Ms 1 Cardiac Diseases

7/31/2019 Ms 1 Cardiac Diseases

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SIGNS AND SYMPTOMS:

1. Chest Pain: maybe cardiac or non-cardiacCardiac: it is accompanied by:

a. Nausea

b. Vomiting

c. Diaphoresis

d. Dyspneae. Fatigue

f. Pallor

g. Syncope

2. Palpitation: irregular heartbeat

It maybe bump, pounding, jumping, flopping, fluttering or raising sensation of theheart (normal: less than 6 minutes; abnormal: last for hours with SOB, pain, severe

lightheadedness)

It is accompanied by:

a. Lightheadedness

b. Syncope


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3. Dyspnea: breathelessness or SOB due to:

a. Cardiac origin:

Maybe felt with exertion also called dyspnea with exertion

Maybe caused by impaired left ventricular function

Leads to: PULMONARY CONGESTION and SOB

If severe: dyspnea occurs at rest

Severe dyspnea includes:

a. Paroxysmal Nocturnal Dyspnea (PND)

b. Orthopnea: breathelessness that is relievd by sitting upright (effective ventilation and

perfusion of the lungs

b. Pulmonary in Origin

Dyspnea relieved by specific breathing pattern (pursed lip breathing)

Relieved by specific body position

4. Cardiac Syncope (Fainting) mild lightheadednessDue to:

Arrythmias (syncope without warning of lightheadedness, dyspnea or nausea)

Orthostatic hypotension

Poor ventricular function

Coronary artery disease (CAD)

Vertebral artery insufficiency


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Non-cardiac origin:

Anxiety

Emotional stress

Medication

5. Fatigue

Cardiac Origin: it is provoked by minimal exertion

It is accompanied by:

a. Dyspnea

b. Chest pain

c. Palpitationd. Headache

6. Cough

Left Ventricular CHF: cough is often hacking with frothy bloodtinged secretion

7. Cyanosis

8. Edema: Congestive Heart Failure

9. Claudication or Leg Pain: TYPES

a. Vascular Claudication: skin discoloration, trophic skin changes, cool skin

b. Intermittent Claudication: normal skin appearance at rest, exercising to the point ofclaudication (marked pallor in the skin)


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CARDIAC DISORDERS

CARDIAC PATHOPHYSIOLOGY:A. Obstruction or restriction

B. Inflammation

C. Dilation or distention

3 COMPONENTS:A. Conditions affecting the Heart Muscles

B. Conditions affecting the Cardiac Valves

C. Conditions affecting the Cardiac Nervous System


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A. Coronary artery disease (Coronary heart disease orIschemic Heart Disease

-Designation for many different conditions that involveobstructed blood flow through the coronary arteries

-A.k.a. Ischemic heart disease or coronary heart disease (CAD)

-And the most common type of coronary artery disease is theCORONARY ATHEROSCLEROTIC HEART DISEASE(CAHD);

-It is an isufficient blood supply to the myocardium secondaryto blocked or narrowed coronary artery that leads to:

Myocardial Infarction

Angina Pectoris


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EPIDEMIOLOGY:Most common cause of death (CAHD)

The incidence is higher in men than in women, in older persons and in the affluent

CAUSES:

A. Atherosclerosis a.k.a. Arteriosclerosis: it is a disease problem involving the

hardening of the arteries

Begins in childhood where the arteries begin to fill with fatty substances or lipid which then

calcify or hardens to become PLAQUES Gradually lines the arterial walls then progressively narrowing the arteries

When fully developed, plaque can cause bleeding, clot formation and rupture of the blood

vessels

B. Thrombus: when the plaque builds up on the arterial wall (THROMBOSIS) blood flow becomes slow and a clot may form in the plaque

C. Spasm: sudden constriction of coronary artery (nicotine, cocaine and cold air)


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RISK FACTORS

NON MODIFIABLE

1. Age

2. Gender

3. Race

4. Family history

MODIFIABLE

MAJOR RISK FACTORS

1. Hyperlipoproteinemia (serum lipid level)

2. Habitual diet (high cholesterol, fat, refined

carbohydrates, sodium)

3. Hypertension

4. Obesity5. Glucose intolerance

6. Cigarette smoking

7. High level of fibrinogen (binds together platelet

cells to form blood clot)

8. Large amount of C-reactive protein: a specialized

protein for tissue repair9. The presence of troponin T (regulatory protein

that help to heart muscle contract

MINOR RISK FACTORS

1. Personality type

2. Sedentary lifestyle

3. Psychologic stress


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PATHOPHYSIOLOGY OF CAHD

The exact cause is unknown Coronary Atherosclerosis

involves a localized accumulation of lipid and fibrous tissue

within the coronary artery

Arterial narrowing and occlusion

As the disease progresses, it is accompanied by vascularchanges (it affects the functional ability of the artery to dilate)

Results in the variable reduction of blood flow to the

myocardium


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SUPPLY

DECREASED

DEMANDUNCHANGEDMyocardial

oxygen

POSSIBLE CAUSES:-coronary artery osbtruction

-hypoxia

-inadequate perfusion-inadequate hemoglobin


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SUPPLY

UNCHANGEDDEMAND

INCREASED

Myocardial

oxygen

POSSIBLE CAUSES:

-increase heart rate-increase contractile state of the

myocardium

-increased afterload

-left ventricular size


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ANGINA PECTORIS-It is characterized by paroxysmal substernal pain, radiatingdown the inner aspect of the left arm

-Patient describes it as:

a. Heaviness or tightness of the chest

b. It maybe interpreted as indigestion

c. Pain is usually diffuse and rarely can be pinpointed at aspecific site

d. Patient maybe gripping the sternum

e. It is associated with exertion and relieve by rest

CAUSE: temporary inadequacy of the blood supply of heartmuscles (an increase in myocardial oxygen demand withinadequate myocardial oxygen supply)


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TYPES OF ANGINA PECTORIS

1. STABLE ANGINA

-Angina caused by exertion or emotion and relieve by rest

-Common in 50-60 y/o (men) and 65-75 y/o (female)

-Characterized by squeezing, central, substernal discomfort usually with

cresendo and decresendo lasting for 1-5 minutes and can radiate to left

shoulder, and to both arms usually on the ulnar surface of FA and hands (ST

SEGMENT DISPLACED)

2. UNSTABLE ANGINA

-angina at rest

-accelarating angina characterized by chronic stable angina who develops

angina that is more frequent, severe, prolonged or precipitated by less exertion

than previously

-3 episodes/ day

3. PRINZMETALSANGINA PECTORIS (ST SEGMENT- ELEVATED)

- Form of angina pectoris, recurrent prolonged attacks of severe angina caused by

episodic, focal spasm of epicardial coronary artery (30-40 y/o)

4. ANGINA DECUBITUS

-nocturnal angina


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MYOCARDIAL INFARCTION

-It is caused by a sudden block (CORONARY

OCCLUSION) of one of the branches of the coronary artery

which leads to necrosis or death of of the portion of the

myocardium with subsequent healing by scar formation orfibrosis

-Causes maybe: Coronary thrombosis, or a sudden progression

of atherosclerotic changes, or prolonged constriction of the

coronary arteries

-A prolonged ischemia (lasting more than 35 to 45 minutes)

produces irreversible cellular damage and necrosis of

myocardial muscle MYOCARDIAL INFARCTION


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MyocardialIschemia

Stimulation of

baroreceptors

Decrease Myocardial

oxygen supply

Increase Cellular hypoxia

Altered cell membraneintegrity

Decrease myocardial

integrity

Decrease cardiac output

Decrease arterial pressure

Increased myocardial oxygen

demand

Decrease coronary perfusion

Decrease diastolic filling

Increase HR

Increase myocardial

contractility

Sympathetic response

Increase

afterload

Peripheral

vasoconstriction


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MANIFESTATIONSAnterior wall myocardial infarction:

a. There is an occlusion of the anterior descending branch of the leftmain coronary artery (supplies the left ventricle)

-Substantial loss of left ventricular muscle mass and can result tosevere hemodynamic disturbances

Inferior wall myocardial infarction:

a. There is an occlusion of right coronary artery and it supplies theAV node and SA node

-ischemia of the AV node, proximal bundle of His and the SA node

(abnormalities in impulse conduction leading arrythmias)Lateral wall myocardial infarction:

a. Occlusion of the left circumflex coronary artery

-same as anterior wall MI


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Pain (most frequent complaint); sudden, severe, crushing

pain in the substernal region which radiates into the left and

sometimes the right arm and up the sides of the neck

Simulates indigestion or a gallbladder attack with abdominal

pain and vomiting

Restlessness and fear

Shortness of breathe and cyanosis Wheezes and crackles upon auscultation

Rapid and barely perceptible pulse

Hypotension

Soft systolic murmurs


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HEART DISEASES

Classification:

a. Congenital heart disease

b,. Acquired heart disease


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A. PERICARDITIS

Result from

bacterial, viral orfungal infection or it

occurs due to

complication of a

systemic disease (RA,

SLE, uremia,scleroderma, MI or

trauma)


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-Inflammatory process of thepericardium

-Characterized by accumulation of

fluid in the pericardial sac CARDIAC

TAMPONADE (COMPRESSION OF

THE HEART)

Effects:

a. Decrease venous return

b. Decrease ventricular emptyingc. Leads to cardiac failure


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A. ACUTE PERICARDITIS

- A predominant clinical manifestation (PERICARDIAL

FRICTION RUB) with severe chest pain (left shoulder which

radiates to the neck and down to the left arm)- Intensified when: lying supine, coughing, swallowing, or

breathing deeply

- Accumulation of fluid (1 L) in the pericardial sac (gradual, the

patient notice little pain)

SYMPTOMS OF CARDIAC TAMPONADE:

1. Diminishes or absent point of maximal impulse

2. Diminished heart sound

3. Tachycardia

4. Paradoxical pulse

5. Narrowed pulse pressure

6. Distended neck veins


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B. CHRONIC PERICARDITIS

-results from fibrosis of the pericardial sac secondary to trauma

or neoplastic disease

-pericardium becomes tighten around the heart and decreases its

efficiency as a pump

-dyspnea, fatigue, exhibits a symptoms of congestive heart

failure (inability of the heart to pump blood)


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MYOCARDITIS

-It is an inflammatory diseaseof the myocardium

-Maybe primary or secondary (drug hypersensitivity or

toxicity and infection)

INFECTION CAN RESULT IN ONE OF 3 WAYS:a. Invasion of the myocardial tissue by an organism (most

common: bacteria and protozoan (worldwide); virus (north

america)

b. Production of toxin

c. Autoimmune reaction


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SYMPTOMS:

ACUTE PHASE OF INFECTION:

a. Flulike symptoms

b. Fever

c. Lymphadenopathy

d. Pharyngitis

e. Myalgia

f. GIT complaints

g. Hepatitis

h. Encephalitisi. Nephritis

j. Orchitis

The most common cardiac symptom:

PERICARDIAL PAIN

Heart failure, pericardial effusion,syncope and ischemia

Preliminary laboratory findings are

non-specific; elevated ESR,

leukocytosis, X-ray may show normal

heart size


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ALCOHOLIC CARDIOMYOPATHY-when a person consumes a

large quantities of alcohol for

more than 5 years (ethanol;

direct toxic effect on cardiac

tissues)

Gradualfatigue

dyspnea on exertion

Pulmonary crackles

Cardiac murmursIncrease BP

Conduction defects

Dysrythmias

X-ray heart is flabby

Left ventricular hypertrophy


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INFECTIVE ENDOCARDITIS

-It is the infection of theendocardium and mostly the

heart valves secondary to

streptococcal infection

(subacute) or staphylococcus

infection

TYPES

a. Acute- occurs rapidly often

on a normal valve and ifuntreated may cause death

b. Sub-acute- occurs in an

already damaged valve

PATHOPHYSIOLOGY


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PATHOPHYSIOLOGY

Previously damaged heart

valve

Allows a turbulent blood flow

and bacteria settling on the

stenotic side of the valve

The organism bombard the

valves, resulting in vegetative

growth, scarring and

proliferates the leaflet

-HALLMARK: (+) platelet-fibrin-bacteria mass

ENDOCARDITIS

Most severe: if the massbreaks free, enters the

bloodstream and become

an emboli


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MANIFESTATIONS

1. Often gradual

2. Malaise and general achiness

3. Low grade fever

4. arthralgia, arthritis, low back pain, myalgias, tenosynovitis,

anorexia, weight loss, chest pain and occasional hemoptysis

4. Reveals splenomegaly, clubbing of fingers, the presence of

OSLERSNODES (small-raised, tender, bluish areas onfingers and toes), petechiae (small capillary hemorrhages

conjunctiva, mouth and extremities)

5. Murmurs over the cardiac valves


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DIGITAL CLUBBING

-also known as "Drumstickfingers," "Hippocratic fingers,"

and "Watch-glass nails

Fluctuation and softening of the nail bed

(increased ballotability)

Loss of the normal


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RHEUMATIC HEART DISEASE

Rheumatic fever: is an

inflammtory disease that affects

the heart, brain, joint and skin

-Usually caused bySTREPTOCOCCAL INFECTION

Symptoms include (but are notlimited to):

sudden onset of sore throat

pain on swallowing

fever, usually 101104F

headache

red throat/tonsils

abdominal pain, nausea and

vomiting may also occur, especially

in children

OTHER SYMPTOMS


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OTHER SYMPTOMS:

fever

painful, tender, red swollen joints

pain in one joint that migrates to

another one

heart palpitations

chest pain

shortness of breath

skin rashesfatigue

small, painless nodules under the

skin

RHEUMATIC HEART DISEASE:

-endocarditis, valvular stenosis,

myocarditis and pericarditis

-damaged in the heart valves


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VALVULAR HEART DISEASE TYPES

A. MITRAL VALVE STENOSIS

The most common and the primary

cause is rheumatic fever

- Thickening of the valve by calcifi-

cation and fibrous tissue formation

- Valve leaflets become stiff, narrows,

and immobile- The chorda tendineae shortens,

thick, and mitral orifice decreases in

size


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LEADS TO:

a. Hypertrophy of the left atriumb. Elevated left atrial pressure

c. Pulmonary hypertension and

congestion (higher pulmonary

pressure)

d. Impede the function of the

right ventricle resulting to right-

sided heart failure

e. Insufficient blood receive by the

left ventricle- decrease Cardiacoutput

f. Left ventricular atrophy


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SYMPTOMS:

a. Dyspnea on exertion

b. Paroxysmal nocturnal dyspnea

c. Orthopnead. Dry cough

e. Dysphagia

f. Brochitis or bronchial irritation

g. Pressure exerted on the laryngeal

nerve causes hoarsness

h. Excessive fatigue and weakness

(decrease CO)

i. Peripheral and facial cyanosis

j. Hemoptysis (later) (rupture ofbronchial veins)

k. Right sided heart failure

l. Distended jugular veins

m. Pitting edema and hepatomegaly


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MITRAL REGURGITATION


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MITRAL REGURGITATION

It is due to papillary muscledysfunction allows the leaflet

to flop in the direction of the

left atrium during systole

causing blood to backflow

MITRAL VALVE

PROLAPSE- is a form of

mitral insufficiency seen most

often in thin, young womenand it is often asymptomatic.


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AORTIC STENOSIS

congenital malformation (the most common etiologic factor)


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g ( g )

LEADS TO:

a. Obstruction of left ventricular outflowb. Left ventricular hypertrophy

c. As the disease progresses, CO decreases

d. Left atrium cannot empty adequately

e. Pulmonary congestion

f. Left ventricle (elevated myocardial oxygen need) (compression of the

coronary arteries) decrease supply

g. Give rise to Myocardial ischemia and angina (severe)

h. Eventually right sided heart failure

Three characteristic symptoms:


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Three characteristic symptoms:

a. Exertional dyspnea

b. Angina pectoris

c. Extertional syncope

Late stage:

a. fatigue

b. Weakness

c. Orthopnea

d. Paroxysmal nocturnal dyspnea

e. Pulmonary edemaf. Symptoms of right-sided heart failure (hepatomegaly, atrial

fibrillations, systemic venous distention)


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2. (L) atrial hypertrophy

Stiffening of the aortic valve

1. Increase (L) atrialpressure

3. Increase pulmonarypressure

4. Pulmonary congestion

5. (R) sided-heart failure

1. (L) ventricular

hypertrophy

2. Decrease cardiac output

2. Compression of

coronary arteries


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AORTIC REGURGITATION

-there is a backflow of blood to the left

ventricle due to incompetent aortic valve

SYMPTOMS:

a. Tachycardia (exertion)b. Premature ventricular beats

c. Exertional dyspnea

d. Angina pectoris (rest or exertion)

e. Hepatomegaly, ankle edema and ascites

(end-stage disease)

f. Aortic diastolic murmursg. Widened pulse pressure

h. ST segment depression and T wave

inversion (left ventricular hypertrophy)


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1. Increase (L) atrialpressure

2. (L) atrial hypertrophy

3. Increase pulmonary

pressure

4. Pulmonary

congestion

5. (R) sided-heart

failure

1. (L) ventricular

hypertrophy

2. (L) sided heart failure

BACKFLOW OF BLOOD TO THE LEFT VENTRICLE


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TRICUSPID STENOSIS


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TRICUSPID REGURGITATION

-backflow of blood to the right

atrium secondary to dilation of

the right ventricle that maycause dilation of the ventricular

ring and displacement of the

papillary muscles

(-) right ventricular output


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PULMONARY STENOSIS

-narrowing of the pulmonary valve

causing less blood to flow towards the

pulmonary circulation

Hypertrophy of the right ventricle

and right atrium

SYMPTOMS

Harsh systolic murmurs

Fatigue and dyspnea on exertion

Have symptoms of right sided heart

failure (hepatomegaly, ascites and

edema)


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PULMONARY REGURGITATION

-the pulmonic valve leaflets becomeincompetent and fails to close which

results in the back flow of blood to

the right ventricle during systole

right atrium and right ventricle

hypertrophies

Px exhibits symptoms of rightsided heart failure


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ACUTE CONGESTIVE HEART CHRONIC CONGESTIVE


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ACUTE CONGESTIVE HEART

FAILURE:

-Develops quickly and often

without warning

CLINICAL PICTURE:

Syncope

ShockCardiac arrest

Sudden death

CAUSE: by myocardium failingto function adequately or

decrease effectiveness of the

heart after myocardial infarction

CHRONIC CONGESTIVE

HEART FAILURE:

-Develops gradually and the

patient is seen initially with

milder symptoms

-The heart is capable to

compensate for the decrease

performance, thus lessening thesymptoms

ETIOLOGY:


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ETIOLOGY:

3 groups:

A. First group: conditions that result in

direct damage to the heart (MI,

Myocarditis, myocardial fibrosis,

Ventricular aneurysm)

B. Second Group: conditions that result

in ventricular overload

Preload: is the ventricular blood

volume at end-diastole or the

maximum blood volume for the beat of

the heart

STARLING LAW: once the preload is

reached a given limit, the effectiveness

of the contraction diminishes, resulting

to HEART FAILURE

Examples: mitral or aortic regurgitation,atrial or ventricular septal defect or

rapid infusion of IV solutions

Afterload: force that the ventricle

must develop to eject blood into the

circulatory system

Examples: aortic and pulmonary stenosis, systemic hypertension, or pulmonary


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p p y , y yp , p y

hypertension

C. Third Group: conditions that can lead to heart failure are does resulting in the

constriction of the ventricles that limits ventricular filling (decrease SV)Example: Cardiac tamponade, constrictive cardiomyopathies, pericarditis


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PATHOPHYSIOLOGY

CARDIAC COMPENSATORY MECHANISMS (ability of the weakenedheart to meet the metabolic demands of the body

Tachycardia- increasing the HR, CO increases; as HR increases diastole is

shortened up to the point where an inadequate filling of the ventricles

occurs (decrease CO)

Ventricular dilation- increase the VR leads to excessive stretching of thecardiac fibers (ventricular dilation), this allows for a more forceful

contraction, increases the SV and CO

Hypertrophy of the myocardium- increase in the diameter of the cardiac

fibers (thickening of the walls); Increase in muscle mass, increases the

effectiveness of the heart to contract, increases the CO (problem: increasein muscle mass limits coronary artery supply leading to hypoxia and

decrease effectiveness)

HOMEOSTATIC COMPENSATORY MECHANISM


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HOMEOSTATIC COMPENSATORY MECHANISM

Vascular system- if circulating blood decreases, SNS releases epinephrine

and norepinephrine (generalized vasoconstriction)

Kidneys- when CO decreases, the glomerular filtration is reduced

(retention of water and sodium), Aldosterone release is stimulated (results

in further reabsorption of sodium and water); ADH release is stimulated

(further increase water reabsorption), the end-result is fluid overload and

edema

Liver- venous volume increases, results to liver congestion (decrease ability

to metabolizes the aldosterone and ADH)

CLASSIFICATION OF HEART FAILURE


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CLASSIFICATION OF HEART FAILURE

1. Backward heart failure: result from the damming up of

blood in the vessels proximal to the heart

2. Forward heart failure: it is the result of the inability of theheart to maintain cardiac output

3. High output heart failure: when the CO remains normal or

above normal but the metabolic needs of the body are not

met4. Low output Heart failure: when cardiac output falls below

normal


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RIGHT-SIDED HEART FAILURE

Peripheral edema or dependent edema (pitting

and non-tender) progresses into bi pedal

edema

Liver congestion and tenderness on the right

upper quadrant of the abdomenAscites (10L)

Displacement of the diaphragm resulting to

respiratory distress

Distended neck veinsIncrease systemic venous pressure (sitting

position)


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LEFT-SIDED HEART FAILURE

Pulmonary congestion leading to

pulmonary edema and pleural effusion

Dyspnea

Orthopnea

Alternating apnea and hyperpnea (Cheyne-

stoke respiration)

Coughing and hemoptysis

Crackles upon auscultation

CARDIAC PAIN IS NOT A TYPICAL

SYMPTOM OF HEART FAILURE

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Ms 1 Cardiac Diseases