This document discusses various cardiac emergencies including myocardial infarction, angina pectoris, congestive cardiac failure, sudden cardiac arrest, cardiac tamponade, and cardiogenic shock. It provides details on the causes, symptoms, diagnostic measures, and management of these conditions. Specifically, it describes angina pectoris as chest pain caused by partial blockage of the coronary arteries, acute myocardial infarction as damage to the heart muscle caused by a blockage of blood supply, and cardiac tamponade as a life-threatening condition where fluid builds up in the space between the heart muscle and the sac surrounding the heart. The document emphasizes the importance of early recognition, CPR, defibrillation and medications in managing cardiac arrest and

1. CARDIAC EMERGENCY
 Prepared by
 Asso.Prof Mr. Vijayreddy .b.v
 M.Sc(N),PGDHA,PGCDE
 Medical-Surgical Nursing dept.

2. CARDIAC EMERGENCY
Myocardial infarction,
Angina pectoris,
Congestive cardiac failure,
sudden cardiac arrest,
cardiac tamponade,
Cardiogenic shock.

3. Angina Pectoris
Coronary arteries
Partial blockage
producing chest pain
Area of decreased
blood supply

4. Acute Myocardial Infarction
Area of Infarct

5. CARDIAC TEMPONADE

6. Sudden cardiac death
 When the heart ceases to beat
effectively and breathing soon ceases, a
person is said to have experienced
sudden cardiac death (SCD).

7. CONTD..
 In order to meet the criteria for this
diagnosis, the critical circulatory collapse
must be;
1) Unexpected,
2) It must relate in some manner to heart
problems, and
3) It should occur with minimal warning or
a complete absence of prelude symptoms.

8. CARDIAC ARREST
Cardiac arrest, also known as
cardiopulmonary arrest or circulatory
arrest, is the end of normal
circulation of the blood due to failure
of the heart to contract effectively.
Medical personnel may refer to an
unexpected cardiac arrest as a sudden
cardiac arrest (SCA).

9. CAUSES
Coronary heart disease
Non-ischemic heart disease
Cardiomyopathy, cardiac rhythm
disturbances, hypertensive heart
disease, congestive heart failure

10. CONTD…
Non-cardiac
The most common non-cardiac causes:
trauma, non-trauma related bleeding
(such as gastrointestinal bleeding,
aortic rupture, and intracranial
hemorrhage), overdose, drowning and
pulmonary embolism

11. MANAGEMENT
Early recognition
Early CPR
Early defibrillation
Medications- This includes the use of
epinephrine, atropine, and amiodarone.
Vasopressin overall does not improve or
worse outcomes but may be of benefit in
those with a systole especially if used early

12. CARDIAC TEMPONADE

13. DEFINITION
Cardiac tamponade, also known as
pericardial tamponade, is an acute type
of pericardial effusion in which fluid
accumulates in the pericardium (the
sac in which the heart is enclosed).

15. CAUSES
 Pericardial
effusion

16. CONTD..
Pericarditis

17. OTHER POSSIBLE CAUSES
Heart tumors
Hypothyroidism
Kidney failure
Leukemia

18. CONTD..
Placement of central lines
Radiation therapy to the chest
Recent invasive heart procedures
Recent open heart surgery
Systemic lupus erythematous

20. MEANING
 Cardiogenic shock is characterized by a
decreased pumping ability of the heart
that causes a shock like state (i.e., global
hypo perfusion). It most commonly
occurs in association with, and as a direct
result of, acute myocardial
infarction(AMI).

21. Pathophysiology
AMI
↓
Dead myocardium does not contract
↓
Marked decrease in contractility
reduces the ejection fraction and
cardiac output.
↓

22. Increased ventricular filling pressures,
cardiac chamber dilatation
↓
Univentricular or biventricular failure
↓
Systemic hypotension and/or pulmonary
edema.

23. A systemic inflammatory response
syndrome
Myocardial infections
↓
Elevated levels of white blood cells, body
temperature, interleukins, and C-reactive
protein. Similarly, inflammatory nitric
oxide synthetase (iNOS) is also released
in high levels during myocardial stress.

24. CONTD…
↓
iNOS induces nitric oxide production,
which may uncouple calcium
metabolism in the myocardium
resulting in a stunned myocardium.
Additionally,
iNOS leads to the expression of
interleukins, which may themselves
cause hypotension.

25. Myocardial ischemia
↓
Decrease in contractile function
↓
Left ventricular dysfunction and decreased
arterial pressure
↓
Exacerbate the myocardial ischemia
↓
Severe cardiovascular decomposition.

26. Other Pathophysiologically
mechanisms
 Papillary muscle rupture leading to
acute mitral regurgitation (4.4%);
 ventricular septal defect (1.5%)
 wall rupture (4.1%) as a
consequence of AMI.

27.  Right ventricular (RV) infarct, by
itself, may lead to hypotension and
shock because of reduced preload
to the left ventricle.
 Cardiac tamponade may result as
a consequence of Pericarditis,
uremic pericardial effusion, or in
rare cases systemic lupus
erythematous.

28. Medications
 Calcium channel blockers may cause
profound hypotension with a normal or
elevated heart rate.
 Beta-blocking agents may also cause
hypotension with or without
bradycardia, or AV node block.

29. CONTD..
Nitroglycerin, Angiotensin-
converting enzyme inhibitors,
opiate, and barbiturates can all cause
a shock state and may be difficult to
distinguish from Cardiogenic shock.

30. Clinical manifestations
The physical examination findings are
consistent with shock.
Patients are in frank distress
profoundly diaphoretic with mottled
extremities
visibly dyspneic

31. A- Airway usually is patent initially.
B- Breathing may be labored, with
audible coarse crackles or wheezing.
C-Circulation is markedly impaired.
Tachycardia, delayed capillary refill,
hypotension, diaphoresis, and poor
peripheral pulses are frequent findings.

32. CONTD…..
Signs of end-organ dysfunction (eg,
decreased mental function, urinary
output) may be present.

33. Diagnostic measures
History collection
General physical examination
Initial vital sign assessment
Neck examination may reveal jugular
venous distention
LV dysfunction, characterized by
pulmonary edema, can be auscultated as
crackles with or without wheezing.

34. Careful cardiac examination may reveal
mechanical causes of Cardiogenic shock.
 Loud murmurs may indicate a valvular
dysfunction, whereas muffled heart
tones with jugular venous distention
and pulsus paradoxus may suggest
tamponade (Beck triad).

35. CONTD..
A gallop may also be heard. The
presence of an S3 heart sound is
pathognomonic of congestive heart
failure. The presence of pulmonary
edema increases the likelihood of
Cardiogenic shock in the setting of
hypotension.

36. Lab Studies
 No one test is completely sensitive,
laboratory studies are directed at the
potential underlying cause.
Following are assessed in cases of
suspected cardiac ischemia:

37. CONTD..
 Cardiac enzymes (eg, creatine kinase,
troponin, myoglobin)
 CBC
 Electrolytes
 Coagulation profile (eg, Prothrombin
time, activated partial
thromboplastin time)

38.  An ABG may be useful to evaluate acid-
base balance because acidosis .
 Elevated serum lactate level is an
indicator of shock.
 Brain Natriuretic peptide (BNP) may be
useful as an indicator of congestive heart
failure and as an independent prognostic
indicator of survival.
A low BNP level may effectively rule
out cardiogenic shock in the setting of
hypotension.

39. Imaging Studies
Portable chest radiograph
Overall impression of the cardiac size
Pulmonary vascularity
Coexistent pulmonary pathology
A rough estimate of Mediastinum and
aortic sizes

40. Other Tests
 ECG
Helpful if it reveals an acute injury
pattern consistent with an AMI
 Echocardiogram
*To reveal a kinetic or dyskinetic areas of
ventricular wall motion.
*To reveal surgically correctable
causes, such as valvular dysfunction and
tamponade.

41. MANAGEMENT
Pre hospital Care: aimed at minimizing any
further ischemia and shock.
All patients require intravenous access, high-
flow oxygen administered by mask, and
cardiac monitoring.
Twelve-lead electrocardiography, The ED
physician, can thus be alerted, and may
mobilize the appropriate resources.

42.  Emergency Department Care:
Aim: making the diagnosis, preventing
further ischemia, and treating the
underlying cause.
 coronary artery bypass is the treatments of
choice within 90 minutes of presentation;
however, it remains helpful, as an acute
intervention, within 12 hours of
presentation.
 If not immediately available, thrombolytic
should be considered which is the second
best.

43. Treatment begins with assessment
and management of the ABCs.
Airway should be assessed for patency.
Breathing evaluated for effectiveness
and increased work of breathing.
Endotracheal intubation and
mechanical ventilation is considered
in patients with excessive work of
breathing.

44. Positive pressure ventilation may improve
oxygenation but may also compromise
venous return, preload, to the heart. In any
event, the patient should be treated with
high-flow oxygen.
supporting myocardial perfusion and
maximizing cardiac output.
 Intravenous fluids should be provided to
maintain adequate preload, guided by
central venous pressure or pulmonary
capillary wedge pressure monitoring .

45. Pharmacotherapy
Aim: To reduce morbidity and to prevent
complications.
Intravenous vasopressors provide Inotropic
support increasing perfusion of the
ischemic myocardium and all body tissues.
Extreme heart rates should be avoided
because they may increase myocardial
oxygen consumption

46. 1. Dopamine may provide vasopressors
support. With higher doses, it has the
disadvantage of increasing the heart
rate and myocardial oxygen
consumption.
Dose:5-20 mcg/kg/min IV continuous
infusion.
 Increase by 1-4 mcg/kg/min q10-30min
to optimal response
 (>50% of patients have satisfactorily
responses with doses <20 mcg/kg/min)

47. 2.Dobutamine, inamrinone (formerly
amrinone), or Milrinone may provide
Inotropic support. In addition to their
positive Inotropic effects, inamrinone
and Milrinone have a beneficial
vasodilator effect, which reduces
preload and after load.
Dose: 5-20 mcg/kg/min IV
continuous infusion.

48. 3. Phosphodiestrase enzyme
inhibitors -improve cardiac output in
refractory hypotension and shock.
Milrinone and inamrinone (formerly
amrinone) may be used.
Loading dose: 50 mcg/kg IV over 10
min
Continuous infusion: 0.375-0.75
mcg/kg/min IV

49. 4.Natrecor (nesiritide)
Should be used with caution in the
setting of Cardiogenic shock because it
has been shown to cause hypotension.
5.Vasodilators
Smooth-muscle relaxants and vasodilators
that can reduce systemic vascular
resistance, allowing more forward flow
and improving cardiac output.

50. 6. Analgesics -- Pain control is essential
to quality patient care. It ensures
patient comfort and promotes
pulmonary toilet.
7. Natriuretic peptide
Nitrates and/or morphine excessive
use of either of these agents can
produce profound hypotension.
Neither of these options has been
shown to improve outcomes in
Cardiogenic shock

51. 8.Diuretics :Cause diuresis to decrease plasma
volume and edema and thereby decrease cardiac
output BP.
The initial decrease in cardiac output causes a
compensatory increase in peripheral vascular
resistance. With continuing diuretic therapy,
extracellular fluid and plasma volumes almost
return to pretreatment levels.
Peripheral vascular resistance decreases below
that of pretreatment baseline.
Lasix: 40-80 mg/d IV/IM

52.  Intra-aortic balloon pump (IABP)
recommended for Cardiogenic shock
not quickly reversed with
pharmacologic therapy.
 It is also recommended as a
stabilizing measure combined with
thrombolytic therapy when
angiography and revascularization
are not readily available.

53. oIABP reduces LV after load and
improves coronary artery blood flow.
oAlthough this procedure is generally
not performed in the ED, planning is
essential, and early consultation with a
cardiologist regarding this option is
recommended.
o Although complications may occur in
up to 30% of patients, extensive
retrospective data support its use.

54. NURSING DIAGNOSIS
 Decreased cardiac output related to shock
as manifested by increased diastolic BP,
tachycardia, dry mucous membrane, pallor,
cyanosis, cool and clammy skin.
 Fear and anxiety related to severity of the
condition as manifested by verbalization of
anxiety about condition and fear of death or
withdrawal with no communication,
increase in heart and respiratory rate.

55. CONTD..
High risk for organ dysfunction related
to decreased tissue perfusion.

56. THANK YOU