PTY316- - Possible areas of radiating pain: neck, jaw, upper • MI location

abdomen, shoulders, and arms. • Resulting EF

Finals Reviewer
CARDIAC DISEASES TYPES OF ANGINA Q WAVE MI
MORTALITY: TEN (10) LEADING CAUSES - the presence of an abnormal Q wave
• Stable angina
• Unstable angina
• Variant angina
• Syndrome X
• Risk Factors: INFARCTION
o Non-modifiable: Age, Sex, Race, Family history of
CAD • Irreversible changes start to appear 20 minutes – 2
o Modifiable: hours from the onset of myocardial ischemia
1. Cigarette smoking • May occur from complete occlusion of the vessel.
2. High blood pressure
TYPES OF PLAQUE
3. Obesity
WHAT IS NON-Q WAVE MI?
WHAT ARE THE PATHOPHYSIOLOGICAL CONDITIONS UNDER 4. Increase cholesterol & LDL levels
• Soft or unstable plaque
5. Inactivity - Was formerly known as nontrans mural or
CVD? • Lipid rich plaque • Hard or stable plaque
6. Stress subendocardial MI because it involve the
• Collagen – rich
• Atherosclerosis 7. DM endocardium
• Altered myocardial muscle mechanics LDL/HDL RATIO
WHAT IS MYOCARDIAL INFARCTION?
• Valvular dysfunction • 2:1 or lower is ideal ANATOMICAL CLASSIFICATION OF MI
• Arrhythmias - as a result of a blocked left anterior descending
• > 4:1 is a risk factor for atherosclerosis and CHD coronary artery
• Hypertension • a lower ratio puts one at risk for sudden death! 1. Inferior MI - Inferior surface of the LV
2. Lateral MI - Involves the lateral surface of the LV
HIGH RISK!! WHAT ARE THE PRECIPITATING FACTORS IN THE DEVELOPMENT OF
CORONARY ARTERY DISEASE 3. Anterior MI - Involves the anterior surface of the LV
• Total cholesterol above 220 MI? 4. Septal MI - septum
An atherosclerotic disease process that narrows the lumen • LDL above 160
1. Atherosclerotic heart disease 5. Posterior MI – posterior wall of LV
of coronary arteries, resulting in ischemia to the • HDL below 35
with thrombus formation
myocardium. EJECTION FRACTION (EF)
WHAT ARE THE MOST COMMON CLINICAL PRESENTATION OF 2. coronary vasospasm or
CAD?
embolism - Ejection fraction (EF) is a measurement, expressed as
PATHOPHYSIOLOGY OF HEART DISEASE
3. cocaine toxicity a percentage, of how much blood the left ventricle
- Failure of any of the three interrelated factors that • Angina Pectoris pumps out with each contraction.
influence pump functioning: • Myocardial Infarction - < 35% ( means 35%) of total blood in the (L) ventricle
1. Oxygen supply to the heart • Arrhythmias is pushed out with each contraction) is considered a
2. Contractility of the ventricles large MI with significant systolic dysfunction and
3. Electrical impulse initiation or conduction WHAT IS ANGINA PECTORIS? with potential for LV failure
ZONES OF INFARCTION
WHAT IS ATHEROSCLEROSIS - a type of chest pain, pressure or discomfort
STEMI: ST ELEVATION MI
- heart is not receiving enough oxygen coronary artery • Zone of infarction
• It is an inflammatory reaction in response to injury - substernal chest pain or pressure • Zone of injury - MI that initially presents with an elevated ST segment
- accompanied by Levine sign (is a clenched fist held • Zone of ischemia on the EKG
over the chest to describe the tightening of pressure - May be an indication for emergent thrombolytic
felt during heart attack) therapy or revascularization
- represents imbalance in myocardial oxygen supply
and demand brought on by:
a. demands on heart by: exertion, emotional stress,
smoking, extremes of temperature (cold), TYPES OF MI
tachyarrhythmias
b. vasospasm – Prinzmetal’s angina • Q wave or non-Q wave
• ST segment ( elevated or not)
SEQUELAE OF IMPAIRED VENTRICULAR FUNCTION • Administration of NTG CORONARY ARTERY BYPASS SURGERY

REVASCULARIZATION PROCEDURES - is an open-heart surgery that is done to reroute or

1. SV, CO & ejection fraction
"bypass" blood around blocked arteries.
2.  end diastolic ventricular pressures - uses an anastomosing graft to bypass the involved
• PTCA with stent
3. Electrical instability lesion & establish an alternate blood supply
• Rotational atherectomy of the lesion
• Laser surgery
MAJOR COMPLICATIONS FOLLOWING MI • CABG
• Thrombolytic agents (ST elevation)
• Recurrence of ischemia ▪ Streptokinase or TPA
• LV failure
• Ventricular arrhythmias MOST COMMON METHODS OF DIAGNOSING MI PATIENT

WHAT IS CARDIOGENIC SHOCK? • EKG findings

• Blood work COMMONLY USED DONOR VESSELS FOR CABG
- inadequate CO and arterial BP to perfuse the major
organs as a result of severe LV failure • saphenous vein
- May necessitate the use of extraordinary medical ENZYME CHANGES ASSOCIATED WITH MI?
• internal mammary artery
interventions such as the intra-aortic balloon pump
1. CPK – MB: peak at 24 hr • radial artery of the
(IABP) WHAT IS THROMBOLYTIC THERAPY?
2. SGOT /AST: peak at 24 – 48 hr nondominant hand
3. LDH: peak at 3 – 6 days - "clot-busting" therapy is used to stop a heart attack in
WOUND HEALING AFTER MI 4. Other markers that may be used to diagnose an acute its tracks
MI: Troponin I, Troponin T, Myoglobin - medications administered to activate body’s
• Wound is established within the first 4-6 wks
fibrinolytic system, dissolve clot, and restore
• During this time the patient may engage in low-level
REVASCULARIZATION PROCEDURES coronary blood flow
activity but aerobic training should be avoided
- This opens the artery and restores the flow of oxygen
• After ETT patient may undergo aerobic & strength • Cardiac Catheterization
and nutrients in the heart muscle.
training program for the next 2 – 4 months • Angiogram – an invasive procedure done to fing the
- For ACUTE MI
blockages in the coronary arteries
DIAGNOSTIC TESTS & MEDICAL MANAGEMENT PLACING THE PATIENT ON ARTIFICIAL HEART-LUNG
THROMBOLYTIC DRUGS
WHAT IS ANGIOPLASTY?
CLASSIC DIAGNOSTIC TOOL FOR EXAMINING PT’S COMPLAINT OF MACHINE (BYPASS PUMP)
SUSPECTED ANGINA PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY (PTCA) • agents which reduce the formation of arterial platelet
thrombi
- The 12-lead EKG - under fluoroscopy, surgical dilation of a blood vessel • Agents include: streptokinase, urokinase and t-PA
o Ischemia: depressed ST segment, inverted T wave using a small balloon-tipped catheter inflated inside
the lumen WHAT IS ATHERECTOMY?
EKG CHANGES WITH TRANSMURAL MI
WHAT IS INTRAVASCULAR STENT - Another type of angioplasty.
• ST segment is initially elevated (area of injury) - The obstructing fibrous plaque is pulverized into
- an endoprosthesis (pliable wire mesh) implanted minute micro particles and washed away into the
• Pathological Q wave within hours
post-angioplasty to prevent restenosis and occlusion bloodstream.
in coronary or peripheral arteries.
EKG CHANGES WITH NON-TRANSMURAL MI PHARMACOLOGICAL MANAGEMENT
REVASCULARIZATION SURGERY (CABG)
• No Q wave • Drug categories
• ST depression • Anti-ischemic – Beta blockes, Calcium channel
blockers, Nitrates
EMERGENCY MANAGEMENT • Afterload reducers – ACE inhibitors (angiotensin
converting enzyme inhibitor), ARBs (angiotensin
- Physiological goal: receptor blocker)
• To decrease MVO2
• Increase myocardial oxygen supply
• Patient is given supplementary O2
 HEART FAILURE WHAT ARE THE PHYSIOLOGICAL ABNORMAL SEEN IN CHF? • Diaphoresis PRINCIPLES OF DRUG MANAGEMENT WITH CHF
• Weakness
• Cardiac failure • ↓ CO A. Increase contractility (positive inotropes) Digitalis
• Tachycardia (resting)
• CHF • ↑ end diastolic pressures (preload) (cardiac glycosides)
• Crackles
• A condition in • ↑ HR - e.g. Digoxin (Lanoxin Inotropic agents, Dopamine,
• Pulsus alternans Dobutamine, Amninone)
which the heart is • Impaired ventricular function
Cardiomyopathy (hypertrophy) • Confusion B. Relieve congestion (diuretics)
unable to maintain •
• Decrease urine output - Furosemide (Lasix)
adequate
• Murmur of mitral insuff. - Hydrochlorothiazide (Esidrix)
circulation of the TYPES OF HEART FAILURE
blood to meet the • Cheyne-stokes resp.
metabolic needs of • Right heart failure MECHANICAL & SURGICAL SUPPORT
the body. • Left heart failure BIVENTRICULAR FAILURE
• Biventricular failure • When left & right heart failure coexist - •Indicated for symptomatic patient in Class III & IV
CAUSE OF HEART FAILURE - Heart transplant
RIGHT HEART FAILURE - LV devices
COMMON SEQUELAE OF CHF - Myoplasty
• CAD
- a.k.a. Backward heart failure
• Valvular diseases
- blood is not adequately returned from the systemic ↓ CO =>> Prerenal failure
• CHD HEART TRANSPLANTATION
circulation to the heart
• Hypertension - due to failure of the RV & Pulmonary hypertension
WHAT IS CARDIOMYOPATHY?
- used in end-stage myocardial disease
• Infections - May occur with pulmonary disease - Is a heart muscle disorder of unknown cause - e.g. cardiomyopathy, ischemic heart disease, valvular
- COPD ⇨ ↑ PA pressures ⇨ Cor pulmonale - Types: Dilated, Hypertrophic, Restrictive heart disease
PATHOPHYSIOLOGY OF CHF - Risk factors: - patient is given immunosuppresive drugs:
SIGNS & SYMPTOMS OF RIGHT-SIDED HEART FAILURE o alcoholism cyclosporine
• Compensatory mechanisms to maintain adequate CO: o pregnancy
1. Increased sympathetic tone. • Nausea o systemic hypertension MYOPLASTY
2. Ventricular remodeling • Anorexia o various infections
3. Activation of renin-angiotensin system - Is a surgical procedure in which an enlarged LV
• Weight gain
4. Redistribution of blood flow away from periphery 3 MAIN TYPES OF NON-ISCHEMIC CARDIOMYOPATHIES undergoes size reduction by removing dilated, scarred
• Ascites
toward central circulation myocardium that is ineffective in contributing to
• RUQ pain contractility
• Dilated
• Hepatomegaly
EFFECTS OF INCREASED SYMPATHETIC TONE • Hypertrophic
• Increased RAP, CVP
• Restrictive WHAT IS BIVENTRICULAR PACING?
• Jugular vein distention
• Increased HR (tachycardia) - Used for patient with intraventricular conduction
• Murmur of tricuspid insufficiency
• Myocardial contractility delay
• Peripheral edema
• Peripheral vascular constriction - Stimulates both the right and left ventricles to make
LEFT HEART FAILURE the heart beat more efficiently.
EFFECTS OF RENIN-ANGIOTENSIN ACTIVATION - Coordinates the contraction of the right & left
- a.k.a. Forward heart failure ventricles
• Water & sodium retention - blood is not adequately
• Peripheral vasoconstriction - pumped into systemic circulation HEART ARRYTHMIAS
- due to an inability of left ventricle to pump ⇨↑
pulmonary artery pressures & Pulmonary Edema NORMAL SINUS RHYTHM

• Rhythm - Regular
SIGNS & SYMPTOMS OF LEFT-SIDED HEART FAILURE PHARMACOLOGICAL MANAGEMENT
• Rate - (60-100 bpm)
• Alpha and beta-blockers • QRS Duration - Normal
• Fatigue
• ACE inhibitors • P Wave - Visible before each QRS complex
• Cough
• Vasodilators • P-R Interval - Normal (<5 small squares. Anything
• SOB
above and this would be 1st degree block)
• DOE
• Indicates that the electrical signal is generated by the
• Orthopnea
sinus node and travelling in a normal fashion in the
• PND
heart.
 • The atria fire electrical impulses in an irregular
fashion causing irregular heart rhythm

E. WOLFF-PARKINSON-WHITE SYNDROME
• caused by an extra
WHAT IS ARRHYTHMIA? WHAT IS ECTOPIC BEAT? C. ATRIAL FLUTTER electrical pathway
- Similar to atrial fibrillation, both can coexist between the atria
Abnormal, disordered rhythm - A beat originates from a site other than the - beats regularly, although at a much faster pace than and the ventricles.
• Caused the heart to beat too fast, too slow or irregularly - sinus node. normal • This pathway may
- •PACs
ETIOLOGY OF ARRHYTHMIA • HR: 250 – 350 bpm allow electrical
- •PVCs current to pass
• Tx: Defibrillation and Beta Blockers
• MI • Rhythm - Regular between the atria
WHAT IS ATRIAL TACHYCARDIA? and the ventricles without passing through the AV
• Electrolyte imbalance • Rate - Around 110 beats per minute
• Acidosis or alkalosis - Rapid and repetitive firing of one or more ectopic foci • QRS Duration - Usually normal node, leading to short circuits and rapid heartbeats.
• Hypoxemia in the atria • P Wave - Replaced with multiple F (flutter) waves, • can cause other types of tachycardia, including atrial
• Hypotension a. Premature Atrial Contractions (PACs) usually at a ratio of 2:1 (2F - 1QRS) but sometimes flutter and atrial fibrillation.
b. Paroxysmal Supraventricular tachycardia (PSVT) 3:1 • Tx: beta blockers and calcium channel blockers
• Emotional stress
• Drugs, alcohol, caffeine c. Atrial flutter • P Wave rate - 300 beats per minute
d. Atrial fibrillation • P-R Interval - Not measurable TACHYCARDIA IN THE VENTRICLES
e. Wolff-Parkinson-White Syndrome - As with SVT the abnormal tissue generating the rapid
TYPES OF ARRHYTHMIA heart rate is also in the atria, however, the • Adversely affects the cardiac output
A. PREMATURE ATRIAL CONTRACTION (PACs) atrioventricular node is not involved in this case. • Types:
1. Tachycardia
- Ectopic beat originates in the atria and may present as a. Premature ventricular contractions (PVCs)
2. Bradycardia
irregular rhythm b. Ventricular tachycardia
- Will not compromise the CO c. Ventricular fibrillation

A. PREMATURE VENTRICULAR
WHAT IS SINUS TACHYCARDIA? D. ATRIAL FIBRILLATION (A-FIB) CONTRACTIONS (PVCS)
- A sinus rhythm of higher than 100/min - Classic irregular rhythm - A premature beat arising from the ventricle
- Impulses originate at S-A node at rapid rate - a rapid, irregular heartbeat - Occurs occasionally in the majority of the normal
- It occurs most often as a physiological response to - HR: >300 bpm population
physical exercise or psychical stress, but may also - is seldom a life-threatening arrhythmia, but over time - On ECG: no P wave; wide bizarre QRScomplexes
PREMATURE ATRIAL TACHYCARDIA (PAT) it can be the cause of more serious conditions such as - Serious: > 6 per minute
result from congestive heart failure.
• Rhythm - Regular stroke.
- A run of PACs occurring at a fast rate (100-200 bpm) - Avoid PT intervention if the patient’s HR is greater
• Rate - More than 100 beats per minute
than 115 bpm
• QRS Duration - Normal B. Paroxysaml Supraventricular Tachycardia (PSVT)
• P Wave - Visible before each QRS complex - a.k.a. paroxysmal atrial tachycardia (PAT).
• P-R Interval - Normal • Rhythm - Regular
- These arrhythmias are common in young people
• The impulse generating the heart beats are normal, but • Rate - Normal
- Common cause is digoxin toxicity
they are occurring at a faster pace than normal. Seen • QRS Duration - Normal
- HR : 140 – 250 bpm
during exercise • Rhythm - Irregularly irregular • P Wave - Ratio 1:1
• Rate - usually 100-160 • P Wave rate - Normal and same as QRS rate
beats per minute but • P-R Interval – Normal
slower if on medication
• QRS Duration - B. VENTRICULAR TACHYCARDIA (V-TACH)
Usually normal • A run of 3 or more PVCs occurring sequentially
WHAT IS SINUS BRADYCARDIA?
SUPRAVENTRICULAR TACHYCARDIA (SVT) • P Wave - Not • fast, regular beating of the heart is caused by
- A sinus rhythm of less than 60/min distinguishable as the abnormal electrical impulses originating in the
- Impulses originate at S-A node at slow rate • Rhythm - Regular atria are firing off all ventricles
- This may be a consequence of increased vagal or • Rate - 140-220 beats per minute over • Very rapid rate (150-200 bpm)
parasympathetic tone. • QRS Duration - Usually normal • P-R Interval - Not • HR =>> ↓ CO
• P Wave - Often buried in preceding T wave measurable
• On ECG: wide bizarre QRS; no P wave WHAT IS CARDIAC ARREST? • Mobitz type I • P Wave rate - Normal but faster than QRS rate
• Medical intervention should be initiated ASAP - A.k.a. Wenkebach phenomenon. • P-R Interval - Variation
- the abrupt loss of the heart's ability to pump blood due - Presents with gradual increase in PR length in the
o No PT intervention • Complete AV block. No atrial impulses pass through
to arrhythmia. preceding beats & then an eventual dropped beat the atrioventricular node and the ventricles generate
o Initiate CPR
o Activating ACLS • Mobitz type II their own rhythm
BRADYCARDIAS - Has N PR intervals in all the beats preceding the
• Rhythm - Regular
• Rate - 180-190 Beats per minute a. Sinus bradycardia dropped beats
• QRS Duration - Prolonged b. Atrioventricular block
• P Wave - Not seen
• Results from abnormal tissues in the ventricles A. SINUS BRADYCARDIA BUNDLE BRANCH BLOCK
generating a rapid and irregular heart rhythm. ◦ sinus node isn't sending impulses properly
• Poor cardiac output is usually associated with this - Conduction delay through the Bundle of His
◦ Causes: hypothyroidism drug side effect
rhythm thus causing the pt to go into cardiac arrest. - Not true arrhythmia because there is no change in the
◦ Treatment: pacemaker c1. Second-degree Block Type 1 (Wenckebach)
• Shock this rhythm if the patient is unconscious and actual rhythm, just in the timing of conduction
• Rhythm - Regularly irregular through the bundle of His
without a pulse. • Rate - Normal or Slow • Rhythm - Regular
• QRS Duration - Normal • Rate - Normal
• P Wave - Ratio 1:1 for 2,3 or 4 cycles then 1:0. • QRS Duration - Prolonged
• P Wave rate - Normal but faster than QRS rate • P Wave - Ratio 1:1
• P-R Interval - Progressive lengthening of P-R • P Wave rate - Normal and same as QRS rate
B. ATRIOVENTRICULAT (AV) BLOCKS interval until a QRS complex is dropped • P-R Interval – Normal
C. VENTRICULAR FIBRILLATION (V-FIB)
- Abnormal delays or failure to conduct through normal
• rapid, chaotic electrical impulses that cause ventricles
conducting system
to quiver uselessly instead of pumping blood
a. First degree
• can originate from many different locations in the
b. Second degree
ventricles
c. Third degree BUNDLE BRANCH BLOCK
• Ventricles do not contract
o Life threatening c2. Second-degree Block Type 2
• No effective CO - is an abnormality in the heart's electrical system that
o Requires medication (atropine) • Rhythm - Regular
• Clinical death within 4-6 min. causes life-threatening arrhythmias.
o Surgical implantation of pacemaker • Rate - Normal or Slow
• On ECG: bizarre, erratic act. QRS complex - occurs most often in young adults.
• QRS Duration - Prolonged
• Activate ACLS with electrical defibrillation & WHAT IS A PACEMAKER
a. First-degree AV block • P Wave - Ratio 2:1, 3:1
medications (lidocaine)
- the P-wave always precedes the QRS-complex but the • P Wave rate - Normal but faster than QRS rate - it is an implanted device that monitors heartbeat and
PR-interval is prolonged over 0.2 s • P-R Interval - Normal or prolonged but constant prevents the heart from beating too slowly
• Rhythm - Regular
• Rate - Normal
• Rhythm - Irregular • QRS Duration - Normal
• Rate - 300+, disorganised • P Wave - Ratio 1:1
• QRS Duration - Not recognisable • P Wave rate - Normal
• P-R Interval - Prolonged (>5 small squares) d. Third-degree AV block
• P Wave - Not seen
- Complete lack of synchronism between the P-wave
• This patient needs to be defibrillated!! QUICKLY
and the QRS-complex
- Impulses originate at AV node and proceed to
ASYSTOLE ventricles AUTOMATIC IMPLANTABLE CARDIOVERTER-DEFIBRILLATORS
(AICD)
• Rhythm - Flat
• Rate - 0 Beats per minute b. Second-degree AV block
- can control abnormal, life-threatening heart rhythms
• QRS Duration - None - the PQ-interval is longer than normal and the QRS-
and prevent cardiac arrest.
P Wave - None complex sometimes does not follow the P-wave
• • Cardioversion - When the ICD detects ventricular
• Carry out CPR!! - If the PR-interval progressively lengthens, leading to
tachycardia, it delivers a mild electrical shock that
the dropout of a QRS-complex • Rhythm - Regular converts the fast heartbeat into a slower, normal
• Rate - Slow heartbeat.
• QRS Duration - Prolonged
• Defibrillation - When the ICD detects ventricular
• P Wave - Unrelated fibrillation, it delivers a strong electrical shock that
 defibrillates or resets your heart to start beating b. Abdominal Aortic Aneurysm (AAA) - aorta • splinter hemorrhages in the nail beds
normally. between renal arteries & iliac branches • recurrent influenza-like illness
• Life Vest Wearable Defibrillator c. Peripheral arterial aneurysm - femoral & popliteal RHEUMATIC FEVER • headaches
arteries • musculoskeletal complications: myalgias, arthralgias,
- Is an infection caused by streptococcal bacteria that back pains
AORTIC DISSECTING ANEURYSM can be fatal or may lead to rheumatic heart disease.
- most common symptoms: fever & joint pain WHAT ARE THE CONGENITAL HEART DEFECTS?
- is an often fatal disorder in which the inner layer - most commonly affects: mitral & aortic valves
(lining) of the aortic wall tears. - Signs and symptoms: - Interventricular septal defect
- blood can surge through, separating (dissecting) the • Arthritis - Interatrial septal defect
middle layer of the wall from the still intact outer • Fever - Patent ductus arteriosus
RADIOFREQUENCY ABLATION
layer. • Carditis - Coarctation of aorta
- a procedure that uses a catheter and a device for - Causes: • Subcutaneous nodules - Tetralogy of Fallot
mapping the electrical pathways of the heart. • high blood pressure • Erythema marginatum - Transposition of the great arteries
- a catheter is inserted into a vein and guided to your • hereditary connective-tissue disorders, especially • Chorea - Valvular stenosis
heart. Marfan syndrome and Ehlers-Danlos syndrome • Abdominal pain - Ebstein’s Anomaly
- Using high-frequency radio waves, doctors can • birth defects of the heart and blood vessels - Hypoplastic (L) heart syndrome
destroy (ablate) the pathways causing the arrhythmia (coarctation of the aorta, patent ductus arteriosus and - Truncus arteriosus
RHEUMATIC CHOREA
defects of the aortic valve)
OTHER CARDIOVASCULAR DISEASES
- a.k.a. St. Vitus’ dance VENTRICULAR SEPTAL DEFECT
A. Pericarditis VALVULAR DISEASES - may occur 1 - 3 months after strep. infection and
always occur after polyarthritis - oxygenated blood leak from the left ventricle into the
- may result into accumulation of fluid in the
- Caused by: - rapid, purposeless nonrepetitive movements that may right ventricle
pericardial sac, preventing the heart from
1. Disease (Rheumatic fever or coronary thrombosis) involve all muscles except the eyes
- expanding & reduces CO
2. Congenital deformity - may last for 1 wk or several months ATRIAL SEPTAL DEFECT
- Signs & Symptoms:
3. Infection (Endocarditis)
• Substernal pain
- Signs & symptoms - allows blood from the left atrium to flow into the right
• Relieve by leaning forward or by sitting upright RHEUMATIC HEART DISEASE
• Easy fatigue atrium, instead of into the left ventricle.
• Aggravated by movement and associated with deep
• Dyspnea - Mitral valve prolapse
• breathing(laughing, coughing, deep inspiration)
• Palpitation - secondary to rheumatic fever PATENT DUCTUS ARTERIOSUS
• Difficulty in swallowing
• Chest pain - may be asymptomatic or may present with symptoms
• History of fever, chills, weakness or heart disease
• Pitting edema that are poorly related - ductus arteriosus connects the pulmonary artery and
• What is Dressler’s syndrome?
• Orthopnea or paroxysmal dyspnea - to exertion and do not subside with rest or the aorta
• Dizziness or syncope nitroglycerin
CARDIAC TAMPONADE - types of valvular disease - mitral regurgitation is present PULMONARY STENOSIS
a. Stenosis - Signs & symptoms:
- Is a life-threatening complication caused by - narrowing or constriction that prevents the valve from • Nonanginal chest pain - the flow of blood from the right ventricle to the
accumulation of fluid in the pericardium opening fully • Palpitations pulmonary
- this fluid accumulates fast enough and in sufficient - may be caused by growths, scars or abnormal deposits • Fatigue - artery is obstructed by narrowing at the pulmonary
quantity to compress the heart and restriction blood on the leaflets • Dyspnea valve
flow in and out of the ventricles. - Aortic Stenosis
- This is a cardiac emergency! b. Insufficiency B. Endocarditis AORTIC STENOSIS
- A.k.a. Regurgitation - Inflammation of the cardiac endothelium caused by
- occurs when the valve does not close properly and infection
ANEURYSM - it is a narrowing or obstruction of the aortic valve
causes blood to flow back into the heart chamber - damages the tricuspid, aortic or mitral valve opening, making it difficult for the heart to pump
c. Prolapse (vegetations)
- Causes: trauma, congenital vascular disease, blood into the aorta
- occurs when enlarge valve leaflets bulge backward - often a consequence of receiving dental treatment
infection, atherosclerosis
into the atrium - Signs & symptoms:
- Types: Saccular, Fusiform, Pseudoaneurysm COARCTATION OF AORTA
- affects only the mitral valve • Fever
- Sites of aneurysm:
a. Thoracic aneurysm - ascending, transverse or • Night sweats - it is a narrowing or constriction, in a portion of the
descending aorta • Petechiae of the skin & mucus of eyes & mouth aorta
 PTY316- • What is the BP? Is it the same in both arms? What is
it sitting and standing?
Finals Reviewer •
TRANSPOSITION OF THE GREAT ARTERIES If the patient has been revascularized. what vessels
CARDIOVASCULAR ASSESSMENT were involved and what is the status of the other
- the positions of the aorta and the pulmonary artery are vessels
CARDIOVASCULAR EXAMINATION
reversed • Does the patient continue to have ischemia after the
- how cardiac impairment has impacted cardiac revascularization?
EBSTEIN’S ANOMALY function?
- plan safe and appropriate exercise interventlons
- it is a defect of the tricuspid valve • V02 is directly related to CO
- The valve is positioned lower than normal into the • an increase in Vo2. such as that with exercise. will
ventricle instead of remaining between the atrium and result in an increase demand for CO
the ventricle • Therefore, anything that limits CO will limit the
amount of systemic energy that the patient has
ATRIOVENTRICULAR CANAL DEFECT avail able

- a large hole in the center of the heart and a single QUESTIONS THAT IS IMPORTANT TO BE ANSWERED
common valve
- A.k.a. atrioventricular septal defect • What is the patient’s cardiac diagnosis and history
(e.g., ischemia. noncomplicated Ml. complicated MI. MEDICAL RECORD REVIEW
- often associated with Down syndrome
CHF) • helpful in understanding patient status and planning
• Does the patient presently have ischemia? If so, how physical therapy interventions
TRUNCUS ARTERIOSUS
does the angina present? • Depending on the type of setting the specific content
• What is the result of the latest exercise tolerance test of the medical record may vary
pulmonary artery and aorta merge into one single great
in order to identify the ischemic RPP
vessel (truncus) arising from the right and left ventricles
• What is the patient’s base line rhythm and rate?
ACUTE IN-PATIENT RECORD
(Identify any ectopy and the EKG interpretation of the
TETRALOGY OF FALLOT rhythm .)
- generally the most thorough regarding
- Named after Etienne-Louis Arthur Fallot (1888) who medical/surgical intervention
described it as "la maladie blue" - Important things to note:
- consists of a number of a number of cardiac defects • Medical problems. past medical history, physician's
possibly stemming from abnormal neural crest examination
migration. • Medications including type. dosage, and schedule
- It is a combination of four (tetralogy) congenital • Laboratory tests
abnormalities: o Blood tests for specific cardiac enzymes that may
1. Stenosis of pulmonary valve indicate an MI has occurred, such as a positive
2. Interventricular septal defect CK-MS or troponin level.
3. Aorta has communication with both ventricles o Electrolytes. especially potassium (K), If
4. (R) ventricular hypertrophy ventricular arrhythmias are present. and albumin
If CHFis present
------------------------------END-------------------------------- o Complete blood count (CBC)
o Presence of CAD risk factors. such as elevated
lipid values (e .g., total cholesterol , low-density
lipoproteins [LDL] triglyceride ), and elevated
blood sugars (glucose)
o Arterial blood gases (ABGs)
• Results of any diagnostic studies or interventions:
CxR, EKGs. EIT, cardiac catheterization, surgical
reports, hemodynamic monitors (e.g. pressure
readings from central line and/or arterial line)
• Nursing and other health care provider notes
 PATIENT INTERVIEW
- formal patient interview should follow the medical
record review.
- determination of overall cognition (e.g. orientation.
memory, learning needs, comprehension) should be
made.
- Patients’ lifestyle, previouslevel of functioning,
recreational interest, work requirements. and goals is
important in establishing the intervention.
- patient 's response to health and illness, coping status
support systems. and knowledge of heart disease.
* not all the information from the Interview need to be
obtained on the first session.
- Patient education can often be woven into the
interview process.
- Patientshould describe on his or her own words, the
quality and location of the symptoms
- Cautious about assuming that the patient‘s symptoms
is pain
• Pressure
• Heaviness
• shortness of breath (dyspnea)
• Aching
• Heartburn
• General malaise
- interview also helps to establish rapport and trust
between therapist and patient
TYPES OF ANGINA
1. Stable
- Response to rest and nitrates
- Predictable during exertion
- Same location of pain overtime
- Can the pt still continue exercise???
2. Unstable
- Preinfarction angina/ progressive angina/ crescendo
angina
- Does not respond to rest and nitrates
- Call for Emergency medical services (EMS)
- Can the pt still continue exercise???
3. Nocturnal angina
- At night during sleep
- (+) exertion 2 to dreams
4. Prinzmetal
- (+) spasm on blood vesselsthat will lead to decrease
blood supply (coronary artery spasm)
- No occlusion but purely spasm
- Common in women in post-menopausal
VITAL SIGNS
- HR and Rhythm
• either by palpation or auscultation it is Important 10
count for a full minute
• When examining the patient’s response to an activity
and no arrhythmia is present an immediate post-
exercise HR can be taken for 10 seconds
• rhythm is regular or irregular and report it as such
(EKG)
• normal respiratory variation in HR: inspiration results
in an increase in HR. expiration in slowing down of
HR
- Respiratory Rate, Rhythm, and Shortness of
Breath
• both rate and rhythm of respiration should be noted,
as well as the breathing pattern and use of accessory
muscles
• Shortness of breath and report that it is anxiety
provoking
o Dyspnea on exertion
o Paroxysmal Nocturnal Dyspnea-assc with LV
failure
▪ Impt to note how many pillow is needed to feel
comfortable breathing
▪ elevating the trunk venous return is slightly
delayed and the work of the LV is temporarily
decreased
▪ Orthophnea
- Blood Pressure
• CO and PVR (BP = CO X PVR)
• increase in either of these factors will increase BP. and
a decrease in either may decrease blood pressure
• slightly higher in supine than in either sitting or
standing because of the increase in venous return in
the gravity-minimized position
• BP usually normalizes within secondsto a minute of
standing
• Orthostatic Hypotension
o sudden prolonged drop in BP that accompanies a
position change from lying to either silting or
standing
o Iightheadedness. dizziness, and loss of balance
o Drop of systolic BP of >20 mmHg
o Standing BP < 100 mmHg systolic
• Risk
o Prolonged bed rest
o Volume depleted.
o PVD
o Muscle atrophy
o Vasodilators or antihypertensive drugs
• Treatment
o Slow, stepwise progression from supine to sit,
gradually elevating the HOB to allow
physiologic adaptation to occur.
o deep breaths and perform ankle pumps.
o support stocking or ace wraps
OBSERVATION, INSPECTION, AND PALPATION
• Cyanosis
- bluish color of the skin . nail beds. and possibly lips
and tongue
- present when arterial oxygen saturation is 85 percent
or less
• Pallor
- absence of a pink rosy color
- indicate a decrease in CO
• Diaphoresis
- Excess sweating cool clammy skin
- excessive effort or inadequate cardiovascular
response
• Cold fingertips
- Compensatory vasoconstriction in response to a
decreased CO or from the suppressed beta
sympathetic response of some bela-blockers.
PALPATION
- Femoral, Dorsalis pedis. and posterior tibialis pulses.
- Compared bilaterally and documented as
• bounding (4 +)
• Normal (3 +)
• weak (2 +)
• •thready ( I +)
• absent (0)
- decrease in CO or a local arterial occlusion.
EDEMA
- LV failure may have an increase in peripheral edema
- owing to the increase in hydrostatic intravascular
pressure associated with increased pressure from the
LV transmitted retrograde through the heart to venous
system
- Bilateral peripheral edema may be a result of CHF
- Edema of one leg. however, is usually associated with
local factors within the same leg such as varicose
veins. lymphedema, or thrombophlebitis
• Auscultation
- listening of the heart sound.
- SI: (lub), which occur, at the time of the closure of the
mitral (and tricuspid) valve and marks the beginning
of systole
- S2: (dub), which occur at the time of aortic (and
pulmonic) valve closure and mark the end of systole
• Abnormal heart sounds
a. Murmurs
- commonly the result of vascular disorder, due to the
changes in blood flow around or through the altered
valve
- Systolic murmur - Present as audible turbulence
between S1 and S2
- Diastolic murmur - Audible turbulence between S2
and S1
b. S3 and S4
- S3 also known ventricular gallop, occurs after S2 and
is clinically associated with LV failure
- S4 also known as an atrial gallop, occurs before S1
and is clinically associated with an MI or chronic
hypertension.
c. Pericardial Friction Rub
- high pitched with a leathery and scratchy quality,
although they may vary in intensity from hour-to-hour
or day-to-day or may even transiently disappear.
- inflammation of the pericardialsac either with or
without excessive fluid
- trauma. infections. tumors. collagen diseases.
anticoagulants. and MI
- Dressler's syndrome
d. Bruit
- carotid and femoral arteries
- Indicates narrowing of arteries
- Probable presence of atherosclerotic disease.
AUSCULTATION SITE:
LOCATION OF THE VALVE:
 DIAGNOSTIC TOOLS PTY316- • Candidates for cardiac rehabilitation
- Post MI
• ECG Finals Reviewer - Post CABG
- P wave CARDIAC REHABILITATION - Post transplant
- QRS complex - Post valvular surgery
- T wave CASE DESCRIPTION
• Chest X-ray Two Primary goals of Cardiac Rehabilitation
A 65 y.o male was admitted to the hospital with acute
- To assess the shape and size of the heart 1. Increase functional capacity
decompensated heart failure for tailored medical therapy
• Myocardial perfusion imaging 2. Alter natural history of cardiac disease to reduce
including dobutamine. When the pt. is medically stable,
- Thalium 201 scan: disease to reduce morbidity and mortality
he is referred to you for exercise training. As a senior PT
o Inject thalium via IV
student, how will you go about designing PT
o Binds to (N) tissue Overall goals of the Cardiac Rehabilitation
intervention?
o (+) cold spots - To reduce myocardial ischemia and the risk of
- Thallium stress test: Use threadmill or bicycle ergo infarction or sudden death
then inject thalium at the peak of exercise CARDIAC REHABILITATION
- To maximize cardiovascular capacity and fitness
• Echocardiogram • A multiphasic program of medical care designed to - To maximize exercise tolerance and activities of daily
- Use US restore the heart diseased to a full productive life living performance
- Internal structure of the heart • Members of the cardiac Team - To establish a patient-controlled and safe aerobic
- Movement of heart wall and valves - Cardiologist exercise program
• Cardiac catherization - Physiatrist - To provide guidelines for safe activities and work
- Injection of catheter in the heart and cinefluroscopy - Physical therapist - To control risk factors for coronary artery disease
- Thru artery(femoral of radial) - Occupational therapist - To help patients cope with perceived stressors
- Nurse - To utilize energy conservation and work
- Psychologist simplification
- Speech and language therapist - To improve quality of life
------------------------------END-------------------------------- - Nutritionist
- Vocational counsellor 4 PHASES OF CARDIAC REHABILITATION

- Phase I (In-hospital phase or acute phase)

BENEFITS OF THE PROGRAM
• Goal
- Improves the quality of life o Prevent complication of bedrest
- Improves circulatory state and pulmonary ventilation o Resume functional activities
- Enhances functional performance • Activities
- Maintain physical, psychological, occupational and o Step ladder program of functional activities
vocational status o Patient’s education
- Intervention modalities • Discharge requirements
• Exercise program o Does self-monitoring of exercise response to
• Vocational counselling activity
• Psychological counselling o Knowledgeable on energy conservation and
• Patient’s education pacing activities
o Simple convalescent phase exercise program has
FUNCTIONAL CLASSIFICATION (NEW YORK HEART ASSOCIATION) prescribed
o Advise on recommended lifestyle changes
reinforced

- Phase II (Convalescent phase)

• Purpose
o Allow a strong scar formation in the myocardium
o Reduce risk for ventricular aneurysm or rupture
• Goal
o Maintain early mobilization
o Gradually increase exercise endurance at the
same intensity as acute phase
• Pre-requisite • Venous distention - Acute systemic illness TYPES OF TREADMILL TESTING PROTOCOLS
o Previous in-patient rehabilitation • Metabolic Equivalent:
o Activity; Walking or bicycling - Energy of the cost of various activitiesto the resting RELATIVE CONTRAINDICATIONS TO EXERCISE TESTING • Bruce
o Intensity-same as target HR used at the end of the state • Cornell
acute phase - 1 met=3.5ml.oxygen/Kg/min - Significant pulmonary hypertension
• Balke-ware
❖ 1.0 (lying) - Significant arterial hypertension
- Tachyarrthymia/ bradyarrythmia • Naughton
- Phase III (training phase 6-8 weeks 3x/wk) ❖ 1.2 – 1.6 (sitting) • Weber
• Pre-requisite ❖ 1.9 – 2.2 (sit with writing) - Moderate valvular disease
o Symptom is limited by exercise tolerance test ❖ 1.4 – 2.0 (standing) - Electrolyte abnormalities
- Left main coronary obstruction FREQUENCY OF THE EXERCISE
ETT ❖ 2.5 – 2.6 (standing plus wash and shave)
❖ 2.3 – 3.3 (Standing plus dress and undress) - Hypertrophic dardiomyopathy • Functional capacity- 3-5x/wk to improve and
• Activity
o Stretching an aerobic exercise ( treadmills, UE ❖ 2.3 (walking 1m/hr) - Psychiatric disease maintain
or LE ergometer, air dynes, rowing machines, ❖ 3.1 (walking 2m/hr) • Functional Capacity
walking, running and calisthenics) ❖ 4.3 (walking 3m/hr) BASIC PRINCIPLES OF EXERCISE STRESS TEST • Cardiopulmonary patients- <3 mets,5
• Intensity ❖ 7.4 (running) - Use the physiological response to exercise to increase min/session/day
o Target HR is computed from the maximum HR ❖ 2.8 (wc to drive) physiological demand on the myocardium which • Persons with Functional Capacity of 3-5 mets, 1-
on ETT ❖ 5.2 (stair descend) increase the MVO2 which can reveal ischemic 2/daily
• Contraindications ❖ 9 (stair ascend) changes via ECG • Persons with Functional Capacity 5-8 mets, 3-5/wk
o Dangerous arrhythmias on ETT ❖ 5.7 (2 steps with climb)
o Decreasing HR with increasing exercise ❖ 1.5 (eating) TYPES OF CARDIAC STRESS TEST INTENSITY OF THE EXERCISE
intensity ❖ 2.0 (washing face)
❖ 3.5 (shower) • electrocardiographic exercise tolerance testing • 60-70% of Functional Capacity - average
o If with benign end-point on EET, can use 85% of
❖ 4 (with bedpan) treadmill stress test conditioning intensity for asymptomatic patients
maximum HR •
❖ 5 (sex with wife) - readily available equipment • 40% FC- cardiac patients
o as target HR
o If serious arrthythmia or ECG changes but no ❖ 8 (extramarital) - well standardized with severaltypes of protocols • Intensities may prescribed thru
chest pain on ❖ 1.73 (light housework) available - HR
o EET lower intensity ❖ 3-6 (heavy housework) • bicycle ergometry o Karvonensformula
❖ 1.3-2.3 (officework) UE ergometry - METS
• Monitoring •
Karvonen’s formula Echocardiograph stress testing o If a patient through exercise stress is identified as
o ECG telemetry if progressing the exercise and • •
borg scale. - THR=RHR+60-80% (MHR-RHR) • Nuclear stress testing having an 8 MET capacity, the prescription for
- MHR=220-age • Pharmalogicalstresstesting exercise is determined by multiplying the MET
o UE MHR=220-age-11 - Uses dypiridamole capacity by the percentage of the FC best
- Phase IV (Maintenance phase)
o Elderly 90-60% - Can be used in all patient even those severely identified fot the training of that person (e.g.
• Exercise program is continued by the patient at home
o Athelete 80-90% decondition and impaired 70%x5.6 mets=3.92 mets)
same as last phase of the three phase of cardiac
Purpose of exercise tolerance testing - Is wellstandardized with good reliability • Rate of Perceived exertion (Borg scale)
rehabilitation program •
- Cardiac risk stratification - Limitations:
CRITERIA FOR MODIFYING OR TERMINATING A CARDIAC ACTIVITY - Determine functional capacity o Not physiological
- Basis for designing an optimal aerobic training o Has risk related to intake of the drugs
- Symptoms program without undue risk to the cardiac patient o Invasive
• Fatigue o Need special imaging equipment
• Light headedness ABSOLUTE CONTRAINDICATIONS TO EXERCISE TESTING • Isometric hand grip test
• Cough and dyspnea • A dynamometer is held isometrically at the ¼ to ¾ of
• Nausea - Unstable angina with recent chest pain the maximum hand strength as long as possible
- Signs - Untreated life threatening arrythythmia
• Confusion, pallor, ataxia and cyanosis - Uncompensated CHF BRUCE PROTOCOL
• Diaphoresis - Advance heart blocks
• Increase HR > 20 bpm above standing HR with - Acute myocarditis/pericarditis THERAPEUTIC CLASSIFICATION OF CARDIAC PATIENTS
activity - Critical aortic stenosis
- Severe hypertrophic obstructive cardiomyopathy • Class A - with cardiac disease whose physical activity
• Excessive BP rise with systolic of 220 and diastolic
- Uncontrolled hypertension need not to be restricted
of 120 mmHg
- Acute myocardial infarction • Class B - with cardiac disease whose ordinary
• Inappropriate bradycardia (> 10 bpm)
- Acute endocarditis physical activity need not be restricted, but advised
• Altered heart sounds or murmur
- Acute pulmonary embolus against severe or competitive efforts
• Class C - with cardiac disease whose ordinary - Individualization of the CV component can be
physical activity need should be moderately restricted achieved by varying; duration spent at each CV
and whose more strenuous effortshould be station, intensity (increase resistance, speed or ROM),
discontinued. period of rest, overall duration of the class
• Class D - with cardiac disease whose ordinary
physical activity should be markedly restricted COOL DOWN
• Class E - with cardiac disease who should be at
complete bedrest or confined to a chair or a bed - The goal is to bring back the body to its pre-exercise
state
DURATION OF EXERCISE - Duration: 10 minutes
- Low intensity exercises like passive stretching of the
• Aerobic period of training - 20-30 minutes
major muscle
• Warm up - 5 to 15 mins
- Goals and expectations with cardiac exercise
• Cooldown - 5 to 10 mins
✓ Lower maximum oxygen consumption during
submaximal workloads
SAMPLE FORMAT OF A CARDIAC REHABILITATION CLASS
✓ Reduced cardiovascular risk, reverse risk factors
1. VC ✓ Develop healthy, productive coping behavioural
2. Warm Up (15 mins) mechanism with improved
3. Main class (30 mins) ✓ quality of life
4. Cool down (10 mins) ✓ Complete return to work
5. Reassessment of vitals ✓ Patient education

------------------------------END--------------------------------
WARM-UP

- Aim: Prepare the body for physical activity by

gradually and safely increasing the heart rate.
- Incorporate activities that elevate the heart rate for 5
minutes; example:
1. marching in place,
2. walking, or
3. engaging in low-intensity cycling.
4. perform stretching targeting major muscle groups for
5 minutes, followed by additional pulse-raising
activities like 1-3

MAIN CLASS

- For group rehab circuit training seems most popular.

- Depending on CV status and functional capacity
patients may adopt an interval or continuous approach
to the circuit.
- Separate stations are set out and participants spend a
fixed amount of time at each aerobic station
- (30secs-2mins) before moving onto the next station
which may be rest or active recovery in the form of
resistance work targeted at specific muscle groups.
- Resistance work as set out by ACSM 2006 – 10-15
reps to moderate fatigue of 8-10 exercises (European
Journal of Cardiovascular Prevention and
Rehabilitation, American College of Sports Medicine
(2006)