Urgent emergency situation . How to handle emergency healthcare situation

1. URGENT CONDITIONS IN
INTERNAL MEDICINE
Perm State Medical University
Department of Faculty Therapy # 1
K.M.N. , Assitant Professor O.R. Parandey

2. True Cardiogenic Shock
• Cardiogenic shock is defined as persistent hypotension (SBP 90 mmHg).
• It is usually associated with extensive LV damage, but may occur in RV
infarction.
• The first step in patients with cardiogenic shock is to identify the
mechanism and to correct any reversible cause such as hypovolaemia,
drug-induced hypotension, or arrhythmias; alternatively, initiate the
treatment of potential specific causes, such as mechanical complications
or tamponade.
• Cardiogenic shock characterization and management do not necessarily
need invasive haemodynamic monitoring, but ventricular and valve
function should be urgently evaluated by transthoracic echocardiography
and associated mechanical complications ruled out.

3. True Cardiogenic Shock
• Invasive monitoring with an arterial line is recommended. A pulmonary artery
catheter may be considered, in order to perform a careful adjustment of filling
pressures and assessment of cardiac output or in cases of shock of unexplained
cause.
• Hypovolaemia should be ruled out first and corrected with fluid loading.
• Pharmacological therapy aims to improve organ perfusion by increasing cardiac
output and blood pressure. Intravenous inotropic agents or vasopressors are
usually required to maintain an SBP >90 mmHg, and to increase cardiac
output and improve vital organ perfusion.
• Dobutamine is the initial therapy for patients with predominant low cardiac
output, whereas norepinephrine may be safer and more effective than
dopamine in patients with cardiogenic shock and severe hypotension.

4. True Cardiogenic Shock
• Levosimendan may be considered as an alternative, especially for
patients on chronic beta-blocker therapy, because its inotropic
effect is independent of beta-adrenergic stimulation.
• Phosphodiesterase III inhibitors are not recommended in STEMI
patients.

5. True Cardiogenic Shock
• Mechanical LV assist devices (LVADs), including percutaneous short-
term mechanical circulatory support devices (i.e. intra-cardiac axial
flow pumps and arterial-venous extracorporeal membrane
oxygenation), have been used in patients not responding to standard
therapy, including inotropes, fluids, and IABP, but evidence
regarding their benefits is limited.
• Therefore, short-term mechanical circulatory support may be
considered as a rescue therapy in order to stabilize the patients and
preserve organ perfusion (oxygenation) as a bridge to recovery of
myocardial function, cardiac transplantation, or even LV assist device
destination therapy on an individual basis.

6. True Cardiogenic Shock in STEMI
• Immediate PCI is indicated for patients with cardiogenic shock if
coronary anatomy is suitable. If coronary anatomy is not suitable for
PCI, or PCI has failed, emergency CABG is recommended
• Invasive blood pressure monitoring with an arterial line is
recommended. Oxygen/mechanical respiratory support is indicated
according to blood gases
• Immediate Doppler echocardiography is indicated to assess
ventricular and valvular functions, loading conditions, and to detect
mechanical complications. It is indicated that mechanical
complications are treated as early as possible after discussion by the
Heart Team

7. True Cardiogenic Shock in STEMI
• In STEMI patients presenting with cardiogenic shock in which PCI-
mediated reperfusion is estimated to occur >120 min, immediate
fibrinolysis and transfer to a PCI centre should be considered.
• Upon arrival at the PCI centre, emergent angiography is indicated,
regardless of the ST resolution and the time from fibrinolysis
administration
• ABP counterpulsation does not improve outcomes in patients with STEMI
and cardiogenic shock without mechanical complications, nor does it
significantly limit infarct size in those with potentially large anterior MI.
Therefore, routine IABP counterpulsation cannot be recommended, but
may be considered for haemodynamic support in selected patients (i.e.
severe mitral insufficiency or ventricular septal defect).

8. True Cardiogenic Shock in STEMI
• B Inotropic/vasopressor agents may be considered for haemodynamic
stabilization.
• Haemodynamic assessment with pulmonary artery catheter may be
considered for confirming diagnosis or guiding therapy.
• Ultrafiltration may be considered for patients with refractory
congestion, who failed to respond to diuretic-based strategies.

9. Acute Left Ventricle Insufficiency.
Pulmonary Edema
• Management Patients with heart failure should be under
continuous monitoring of heart rhythm, blood pressure,
and urinary output.
• The mechanism of heart failure should be assessed early by
physical examination, ECG, echocardiography, and (when
not rapidly controlled) with invasive haemodynamic
monitoring, and corrected as soon as possible.

10. Recommendations for the management of left ventricular dysfunction
and acute heart failure in ST-elevation myocardial infarction
• Oxygen is indicated in patients with pulmonary oedema with SaO2 95%. I C
• Nitrates are recommended in patients with symptomatic heart failure with SBP >90
mmHg to improve symptoms and reduce congestion. I C
• Intravenous nitrates or sodium nitroprusside should be considered in patients with heart
failure and elevated SBP to control blood pressure and improve symptoms. II А
• Loop diuretics are recommended in patients with acute heart failure with
symptoms/signs of fluid overload to improve symptoms - I C
• ACE inhibitor (or if not tolerated, ARB) therapy is indicated as soon as haemodynamically
stable for all patients with evidence of LVEF - I A
• An MRA is recommended in patients with heart failure and LVEF < 40 % in patients
without renal failure and/or hyperKaliemia to reduce recurrent hospitalization and death
- I B

11. Recommendations for the management of left ventricular
dysfunction and acute heart failure in ST-elevation myocardial
infarction
• Opiates may be considered to relieve dyspnoea and anxiety in patients with
pulmonary oedema and severe dyspnoea. Respiration should be monitored. II B
• Non-invasive positive pressure ventilation (continuous positive airway pressure,
biphasic positive airway pressure) should be considered in patients with
respiratory distress (respiratory rate >25 breaths/min, SaO2 < 90 % without
hypotension II А
• Patient intubation is indicated in patients with respiratory failure or exhaustion,
leading to hypoxaemia, hypercapnia, or acidosis, and if non-invasive ventilation
is not tolerated I C
• Inotropic agents may be considered in patients with severe heart failure with
hypotension refractory to standard medical treatment. IIb C
• Beta-blocker therapy is recommended in patients with LVEF < 40 % in patients
with HF after stabilization, to reduce risk of death, reccurent MI and HF - I A

12. Acute Right Ventricle Insufficiency.
Diagnostic work-up
• In 1616, Sir William Harvey was the first person to describe the importance
of right ventricular function.
• However, only since the early 1950s, the prognostic significance of RV
function has been recognised in several conditions, primarily those
involving the LV (e.g. chronic LV failure), the lungs and their vascular bed
(e.g. pulmonary embolism, chronic pulmonary disease and pulmonary
arterial hypertension) or the right-sided chambers (e.g. RV infarction, RV
cardiomyopathies and congenital heart diseases).
• Recent advances in imaging techniques have created new opportunities
to study RV anatomy, physiology and pathophysiology, and contemporary
research efforts have opened the doors to new treatment possibilities

13. Acute Right Ventricle Insufficiency.
Diagnostic work-up
• Nevertheless, the treatment of RV failure remains challenging.
• The RV is a unique chamber with distinct anatomy and physiology.
• It is coupled to systemic venous return and the pulmonary
circulation. Since the pressure in the pulmonary circulation is
generally much lower than it is in the systemic circulation, less muscle
power is needed (a quarter of the LV stroke work)and RV muscle is
much thinner than the LV, having about one-third of the thickness.
• Furthermore, venous return fluctuates, so the RV is much more
compliant and is slightly larger (approximately 10–15%) than the LV,
which allows it to accommodate large variations in venous return
without altering end-diastolic pressure

14. Acute Right Ventricle Insufficiency.
Diagnostic work-up
• The right coronary artery, at least in most individuals, perfuses the RV free
wall and the posterior third of the interventricular septum. The left
anterior descending artery perfuses the apex and the anterior part of the
septum. Unlike the LV, RV perfusion occurs both in systole and diastole
and the collateral vessels of the RV are denser than those of the LV.
• One of the main characteristics of the RV is its greater sensitivity to
changes in afterload. Brisk increases in afterload are poorly tolerated and
lead to RV dilatation and to decrease of stroke volume
• A further important characteristic is ventricular interdependence.
Excessive RV volume loading is constrained by the pericardium and
therefore results in compression and D-shaping of the LV. Volume overload
in the RV therefore indirectly leads to a decrease in LV stroke volume.

15. Acute Right Ventricle Insufficiency.
Diagnostic work-up
Mechanism Cause
Increased afterload LV backward failure (pulmonary hypertension associated with left-sided heart
disease)
Pulmonary embolism, chronic thromboembolic pulmonary hypertension
Pulmonary artery hypertension
(Exacerbated) chronic pulmonary disease
Acute lung injury/acute respiratory distress syndrome
Sleep-related breathing disorders, obesity-hypoventilation syndrome
Mechanical ventilation
(Repaired) congenital heart disease with systemic RV or RV outflow obstruction
Reduced contractility RV ischaemia/RV infarction
RV injury, systemic inflammatory response (SIRS)
Myocarditis
Cardiomyopathies (e.g. dilated cardiomyopathy or hypertrophic cardiomyopathy)
Arrhythmogenic RV cardiomyopathy, Uhl’s anomaly
Abnormal preload Hypo- or hypervolaemia
LV forward failure
Pericardial tamponade
Mechanical ventilation
Chronic left-to-right shunt
Altered interdependence Pericardial tamponade
Pericardial disease
Septal shift
Altered rhythm Bradyarrhythmia
Tacharrhythmia
Table 1:
Mechanisms and Causes of Right Ventricular Failure

16. Acute Right Ventricle Insufficiency.
Diagnostic work-up : Clinical signs
• The clinical signs of RV failure are mainly determined by backward
failure causing systemic congestion
• In severe forms, the right heart dilates and, through interventricular
dependence, can compromise LV filling, reducing LV performance and
causing forward failure (i.e. hypotension and hypoperfusion)
• Backward failure presents as elevated central venous pressure with
distension of the jugular veins and may lead to organ dysfunction and
peripheral oedema
• The association between systemic congestion and renal, hepatic and
gastrointestinal function in heart failure has been extensively studied.

17. Acute Right Ventricle Insufficiency.
Diagnostic work-up : Clinical signs
• Elevated central venous pressure is the main determinant of impaired
kidney function in acute heart failure.
• Hepatic dysfunction is also highly prevalent in acute heart failure;
systemic congestion frequently presents with a cholestatic pattern,
while hypoperfusion typically induces a sharp increase in circulating
transaminases.
• Finally, systemic congestion may alter abdominal function, including
reduced intestinal absorption and impaired intestinal barrier.

18. Acute Right Ventricle Insufficiency.
Diagnostic work-up : ECG
• Right axis deviation
• RS-ratio in lead V5 or V6 ≤1, SV5 or V6≥7 mm
• P-pulmonale
• SI – QIII pattern which is an initial S deflection in I, an initial Q-
deflection in III and T-Inversions in III, this pattern is very sensitive in
in massive pulmonary embolism
• Moreover, RV failure is often accompanied by atrial flutter or AF.
an initial S deflection in I, an initial Q-deflection in III and T-
Inversions in III

19. Acute Right Ventricle Insufficiency.
Diagnostic work-up : Imaging
• The primary working tool for imaging the (failing) RV is echocardiography.
In most patients, transthoracic assessment by echocardiography is
sufficient to describe RV morphology and function adequately.
• Newer imaging techniques, such as 3D-echocardiography and strain
imaging, have proven to be useful and accurate imaging modalities but
have limitations because they depend on good image
• Cardiac MRI has become the standard reference method for right heart
acquisition as it is capable of visualising anatomy, quantifying function and
calculating flow. In addition, it is useful in cases where image quality by
echocardiography is limited. Moreover, it can provide advanced imaging
with tissue characterisation, which is useful in different cardiomyopathies,
such as arrhythmogenic RV cardiomyopathy, storage disease and cardiac
tumours

20. Acute Right Ventricle Insufficiency
Medical Treatment of Acute Right Ventricular Failure
• The Heart Failure Association and the Working Group on Pulmonary Circulation
and Right Ventricular Function of the European Society of Cardiology recently
published a comprehensive statement on the management of acute RV failure
• Management of acute RV failure requires not only an understanding of the
anatomical and physiological particularities of the RV but also rapid
identification and treatment of the underlying causes and related
pathophysiological disorders
• In patients presenting with severe RV failure, rapid initiation of treatment to
restore haemodynamic stability is essential to prevent significant, potentially
irreversible end-organ damage.
• Acute treatment consists of four elements: volume optimisation; restoration of
perfusion pressure; improvement of myocardial contractility; and advanced
options

21. Acute Right Ventricle Insufficiency
Medical Treatment of Acute Right Ventricular Failure
Figure 3:
Algorithm for the Treatment of Acute Right Ventricular Failure

22. Acute Right Ventricle Insufficiency
Medical Treatment of Acute Right Ventricular Failure
• A common misconception is that RV failure should consistently be treated with
volume supplementation. First, volume status need to be identified with volume
bolus; in case the condition is improved, then another volume can be infused
• In patients with RV failure and signs of venous congestion, diuretics are often the
first option to optimise volume status. Early evaluation of the diuretic response
(by measuring urine output or post-diuretic spot urinary sodium content) to
identify patients with an inadequate diuretic response is even more important
than it is in other forms of acute heart failure. If decongestion is insufficient, rapid
intensification of loop diuretic dose, starting a sequential nephron blockade
(combining diuretics with a different mode of action) or the use of renal
replacement therapy/ultrafiltration should be considered.

23. Acute Right Ventricle Insufficiency
Medical Treatment of Acute Right Ventricular Failure
• Vasopressors are primarily indicated to restore arterial blood pressure and
improve organ perfusion. Restoration of coronary perfusion pressure by
vasopressors is a mainstay of therapy since the failing RV dealing with volume
and/or pressure overload is particularly susceptible to ischaemic injury.
Furthermore, vasopressors restore cerebral, renal and hepato-splanchnic
perfusion pressures
• Noradrenaline can restore systemic haemodynamics without increasing RV
afterload (i.e. there is no effect on pulmonary vascular resistance)
• Dobutamine, levosimendan and phosphodiesterase III inhibitors improve
contractility and increase cardiac output and are indicated in patients with severe
RV failure causing cardiogenic shock despite treatment with vasopressors

24. Acute Right Ventricle Insufficiency
Medical Treatment of Acute Right Ventricular Failure
• In patients with refractory RV failure despite treatment with vasopressors and inotropes,
advanced therapeutic options including fibrinolysis for pulmonary embolism or
mechanical circulatory support should be considered
• Mechanical circulatory support with RV assist devices (RVADs) should be considered
when RV failure persists despite treatment with vasopressors and inotropes
• Conclusion
• The assessment of RV failure should consider the anatomical and physiological
particularities of the RV and include appropriate imaging techniques to understand the
underlying pathophysiological mechanisms.
• Treatment should include rapid optimisation of volume status, restoration of perfusion
pressure, and improvement of myocardial contractility and rhythm and, in case of
refractory RV failure, mechanical circulatory support.

25. Acute Pulmonary Embolism : clinical signs
and symptoms
• 2019 ESC Guidelines for the diagnosis and management of acute
pulmonary embolism developed in collaboration with the European
Respiratory Society (ERS): The Task Force for the diagnosis and
management of acute pulmonary embolism of the European Society
of Cardiology (ESC)
• These Guidelines focus on the diagnosis and management of acute
PE in adult patients. For further details specifically related to the
diagnosis and management of deep vein thrombosis (DVT), the
reader is referred to the joint consensus document of the ESC
Working Groups of Aorta and Peripheral Vascular Diseases, and
Pulmonary Circulation and Right Ventricular Function.1

26. Epidemiology
• Venous thromboembolism (VTE), clinically presenting as DVT or PE, is globally
the third most frequent acute cardiovascular syndrome behind myocardial
infarction and stroke.
• Cross-sectional data show that the incidence of VTE is almost eight times higher
in individuals aged ≥80 years than in the fifth decade of life.
• Together with the substantial hospital-associated, preventable, and indirect
annual expenditures for VTE (an estimated total of up to €8.5 billion in the
European Union),8 these data demonstrate the importance of PE and DVT in
ageing populations in Europe and other areas of the world
• Time trend analyses in European, Asian, and North American populations suggest
that case fatality rates of acute PE may be decreasing due to use of more
effective therapies and interventions, and possibly better adherence to
guidelines

27. Predisposing factors
Strong risk factors (OR > 10)
• Fracture of lower limb
• Hospitalization for heart failure or atrial fibrillation/flutter (within previous 3 months)
• Hip or knee replacement
• Major trauma
• Myocardial infarction (within previous 3 months)
• Previous VTE
• Spinal cord injury
Moderate risk factors (OR 2–9)
• Arthroscopic knee surgery
• Autoimmune diseases
• Blood transfusion
• Central venous lines
• Intravenous catheters and leads
• Chemotherapy
• Congestive heart failure or respiratory failure
• Erythropoiesis-stimulating agents
• Hormone replacement therapy (depends on formulation)
• In vitro fertilization
• Oral contraceptive therapy
• Post-partum period
• Infection (specifically pneumonia, urinary tract infection, and HIV)
• Inflammatory bowel disease
• Cancer (highest risk in metastatic disease)
• Paralytic stroke
• Superficial vein thrombosis
• Thrombophilia
Weak risk factors (OR < 2)
• Bed rest >3 days
• Diabetes mellitus
• Arterial hypertension
• Immobility due to sitting (e.g. prolonged car or air travel)
• Increasing age
• Laparoscopic surgery (e.g. cholecystectomy)
• Obesity
• Pregnancy
• Varicose veins

28. Pathophysiology and determinants of outcome
• Acute PE interferes with both circulation and gas exchange. Right
ventricular (RV) failure due to acute pressure overload is considered the
primary cause of death in severe PE.
• Pulmonary artery pressure (PAP) increases if >30–50% of the total cross-
sectional area of the pulmonary arterial bed is occluded by
thromboemboli.57
• PE-induced vasoconstriction, mediated by the release of thromboxane A2
and serotonin, contributes to the initial increase in pulmonary vascular
resistance (PVR) after PE.58
• Anatomical obstruction and hypoxic vasoconstriction in the affected lung
area lead to an increase in PVR, and a proportional decrease in arterial
compliance.59

29. Eur Heart J, Volume 41, Issue 4, 21 January 2020, Pages 543–603, https://doi.org/10.1093/eurheartj/ehz405
The content of this slide may be subject to copyright: please see the slide notes for details.
Figure 2 Key factors contributing to haemodynamic collapse and
death in acute pulmonary embolism (modified from ...

30. (1) Cardiac arrest (2) Obstructive shock68–70 (3) Persistent hypotension
Need for cardiopulmonary resuscitation Systolic BP < 90 mmHg or
vasopressors required to achieve a BP
≥90 mmHg despite adequate filling
status
Systolic BP < 90 mmHg or systolic BP
drop ≥40 mmHg, lasting longer than 15
min and not caused by new-onset
arrhythmia, hypovolaemia, or sepsis
And
End-organ hypoperfusion (altered
mental status; cold, clammy skin;
oliguria/anuria; increased serum
lactate)
Definition of haemodynamics instability in PE

31. • The clinical signs and symptoms of acute PE are non-specific.
• In most cases, PE is suspected in a patient with dyspnoea, chest pain,
pre-syncope or syncope, or haemoptysis.
• Haemodynamic instability is a rare but important form of clinical
presentation, as it indicates central or extensive PE with severely
reduced haemodynamic reserve.
• Syncope may occur, and is associated with a higher prevalence of
haemodynamic instability and RV dysfunction. According to the results
of a recent study, acute PE may be a frequent finding in patients
presenting with syncope (17%), even in the presence of an alternative
explanation.
Clinical presentation

32. Clinical presentation – continue
• In some cases, PE may be asymptomatic or discovered incidentally during
diagnostic workup for another disease.
• Dyspnoea may be acute and severe in central PE; in small peripheral PE it
is often mild and may be transient. In patients with pre-existing heart
failure or pulmonary disease, worsening dyspnoea may be the only
symptom indicative of PE.
• Chest pain is a frequent symptom of PE and is usually caused by pleural
irritation due to distal emboli causing pulmonary infarction. In central PE,
chest pain may have a typical angina character, possibly reflecting RV
ischaemia, and requiring differential diagnosis from an acute coronary
syndrome or aortic dissection.

33. Assessment of clinical (pre-test) probability
• In addition to symptoms, knowledge of the predisposing factors for
VTE is important in determining the clinical probability of the
disease, which increases with the number of predisposing factors
present
• The combination of symptoms and clinical findings with the
presence of predisposing factors for VTE allows the classification of
patients with suspected PE into distinct categories of clinical or pre-
test probability, which correspond to an increasing actual prevalence
of confirmed PE.

34. The revised Geneva clinical prediction rule for
pulmonary embolism ( Geneva score )
Items Clinical decision rule points
Original version91 Simplified version87
Previous PE or DVT 3 1
Heart rate
75–94 b.p.m. 3 1
≥95 b.p.m. 5 2
Surgery or fracture within the past month 2 1
Haemoptysis 2 1
Active cancer 2 1
Unilateral lower-limb pain 3 1
Pain on lower-limb deep venous palpation and unilateral oedema 4 1
Age >65 years 1 1
Clinical probability
Three-level score
Low 0–3 0–1
Intermediate 4–10 2–4
High ≥11 ≥5
Two-level score
PE-unlikely 0–5 0–2
PE-likely ≥6 ≥3

35. Score’s value
• Regardless of the score used, the proportion of patients with
confirmed PE can be expected to be ∼10% in the low-probability
category, 30% in the moderate-probability category, and 65% in the
high-probability category.
• When the two-level classification is used, the proportion of patients
with confirmed PE is ∼12% in the PE-unlikely category and 30% in the
PE-likely category. A direct prospective comparison of these rules
confirmed a similar diagnostic performance.

36. Criteria of PE Rule –out
• Searching for PE in every patient with dyspnoea or chest pain may lead to high
costs and complications of unnecessary tests.
• The Pulmonary Embolism Rule-out Criteria (PERC) were developed for emergency
department patients with the purpose of selecting, on clinical grounds, patients
whose likelihood of having PE is so low that diagnostic workup should not even
be initiated.
• They comprise eight clinical variables significantly associated with an absence of
PE: age < 50 years; pulse < 100 beats per minute; SaO2 >94%; no unilateral leg
swelling; no haemoptysis; no recent trauma or surgery; no history of VTE; and no
oral hormone use.
• The results of a prospective validation study, suggested safe exclusion of PE in
patients with low clinical probability who, in addition, met all criteria of the
PERC rule.

37. D-dimer testing
• D-dimer levels are elevated in plasma in the presence of acute
thrombosis because of simultaneous activation of coagulation and
fibrinolysis.
• The negative predictive value of D-dimer testing is high
• The positive predictive value of elevated D-dimer levels is low and D-
dimer testing is not useful for confirmation of PE, because D-dimer is also
frequently elevated in patients with cancer, in hospitalized patients, in
severe infection or inflammatory disease, and during pregnancy.
• In the emergency department, a negative ELISA D-dimer can, in
combination with low clinical probability, exclude the disease without
further testing in patients with suspected PE.
• So, D- dimer is used To Exclude PE ( if this test is negative)
• When it is positive, then further investigations are needed

38. Assessment of pulmonary embolism severity
and the risk of early death
• Risk stratification of patients with acute PE is mandatory for determining
the appropriate therapeutic management approach.
• As described in above, initial risk stratification is based on clinical
symptoms and signs of haemodynamic instability, which indicate a high
risk of early death.
• In the large remaining group of patients with PE who present without
haemodynamic instability, further (advanced) risk stratification requires
the assessment of two sets of prognostic criteria: (i) clinical, imaging, and
laboratory indicators of PE severity, mostly related to the presence of RV
dysfunction; and (ii) presence of comorbidity and any other aggravating
conditions that may adversely affect early prognosis.

39. Clinical parameters of pulmonary embolism
severity
• Acute RV failure defined as a rapidly progressive syndrome with
systemic congestion resulting from impaired RV filling and/or
reduced RV flow output
• It is a critical determinant of outcome in acute PE.
• Tachycardia, low systolic BP, respiratory insufficiency (tachypnoea
and/or low SaO2), and syncope, alone or in combination, have been
associated with an unfavourable short-term prognosis in acute PE.

40. Imaging of right ventricular size and function.
1. Echocardiography
• Echocardiographic assessment of the morphology and function of
the RV is widely recognized as a valuable tool for the prognostic
assessment of normotensive patients with acute PE in clinical
practice (see next slide)
• Of these, an RV/LV diameter ratio ≥1.0 is the finding for which an
association with unfavourable prognosis has most frequently been
reported.
• In addition to RV dysfunction, echocardiography can identify right-
to-left shunt through a patent foramen ovale and the presence of
right heart thrombi, both of which are associated with increased
mortality in patients with acute PE.

41. Echocardiographic parameters used to stratify
the early risk of patients with PE

42. Imaging of right ventricular size and function.
2. Computed tomographic pulmonary angiography
• Four-chamber views of the heart by CT angiography can detect RV
enlargement (RV end-diastolic diameter and RV/LV ratio measured
in the transverse or four-chamber view) as an indicator of RV
dysfunction.
• RV enlargement (defined as an RV/LV ratio ≥0.9) is an independent
predictor of an adverse in-hospital outcome, both in the overall
population with PE and in haemodynamically stable patients
• Apart from RV size and the RV/LV ratio, CT may provide further
prognostic information based on volumetric analysis of the heart
chambers and assessment of contrast reflux to the inferior vena
cava (IVC).

43. Laboratory biomarkers
1. Markers of myocardial injury
• Elevated plasma troponin concentrations on admission may be
associated with a worse prognosis in the acute phase of PE.
Elevated troponin concentrations were associated with an increased
risk of mortality, both in unselected patients and in those who were
haemodynamically stable at presentation.
• Heart-type fatty acid-binding protein (H-FABP), an early and
sensitive marker of myocardial injury, provides prognostic
information in acute PE, both in unselected198,199 and normotensive
patients.

44. Laboratory biomarkers
2 Markers of right ventricular dysfunction
• RV pressure overload due to acute PE is associated with increased
myocardial stretch, which leads to the release of B-type natriuretic
peptide (BNP) and N-terminal (NT)-proBNP.
• Thus, the plasma levels of natriuretic peptides reflect the severity of
RV dysfunction and haemodynamic compromise in acute PE.
• Low levels of BNP or NT-proBNP are capable of excluding an
unfavourable early clinical outcome, with high sensitivity and a
negative predictive value.

45. Integration of aggravating conditions and comorbidity
into risk assessment of acute pulmonary embolism
• In addition to the clinical, imaging, and laboratory findings, which
are directly linked to PE severity and PE-related early death, baseline
parameters related to aggravating conditions and comorbidity are
necessary to assess a patient’s overall mortality risk and early
outcome.
• The Pulmonary Embolism Severity Index (PESI) (see next slide) is the
one that has been most extensively validated to date.
• The principal strength of the PESI lies in the reliable identification
of patients at low risk for 30 day mortality (PESI classes I and II). One
randomized trial employed a low PESI as the principal inclusion
criterion for home treatment of acute PE.

46. Original and simplified Pulmonary Embolism
Severity Index ( PESI and sPESI score )
Parameter Original version226 Simplified version229
Age Age in years 1 point (if age >80 years)
Male sex +10 points –
Cancer +30 points 1 point
Chronic heart failure +10 points 1 point
Chronic pulmonary disease +10 points
Pulse rate ≥110 b.p.m. +20 points 1 point
Systolic BP <100 mmHg +30 points 1 point
Respiratory rate >30 breaths per min +20 points –
Temperature <36°C +20 points –
Altered mental status +60 points –
Arterial oxyhaemoglobin saturation <90% +20 points 1 point
Risk strata
a
•Class I: ≤65 points
•very low 30 day mortality risk (0–1.6%)
•Class II: 66–85 points
•low mortality risk (1.7–3.5%)
•0 points = 30 day mortality risk 1.0%
•(95% CI 0.0–2.1%)
•Class III: 86–105 points
•moderate mortality risk (3.2–7.1%)
•Class IV: 106–125 points
•high mortality risk (4.0–11.4%)
•Class V: >125 points
•very high mortality risk (10.0–24.5%)
≥1 point(s) = 30 day mortality risk 10.9% (95% CI 8.

47. Prognostic assessment strategy
• The classification of PE severity and the risk of early (in-hospital or 30 day)
death is summarized in Table below ( next slide)
• Risk assessment of acute PE begins upon suspicion of the disease and
initiation of the diagnostic workup.
• At this early stage, it is critical to identify patients with (suspected) high-
risk PE.
• This clinical setting necessitates an emergency diagnostic algorithm and
immediate referral for reperfusion treatment. Testing for laboratory
biomarkers such as cardiac troponins or natriuretic peptides is not
necessary for immediate therapeutic decisions in patients with high-risk
PE.

48. Classification of pulmonary embolism severity and
the risk of early (in-hospital or 30 day) death

49. Steps for assessing of PE and its severity
• 1. If a patient have clinical signs of PE we should assess
predisposing factors of PE ( Geneva score)
• 2. If a patient have clinical sighs + high Geneva score = suspect PE
• 3. If we suspect PE we should access its severity by assessing
stability of patient’s hemodynamics + PESI score ( Pulmonary
Embolism Severity Index)
• 4. If hemodynamics is unstable and PESI class from III to V
( or sPESI >1) – the patient is on highest risk of mortality and needs
immediate reperfusion

50. Treatment in the acute phase.
Reperfusion treatment. Systemic thrombolysis
• A meta-analysis of thrombolysis trials that included (but were not confined to)
patients with high-risk PE, defined mainly as the presence of cardiogenic shock,
indicated a significant reduction in the combined outcome of mortality and
recurrent PE
• Thrombolytic therapy leads to faster improvements in pulmonary obstruction,
PAP, and PVR in patients with PE, compared with UFH alone; these
improvements are accompanied by a reduction in RV dilation on
echocardiography.
• The greatest benefit is observed when treatment is initiated within 48 h of
symptom onset, but thrombolysis can still be useful in patients who have had
symptoms for 6–14 days.
• Unsuccessful thrombolysis, as judged by persistent clinical instability and
unchanged RV dysfunction on echocardiography after 36 h, has been reported in
8% of high-risk PE patients.

51. Thrombolytic regimens, doses, and
contraindications
Molecule Regimen Contraindications to fibrinolysis
rtPA 100 mg over 2 h
•Absolute
•History of haemorrhagic stroke or stroke of
unknown origin
•Ischaemic stroke in previous 6 months
•Central nervous system neoplasm
•Major trauma, surgery, or head injury in previous
3 weeks
•Bleeding diathesis
•Active bleeding
•Relative
•Transient ischaemic attack in previous 6 months
•Oral anticoagulation
•Pregnancy or first post-partum week
•Non-compressible puncture sites
•Traumatic resuscitation
•Refractory hypertension (systolic BP >180
mmHg)
•Advanced liver disease
•Infective endocarditis
•Active peptic ulcer
0.6 mg/kg over 15 min (maximum dose 50 mg)
a
Streptokinase 250 000 IU as a loading dose over 30 min, followed by 100 000 IU/h over 12–24 h
Accelerated regimen: 1.5 million IU over 2 h
Urokinase 4400 IU/kg as a loading dose over 10 min, followed by 4400 IU/kg/h over 12–24 h
Accelerated regimen: 3 million IU over 2 h

52. Recommendations for acute-phase treatment of high-risk
pulmonary embolism

53. Suggestions for the anticoagulation and overall management of
acute PE in specific clinical situations

54. Combined parameters and scores for
assessment of pulmonary embolism severity
• To date, only a combination of RV dysfunction on an echocardiogram
(or CTPA) with a positive cardiac troponin test has directly been
tested as a guide for early therapeutic decisions (anticoagulation plus
reperfusion treatment vs. anticoagulation alone) in a large
randomized controlled trial (RCT) of PE patients presenting without
haemodynamic instability.224

55. ASCIA Guidelines - Acute Management of
Anaphylaxis – 2023
• ASCIA defines anaphylaxis as:
• Any acute onset illness with typical skin features (urticarial rash or
erythema/flushing, and/or angioedema), plus involvement
of respiratory and/or cardiovascular and/or persistent
severe gastrointestinal symptoms; or
• Any acute onset of hypotension or bronchospasm or upper airway
obstruction where anaphylaxis is considered possible, even if typical skin
features are not present.
• The ASCIA definition is consistent with the following criteria published in
the World Allergy Organisation Anaphylaxis Guidance Position Paper 2020.

56. Anaphylaxis is highly likely when any one of the
following two criteria are fulfilled:
• Criteria 1.
Acute onset of an illness (minutes to several hours) with simultaneous involvement of the skin,
mucosal tissue, or both (e.g. generalized hives, pruritus or flushing, swollen lips-tongue-uvula),
and at least one of the following:
a) Respiratory compromise (e.g. dyspnea, wheeze-bronchospasm, stridor, reduced peak
expiratory flow, hypoxemia).
b) Reduced blood pressure or associated symptoms of end-organ dysfunction (e.g. hypotonia
[collapse], syncope, incontinence).
c) Severe gastrointestinal symptoms (e.g. severe crampy abdominal pain, repetitive vomiting),
especially after exposure to non-food allergens.
• Criteria 2.
Acute onset of hypotension or bronchospasm or laryngeal involvement after exposure to a known
or highly probable allergen for that patient (minutes to several hours), even in the absence of
typical skin involvement.

57. Signs and symptoms of allergic reactions (1)
• Mild or moderate reactions (may not always occur before
anaphylaxis):
• Swelling of lips, face, eyes
• Hives or welts
• Tingling mouth
• Abdominal pain, vomiting - these are signs of anaphylaxis for insect
sting or injected drug (medication) allergy

58. Signs and symptoms of allergic reactions (2)
• Anaphylaxis – Indicated by any one of the following signs:
• Difficult or noisy breathing
• Swelling of tongue
• Swelling or tightness in throat
• Difficulty talking or hoarse voice
• Wheeze or persistent cough - unlike the cough in asthma, the onset of
coughing during anaphylaxis is usually sudden
• Persistent dizziness or collapse
• Pale and floppy (young children)
• Abdominal pain, vomiting - for insect stings or injected drug (medication)
allergy.

59. Immediate actions for anaphylaxis
• Remove allergen (if still present), stay with person, call for
assistance and locate adrenaline injector.
• LAY PERSON FLAT - do NOT allow them to stand or walk
• • If unconscious or pregnant, place in recovery position - on left side
if pregnant, as shown below
• If breathing is difficult allow them to sit with legs outstretched
• • Hold young children flat, not upright

60. Immediate actions for anaphylaxis – continue
• GIVE ADRENALINE INJECTOR - Give intramuscular injection (IMI) adrenaline into
outer mid-thigh without delay using an adrenaline autoinjector if available OR
adrenaline ampoule/syringe. Adrenaline (epinephrine) is the first line treatment
for anaphylaxis
• Give oxygen (if available).
• Phone ambulance - to transport patient if not already in a hospital setting.
• Phone family/emergency contact.
• Further adrenaline may be given if no response after 5 minutes.
•
IF IN DOUBT GIVE ADRENALINE
• Transfer person to hospital for at least 4 hours of observation.
• Commence CPR at any time if person is unresponsive and not breathing
normally

61. Adrenaline administration and dosages
•Adrenaline is the first line treatment for
anaphylaxis and acts to reduce airway
mucosal oedema, induce
bronchodilation, induce
vasoconstriction and increase strength
of cardiac contraction.

62. Adrenaline (epinephrine) dose chart
Age (years) Weight (kg)
Volume (mL) of adrenaline
1:1,000 ampoules*
Adrenaline injector devices (for
use instead of ampoules)
~<1 <7.5 0.1 mL Not available
~1-2 10 0.1 mL 7.5-20 kg (~<5yrs)
150 microgram device**
~2-3 15 0.15 mL
~4-6 20 0.2 mL
~7-10 30 0.3 mL >20 kg (~>5yrs)
300 microgram device***
~10-12 40 0.4 mL
~>12 and adults >50 0.5 mL
>50 kg (~12 years)
300 microgram or 500 microgram****
device
Adrenaline administration and dosages

63. Adrenaline administration and dosages -continue
• *Adrenaline 1:1,000 ampoules contain 1mg adrenaline per 1mL
• Note:
• If multiple doses are required for a severe reaction (e.g. 2-3 doses
administered at 5 minute intervals), consider adrenaline infusion if
skills and equipment are available.
• For emergency treatment of anaphylaxis, ampoules of adrenaline
1:1,000 should be used for both IM doses and infusion if required
(adrenaline 1:10,000 should not be used).

64. Additional measures - IV adrenaline infusion
in clinical setting:
• If there is an inadequate response after 2-3 adrenaline doses, or
deterioration of the patient, start IV adrenaline infusion, given by staff
trained in its use or in liaison with an emergency specialist.
• IV adrenaline infusions should be used with a dedicated line, infusion
pump and anti-reflux valves wherever possible.
• CAUTION: IV boluses of adrenaline are NOT recommended without
specialised training as they may increase the risk of cardiac
arrhythmia.

65. Additional measures to consider if IV
adrenaline infusion is ineffective
For upper airway obstruction
 Nebulised adrenaline (5mL e.g. 5 ampoules of 1:1000).
 Consider need for advanced airway management if skills and equipment
are available.
For persistent hypotension/ shock  Give normal saline (maximum of 50mL/kg in first 30 minutes).
 Glucagon
 In adults, selective vasoconstrictors only after advice from an emergency
medicine/critical care specialist.
For persistent wheeze Bronchodilators: Salbutamol 8-12 puffs of 100microgram (spacer) or 5mg
(nebuliser).
Note: Bronchodilators must not be used as first line medication for anaphylaxis as
they do not prevent or relieve upper airway obstruction, hypotension or shock.
Corticosteroids: Oral prednisolone 1 mg/kg (maximum of 50 mg) or intravenous
hydrocortisone 5 mg/kg (maximum of 200 mg).
Note: Steroids must not be used as a first line medication in place of adrenaline as
the benefit of corticosteroids in anaphylaxis is unproven.

66. Actions after administration of adrenaline
• Observation of patient for at least 4 hours after last dose of adrenaline
• Relapse, protracted and/or biphasic reactions may occur and overnight
observation is strongly recommended if they:
• Had a severe or protracted anaphylaxis (e.g. required repeated doses of
adrenaline or IV fluid resuscitation), OR
• Have a history of severe/protracted anaphylaxis, OR
• Have other concomitant illness (e.g. severe asthma, history of arrhythmia,
systemic mastocytosis), OR
• Live alone or are remote from medical care, OR
• Present for medical care late in the evening.
• True biphasic reactions are estimated to occur following 3-20% of
anaphylactic reactions.

67. Advanced Acute Management of Anaphylaxis
• Supportive management (when skills and equipment available)
• Monitor pulse, blood pressure, respiratory rate, pulse oximetry, conscious state.
• Give high flow oxygen (6-8 L/min) and airway support if needed.
• Supplemental oxygen should be given to all patients with respiratory distress,
reduced conscious level and those requiring repeated doses of adrenaline.
• Supplemental oxygen should be considered in patients who have asthma, other
chronic respiratory disease, or cardiovascular disease.
• Obtain intravenous (IV) access in adults and in hypotensive children.
• If hypotensive:
• Give intravenous normal saline (20 mL/kg rapidly under pressure), and repeat bolus if
hypotension persists.
• Consider additional wide bore (14 or 16 gauge for adults) intravenous access.

68. Advanced Acute Management of Anaphylaxis
•During severe anaphylaxis with
hypotension, marked fluid
extravasation into the tissues can
occur: DO NOT FORGET FLUID
RESUSCITATION.

69. Advanced Acute Management of Anaphylaxis
• If there is inadequate response to IMI adrenaline or deterioration, start an
intravenous adrenaline infusion. IV adrenaline infusions should only be
given by, or in liaison with, an emergency medicine/critical care specialist.
• The protocol for 1,000 mL normal saline is as follows:
• Mix 1 mL of 1:1,000 adrenaline in 1,000 mL of normal saline.
• Start infusion at ~5 mL/kg/hour (~0.1 microgram/kg/minute).
• If you do not have an infusion pump, a standard giving set administers ~20
drops per mL; therefore, start at ~2 drops per second for an adult.
• Titrate rate up or down according to response and side effects.
• Monitor continuously – ECG and pulse oximetry and frequent non-invasive
blood pressure measurements as a minimum to maximise benefit and
minimise risk of overtreatment and adrenaline toxicity.

70. Advanced Acute Management of Anaphylaxis
• Assess circulation to reduce risk of overtreatment
• Monitor for signs of overtreatment (especially if respiratory distress or
hypotension were absent initially) – including pulmonary oedema, hypertension.
• In this setting (anaphylaxis) it is recommended that if possible a simple palpable
systolic blood pressure (SBP) should be measured:
• Attach a manual BP cuff of an appropriate size and find the brachial or radial pulse.
• Determine the pressure at which this pulse disappears/reappears (the "palpable" systolic BP).
• This is a reliable measure of initial severity and response to treatment
• Measurement of palpable SBP may be more difficult in children.
• Note: If a patient is nauseous, shaky, vomiting, or tachycardic but has a normal or
elevated SBP, this may be adrenaline toxicity rather than worsening anaphylaxis.

71. Advanced airway management
• Oxygenation is more important than intubation.
• Always call for help from the most experienced person available.
• If airway support is required, first use the skills you are most familiar with (e.g.
jaw thrust, Guedel or nasopharyngeal airway, bag-valve-mask with high flow
oxygen attached). This will save most patients, even those with apparent airway
swelling (these patients have often stopped breathing due to circulatory collapse
rather than airway obstruction and can be adequately ventilated with basic life
support procedures).
• DO NOT make prolonged attempts at intubation - remember the patient is not
getting any oxygen while you are intubating.
• If unable to maintain an airway and the patient's oxygen saturations are falling,
further approaches to the airway (e.g. cricothyrotomy) should be considered in
accordance with established difficult airway management protocols. Specific
training is required to perform these procedures.

72. Overwhelming anaphylaxis (cardiac arrest)
• Massive vasodilatation and fluid extravasation.
• Unlikely that IMI adrenaline will be absorbed in this situation due to poor
peripheral circulation.
• Even if absorbed, IMI adrenaline on its own may be insufficient to
overcome vasodilatation and extravasation.
• Need both IV adrenaline bolus (cardiac arrest protocol, 1 mg every 2-3
minutes) AND aggressive fluid resuscitation in addition to CPR (Normal
Saline 20mL/kg stat, through a large bore IV under pressure, repeat if no
response).
• Do not give up too soon - this is a situation when prolonged CPR should be
considered, because the patient arrested rapidly with previously normal
tissue oxygenation, and has a potentially reversible cause.

73. Emergency Care for Hyperkalemia
• Hyperkalemia is a common electrolyte disorder observed in the
emergency department.
• It is often associated with underlying predisposing conditions, such as
moderate or severe kidney disease, heart failure, diabetes mellitus, or
significant tissue trauma
• Such medications as inhibitors of the renin-angiotensin-aldosterone
system, potassium-sparing diuretics, nonsteroidal anti-inflammatory
drugs, succinylcholine, and digitalis, are associated with hyperkalemia

74. INTRODUCTION
• In 2018 Assoaciation “Kidney Disease: Improving Global Outcomes”
(KDIGO) Controversies Conference was held in Miami, Florida, USA, to
address potassium homeostasis and management of dyskalemia in
kidney disease
• The following text represents consensus suggestions based on a
review of the current literature and conference discussions of acute
hyperkalemia, with the goal of facilitating knowledge translation of
the key conclusions for health care professionals who work in
emergency departments (EDs) and in the acute care settings.

75. Definitions
• Hyperkalemia refers to an elevation in potassium concentration, although a
universal definition does not exist.
• Commonly, hyperkalemia is defined as a potassium concentration ≥5.5
mmol/l, but this cutoff varies depending on the individual laboratories and
differs between plasma and serum measurements
• There is not a common and standardized definition for grading of the
severity of hyperkalemia as mild, moderate, or severe; potassium
concentrations vary depending on whether serum or plasma potassium
was analyzed, with serum potassium concentrations usually being higher
than plasma concentrations
• So, acute hyperkalemia is defined as a potassium concentration above the
upper limit of normal, not known to be chronic.

76. Risk factors of Hyperkalemia

77. Severity of Hyperkalemia

78. Symptoms and consequences
of hyperkalemia
• While many patients are asymptomatic, hyperkalemia may manifest
clinically by muscle weakness.
• Paresthesias and muscular fasciculations in the arms and legs might
be earlier signs of hyperkalemia .
• Paralysis, cardiac conduction abnormalities, and cardiac arrhythmias
can be lethal.
• Usually, the muscle weakness associated with hyperkalemia is
ascending, starting at the legs and progressing to the trunk,
sometimes resembling Guillain–Barré syndrome

79. ECG – changes of hyperkalemia
• The cardiac manifestations of hyperkalemia are caused by its
depolarizing effects on the heart muscle cells and are usually
progressive
• Tall, peaked T waves can, however, be early ECG signs of hyperkalemia
• Decreased amplitudes of the P waves, prolonged PR interval, and
widening of the QRS complex are also sometimes observed, caused
by a diminished sodium influx into the cardiac myocytes
• The classic ECG pattern of hyperkalemia : severe QRS broadening and
fusion of the QRS complex with broadened ST-T segments

80. ECG patterns depending of K concentration

81. Important!
• It is important to note that ECG changes may not correlate closely
with serum potassium concentration or be useful in predicting
outcomes.
• However, recently, computerized-analysis algorithms have been
shown to be able to diagnose hyperkalemia from the ECG and may in
future have a role in rapid diagnosis, especially in patients with
chronic kidney disease, heart failure, or patients otherwise at risk for
development of this serious electrolyte disorder

82. Management of acute hyperkalemia in the ED
• Physical examination and history taking : medical history along with
history of previous medical conditions may help to assess the cause of
hyperkalemia.

83. Management of acute hyperkalemia in the ED
• Monitoring : continuous ECG monitoring, interval blood pressure
monitoring at a frequency appropriate to the clinical context, and
measurement of oxygen saturation should be established in patients
with hyperkalemia
• The fact that severe hyperkalemia may not necessarily be associated
with ECG changes and that hyperkalemia can lead to ‘atypical’ ECG
changes under certain circumstances must always be kept in mind .
Therefore, one should put all hyperkalemic patients on continuous
monitoring even if no typical ECG changes appear initially.

84. Treatment of hyperkalemia
1.Cellular membrane stabilization
• Intravenous calcium salts should be administered immediately in
hyperkalemic patients presenting with ECG changes suggesting
hyperkalemia
• It is crucial to note that the concentration of calcium is approximately three
times higher in calcium chloride than in calcium gluconate (6.8 mmol
Ca2+ per 10 ml of 10% calcium chloride vs. 2.3 mmol Ca2+ per 10 ml/10%
calcium gluconate)
• Thus, to administer the same amount of calcium to the patient one has to
use 30 ml of 10% calcium gluconate compared with 10 ml of 10% calcium
chloride.
• The European Resuscitation Council recommends use of 10 ml 10% calcium
chloride over 2–5 minutes in hyperkalemic patients with ECG changes

85. 1.Cellular membrane stabilization - continue
• Calcium prevents ventricular fibrillation/tachycardia by stabilizing the
cardiac cell membrane and is effective within 1–3 minutes after
administration [2]. Another dose can be administered within 5–10
minutes if no effect is seen, and repeated doses may be necessary if
cardiac abnormalities resolve then recur.
• If the potassium concentration is known but an ECG or placement on
a monitor is not immediately possible, we suggest giving calcium to all
patients with potassium concentration above 6.5 mmol/l

86. 2. Potassium shift to the intracellular
compartment
• Since administration of calcium salts does not result in a lowering of potassium
concentrations, other measures have to be taken to shift potassium from the
extracellular to the intracellular compartment, including use of insulin and β-adrenergic
agonists.
• Because of the risk of hypoglycemia, blood glucose concentrations should be closely
monitored. With glucose concentrations greater than 200 mg/dl (11.1 mmol/l), insulin
may be given without additional glucose
• Use of 10 mg salbutamol via nebulizer results in a significant reduction of potassium at a
peak of 120 minutes after application (90 minutes for 20 mg). The effects of salbutamol
and insulin are potentially additive and are currently under investigation
• Sodium bicarbonate activates the Na+-K+-pump and corrects an underlying metabolic
acidemia, potentially resulting in a lowering of serum potassium values [65], but data on
its effectiveness are conflicting [66]. We suggest using sodium bicarbonate only in
patients with metabolic acidemia who are expected to tolerate the sodium load involved.

87. 3. Potassium elimination
• Potassium-binding agents, dialysis and loop diuretics, are the only means
to remove potassium from the body
• Loop diuretics are commonly used in management of acute hyperkalemia;
however, to date, Loop diuretics are likely useful in hyperkalemic patients
with volume overload, such as in heart failure, and potentially useful after
fluid resuscitation in other patients.
• Novel potassium binders such as patiromer and sodium zirconium
cyclosilicate have recently been approved with promising results in
eliminating potassium
• Dialysis eliminates potassium from the blood in patients with
hyperkalemia. We recommend nephrology consultation in all patients
presenting to the ED with hyperkalemia and receiving dialysis therapy

88. 4. Reassessment
• Frequent assessment of potassium concentrations is indicated in patients with
acute hyperkalemia. Because the onset of action of potassium-shifting agents
insulin-glucose and β-adrenergic agonists is 30–60 minutes, a reevaluation of
potassium can be performed at 60 minutes after administration
• Since these medications do not excrete potassium but only shift it to inside the
cell, a recurrence of hyperkalemia is expected and therefore reevaluation is
crucial. Rebound towards higher values may occur at 2–3 hours if potassium has
not been eliminated from the body during that period
• Additionally, blood glucose should be checked in patients receiving insulin-
glucose because of the risk of hypoglycemia.
• The duration of frequent monitoring of potassium concentration, continuous
cardiac monitoring, and frequent blood pressure monitoring will depend upon
the severity of the hyperkalemia, the severity of its manifestations, the likelihood
of rebound, and the patient’s overall clinical context and response to treatment.

89. Treatment algorithm for management of acute
hyperkalemia in the emergency department.

90. Hypertensive Emergencies.
Pathogenesis
• Hypertensive crisis - a sharp increase in blood pressure due to spasm
of arterioles - can occur at any stage.
• Morphological changes during a crisis:
1)Spasm of arterioles: corrugation and destruction of the basement
membrane of the endothelium with its peculiar arrangement in the
form of a stockade.
2) Plasma impregnation.
3)Fibrinoid necrosis of the arteriolar wall.
4)Thrombosis.
5) Diapedetic hemorrhages.

91. Hypertensive Emergencies
Classification
• 75 % of Hypertensive crises are uncomplicated
• 25 % are complicated
Complications of Hypertensive Crises
- cerebral strokes ( ischemic or/and hemorrhagic)
- acute cerebral unsufficiency
- acute pulmonary edema
- acute coronary syndrome
- aortic dissection
- eclampsia

92. Emergency treatment of Hypertensive Crisis
• Uncomplicated HC : gradual decrease 20-25 % of blood pressure
level within 2-6 hours with a subsequent selection of a constant
antihypertensive therapy (oral drugs)
• Complicated HC : rapid decrease 15-25 % of blood pressure level
within 30 to 120 min with parenteral medications.
Then during next 2-6 hours the blood pressure level should slowely
get down up to 160/100 mmHg.