.
1. What is the diagnosis?
2. What is the therapeutic approach?

Situation task № 3
A 72-year-old patient V. suffered from essential hypertension for 20 years. It was treated in the
cardiology department at the frequent attacks of dyspnea. In 2000 he had a myocardial infarction.
At night, he was awakened by the inspiratory dyspnea attack, dry cough, which was intensified in a
horizontal position. He has called the doctor on duty.
Physical exam: the patient's condition is severe. The forced position – ortopnoe; skin is pale. During
cough the foamy pink sputum is expectorated.
Pulse - 120/min, rhythmical. BP - 180/120 mm Hg. The left border of the heart is 2 cm outwards from
the left l. sternocleidomastoideus. At the apex and 5-th point - the protodiastolic gallop rhythm.
Breathing rate - 36 min. Above the lungs – decrease vesicular breathing, fine and moist rales over 50%
of the lung. The liver +2 cm from the right subcostal area.
ECG: sinus rhythm, rhythmical, heart rate - 120/min, levogram; QS complexes in I, V2, V4 leads; ST
segment on the isoline, T wave is slight negative.
ECHO - dilated left atrium and ventricle, posterior and septum thickness - 1,3 cm, ejection fraction -
32%.
1. Make a diagnosis.
2. Emergency treatment.
 18

Situation task №4
A 58-year-old patient complains of a headache in the occipital region, nausea, choking, opplotentes.
The presentations appeared after a physical exertion. Objectively: the patient is excited. Face is
hyperemic. Skin is pale. Heart sounds are regular, the 2nd aortic sound is accentuated. AP- 240/120 mm
Hg, HR- 92/min. Auscultation reveals some fine moist rales in the lower parts of the lungs. Liver is not
enlarged. ECG shows signs of hypertrophy and left ventricular overload. What is the most likely
diagnosis?
1. Make a diagnosis.
2. Emergency treatment.

Methodical recommendation made by Ph.D. Berko G.K.

Ph.D Ostapchuk O.I.