This document provides information about cardiac emergencies presented by Mrs. Shalini, an Assistant Professor of Nursing. It defines cardiac emergencies and lists the learning objectives. The major cardiac emergencies discussed include acute myocardial infarction, heart failure, sudden cardiac death, cardiac tamponade, hypertensive emergencies, and dysrhythmias. For each emergency, the document provides definitions, causes, signs and symptoms, diagnostic tests, management, and nursing care considerations.

1. MRS.SHALINI
MSC (N),MEDICAL SURGICAL NURSING
ASSISTANT.PROFESSOR
GANGA COLLEGE OF NURSING
COIMBATORE

2. CARDIAC EMERGENCY
PRESENTED BY
MRS.SHALINI, MSC(NURSING),
ASST.PROFESSOR,
GANGA COLLEGE OF NURSING

3. At the end of the Lecture ,the students will be able to
1.Definecardiacemergencies
2.Compare the causes of various cardiac emergencies
3.Identify the signs and symptoms of various cardiac emergencies
4.Enumerate the diagnostic tests used for cardiac emergencies
5.Describe an assessment of patients with cardiac emergencies
6.Recognize the emergency management of cardiac emergencies

4.  Cardio vascular disease is the number one killer of
adults. Prompt recognition and initiation of
appropriate treatment can save lives during the
most deadly cardiac emergencies("Heart Disease
and Stroke Statistics",2013)
 Cardio vascular emergencies and symptoms are
one of the most common reasons for patients’
attendance in any emergency department(ED)

6.  1)AcuteMyocardialinfarction(AMI)
 2)Heartfailure(HF)
 3)Suddencardiacdeath(SCD)
 4)CardiacTamponade
 5)Hypertensiveemergencies
 6)Dysrhythmias

7. DEFINITION
•Myocardial Infarction(MI) or Heart attack
are terms used anonymously, but the preferred term
is MI
•MI is defined as cell death and necrosis
•Myocardial infarction occurs as a result of sustained
ischemia, causing a irreversible myocardial cell death
(necrosis).
•MI is usually caused by reduced or decreased blood
flow in a coronary artery due to rupture of an
atherosclerotic plaque and subsequent occlusion of
the artery by a thrombus

8.  Descriptions are used to further identify MI: the
type of MI (ST segment elevation myocardial
infraction STEMI and non-ST elevation MI NSTEMI
 Infarctions are usually described based on
location of damage (anterior, inferior, posterior, or
lateral wall)

9.  Atheroscleros is (causes luminal narrowing and
reduced blood flow)
 Eighty percent to 90% of all acute MI are
secondary to thrombus formation
 The three mechanisms that are primarily
responsible for acute reduction in O2 delivery to
the myocardium are
-Coronaryarterythrombosis
-Plaquefissureorhemorrhage
-Coronaryarteryspasm

10. Due to risk factor (Coronary atherosclerotic heart disease, coronary
thrombosis and embolism)
Decrease blood flow to coronary artery
Decrease myocardial oxygen supply and
ischemia
Stimulation of baroreceptor and sympathetic
receptors
Decrease myocardial contractility and
cardiac output

11. I Increase myocardial contractility and Heart
rate
Decrease diastolic filling and myocardial tissue
perfusion
Prolong ischemia of myocardial cell
Severe cellular damage and necrosis of cardiac
muscle
Myocardial infarction

12.  Chest pain
 Nausea
 Vomiting
 Diaphoresis

13.  History and physical examination
 12 lead ECG,
 Cardiac enzyme level
 Chest X-Ray,
 Serum cardiac markers,
 echocardiography,
 Scintigraphy
 CT angiography
ECG Changes for Acute MI

14.  Goal is early revascularization and reperfusion using either
fibrinolysis or primary angioplasty.
 Oxygen should be administered when blood oxygen saturation is
90% or if the patient is in respiratory distress
 Nitroglycerine:It is a coronary vasodilator and reduces
myocardial pre-load and after load
 Beta-blockers
 Calcium channel blockers(CCBs)
 ACE inhibitors
 Anti platelet therapy reduces progression
to acute infarction in patients with
non-AMIACS patients
 Anticoagulation

15. Reperfusion therapy
 Thrombolytics or primary Percutaneous coronary
intervention (PCI),increases the opportunity to salvage
ischemic myocardium
 Fibrinolytic therapy improves coronary flow,limits infarct
size and improves survival
- Initiated within 30minute(Door to needl etime)
- Not interventional cardiac catheterization lab
- Know the contraindication of fibrinolytic therapy
- Medication of fibrinolytic therapy
= Recombinant plasminogen activator (rPA)-
Reteplase
= Tissue plasminogen activator (tPA)-Alteplase
 Prefibrinolytic therapy care
 Post fibrinolytic therapy care

16. Emergency PCI (Percutaneous coronary intervention)
Percutaneous Transluminal
coronary angioplasty (PTCA)
Coronary Artery Stent

17.  Dysrhythmias (The most common complications
after an MI in 80% of MI cases)
 Ventricular aneurysm
 Ventricular septal defect
 Acute pulmonary edema
 Heart failure
 Cariogenic shock
 Papillary muscle dysfunction
 Pericarditis and cardiac tamponade

18.  Ineffective cardiac tissue perfusion related to coronary
artery occlusion
 Decrease Cardiac output related to impaired
contractility
 Acute chest pain related to decrease oxygen supply to
myocardial tissue
 Activity intolerance related to insufficient oxygenation
to perform activities of daily living
 Anxiety related to chest pain & threatening environment
 Ineffective coping related to threats to self esteem & lack
of significant support system
 Risk for injury (Bleeding) related to dissolution of
protective clots

19. Definition
 It is defined as the path physiologic
state in which the heart is not capable of
pumping sufficient supply of blood to meet the
body requirements or else requires elevated
ventricular filling pressures to accomplish this goal.
 The inability of the heart to pump sufficient blood to
meet the needs of the tissues for oxygen and
nutrients; signs and symptoms of pulmonary and
systemic congestion may or may not be present.

20. LEFT VENTRICULAR FAILURE RIGHT VENTRICULAR FAILURE
 -Tachypnea
 -Tachycardia
 -Cough,crackles
 -Hemoptysis
 -Cyanosis
 -Pulmonaryedema
 -Dyspnea orthopnea
paroxysmal nocturnal
dyspnea
 Peripheraledema
 Hepatomegaly,
splenomegaly
 Ascites,jugularvenousdiste
ntion
 -IncreasedCVP
 -Pulmonaryhypertension
 -Anorexia,weakness
 -Indigestion

21.  Stabilization of patient and resuscitation
 Identify the underlying and precipitating cause and
treat it,
 Control the symptoms and acute congestive state by
reducing the cardiac work load(reducing pre-and
after load),controlling excessive salt and water
retention and improving cardiac contractility

22.  Optimize cardio pulmonary function:-auscultate
breath sounds, administer O2, diuretics/vasodilators,
prepare for ET intubation and mechanical ventilation
and obtain daily weight
 Promote rest:-restrict activity and prescribe bed rest,
elevate the head end of the bed, monitor vital signs,
and activity intolerance.
 Pharmacologic therapy:-administer diuretics,
positive inotropes, vasodilators as ordered. Monitor
hemodynamic parameters and fluid restrictions
 Provide nutrition:-provides mall frequent meals.

23. Definition:
 SCD occur in patients with pre existing
ventricular dysfunction secondary to multi vessel
cardiac disease with or without history of MI
Risk factors:
 VT, VF, dilated cardiomyopathy, aortic stenosis, AV
block
Management:
 Anti dysrhythmic agents,internal cardioverter
defibrillator(ICD)

24. Definition
 A built-up of blood or other
fluid in the pericardial sac
puts pressure on the heart,
which may prevent it from
pumping effectively
 Pericardial layers
 •Visceral layer
 •Parietal layer
 •Fibrous pericardium

25. The common causes are;
 Bacterial /Mycobacterial
Fungal
 Hemopericardium
-Traumatic Iatrogenic
-Aortic Dissection
 HIV
 Uremia /Dialysis
associated
 Malignancy

27.  Tachycardia-Exceptions include
patients with bradycardia
during uraemia and patients
with hypothyroidism
 Tachypnea
 Jugular venous distension
 Quiet pre cordium with both
inspection and palpation
 Impure muffled heart sounds
 Rub
 Peripheral Cyanosis
 Beck Traid

28. Cardiac tamponade X –ray

29.  Oxygenation
 Increasing the volume may help only in patients with
Hypovolemic
 Bed rest and legelevation
 Inotropic drugs (Dobutamine)
 Mechanical ventilation with positive airway pressure
should be avoided in patients with tamponade,
because this further decreases cardiac output

30. Pericardiocentesis: The treatment of cardiac
tamponade is drainage of the pericardial contents,
preferably by needle paracentesis, with the use of
echocardiography or another type of imaging, such
as fluoroscopy or CT

31. In the Emergency Department hypertension presents as
one of the four varieties:
 Hypertensive emergency or crisis with acute end organ
ischemia
 Hypertensive urgency: Patients with poorly controlled
hypertension
 Mild hypertension
 Transient hypertension which is related to anxiety or
complaint
 Hypertensive crisis is characterized by arise in diastolic
BP to>120to130 mm Hg
 Only hypertension crisis requires treatment in the
emergency department within 90min of their
presentation

32. ETIOLOGY
 No history or non compliance to drug
 Acute renal failure
 Acute CNS events
 Drug induced hypertension
 Ingestion of tyramine containing food or beverages
during treatment with amonoamine oxidase
inhibitor (MAOI)
 Pregnancy induced eclampsia

33. CLINICAL MANIFESTATION
 CNS compromise
-headache, papilledema, coma
 CVScompromise
-angina ,MI
-Chestpain causes unstable angina, MI, aortic
dissection
-Acute heart failure-MI, severe HT
-Hypertension after vascular surgery-aortic
aneurysmectomy, carotid endarterectomy, CABG

34. DIAGNOSTIC TEST
 BP measurement in both arms, intra arterial line
monitoring
 12leadECG
MEDICAL MANAGEMENT
 Antihypertensive therapy
 Vasodilators-SNP, NTG, hydralazine
 Short acting beta blockers-betalol, esmolol
 IV ACE in hibitor
 IV Furosemide
 Hypertensive urgencies-calcium
channel blockers-nifedipine oral.
 Captoprilan ACE inhibitor,beta blocker.

35. Goal-To return the BP to normal
 Altered cerebral tissue perfusion related to
vasospasm or haemorrhage
 Altered myocardial tissue perfusion related to acute
myocardial ischemia
 Anxiety related to threat to biologic ,and social
integrity.

36. Dysrhythmias present in the emergency
department as chest pain, breathlessness,
palpitation,sweating, pre-syncope,syncope and thrombo
embolic complications
Definition:
An arrhythmiais an abnormality of rate,
regularity, or site of origin of the cardiac impulse or a
disturbance in conduction that causes an abnormal
sequence of activation.
-Irregular rhythm
-Abnormal Rate
-Conduction abnormality

37. Many MI patients experience
complications due to electrical dysfunction which
include bradycardia, bundle branch block, and heart
block.
Etiology of dysrhythmias in MI
 Tissue ischemia, hypoxemia
 Metabolic derangements
–acid base imbalances
 Electrolyteim balances
 Cardio myopathy
 Drugs

38.  Administer O2 to reduce myocardial hypoxia
 Administer bolus IV Lidocaine and infusion
 Correcting electrolyte and acid base imbalance

39.  History and physical examination
 ECG
 Ambulatory ECG recording: Holter recording
 Exercise ECG: tread milltest
 Trans-esophageal electro physiological study
 Invasive electrophysiological study(EPS)

40. DEFINITION
A run of three or more premature ventricular
contractions define VT. It is a life threatening dysrhythmia
because of decreased cardiac output and the possibility of
development of ventricular fibrillation (VF), which is a
lethal dysrhythmia
 FORMS OF VT: Monomorphic, polymorphic
 CLINICAL ASSOCIATION: VT is associated with MI, CAD,
significant electrolyte imbalances, cardiomyopathy, mitral
valve prolapse, long QT syndrome, drug toxicity, and CNS
disorders

41.  ECG Characteristics: ventricular rate is150 to 250 beats /minute,
rhythm may be regular or irregular. AV dissociation may be present
with p wave occurring independently of the QRS complex. The QRS
complex is distorted in appearance, with a duration >0.12 sec and with
the ST-T wave in the opposite direction of the QRS complex .The R-R
interval may be regular or irregular
 Clinical significance: VT can be stable (patient has a pulse) or
unstable (patient is pulseless). VT causes decreased cardiac out put
results in hypotension, pulmonary edema, decreased cerebral blood
flow, and cardio pulmonary arrest

42. Treatment:
 Identify the cause and
treat
 -If pulse is present IV
procainamide, sotalol,
amiodarone, or lidocaine
 -If Vt with out pulse-CPR
and rapid defibrillation
followed by
administration of
vasopressors and
antidysrhythmics

43. Definition:
VF is a severe derangement of the heart
rhythm characterized on ECG by irregular wave
forms of varying shapes and amplitude.
Clinical associations:
VF occurs in acute MI, myocardial ischemia,
and in chronic diseases such as HF and
cardiomyopathy. Other clinical associations are
accidental electrical shock, hyperkalemia, acidosis,
and drug toxicity.

44. ECG characteristics:
 HR not measurable, rhythm is irregular and chaotic,
the p wave is not visible, and the PR interval and the
QRS interval not measurable

45. Clinical significance:
VF results in an unresponsive, pulse less, and
apneic state. If not treated patient will die
Treatment:
immediate initiation of CPR and advanced
cardiac life support (ACLS) measures with the use of
defibrillation and definitive drug therapy

46. Definition
A systole represents the total absence of
ventricular electrical activity, occasionally p waves
are seen. Patients are unresponsive, pulse less and
apneic requires immediate treatment.
Clinical association:
Result of advanced cardiac disease, conduction
system disturbance or end stage HF

47. Clinical significance:
 Generally patient has a prolonged arrest and cannot be
resuscitated
Treatment:
 CPR with initiation of ACLS which includes definitive
drug therapy, intubation and possibly a transcutaneous
temporary pacemaker


48. Definition: no mechanical activity of the ventricles
and the patient has no pulse.The most common
cause include hypovolemia, hypoxia, metabolic
acidosis, hyper kalemia, or hypo kalemia,
hypothermia, drug over dose, cardiac tamponade,
MI,Tension pneumothorax, trauma and pulmonary
embolism. Treatment begins with CPR followed by
drug therapy (epinephrine) and intubation.
Atropine is used if the ventricular rate is slow.

49. Every patient diagnosed with life threatening
cardiac emergency like acute myocardial infarction,
SCD, HF, Cardiac tamponade, Dysrhythmias and
hypertensive emergencies should receive the
emergency care as early as possible including
oxygenation, ventilator support and appropriate
pharmacotherapy which would help in saving
patients life and preventing complications

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