Cardiovascular emergencies are life-threatening disorders that must be recognized immediately to avoid delay in treatment and to minimize morbidity and mortality. Patients may present with severe hypertension, chest pain, arrhythmia, or cardiopulmonary arrest

1. Cardiovascular Emergencies

2. Pay attention
I am not kidding
I am reading
“You” the distraction
I am heading

3. Tamponade :A prototype of cardiac
emergency
• Blood pressure 80/50 mm Hg
• Heart rate 135 beats per minute
• Neck veins were distended
• Heart sounds were muffled
• Electrocardiogram :Low-voltage complexes in
the limb and precordial leads and QRS
alternance

4. Bird’s eye view

5. CONTENTS
• DYSRHYTHMIA
• CARDIOPULMONARYARREST
• HYPERTENSION EMERGENCY
• ACUTE MYOCARDIAL INFARCTION
• ACUTE AORTIC DISSECTION
• CARDIACTAMPONADE
• Life-threatening disorders
• Must be recognized
immediately to avoid delay in
treatment and to minimize
morbidity and mortality

6. Cardiopulmonary arrest
• Sudden and unexpected loss of perfusing
pulsatile blood flow
• Cessation of cardiac mechanical activity
• It occurs as a result of a multitude of
cardiovascular, metabolic, infectious,
neurologic, inflammatory, and traumatic
diseases

7. Aetiology
5 H
• Hypovolemia
• Hypoxemia
• Hydrogen ion (acidosis)
• Hypo- or Hyperkalaemia
• Hypothermia
5T
• Tension pneumothorax
• Tamponade
• Toxins
• Thrombosis-ACS
• Thrombosis–Pulmonary

8. Abnormal electrolyte level
Hyperkalaemia Hypokalaemia

9. Short QT in hyper and Long QT in Hypo
Hypercalcaemia Hypocalcaemia

10. The
endpoints
of CPA
Pulseless ventricular
tachycardia (VT)
Ventricular fibrillation
(VF)
Pulseless electrical
activity or asystole

11. VT andVF

12. VT/VF
• EMS-treated out-of-hospital cardiac arrests, 23% -VF/VT
• Early bystander cardiopulmonary resuscitation (CPR) and immediate
defibrillation is extremely useful
• Increased use of automated external defibrillators by EMS, businesses, and
airports for patients withVT orVF has improved survival
• Without defibrillation, mortality fromVT,VF, or both increases by
approximately 10% / min

13. Diagnosis and therapy
• Call EMS[108]
• Perform basic life support (CPR)
• Early defibrillation if indicated
• Advanced cardiac life support, such as
intubation, establishment of intravenous (IV)
access, and transfer to a medical center or
intensive care unit.

14. The new changes are as follows
• Changing the Airway (A) – Breathing (B) – Circulation (C) sequence to C-A-
B[2010 American HeartAssociation guidelines ]
•

15. • "Look, listen and feel" has also been removed
• Quality of CPR
• Professional healthcare rescue teams

16. PulselessVT orVF
• Early CPR
• ACLS if required
• Rectify 5 H's and 5T’s

17. On arrival to an unwitnessed cardiac arrest or
downtime longer than 4 minutes
• 5 cycles (~2 min) of CPR
• Each cycle is 30 compressions at a rate of ~100 compressions per minute) are to be
initiated before evaluation of rhythm
•

18. If the cardiac arrest is witnessed or downtime
is shorter than 4 minutes
• One shock may be administered immediately if the patient is inVF or
pulselessVT followed by five cycles of CPR.

19. If the patient is inVF or pulselessVT If the
patient is inVF or pulselessVT
• Shock the patient once using 200 J [Biphasic ]

20. • Resume CPR immediately after attempted defibrillation
• CPR should be started with beginning with chest compressions
• Rescuers should not interrupt chest compression to check circulation (e.g.,
evaluate rhythm or pulse) until five cycles or 2 minutes of CPR have been
completed.

21. If there is persistent or recurrentVT orVF
despite several shocks and cycles of CPR
• Secondary ABC survey
• Assessments and pharmacologic therapy
• Epinephrine (1 mg IV push, repeated every 3-5 min)
• Vasopressin (a single dose of 40 U IV, one time only).

22. Antiarrhythmics for persistent or recurrent
pulselessVT orVF
• Use antiarrhythmics for persistent or recurrent pulselessVT orVF
• Amiodarone, lidocaine, magnesium, and procainamide
• Resume CPR and attempts to defibrillate
• .

23. If spontaneous circulation returns
• Start immediate post-cardiac arrest care
• optimization of oxygenation and ventilation with emphasis on avoiding
hyperventilation
• Treating hypotension by starting vasopressor infusion or inserting intra-aortic balloon
pump
• Neurologic status and starting induced hypothermia if indicated
• Need for coronary reperfusion if high suspicion for acute coronary syndrome

24. Pulseless
electrical
activity or
asystole
Assess the patient and begin chest compressions
immediately.
Assess
Administer epinephrine (1 mg IV push repeated every 3-5
min). Consider transcutaneous pacing if asystole.
Administer
Conduct a secondary ABC survey and consider reversible
causes (5 H's and 5T's).Conduct
Resume immediate post-cardiac arrest care if there is a
return of spontaneous circulation as above.
Resume

25. Bradycardia

26. • Heart rate <50/ minute
• Rectify 5 H's and 5T's
• Check for serious signs of low cardiac output due to bradycardia such as cyanosis,
hypotension, altered mental status, or acute heart failure
• If serious signs or symptoms are present, begin the following intervention
sequence:
• Atropine, 0.5 mg, up to a total of 3 mg IV
• Transcutaneous /IV pacing

27. • Dopamine, 5 to 20 µg/kg/min
• Epinephrine, 2 to 10 µ/min
• Isoproterenol, 2 to 10 µ/min

28. Advance
care for
brady
Glucagon for beta-blocker
toxicity, calcium infusion for
calcium channel blocker
toxicity
If no serious signs or
symptoms are present,
evaluate for a type II second-
degree atrioventricular block
or third-degree
atrioventricular block.
If one of these types of heart
block is present, prepare for
transvenous pacing.
Resume immediate post-
cardiac arrest care if there is
a return of spontaneous
circulation as above.

29. Hypertensive
emergency
A hypertensive
emergency is sudden
rise of BP to >180/120
Accompanied by end-
organ compromise

30. End-organs
• Acute renal failure
• Ocular involvement :retinal exudates, hemorrhages, or papilledema
• Encephalopathy
• Acute stroke or intracranial hemorrhage
• Acute myocardial infarction
• Aortic dissection
• Eclampsia

31. CAUSES
• ESSENTIAL HYPERTENSION
• Renal causes
• Renal artery stenosis
• Glomerulonephritis
• Vascular causes
• Vasculitis
• Hemolytic-uremic syndrome
• Thrombotic thrombocytopenia purpura
• Pregnancy-related causes
• Preeclampsia
• Eclampsia
• Pharmacologic causes
• Sympathomimetics
• Clonidine withdrawal, beta blocker withdrawal
• Cocaine
• Amphetamines
• Endocrine causes
• Cushing's syndrome
• Conn's syndrome

32. • Pheochromocytoma
• Renin-secreting adenomas
• Thyrotoxicosis
• Neurologic causes
• Central nervous system trauma
• Intracranial mass
• Autoimmune cause
• Scleroderma renal crisis

33. Prevalence
• The prevalence of hypertension rises substantially with increasing age
• Less than 1% of patients with primary hypertension progress to
hypertensive crisis

34. Pathophysiology
• Any syndrome that produces an acute rise in blood pressure may lead to a hypertensive crisis. Cerebral
vasomotor autoregulation is a key facet of a patient's symptomatic presentation. Patients without chronic
hypertension generally develop hypertensive crises at a lower blood pressure than those with chronic
hypertension.
• An initial rise in vascular resistance mediated by vasoconstrictors such as angiotensin II, acetylcholine, or
norepinephrine is responsible for the acute increase in blood pressure.This cascade exceeds the
vasodilatory response of the endothelium, mediated primarily by nitric oxide
• Mechanical destruction of the endothelium by shear stress leads to further vasoconstriction, platelet
aggregation, inflammation, and subsequent blood pressure elevation.The rate at which this occurs
determines the rate of increase in systemic vascular resistance as well as the acuity of a patient's
presentation.

35. • Understanding autoregulation is key to the safe management of
hypertensive crises. In patients with chronic hypertension, the vascular bed
auto-regulates at higher blood pressure ranges compared with those with
newly diagnosed hypertension.Therefore, blood pressure should not be
aggressively lowered in those with chronic hypertension, in whom a SBP of
130 mm Hg, for example, may cause end-organ hypoperfusion.

36. Clinical evaluation
• Symptoms :Headache, blurred vision, confusion, chest pain, shortness of breath,
back pain (e.g., aortic dissection), seizures, and altered consciousness
• Physical examination
• fundoscopic, neurologic, and cardiovascular examinations, with emphasis on the presence
of congestive heart failure and bilateral upper extremity blood pressure measurements.
• Laboratory evaluation
• complete blood count with differential and smear evaluations, measurements of
electrolyte, blood urea nitrogen, and creatinine levels, and electrocardiography, chest
radiography, and urinalysis.

37. Treatment
• All patients with end-organ involvement should be admitted for intensive
monitoring and have an arterial blood pressure line placed
• Pharmacologic therapy
• IV vasodilator therapy to achieve a decrease in mean arterial pressure (MAP) of 20% to
25% or a decrease in DBP to 100 to 110 mm Hg within the first 24 hours is
recommended. Decreasing the MAP and DBP further should be done more slowly, over
a period of days, because of the risk of decreasing perfusion of end organs. Several
drugs have proved beneficial in achieving this goal

38. IntravenousVasodilatorTherapy for
Hypertensive Crisis

39. • In cases of marked catecholamine level elevation, large doses of IV beta-
blockers may be required to achieve blood pressure reduction. An exception
to this rule is the treatment of cocaine-induced hypertension, for which
beta-blockers can induce unopposed alpha-mediated vasoconstriction, so
direct-acting vasodilators and benzodiazepines are instead the mainstays of
therapy.

40. • Type A dissection : Reduction in shear stress is best achieved with IV beta
blockade, SNP and Surgery
• IV bolus hydralazine therapy must be monitored because sudden
hypotension
• IV magnesium: Eclampsia

41. Antihypertensive therapy in the context of
ischemic stroke
• Antihypertensive medications are generally not used during the first 24
hours, as long as the SBP does not exceed 220 mm Hg, and the DBP does
not exceed 120 mm Hg.This is because maintenance of a moderately-high
cerebral perfusion pressure theoretically could confer neurological benefits
• Pients treated with recombinant tissue plasminogen activator, blood
pressure should be controlled (SBP ≤185 mm Hg and DBP ≤105 mm Hg) to
reduce the risk of hemorrhagic conversion

42. Aortic dissection
• Aortic dissection is a tear of the aortic intima that allows the shear forces of blood
flow to dissect the intima from the media and, in some cases, penetrate the
diseased media with resultant rupture and hemorrhage
• Site of dissections
• 65% of dissections originate in the ascending aorta
• 20% in the descending aorta
• 10% in the aortic arch
• 5% in the abdominal aorta

43. Classification
• chronicity
• acute :<2 weeks
• Chronic:>2 weeks
• mortality peaks at 80% after 2 weeks and then
levels off

44. Aetiology
• Aging
• hypertension
• Marfan syndrome
• Ehlers-Danlos syndrome
• Loeys-Dietz syndrome
• bicuspid aortic valve
• coarctation, andTurner's syndrome
•
• Pregnancy : increased blood volume, cardiac
output, and shear forces on the aorta. In
women younger than 40 years, 50% of
dissections occur in the peripartum period
• Iatrogenic trauma from catheters or intra-
aortic balloon pumps may initiate dissection
between the aortic intima and media
• Blunt trauma or acceleration-deceleration
injury, as can occur in motor vehicle accidents

45. Clinical presentation
• “Tearing" or "ripping" in nature of pain
• ACS
• TAMPONADE
• SHOCK
• ALI
• PARAPLEGIA

46. • Chest radiographs- widened mediastinum or loss of the demarcation of the
aortic knob, pleural effusion, or pulmonary edema.Importantly, a normal
chest radiograph does not rule out aortic dissection
• The electrocardiogram (ECG) : left ventricular hypertrophy, ST depression,
T wave inversion, or ST elevation when the coronary arteries are involved.
The right coronary ostium is involved in 1% to 2% of aortic dissection cases,
leading to an inferior myocardial infarction.

47. Diagnosis
• It is essential to recognize several key signs in the imaging of aortic dissection, because they dramatically affect treatment and outcome:
• Involvement of the ascending aorta
• Location of dissection flap, intimal tear and the major vessels involved
• Presence of pericardial effusion or cardiac tamponade
• Involvement of coronary ostia
• The sensitivity of computed tomography angiography (CTA) for detecting aortic dissection is approximately 83% to 100%, and its specificity
ranges from 87% to 100%, depending on the study.35,36 In the current age of ECG-gated CTA, the sensitivity and specificity for detecting
dissections approaches 100%, and thus it is the diagnostic imaging modality of choice. Transesophageal echocardiography has a sensitivity
of approximately 98%; however, its lower specificity of 77% to 97%, reflects differences in operator experience.30,36 Magnetic resonance
imaging has a sensitivity and specificity of approximately 98% for detection of dissection but its lack of portability, limited access, and long
duration of imaging make this a less favorable option in the care of acute aortic dissection.37 Choice of testing should be based on the
medical center's expertise, hemodynamic stability of the patient, and access to the imaging modality.35-37

48. Treatment
• Surgery
• Surgical therapy is the best option for acute aortic dissection involving the ascending aorta. Studies have shown that delaying surgical intervention, even to carry out
left heart catheterization, aortography, or both, results in worse outcomes.38-40 Mortality increases by 1% per hour while waiting for surgery. Surgical repair in
patients with type B dissection is generally reserved for those with end-organ compromise or those who do not respond to medical therapy.
• Medical therapy
• Medical therapy should be initiated in all patients with acute dissection. Reductions of shear force and blood pressure should be the primary goals. Beta-blockers
should be given intravenously and titrated to the desired effect. In our institution, we typically start by using boluses of IV metoprolol to achieve a heart rate of 50 to
60 beats/min, which may require very high doses of 200 to 1,000 mg. We then add SNP if needed because of its rapid onset and ease of titration, aiming for a MAP of
65 to 75 mm Hg.
• In the hypotensive patient, diagnoses of pericardial tamponade, aortic rupture, aortic insufficiency, myocardial infarction, or a combination of these should be
suspected and tested for. Volume replacement and early surgical intervention should be pursued. Pericardiocentesis should be avoided if tamponade is present,
because immediate surgical intervention is the therapy of choice. If hypotension persists, norepinephrine and phenylephrine are the vasopressors of choice because of
their limited effects on increasing cardiac contractility. Endovascular stenting, a rapidly growing field, remains investigational in this acute setting and is sometimes
used in very high-risk surgical patients with type B aortic dissections or aneurysms.

49. Acute pulmonary oedema
• Cardiogenic pulmonary edema results from an absolute increase in left atrial
pressure, with resultant increases in pulmonary capillary and venous
pressures. In the setting of normal capillary permeability, this increased
pressure causes extravasation of fluid into the alveoli and overwhelms the
ability of the pulmonary lymphatics to drain the fluid, thus impairing gas
exchange in the lung

50. Aetiology and pathophysiology
• Left ventricular systolic dysfunction, left ventricular diastolic dysfunction, and obstruction of the left atrial outflow tract
are the primary causes of increased left atrial pressure. Left ventricular systolic dysfunction is the most common cause of
cardiogenic pulmonary edema.41This dysfunction can be the result of coronary artery disease, hypertension, valvular
heart disease, cardiomyopathy, toxins, endocrinologic or metabolic causes, or infections.
• Diastolic dysfunction results in impaired left ventricular filling and elevation in left ventricular end-diastolic pressure. In
addition to myocardial ischemia, left ventricular hypertrophy, hypertrophic obstructive cardiomyopathy, and infiltrative
or restrictive cardiomyopathy are all causes of diastolic dysfunction.
• Left atrial outflow obstruction is often a result of valvulopathy, such as mitral stenosis or mitral regurgitation, but also can
be caused by tumors (atrial myxoma), dysfunctional prosthetic valves, thrombus, and cor triatriatum. It is imperative to
distinguish between mitral regurgitation and mitral stenosis, given their very different treatments.

51. Diagnosis
• Pulmonary edema is diagnosed by the presence of various signs and symptoms, including tachypnea, tachycardia,
crackles (reflecting alveolar edema), hypoxia (secondary to alveolar edema), and the S3 or S4 heart sounds, individually or
in combination. Additionally, if hypertension is present, it may represent diastolic dysfunction, decreased left ventricular
compliance, decreased cardiac output, and increased systemic vascular resistance. The presence of increased jugular
venous pressure indicates increased right ventricular filling pressure secondary to right ventricular or left ventricular
dysfunction. Finally, the presence of peripheral edema indicates a certain degree of chronicity to the patient's condition.
• Laboratory data associated with pulmonary edema include hypoxemia on arterial blood sampling and a chest radiograph
showing bilateral perihilar edema and cephalization of pulmonary vascular marking. Cardiomegaly, pleural effusion, or
both may be present.Two-dimensional transthoracic echocardiography is usually helpful in the acute setting to assess
biventricular size and function, to identify valvular stenosis or regurgitation, and to determine the presence or absence of
pericardial pathology. The ECG may reflect ongoing ischemia, injury, tachycardia, and atrial or ventricular hypertrophy. In
many cases, differentiating cardiogenic and noncardiogenic pulmonary edema can be challenging and requires the
insertion of a pulmonary artery catheter to measure the pulmonary capillary wedge pressure

52. Treatment
• The pharmacologic agents most commonly used in the treatment of acute
pulmonary edema are nitroglycerin, SNP, and diuretics.45
• Nitroglycerin acts immediately to decrease preload and afterload.46 It should be
used for the management of patients with pulmonary edema who are not
hypotensive. Sublingual administration allows rapid delivery, which is often
required to decrease preload. IV administration of nitroglycerin also should be used
in the nonhypotensive patient and, based on symptoms, titrated to a MAP of
approximately 70 to 75 mm Hg.

53. • SNP is an effective vasodilator that is often required for the treatment of the hypertensive
patient with pulmonary edema.47 Due to the rapid and potent effects of SNP, its use requires
continuous invasive monitoring of arterial blood pressure.The issues of methemoglobinemia,
cyanide, and thiocyanate toxicity rarely become significant, but since patients receiving
continuous infusions will often develop tachyphylaxis—a progressive resistance to the drug's
effects—frequent blood testing is necessary. SNP should be used with caution in the setting of
hepatic dysfunction, since the liver is responsible for transformation of the cyanide radical into
thiocyanate. Patients with renal dysfunction will tend to accumulate thiocyanate more rapidly
than those with normal kidney function, since thiocyanate is excreted in the urine. Finally,
through its effects on coronary arteriolar resistance vessels, SNP can potentially cause coronary
"steal," drawing blood flow away from ischemic myocardium. We generally co-administer
nitroglycerin along with SNP to dilate conductance vessels and lessen this theoretical risk.

54. • V diuretics are most helpful for the treatment of volume overload in chronic
congestive heart failure.Their vasodilative and diuretic properties also are useful in
the management of pulmonary edema. Diuretics should be used with caution in
the euvolemic patient to avoid compromising cardiac output and oxygen delivery.
• IV morphine can be used in certain select patients to decrease their "air hunger,"
anxiety, and sympathetic tone, which can in turn help reduce their afterload.

55. SUMMERY

56. Cardiopulmonary arrest
• Address the causes
• Prompt resuscitative efforts
• The 2010 American Heart Association guidelines have proposed changes
that make chest compressions a priority before assessment of airway and
breathing, in order to minimize time delays

57. Hypertensive emergency
• Protect End-organs
• Intensive monitoring
• Continuous arterial blood pressure
• Compelling treatment

58. Aortic dissection
• Stanford type A requires emergent surgery
• Type B is generally managed medically unless
end-organ damage can be demonstrated

59. Acute pulmonary edema
• Improving oxygen delivery to end organs
• Decreasing myocardial oxygen consumption
• Decreasing preload
• Decrease afterload

60. Thank you