ACUTE CARDIOLOGY

Budi Yuli Setianto

Fakultas Kedokteran, Kedokteran Masyarakat dan Keperawatan
Universitas Gadjah Mada
Acute Cardiology: Cardiac Emergencies
Definition:
There is no unique definition, and clinical presentation may be different.

“Clinical presentation may vary from cardiac arrest and loss of consciousness to asymptomatic cardiac standstill”.

Mostly is associated detoriation of normal electrical and hemodynamic physiology.

Clinical endpoints:
1. Acute symptoms and events
2. Chronic clinical events: High mortality and morbidity.

Physiopathology:
A. Low cardiac output and systemic hypoperfusion
B. Severe myocardial ischemia and its results.
Acute Cardiology: Symptoms
Diagnosis of cardiac emergencies:
Synthesis of symptoms and physical examination and combination with laboratory findings,
and appealing an expert opinion.

Main symptoms:
1. Chest pain and chest discomfort
2. Dyspnea
3. Shock
4. Fatigue
5. Palpitation
6. Syncope, Presyncope
7. Sudden death
Acute Cardiology: Clinical Presentations
CLINICAL KEY POINTS OF PHYSICAL EXAMS:
History.
1. Blood pressure: Low, high
2. Peripheral pulses: Rapid, slow, rhythmic, arrhyrthmic.
3. Signs of systemic hypoperfusion: Consciousness, skin color, warmness of
the skin, urinary output.
4. General posture of the patient: Inspection, orthopnea, supine position, pale,
sweating.
5. Killip class. (I-IV).
Chest Pain
Classification of myocardial ischemi
1. Transient myocardial ischemia
Stable angina pectoris (chronic)
Unstable angina
Prinzmetal angina (variant)
Post MI angina
2. Long lasting myocardial ischemia
AMI (objective documentation – symptomatic/ asymptomatic)
3. Sudden death.
Main Causes of Chest Discomfort and Pain:

A. Cardiac:
Angina
ACS
Aortic dissectıon
Pericarditis, myocarditis
Mitral valve prolapse
HCM, Aortic Stenosis
B. Noncardiac Causes of Chest Pain:
Esophagitis, oesophageal spasm. Pneumonia.
Peptic ulcer. Pulmonary embolus.
Gallblader disease. Pneumotorax.
Musculoskletal causes (osteochondritis, Pulmonary hypertension.
cervical disk, thoracic outlet syndrome).
Hyperventilatıon, anxiety.
ACUTE CORONARY SYNDROME
Acute Coronary Syndrome
 Unstable Angina
 Non ST Elevation MI
 ST Elevation MI

Biomarker elevation in the prescence of two of the criteria below:

a. ECG and ischemic symptoms.
b. Old MI Q waves on ECG.
c. ECG findings of acute ischemia: ST- T wave changes. (ST elevation, depression,
new LBBB).
d. History of Recently performed PCI or ACBG.
Acute Coronary Syndromes
PQRST: Eliciting
pain information
P: Placement/
provocation/
precipitating factors
Q: Quality
R: Radiation, relief and
reproducibility
S: Severity (0-10 scale)
T: Time of onset
Diagnosis

1. Clinical presentation – Chest Pain in ACS

- Prolonged (20 min) anginal pain at rest
- New onset (de novo) angina
- Crescendo angina
- Post-MI angina.

2. Diagnostic tools
- Physical examination
- EKG
- Biomarkers
- Imaging

12 Hamm CW, et al. European Heart Journal (2011) 32, 2999–3054

The spectrum of ACS

9
Hamm CW, et al. European Heart Journal (2011) 32, 2999–3054
ESC Guidelines 2017
ESC Guidelines 2017
ESC Guidelines 2017
ACUTE HEART FAILURE
Acute Dyspnea

A. Cardiac dyspnea: Pulmonary venous hypertension/

congestion.
1. Exertional dyspnea
2. Paroxysmal nocturnal dyspnea
3. Orthopnea
4. Cheyne Stokes

B. Pulmonary causes:
1. Bronchial asthma
2. Pneumonia
3. Pulmonary embolus, fat embolism, shock
4. Acute Respiratory Distress
Heart Failure: Definition
HF is a clinical syndrome characterized by typical symptoms (e.g. breathlessness, ankle
swelling and fatigue) that may be accompanied by signs (e.g. elevated jugular venous
pressure, pulmonary crackles and peripheral edema) caused by a structural and/or
functional cardiac abnormality, resulting in a reduced cardiac output and/or elevated
intra-cardiac pressures at rest or during stress.
Heart Failure: Sign and Symptoms
Heart Failure: Terminology
The main terminology used to describe HF is historical and is based on measurement
of the LVEF
Heart Failure: Pharmacological treatment of heart
failure with reduced ejection fraction

A new therapeutic class of agents acting on the RAAS

and the neutral endopeptidase system has been
developed [angiotensin receptor neprilysin inhibitor
(ARNI)]. The first in class is LCZ696, which is a molecule
that combines the moieties of valsartan and sacubitril
(neprilysin inhibitor) in a single substance. By inhibiting
neprilysin, the degradation of NPs, bradykinin and
other peptides is slowed. Physiologic effects through
binding to NP receptors and the augmented
generation of cGMP, thereby enhancing diuresis,
natriuresis and myocardial relaxation and anti-
remodelling.
Acute Heart Failure: Definition
 Acute heart failure includes systolic or diastolic dysfunction, heart rhythm disturbances
or preload-afterload mismatch.
 Characteristic gradually or quickly and fill in sudden hospitalization.(1,2)

1. Gheorghiade M, et al. Patophysiologic targets in the early phase of acute heart failure syndromes. Am J Card, 2005. 96(6A): 11G-17G.
2. Nieminen MS, et al. Executive summary of the guidelines on the diagnosis and treatment of acute heart failure: the Task Force on Acute Heart Failure of the
European Society of Cardiology. Eur Heart J. 2005 Feb;26(4):384-416
Etiology
Decompensation in previous chronic heart Severe myocarditis
disease
Cardiac tamponade
Acute coronary syndrome
Aortic dissection
Hypertension crisis
Post partum cardiomyopathy
Acute arrhythmias
Non-cardiac causes
Valvular disorders that worsening
High output syndrome

Nieminen MS, et al. Executive summary of the guidelines on the diagnosis and treatment of acute heart failure: the Task Force on Acute Heart Failure
of the European Society of Cardiology. Eur Heart J. 2005 Feb;26(4):384-416
Pathophysiology
Vicious Circle on Acute Heart Failure
The inability of the myocardium to maintain cardiac output in order to meet peripheral
tissue metabolic needs. If this circle is not overcome, there will be chronic heart
failure.
Myocardial stunning:
The condition of myocardial dysfunction due to prolonged and persistent myocardial
ischemia occurs even though myocardial perfusion occurs. This event is based on
oxidative stress, changes in Ca2 ++ homeostasis, desensitization of myocardial
contractile proteins. This situation depends on the myocardial ischemia that preceded
it.
Myocardial hibernation
Impaired myocardial function due to impaired coronary blood flow. So that with blood
flow and oxygenation, myocardial muscles can return to function. Is a mechanism of
adaptation to oxygen deprivation to prevent ischemia and irreversible myocardial
necrosis.

Nieminen MS, et al. Executive summary of the guidelines on the diagnosis and treatment of acute heart failure: the Task Force on
Acute Heart Failure of the European Society of Cardiology. Eur Heart J. 2005 Feb;26(4):384-416
Clinical Assessment
1. Acute decompensated heart failure
◦ Minor complaints and symptoms that do not meet the criteria of cardiogenic shock,
pulmonary edema, or hypertensive crisis

2. Acute heart failure with hypertensive crisis

◦ Complaints and clinical symptoms of Acute Heart Failure are accompanied by high blood
pressure, pulmonary edema evidenced by chest X-ray, but with good left ventricular
function.

3. Acute heart failure with pulmonary edema

◦ Accompanied by severe shortness of breath, the presence of wet rhonchi in all lung fields,
and orthopnea.
◦ O2 saturation <90% without oxygen
4. Cardiogenic shock
◦ Tissue hypoperfusion due to heart failure.
◦ Characterized by systolic blood pressure <90mmhg or MAP> 30mmhg and or low urine production (<0.5
ml / kg body weight / hour), heart rate> 60x / minute with or without evidence of organ edema.

5. High output heart failure

◦ Clinically characterized by high cardiac output.
◦ Can be caused by anemia, thyrotoxicosis, arithmetic, or other causes.
◦ Clinical signs are temperature of warm extremities, sometimes accompanied by a decrease in systolic
blood pressure.

6. Right Heart Failure

◦ Marked low cardiac output syndrome with peripheral dam signs in the form of increased jugular venous
pressure, hepatomegaly, and hypotension.
Clinical Presentation
Symptoms: Symptoms that are less specific
 Shortness at rest or activity  Nausea and vomiting
 Reduced activity ability  Abdominal discomfort
 Orthopnea  Wheezing breath sounds
 Paroxysmal nocturnal dyspnea (PND)  Fatigue
 Ascites  Delirium
 Scrotum edema

Lindenfeld J, et al. Executive Summary: HFSA 2010 Comprehensive

Heart Failure Practice Guideline. J Card Fail, 2010. 16(6).
Clinical Presentation
Increased left ventricular filling pressure:
 Increased jugular venous pressure
 S3 gallop sound
 Rhonchi
 Hepatojugular reflux
 Enlargement of the heart
Heart Failure: Diagnosic flowchart for patients with
suspected heart failure
Heart Failure: Algorithm for the diagnosis of heart
failure
SUDDEN CARDIAC DEATH
SUDDEN CARDIAC DEATH

Definition:
Sudden halt of the pump function of the heart.
If rapid intervention is carried out, the event may be reversible Otherwise lethal.

► The most frequent mechanism of SCD:

(a) ”Ventricular Tachyarrythmia; VT, VF.
(b) Non-Tachyarrythmic events (relatively infrequent): Pulseless electrical activity (AV-
dissosiation). Asystoly (due to cardiac rupture). Bradycardyarythmia.
Cardıovascular Causes of SCD:

1. Coronary artery disease (acute ischemic events,chronic ischemic heart disease).

2. Dilated Cardiomyopathy (CMP).
“These two diseases are >%90 cause of SCD”.

3. 3. Other CMP
4. (a) Hypertrophic CMP
5. (b) Arrythmogenic right ventricular CMP.
6. 4. Primary “Electrical” disorders.
7. 5. Mechanic cardiovascular disorders
Electrical Causes of SCD:

(a) Long QT syndrome.

(b) Brugada syndrome.
(c) Catecolaminergic polymorphic VT.
(d) Wolf-Parkinson-White syndrome (WPW).
(e) Sinus and AV node, conduction defect.
 PATOPHYSIOLOGY
TRIGGERS
VT
AUTONOMIC CHANGES
VF
ACUTE ISCHEMIA
ELECTROLYTE ABN ASYSTOLE
PHYSICAL EXERTION EMD
MENTAL STRESS FUNCTION
DRUGS
ELECTROLYTE SHIFTS
ELECTRICAL INSTABILITY
PLATELET AGREGATION
SUBSTRATE VASOCONSTRICTION
HYPERTROPHY
MYOCARDIAL SCAR SUDDEN
ATHEROSCLEROSIS CARDIAC
CORONARY ANOMALIES DEATH
MYOCARDITIS
ETIOLOGY
RISK FACTORS
HYPERTENSION & LVH
LIPIDS
DIETARY FACTOR
PHYSICAL ACTIVITY
HEART RATE
SMOKING
DIABETES MELLITUS
ECG CHANGES

GENETICS
Neurocardiogenic syncope:

Definitıon:
Defined as transient loss of consciousness associated with the loss of postural tone that is a
result of sudden, transient, and inadequate cerebral flow an systolic blood pressure to less than
70 mm Hg causes an interruptıon of blood flow more than 8 seconds.

ABC of syncope:
A. Clinical conditıon: Generally, loss of postural tonus that is associated with sudden

fall down and recover spontaneously.

B. Presentation: Generally attack occur abruptly, then sudden and full clinical recovery is seen.

C. Mechanism: Sudden / short interval of transient cerebral hypoperfusion.

Neurocardiogenic syncope: Cardiac Causes

Anatomic causes: Arrythmic causes:

Aortic stenosis Tachyarrythmia
Hypertrophic CMP - SVT
Miocardial ischemia /AMI - VT
- Long QT
Aortic dissection
- Brugada
Cardiac tamponade
Bradyarrythmia.
Atrial mixoma
- Atrioventricular block.
Pulmonary hypertension
- Pace-maker dysfunction.
Pulmonary emboli - ICD dysfunction.
Subclavian steal send - Sinus dysfunction
Fallot tetralogy. Sick Sinus Syndrome.
Neurocardiogenic syncope: Absolute Diagnostic
Criteria

Vasovagal Syncope. Diagnosed if precipitating events such as fear, severe pain, emotional
distress, instrumentation or prolonged standing are associated with typical prodromal
symptomps.

Situational syncope: Diagnosed if syncope occurs during or immediately after urinatıon,

defeaecation, coughing or swallowing.

Orthostatic Syncope: Associated with syncope or presyncope.

Documentation of orthostatic syncope: A decrease in Systolic BP > 20 mmHg or a

decreased Systolic BP below 90 mmHg.

Presyncope (“near- syncope): Condition in which patients feel as syncope imminent

Cardiac ischemia related syncope is diagnosed when symptomps are present with ECG evidence of
acute ischemia with or without Mİ.
However, in this case, the further determination of the specific ischemia- induced etiology may be
necessary (tachyarrhytmia-induced AV block).

Arrhytmia syncope was diagnosed by ECG when there is:

a. Sinus bradycardia: < 40/min or repetitive SA blocks or sinus pauses >3s in the absence of
medications known to have negative chronotropic effect.
b. Second- degree Mobitz II or III degree AV block.
c. Alternating left and right bundle branch block.
d. Rapid PSVT or VT.
e. Pace maker malfunctıon.
Cardiogenic Shock
Definition:
a) Systemic hypoperfusion.
b) Despite IV volume replacement, in order to maintain systolic blood pressure >90
mmHg needed İV vasopressor and/or IABP support.

Characteristics:
a) Systolic BP: <90 mmHg.
b) Pulmonary Capilary Wedge Pressure : >20 mmHg.
c) Cardiac index: <1.8 Lt/min.

Clinical findings and diagnosis:

a) Pump failure, and clinical signs and Lab findigs of MI.
b) SBP: <90mmHg, urine output: <20- 30 ml/hr.
c) Exclusion of other causes of hypotension .
d) Clinical shock. (loss of consciousness, cold and wet skin, palor).
Hypertensive Emergency

Hypertensive Emergency :
 Sudden rise in blood pressure. : “DBP >120 mmHg. SBP >220 mmHg”.
 Sudden rise: SBP (mm Hg)  From 160- 170 to >220 is significant for crisis.

Basic Principle:
a) Degree of rise in BP is more signifficant than measured BP.
b) Is related with life threatening acute end- organ injury or dysfunction (retinal hemorrhage,
papilla edema, acute pulmonary edema, renal dysfunction, SVA, hypertensive
encephalopathy)

Principle of management:
Arterial BP must fall within a few minutes with IV treatment.
 Aortic Dissection

Intımal flaw and seperation from media towards luminal

surface.
Signs of clinical diagnosis:
a. Sudden onset chest or interscapular pain.
b. CP of unknown origin, back pain, upper abdominal
pain, CP+ pulse difference between
extremities+atypical stroke, extremity malperfusion
(asymmetric).
c. Signs of dissection radiation: Shock like condition,
irrespective of arterial blood pressure.
Aortic Dissection

Gold standart of diagnosis: TEE, CT,

MRI. Coronary angiography and
artography .