CARDIOVASCULAR EMERGENCIES

Erwin Azmar
Cardiology Division Dept of Internal Medicine
Faculty of Medicine University of Sriwijaya
2016
Cardiovascular emergencies

 Life-threatening
 Immediately recognized
 Avoid delayed treatment
 Minimize morbidity and mortality
Cardiac anatomy

9. Right Atrium
1.Left Anterior Descending
10. Right Ventricle
2.Left Circumflex
11. Left Atrium
3.Superior Vena Cava
12. Left Ventricle
4.Inferior Vena Cava
13. Papillary Muscles
5.Aorta
14. Chordae Tendineae
6.Pulmonary Artery
15. Tricuspid Valve
7.Pulmonary Vein
16. Mitral Valve
8.Right Coronary
17. Pulmonary Valve
Aortic Valve (Not pictured)
Etiology and underlying diseases
 Congenital heart diseases
 Valvular heart diseases
 Hypertensive heart disease
 Coronary artery disease
 Cardiac dysrhythmia
 Trauma, myopathy, infection, tumor, toxin
 Vascular diseases
 Systemic diseases
Diagnostic
 History : chest pain, shortness of breath,
palpitation, racing heart beat, syncope, dizziness,
epigastric pain, leg pain, vomitus, convulsion,
numbness.
 Physical exam : BP HR RR PR consciousness,
Temperature, pallor, sweating, heart sounds,
pulmonary sounds, JVP, pulsation, struma, vessel
dilation.
 Modalities : ECG, Echo, Imaging, Blood, cardiac
biomarkes, urinalysis.
Acute cardiac emergencies
 Cardiac arrest : anaphylactic, electrocution, hypothermia, drug overdose,
pregnancy
 Cardiogenic shock
 Peri-arrest arrhythmia : bradycardia, broad-complex tachycardias, narrow
complex tachycardias
 Cardiac tamponade : pericardial effusion
 Valve and Septal Rupture : after AMI, trauma
 Sinus of valsava rupture : congenital aneurysm, infective endocarditis
 Acute aortic dissection
 Acute prosthetic valve rupture
 ACS
 Acute cardiac failure
 Hypertensive emergency
 Vascular thrombosis
Emergency cardiological procedures

 Central venous access

 Pulmonary artery catheterization
 Temporary cardiac pacing
 Pericardial aspiration
 Intra aortic ballon pump insertion
Intra Aortic Balloon Pump
 Indications for IABP therapy
Increase coronary artery
perfusion Reduction in afterload

 Refractory unstable angina  Ventricular failure

 Impending infarction unresponsive to
 Acute myocardial infarction pharmacological therapy
 Support during PCI  Cardiogenic shock
 Complications post myocardial  Post-surgical myocardial
infarction (VSD, papillary muscle dysfunction/low cardiac
rupture, acute mitral regurgitation) output syndrome
 Myocardial contusion  Bridge to cardiac
 Ischaemia related intractable transplantation
ventricular arrhythmias  Bridge to other form of
 Bridge to cardiac surgery circulatory support
Cardiac pacing
Central venous accsess
Pulmonary artery catheterization
Pericardial aspiration
CARDIOGENIC SHOCK
Cardiogenic Shock

 Hypotension and end-organ hypoperfusion as a result

of low cardiac output
 Most common COD after presentation of MI
 Occurs in 5% to 8% with STEMI, 2,5% Non –STEMI
 Incidence of CS has decreased only slightly over time
 Mortality rate remains high at near 50%
Etiology

 CS after an MI  secondary to severe LV dysfucntion

 Acute hemodynamic collapse (rupture)
 Iatrogenic  inappropriate administration of
medications ( Beta-blocker)
 Occult hemorrhage due to procedure-related
complication/medication (antithrombotic, antiplatelet,
fibrinolytic)
Differential Diagnosis

 Non ischemic and extracardiac

 Acute myocarditis ec infection or toxin
 Apical balloning syndrome (Takotsubo
cardiomyopathy  acute LV dysfunction, as a
response to emotional/physical stress)
 Acute aortic dissection, coronary artery dissection,
aortic rupture, tamponade
 Myocardial depression ec septic shock
Pathogenesis
 Predominant LV failure (SBP < 90 mmHg, normal to
elevated LV filling pressure, evidence of end-organ
hypoperfusion )
 RV failure (infarction of territory supplied by cute
marginal branches of RCA ( hypotension, clear lung
fields, bradyarrhytmic complication)
 MR
 Ventricular Septal Rupture
 Free Wall Rupture
Pathophysiology
Clinical Presentation
 Derive from underlying pathophysiology
 Chest pain, nausea, emesis,restlessness, agitation
 Cool and clammy peripheries
 Decreased of urine output
 Mental status changes
 Pulmonary edema,dyspnea, tachypnea, bilateral
rales,respiratory failure
Clinical Presentation
 Hemodynamic collapse
 Diffuse point of maximal impulse
 Loud S3 gallop, elevated JVP
 Rales
 New holosystolic murmupresence of cardiac
tamponade
Diagnostic Approach

 Clinical signs and symptoms of CS

 Echocardiography
Management and Therapy
 Optimum treatment ( to stabilize oxygenation, BP
and rhythm while proceeding urgently to coronary
angiography )
 Hemodynamic monitoring with SGC
 IABP (creates a vacuum effect during systole 
reduces afterload on LV, augment DBP  increase
coronary perfussion pressure )
 Early reperfusion of occluded coronary artery
 Avoiding treatmen errors
Future Directions

 Persistent shock  Poor prognosis

 Adequate CO prevent end-organ dysfunction
 Cardiac tranplantation
 Mechanical support (devices implanted
percutaneously)
 Stem cell therapy
Cardiac dysrhythmia
Dis- /Arrhythmias :

 Disorders of the regular rhythmic beating the heart.

 Common — 2.2 million Americans are living with AF
(one type of rhythm problem).
 Can occur in a healthy heart and be of minimal
consequence.
 Also may indicate a serious problem and lead to
heart disease, stroke or sudden cardiac death.
 The goal : ultimately reduce disability and death from
heart disease and stroke.
Causes
 Common : heart disease, high BP, DM, smoking,
excessive alcohol or caffeine, drug abuse, stress
 Scarring — most commonly, from a previous heart
attack — disrupt the initiation or conduction of
electrical impulses.
 In a healthy person with a normal, healthy heart, a
sustained arrhythmia to develop caused by outside
trigger: an electrical shock or the use of illicit drugs.
Any pre-existing structural heart condition
can lead to arrhythmia development due to:
 Inadequate blood supply.

It can alter the ability of heart tissue — including

the cells that conduct electrical impulses — to
function properly.

 Damage or death of heart tissue.

This can affect the way electrical impulses spread in
the heart.
These pre-existing heart conditions may
include:

 Coronary artery disease (CAD).

 Cardiomyopathy.

 Valvular heart diseases.

Complications
Stroke.
When your atrial chambers fibrillate, they're unable
to pump blood effectively. Stagnant blood in the atria
can form blood clots. If a clot breaks loose, it can
travel to and obstruct a brain artery, causing an
ischemic stroke. This may damage or kill a portion of
your brain or lead to death.

Congestive heart failure.

This can result if your heart is pumping ineffectively
for a prolonged period due to a bradycardia or
tachycardia, such as AF. Sometimes, controlling the
rate of an arrhythmia that's causing CHF can lead to
improved heart function.
SUMMARY
Ventricular Arrhythmias
Rules of Malignancy for PVCs :

 Frequent PVCs
 Consecutive PVCs
 Multiform PVCs
 R-on-T phenomenon
 Any PVC occurring during an acute
myocardial infarction (or in any patient with
underlying heart disease)
RBBB

• Sinus rhythm with a normal PR interval

• RSR1 pattern in V1
• The dominant R wave is characteristic of RBBB, and does not
indicate RV hypertrophy
• Wide and slurred S wave in V6
LBBB

• Sinus rhythm
• Broad QRS complexes with notch in the R wave in I, VL, V5, V6
• Inverted T waves are associated with bundle branch block, and
have no other significance.
Acute coronary syndrome
Hypertensive crise
Clinical Vignette
 65 y/o M with past medical history of Type II DM (on oral
hypoglycemics), presenting with headache, chest pain and
shortness of breath that developed after lunch the day of
admission; non-exertional; no alleviating factors.
 Physical Exam:
 Vitals: 37.3, 195/125, 92, 24, 93% on RA
 HEENT: Decreased A:V on retinal exam (<25%)
 Heart: S4 heard on exam, no m/r/g
 Lungs: mild resp distress, otherwise clear to auscultation

What’s the diagnosis and next best step in management?

Definitions:
 Hypertension:
 Stage I: 140-159/90-99
 Stage II: >160/100

 Hypertensive Urgency:
 Systolic
BP >180 or Diastolic BP >120 in the absence
of end-organ damage
Definitions Continued:
 Hypertensive Emergencies:
 SBP>180 OR DBP>120 in the presence of end-organ
damage
 Malignant Hypertension: End-organ damage--eyes, kidneys,
brain (hemorrhage/infarct) affected
 Hypertensive encephalopathy: Cerebral edema leading to
neurological symptoms
Signs and Symptoms:
 Hypertensive Urgency:
 Can be completely asymptomatic
 Some symptoms include:
 Severe headache
 Shortness of breath
 Nosebleeds
 Severe anxiety
 Signs:
 Elevated BP on consecutive readings
S&S Continued
 Hypertensive Emergencies
 Symptoms:
 nausea, vomiting (cerebral edema)
 Chest Pain
 SOB
 Blurry vision
 Confusion
 Loss of consciousness
 Signs:
 Retinal hemorrhages, exudates, or papilledema
 Renal involvement (malignant nephrosclerosis) with AKI,
proteinuria, hematuria
 Cerebral edema  seizures and coma

 Pulmonary Edema

 Myocardial Infarction

 Hemorrhagic Stroke, lacunar infarcts

Treatment Options
 Hypertensive Urgency:
 Goal: Reduce BP to <160/100 over several hours to
day
 Elderly at high risk of ischemia from rapid reduction of BP,
therefore slower reduction in BP in this patient population
 Previously treated hypertension:
 Increase dose of existing med or add another med
 Reinstitution of med in non-compliant patients
Treatment continued
 Hypertensive Urgency continued:
 Previously untreated hypertension:
 Slowreduction of BP (one to two days): Amlodipine,
Metoprolol XL, lisinopril (po anti-hypertensives usually
enough)
 Experts recommend: Initiate two agents or a combination
agent (one being a thiazide diuretic)
 Rationale: Most patients with BP >20/10 above goal will require
two agents to control their BP
Treatment Continued
 Hypertensive Emergency:
 Goal: Lower Diastolic BP to approximately 100-105 over 2-
6 hours; max initial fall not to exceed 25%
 More aggressive decrease can lead to ischemic stroke and
myocardial ischemia
 If focal neurological sx presentobtain MRI to r/o acute
stroke (rapid BP correction contraindicated)
 Parenteral antihypertensives (IV Drip) recommended over
oral agents in hypertensive emergency
Treatment
 Recommended parenteral antihypertensive agents
(IV drip) for Hypertensive Emergencies and
admission to ICU
 Nitroprusside (cautious about cyanide toxicity),
Nicardipine, and Labetalol.
 Once BP controlled, switch to oral anti-hypertensives
and follow-up closely
Summary
 Hypertensive Crises are common
 Differentiate Hypertensive Urgency from Emergency
on the basis of end-organ damage
 Can treat hypertensive urgency with oral
antihypertensives, but parenteral medications
required for hypertensive emergencies
 25% reduction in diastolic BP over 2-6 hours for
hypertensive emergencies
 Don’t forget to start Oral antihypertensives and
follow-up closely!
Heart failure
DEFINITION
“The situation when the heart is
incapable of maintaining a cardiac
output adequate to accommodate
metabolic requirements and the
venous return."
E. Braunwald
 PUMP
DYSFUNCTION MYOCARDIAL
HORMONAL REMODELING

CIRCULATORY NEUROREGULATORY
CYTOKINE
INSUFFICIENCY

HEART FAILURE
 PATHOPHYSIOLOGY
 Heart Failure is a Dropsical Condition with
Generalized Edema from Fluide Retention.
 Heart Failure is Due to a Central Cardiac Pump inadequacy.
 Heart Failure is Precipitated by Decompansated Ventricular
Hypertrophy.
 Heart Failure is due to Circulatory Dysfunction.
 Heart Failure is an Endocrinopathy.
 Heart Failure is a Fever
DIAGNOSIS

 HISTORY.
 PHYSICAL EXAMINATION.
 APPROPRIAT INVESTIGATION.
1. SYMPTOMS OF HEART FAILURE(AT REST OR DURING EXERCISE).
2.Objective evidence of cardiac dysfunction.
3.Response to treatment directed towards heart failure.
 CRITERIA FOR CONGESTIVE HEART FAILURE

 MAJOR CRITERIA  MINOR CRITERIA

1.Paroxysmal nocturnal dyspnea 1.Ankle edema.
or orthopnea. 2.Night cough.
2.Rales. 3.Dyspnea on exertion.
3.Cardiomegaly. 4.Pleural effusion.
4.Acute pulmonary edema. 5.Vital capacity decreased 1/3 from
5.S3 Gallop. maximum.
6.Increased venous pressure>16 cm of 6.Tachycardia (rate>120/min).
water.
 MAJOR OR MINOR
7.Circulation time>25 sec.
Weight loss>4.5 Kg in 5 days in
8.Hepatojugular reflux. response to treatment.
Symptomatic classification of exercise tolerance
New York Heart Association (NYHA)

NYHA Class I: No complaints under

heavy physical load.
NYHA Class II: Complaints under
heavy physical load.
NYHA Class III: Complaints under light
physical load.
NYHA Class IV : Complaints at rest.
 Descriptive terms in heart failure

Acute vs Chronic heart failure.

Systolic vs Diastolic.

Right vs Left heart failure.

Etiology of Chronic Heart Failure

It is important to know the etiology

of heart failure.
Look for other diseases that may an important
influence on management of heart failure.
Identify potentially reversible exacerbatiry factor.
 Causes of ChronicHeart Failure

Systolic dysfunction:
Coronary artery disease.
Hypertension.
Dilated Cardiomyopathy.
Myocarditis.
 Causes of Chronic Heart Failure cont.

Diastolic Dysfunction:
Coronary artery disease.
Systemic Hypertension.
Diabetis Mellitus.
Aortic stenosis.
Hypertrophic cardiomypathy.
Infiltrative cardiomypathy
Endocardial fibrosis.
Normal aging process.
Causes of worsening Heart Failure
Non- cardiac:

 Non compliance to the prescribed

regimen(salt,liquid,medication).
 Recently co-prescribed drugs
(antiarrhythmic,beta-blockers,non steroidal anti-
inflmatory drugs,verapamil,diltiazem).
 Renal dysfunction.
 Infection.
 Pulmonary embolism.
 Thyroid dysfunction.
 Anemia.
 Alcohol abuse.
Causes of worsening Heart Failure cont.
Cardiac:

 Atrial fibrillation.
 Other supraventricular or ventricular arrhythmias.
 Bradycardia.
 Appearance or worsening mitral or ticusped
regurgitation.
 Myocardial ischaemia.
 Excessive preload reduction(diuretics,ACE inhibitors).
 The Heart Failure Milieu :
Clinical Presentation Physical findings
Peripheral edema
Disease Ascites
process Vascular congestion
Jugular venous distension
Rales
Ventricular Tachycardia
dysfunction
Hypotension
Cachexia
Disease-specific findings
Hemodynamic
abnormalities
Physical findings
Azotemia Metabolic
Hyponatremia changes
Hypocalemia Compensatory
Hypomagnesemia mechanisms Symtoms and
Symptoms
Hyperuricemia physical findings Fatique and weakness
Acidosis/alkalosis Dyspnea and fluid
Hypoxia/O2 desaturatuion retention syndromes
Decreased MVO2 Nocturia
Gastrointestinal symptoms
Diminished mentation
 The Heart Failure Milieu :
Disease
End-Organ Failure and Death
process
Systemic organ failure
Renal failure
Ventricular Hepatic failure
dysfunction
Respiratory failure
Multi-organ failure
Pulmonary embolism
Hemodynamic Peripheral (cerebral embolism)
abnormalities

Metabolic Death
changes
Compensatory
Sudden
mechanisms End-Organ Death
Failure

Lethal arrhythmia Symtoms and

Electrolyte abnormalities physical findings
Elevated catecholamine levels
Ischemia
Drug-proarrhythmia
 Responses to Hemodynamic Overload

Pressure overload Volume overload

Systolic wall stress Diastolic wall stress

Mechanical transducers

Intracellular signals

Ventricular remodeling

Paralel sarcomeres Series sarcomeres

Concentric hypertrophy Normal Eccentric hypertrophy

Evaluation of heart failure patient

Physical
Laboratory
Examination
tests

History

Diagnostic
studies
 Assessment of heart failure

Patient history: Physical examination :

Cardiac Cardiac
Pulmonary Pulmonary
Gastrointestinal Abdominal
Renal Neurological
Neuro-psychatric Systemic

Diagnostic studies:
Laboratory tests,ECG,Chest X ray,Echo,Exercise testing,
Cardiac catheterization,Radionuclited studies
 Investigation :Laboratory
 Complete Blood Count.
 Serum electrolytes, blood urea nitrogen,serum creatinine.
 Liver function test.
 Prothrombin time.
 Lipid profile.
 Thyroid function test.
 Anaemia evaluation.
 Arterial blood gases.
 Serum drug levels(digoxin,phenytoin).
 Atrial natriuretic peptides.
 Urin analysis.
Chest X- ray
 Other investigation
 Transthoracic Echocardiography.
 Stress Echo.
 Exercise stress testing.
 24- hour Holter monitoring.
 Nuclear imaging,thallium perfusion scan,cardiac
MRI.
 Coronary angiography
 Chronic Congestive Heart Failure

EVOLUTION OF
CLINICAL STAGES
NORMAL
No symptoms
Normal exercise
Asymptomatic
Normal LV fxn LV Dysfunction
No symptoms
Normal exercise
Compensated
Abnormal LV fxn CHF
No symptoms Decompensated
Exercise
Abnormal LV fxn CHF
Symptoms
Exercise
Refractory
Abnormal LV fxn CHF
Symptoms not controlled
with treatment
TREATMENT OBJECTIVES

Survival
Morbidity
Exercise capacity
Quality of life
Neurohormonal changes
Progression of CHF
Symptoms
 Treatment Options
 Non-pharmacological.
General advice and measures.
Exercise and exercice training.
 Pharmacological therapy.
Angiotensin-converting enzyme inhibitors(ACI).
Beta-adrenoreceptor antagonists.
Cardiac glycosides.
Diuretics.
Vasodilators(nitrats,hydralazine).
Antiarrhythmic agent.
Anticoagulantion.
Oxyggen.
 Divices and surgery.
Revascularization.
Pacemaker.
Implantable cardioverter defibrillator(ICD).
Cadiac trnsplantation.
Ultrafiltration,haemodialysis.
 TREATMENT
Correction of aggravating factors

Pregnancy Endocarditis
Arrhythmias (AF) Obesity
Infections Hypertension
Hyperthyroidism Physical activity
Thromboembolism Dietary excess
MEDICATIONS
 TREATMENT
PHARMACOLOGIC THERAPY

DIURETICS

INOTROPES

VASODILATORS

NEUROHORMONAL ANTAGONISTS

OTHERS (Anticoagulants, antiarrhythmics, etc)

Normal
TREATMENT
Asymptomatic
LV dysfunction
EF <40%
Symptomatic CHF
ACEI NYHA II Symptomatic CHF
Diuretics mild NYHA - III
Neurohormonal Symptomatic CHF
inhibitors Loop
Diuretics NYHA - IV
Digoxin?
Inotropes
Specialized therapy
Transplant
Secondary prevention
Modification of physical activity
 Take Home Messages
 Cardiac emergencies is the life threatening
condition
 Many etiologies and underlying diseases
 Dx base on history, Physical Exam, Additional exam
 Management is depend on the etiology
 Early Dx and treatment reduce morbidity and
mortality
 Reaching Level of competence need a good skill
and knowledge
Terima kasih