altin oxygenation_heart as a pump

8/10/2019 Altin Oxygenation_Heart as a Pump

1/31

8/7/20

Disturbances in HEART as a Pump

Jenniffer TorralbaPaguio, RN

Review of Cardiac Physiology


Jenniffer TorralbaPaguio, RN 9

Hollow, muscular organ

300 grams (size of a fist) 4 chambers

found in chest between lungs

surrounded by membrane called Pericardium

Pericardial space is fluid-filled to nourish and

protect the heart.

CARDIAC ANATOMY



CARDIAC ANATOMY



CARDIAC FUNCTIONS

Generates blood pressure

Routes blood

Heart separates pulmonary and systemic circulation

Ensures one-way blood flow

Heart valves ensure one-way flow



CARDIAC FUNCTIONS

Regulates blood supply Changes in contraction rate and force match blood delivery

to changing metabolic needs

Most healthy people can increase cardiac output by 300500%



The heart is acomplex muscularpump that

maintains bloodpressure and flowthrough the lungsand the rest of thebody.

The heart pumpsabout 100,000times and moves7200 liters (1900gallons) of bloodevery day.


2/31

8/7/20





CARDIAC ANATOMY



Layers of the Heart:

Epicardium

Lines the pericardial

cavity

Myocardium

Muscle layer

Endocardium

Lines the chambers of the heart

CARDIAC ANATOMY




Pericardium

Physical protection & barrier

Highly resistant to distension

Epicardium: visceral layer covering the heart &

great vessels

Contains the pericardial cavity (bet the visceral &

parietal layers)

CARDIAC ANATOMY




Myocardium

Muscular portion of the

heart

Cardiac muscle cells

behaving as a single unit d/t:

Intercalated disks low

resistance for passage of

ions & electrical impulses

CARDIAC ANATOMY




Endocardium

Membrane that lines the

heart

Lines with blood vessels,

connective tissues with

elastic fibers & branches

of the conduction system

of the heart

CARDIAC ANATOMY


3/31

8/7/20



CARDIAC ANATOMY

Heart Valves:

2 Atrioventricular

Tricuspid & Mitral

Has cordae tendinae

2 Semilunar

Pulmonic & Aortic



CARDIAC ANATOMY & PHYSIOLOGY



Contraction of Cardiac Muscle



Electrical Activity of Cardiac Muscle



Conducting System of the Heart



Steps in Impulse

Conduction


4/31

8/7/20



CARDIAC CYCLE

The heart is two pumps that work together, right

(pulmonary) and left (systemic) half

Repetitive, sequential contraction (systole) and

relaxation (diastole) of heart chambers

Blood moves through circulatory system from areas

of higher to lower pressure.

o Contraction of heart produces the pressure



CARDIAC CYCLE

The rhythmic pumping action of the heart

Phases:

Sytole

The period at which the ventricles are contracting

Diastole

The period at which ventricles are relaxed & filled with

blood



The Electrocardiogram





CARDIAC CYCLE



CARDIAC CYCLE


5/31

8/7/20



CARDIAC CYCLE



CARDIAC PREFORMANCE REGULATION

Cardiac Output Measure used to determine efficiency of cardiacperformance

Amount of blood the heart pumps each minute

CO = SV x HR

Varies with body size & metabolic needs

Increased in stress & physical activity

Decreased in sleep & rest

Average: 3.5 8L/min



Regulation of Cardiac Output

Cardiac Output is

determined by

stroke volume and

heart rate each

can be regulated!!




Cardiac Reserve

Maximum percentage of increase in cardiac output

that can be achieved above the normal resting level

N: 300-400%

Dependent on:

1. Preload

2. Afterload

3. Cardiac contractility

4. Heart Rate






Preload Represents the amount of blood that the heart must pump

with each beat

Determined by venous return to the heart & stretch of the

muscle fibers

Frank-Starling mechanism


6/31

8/7/20




Afterload

The pressure that the heart must generate to move blood

into the aorta

Sources of afterload:

o L Heart: Systemic arterial BP

oR Heart: Pulmonary arterial pressure




Contractility

The ability of the heart to change its force of contraction

without changing its resting length

Influenced by number of calcium ions available in the

contractile process

SNS stimulation: + inotropic effect by increasing Ca+

available




Heart Rate

Determines the frequency with which blood is ejected

from the heart

HR CO

HR time spent in diastole, less time to fill

ventricles BUT same time in systole

EFFECT: SV but CO



Review of Cardiac Output



Pump Failure



PUMP FAILURE

Inability to pump blood, oxygen and nutrients tomeet metabolic needs

NOT a disease per se BUT a syndrome due to a

variety of disruptions that place an increased

demand to the heart


7/31

8/7/20



OUTLINE

1. Disturbances of BP regulation

2. Conduction disturbances (Arrythmia)3. Perfusion disturbances (Coronary Artery Disease &

Acute Coronary Syndrome, Cardiomyopathy)

4. Structural defects (Congenital Heart Disease,

Valvular Heart Disease)

5. Heart Failure (Heart Failure & Cardiogenic Shock)



DISORDERS OF BP REGULATIONHypertension



Diastolic BP

Maintained by the energy that has been stored in

the elastic walls of the aorta during systole

Based on:1. Condition of the vessel wall

2. Ability to stretch

3. Competency of the aortic valve4. Arteriolar resistance

Diastolic BP

Maintained by the energy that has been stored in

the elastic walls of the aorta during systole

Based on:1. Condition of the vessel wall

2. Ability to stretch

3. Competency of the aortic valve4. Arteriolar resistance

BLOOD PRESSURE

Determined by CO and PVR, where

BP = CO X PVR

Systolic BP

Reflects the rhythmic ejection of blood into the aorta

Increases with rapid ejection of large SV or when SV is

ejected into a rigid aorta



Regulatory Mechanisms of BP Maintenance

Short-Term

Vagal stimulation

ANS, barroreceptors

Renin-Angiotensin-Aldosteronemechanism

Vasopressin (ADH)

Long-Term

Renal Mechanisms

Extracellular fluid volume






8/31

8/7/20





What is NORMAL?



Specific Factors - Sites of Blood Pressure Control

Renal sodium and water excretion

Arterial resistance

Venous capacitance

Tissue remodeling

CNS influence on the autonomic

nervous system.

HR can be affected by

multiple factors

SV can be affected by venous return

RAS



Increased arterial

resistance

renin release

blood volume by directly promotingsodium and water retention

increased cardiac rate

and force

venous

compliance

Specific Factors - Sites of Blood Pressure Control



Risk Factors

Family history of hypertension

Race

Age-related increases in BP

Insulin Resistance & Metabolic Abnormalities

Lifestyle Factors

High Salt Intake

Excess alcohol consumption

Dietary intake of potassium, calcium & magnesium

Stress

Obesity



HYPERTENSION

Classification:1. Essential chronic elevation in BP that

occurs without evidence of other disease

Systolic

Diastolic

2. Secondary HPN resulting from other

diseases (eg. Kidney disease)


9/31

8/7/20



HYPERTENSION cascade




Elevated BP

(systole)

LV hypertrophy

Increased myocardialO2 demand

L heart failure




L heart failure

End-Organ Damage:

Heart, Brain, CKD, PeripheralVascular Disease,

Retinopathy



Secondary Hypertension




1. Renal Hypertension d/t reduced blood flowexcessive release of

Renin Angiotensin II PVR & aldosterone

& Na retention

2. Adrenocorticosteroid Hormone-Related HPN

d/t increased sodium retention SV




3. Pheochromocytoma d/t increased catecholamine release

4. Coarctation of the aorta

Narrowing of the aorta

Reduced blood flow from the lower part of the body

& kidneys SV CO BUT supplying only to the

upper parts of the body


10/31

8/7/20



CONDUCTION DISTURBANCESArrythmias



Cardiac Conduction System

Controls the rate and direction of electric impulse

conduction of the heart

SA AV His Bundle Purkinjie Fibers



Cardiac Conduction System

Phases of Cardiac Action Potential

Phase 0 - r apid upstroke

Phase 1 - early repolarization

Phase 2 - the Plataeu

Phase 3 - final repolarization period

Phase 4 - diastolic repolarization period






Mechanisms of Conduction Disorders

REVIEW!!

Properties of the Cardiac Muscle

1. Automaticity

Ability of the cells in the conduction system to initiate

impulse spontaneously

2. Excitability

Ability of the cell to respond to an impulse & generate

action potential




REVIEW!!

Properties of the Cardiac Muscle

3. Conductivity

Ability to conduct impulses

4. Refractoriness

The extent to which the cell is able to respond to an

incoming stimulus

Represents temporary interruptions in conductivity r/t

repolarization phase of the action potential


11/31

8/7/20







Automaticity Problems

Arise when the SA node does not fire, fires slowly or

SA node is blocked where another site takes over

Possible that the SA is functioning we BUT cardiac

cells assume accelerated properties of automaticity

generating impulses independently

Conduction System Firing Rate

SA Node 60 100 beats/ minute

AV Node 40 60 beats/ minute

Purkingie system 20 40 beats/ minute




Automaticity Problems

Promotive Factors

Myocardial tissue injury, hypoxia

Electrolyte disturbances

Hypertrophy (atrial/ventricular)

Medications

Ectopic Pacemaker




Premature Atrial Contractions

Premature Ventricular Contractions




Excitability Problems

Requires normal functioning myocardial cells

Ex. Injured myocardium 2 to ischemia

Injured myocardium

Depolarization of myocardial cells

Ischemic cells remain depolarized

Induces re-excitation of other Normal myocardium




Conductivity & Refractoriness Problems

Re-entry

Fibers that are inactive are activated

BEFORE the initial impulse dies out

re-excites areas of the heart that were

JUST discharged and have already

recovered

Requires a stimulus


12/31

8/7/20





Re-entry Contributing Factors

Ischemia

Infarction

Elevated serum K+





Re-entry

Injured myocardium

Increased resistance to impulse

Slow impulse transmission

Asynchronous myocardial activation

Predisposition to BLOCKS





Re-entry





Re-entry



PERFUSION DISTURBANCES

Coronary Artery DiseaseAcute Coronary Syndrome



Coronary Artery Disease

An abnormal accumulation of lipid, or fatty,substances and fibrous tissue in the vessel wall

Involves a repetitious inflammatory response to

artery wall injury and an alteration in the

biophysical & biochemical properties of the walls

Progressive disease resulting in coronary arterial

narrowing or complete occlusion

Preventable and Manageable


13/31

8/7/20




Etiology:

Exists even at childhood as fatty streaks Becomes symptomatic once occlusion is at

75%, usually at middle age

Epidemiologic data demonstrate association

between specific Risk Factors and CAD

development







RISK FACTORS

Major:

1. Tobacco Use

2. Hypertension

3. Elevated Blood lipid levels (LDL)

4. Family history of premature CVD (1st degree

relative w/ CVD at 55 or younger for men & 65 or

younger in women)

5. Age (>45 for men & >55 for women)Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High BloodCholesterol in Adults (Adult Treatment Panel III ; 2001)




RISK FACTORS

CAD Risk Equivalents (High risk for cardiac event in 10

years):

6. Diabetes

7. Peripheral Arterial Disease

8. Abdominal Aortic Aneurysm

9. Carotid Artery Disease

Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood

Cholesterol in Adults (Adult Treatment Panel III ; 2001)




RISK FACTORS Minor:

1. Physical Inactivity

2. Obesity

3. Metabolic Syndrome (composite of lipid & non-

lipid RFs of metabolic origin: abdominal obesity,

elevated triglyceride levels, low HDL, elevated BP, &

impaired insulin function)

4. StressThird Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood





RISK FACTORS

Minor:

5. Gender & Estrogen Levels

Women tend to have a higher incidence of

complications from CAD (AHA, 2002)

Women tend to not recognize the symptoms as early as

men & wait longer to report and seek medical

assistance (Meische et al.,1999;Penque et al., 1998)

Long-tern HRT may have more risks than benefits, &

that HRT should not be initiated or continued for

primary prevention of CAD (Womens Health Initiative,

Gebbie, 2002)


14/31

8/7/20




RISK FACTORS

Minor:

6. Behavioral Patterns (Type A personality:excessive competitiveness, sense of time urgency,

aggressiveness, hostility)

Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood




Risk Factors:

Explored in the Framingham Study

Non-Modifiable FRAG

1. Family History

2. Race

3. Age

4. Gender




Risk Factors:

Modifiable OCHIPED

1. Obesity

2. Cigarette Smoking

3. Hypertension

4. Impaired glucose tolerance

5. Physical Inactivity (Sedentary Lifestyle)

6. Elevated Serum lipids

7. Diet high in saturated fat, cholesterol and calories







Atherosclerotic Plaque Development




Deposition of fattystreaks in the

arterial wall intima

inflammatoryresponse

development offibrous capATHEROMA

narrowing of bloodvessel &

obstruction ofblood flow

decreased O2 in themyocardium(ISCHEMIA)

chest pain(ANGINA)

thrombusformation may

develop

myocardialinfarction


15/31

8/7/20





This coronary artery

demonstrates yellowish

atherosclerotic p laques grossly.

This coronary artery

opened longitudinally

demonstrates severe

atherosclerosis.



HEMODYNAMIC EFFECTS

Imbalance in myocardial oxygen supply and demand

1. Flow restricted under normal conditions

2. Stiffened vessels and inability to dilate causing

decreased driving pressure beyond the site of lesion

and less oxygenated blood available to the myocardial

cells perfused by the affected vessel

AerobicAnaerobic MetabolismTISSUE HYPOXIA




ACUTE CORONARY SYNDROMES



ANGINA A clinical syndrome usually characterized by

episodes of paroxysms of pain or pressure on the

anterior chest

Usually d/t insufficient blood flow that results to a

decreased O2 supply to meet an increased

myocardial demand for O2 in response to physical

exertion or emotional stress




ANGINA

Urden, et al.

Thelans Critical Care Nursing.2002


16/31

8/7/20



ANGINA

Types:

1. Stable Angina2. Unstable Angina

3. Variant Angina

4. Silent Ischemia



ANGINA

Types:

1. Stable Angina

Predictable, caused by similar risk factors

(eg. Exercise, emotional upset,

tachycardia)

Occurs when myocardial O2 demand

exceeds supply

usual chest pain

Relieved by rest, NTG



ANGINA

Types:

2. Unstable Angina

Change in previously established pattern

of angina OR a new onset of severe

angina

More intense

Preinfarction or cresendo unstable

angina unrelieved for >15 minutes

Atherosclerotic plaque instability Admitted as NSSTSE r/o MI



ANGINA

Types:

3. Variant Angina

Caused by coronary artery spasm

Commonly occurs when the patient is at

rest and can be cyclic

Associated with ST segment elevation &

transient abnormal Q waves



ANGINA

Types:

4. Silent Ischemia

Defined as objective evidence of

myocardial ischemia (ST segment

changes) WITHOUT the patient

experiencing any symptoms of angina



ANGINA

PATHOPHYSIOLOGYPathogenic Mechanisms causing chest pain d/t ischemia:

1. Atherosclerosis

2. Platelet aggregation in diseased vessels

3. Transient coronary artery thrombosis

4. Hemorrhage into atheromatous plaque

5. Abnormal vassoconstriction(spasm) of a

coronary artery

6. Extracardiac factors (anemia, thyrotoxicosis)


Decreased coronary perfusion OR increased oxygen demand

chest pain


17/31

8/7/20



ANGINADIAGNOSTIC FINDINGS

1. ECG: may be normal (ST segment depression

with/without T wave inversion; ST segment may

be elevated during episode)

2. Positive Stress Test (at least 1mm horizontal

depression or down sloping ST segment lasting

0.08 sec)

3. No changes in serum electrolytes

4. Elevated C-reactive protein (marker for

inflammation of vascular endothelium)




ACUTE CORONARY SYNDROMES



MYOCARDIAL INFARCTION

Describes irreversible myocardial necrosis resulting

from an abrupt decrease or total cessation of coronary

blood flow to a specific area of the myocardium.

ETIOLOGY:

1. Plaque rupture

2. New coronary artery thrombosis

3. Coronary artery spasm



Deposition of fatty streaks

in the arterial wall intima

inflammatory

response

development of fibrous cap

ATHEROMA

narrowing of blood vessel &

obstruction of blood flow

chest pain (ANGINA)

decreased O2 in the myocardium

(ISCHEMIA)

thrombus formation may develop

myocardial infarction

Complete & irreversible

myocardial necrosis in

3-4 hours



MYOCARDIAL INFARCTION




MYOCARDIAL INFARCTIONLOCATION

1. Anterior wall

2. Anteroseptal

3. Anterolateral

4. Inferior wall

5. Right ventricular

6. Posterior wall


18/31

8/7/20



MYOCARDIAL INFARCTIONCLINICAL PRESENTATION

Cardiovascular Chest pain, palpitations

S3, S4, new onset murmur

JVD

BP (may be elevated/decreased)

Pulse deficit (Af)

ECG (dysrythmias, ST, T wave changes, Q wave

presence)






Respiratory SOB

Dyspnea

Tachypnea

Crackles





Gastrointestinal

Nausea & vomiting

GUT

Decreased UO (maybe d/t

cardiogenicshock)

Skin

Cool,clammy,diaphoretic, pallor Dependent edema





Neurologic

Anxiety,restlessness, light-headedness

Headache, visual disturbances

Altered speech, motor functions

Changes in LOC





Electrocardiogram:

T wave inversion

ST segment elevation

Development of abnormal Q wave



MYOCARDIAL INFARCTIONPOSSIBLE COMPLICATIONS

1. Dysrhythmias

Sinus dysrhythmias

Ventricular/Atrialdysrhythmias

AV Heart Block

2. Acute MI



19/31

8/7/20



MYOCARDIAL INFARCTIONPOSSIBLE COMPLICATIONS

3. Structural Problems

Ventricular aneurysm

VSD

Papillary Muscle rupture

Cardiac wall rupture

Pericarditis




STRUCTURAL DEFECTS

Congenital Heart Defects

Valvular Defects



Valvular Heart Disease

TYPES:

1. Mitral valve stenosis

2. Mitral Valve Regurgitation

3. Aortic Valve stenosis

4. Aortic valve regurgitation

5. Tricuspid valve stenosis

6. Tricuspid valve regurgitation







Describes structural and/or functionalabnormalities of single or multiple cardiac valves

Causes alteration in blood flow across the valve

Types:

1. Stenotic

2. Regurgitant

Usual reason for ICU admission if for Heart Failure or for

cardiac surgical valve replacement




Etiology:

Secondary to Rheumatic Heart Disease

Direct result of damage caused by

hemolytic streptococcal pharyngitis

Secondary to degenerative valve changes


20/31

8/7/20




Rheumatic Heart Disease:

Inflammatory process that may affect the

myocardium, pericardium and or endocardium Usually results in distortion and scarring of the valves

Subjective Symptoms Objective Symptoms

Prior history of rheumatic fever

General malaise

Pain may or may not be present

Temperature

Murmurs

Dyspnea

Polyarthritis




Mechanisms:

Obstruction to forward flow (stenosis) or

insufficiency of the valve, allowing backwardflow (regurgitation).

Caused by sclerosing, thickening and calcificationof the valve leaflets.

May be caused by rheumatic heart disease,dilatation of the valve ring, or damage to thenearby valve structures




Recall of Normal Flow




Mitral Valve Stenosis

LA must generate more pressure

to propel blood beyondthe lesion

Rise in LA pressure & volume is

reflected retrograde into

pulmonaryvessels

RV hypertrophy

RV failure




Mitral Valve StenosisManifestations:

Exertionaldyspnea

Weakness, fatigue

Pronounced respiratory

symptoms (orthopnea, PND)

Mild hemoptysis with bronchial

capillary rupture

Susceptibility to pulmonary

infections




Mitral Valve Stenosis

Manifestations

1. CXR: pulmonary congestion, redistribution of blood

flow to upper lobes

2. ECG: Atrial Fib & other atrial dysrrhythmias

3. Auscultation: Diastolic murmur, accentuated S1,

opening snap


21/31

8/7/20




Mitral Valve Regurgitation

Pathophysiologic Consequences

LVdilation & hypertrophy

Left atrial dilation and

hypertrophy




Mitral Valve Regurgitation

MANIFESTATIONS

Weakness & fatigue

Exertionaldyspnea

Palpitations

Severe symptoms precipitated

by LV fai lure, with low output

and pulmonary congestion




Aortic Valve Stenosis

PathophysiologicConsequence

LV hypertrophy

Progressive failure of ventricular

emptying

Pulmonary congestion

Failure of R-side of heart, with

systemicvenous congestion Sudden Cardiac Death




Aortic Valve Stenosis

Manifestations

Exertionaldyspnea

Exercise intolerance

Syncope

Angina

HF (left-ventricular failure)




Aortic Valve Regurgitation


Increased volume load imposed

on left ventricle

LVdilation and hypertrophy

Manifesting

Fatigue

Exertionaldyspnea

Palpitations




Tricuspid Valve Stenosis

PathophysiologicMechanisms

RA must generate higher

pressure to eject blood

beyondthe lesion

Right atrial dilation

Systemic venous

engorgement

Increasedvenous pressures


22/31

8/7/20




Tricuspid Valve Stenosis

Manifestations

Venousdistension

Peripheral edema

Ascites

Hepatic engorgement

Anorexia




Tricuspid Valve Regurgitation


RV dilation and hypertrophy

Manifestations

Decreased CO

NVE

Hepatic engorgement

Ascites

Edema

Pleural effusion




Diagnostic Tests:1.Cardiac catheterization

assist in visualization of blood flow.

Measurement of chamber assists in determining

type of disorder present and the degree of

severity.

2.Echocardiography

determine ventricular function, chamber size,

and valve function



Congenital Heart Diseases

Classification based on effect:

1. Acyanotic

Ventricular Septal Defect (VSD)

Atrial Septal Defect (ASD)

Patent Ductus Arteriosus (PDA)

2. Cyanotic

Tertralogy of Fallot




Classification based on hemodynamic & blood

flow patterns:

1. Increased pulmonary blood flow

2. Obstruction to blood flow leaving the heart

3. Mixed blood flow (oxygenated &

deoxygenated blood mixing in the heart or

great vessels)

4. Decreased pulmonary blood flow




Acyanotic Congenital Heart Disease

LeftRight SHUNT (oxygenated unoxygenated)

Involves heart & circulatory anomalies on:

Stricture to the flow of blood; OR

Shunt that moves blood from the arterial to the

venous system

Causes the heart to become an INEFFECTIVE

PUMP and predisposes the child to HF


23/31

8/7/20




Ventricular Septal Defect

Opening is present in the septum between the 2ventricles.

LV pressure > RV pressure blood flows from the

L to the R across the septum

Impairment of the effort of the heart to the

systemic circulation

L R back to pulmo circulation ventricular

hypertrophy &pulmonary arterial pressure




Atrial Septal Defect

Abnormal communication between the 2 atria shift of blood from L to R

Types:

1. Ostrium Primum opening at the lower end

of the septum

2. Ostrium Secundum opening near the center

of the septum




Patent Ductus Arteriosus

DA is an accessory fetal structure that connects the

pulmonary artery to the aorta closes at birth

Blood shunts from the aorta (oxygenated blood) to

the pulmonary artery (unoxygenatedblood)




Cyanotic Congenital Heart Disease

Right Left SHUNT (unoxygenated oxygenated)

Presence of strictures in this disease causes blood

to be shunted from the venous arterial system

as a result of abnormal communication between

the L & R side of the heart




Tetralogyof Fallot

Four Anomalies:

1. Pulmonary stenosis

2. VSD

3. Dextropositionof the aorta

4. RV hypertrophy

Causes blood to shunt from the R L and

overriding the aorta CYANOSIS



HEART FAILURE

Heart Failure & Cardiogenic Shock


24/31

8/7/20



Heart Failure

A response to cardiac dysfunction

A condition where the heart cannot pumpblood at a volume required to meet the

bodys needs

Results in failure to deliver blood to the

pulmonary and arterial circulations



Heart Failure



Heart Failure

Precipitating Factors Reduction or cessation of medication

Dysrrhythmias

Systemic infection

Pulmonary embolism

Physical, environmental and emotional stress

Pericarditis, myocarditis and endocarditis

High ventricular output states

Development of serious systemic illness

Administration of cardiac depressant or salt -retaining

drug

Development of a second form of heart disease



Heart Failure

Classifications:

1. Using the NYHA classification

2. Based on primary ventricular involvement (Left

vs. Right)

3. As pressure extending backward or forward

4. Based on chronicity (Acute vs. Chronic)

5. As primary Systolic or Diastolic LV dysfunction





NEW YORK HEART ASSOCIATION

Functional Classification

Heart Failure


25/31

8/7/20



NEW YORK HEART ASSOCIATION

Functional Classification

Sources: American Heart Association. Heart and Stroke Facts; National Heart, Lung, and Blood Institute. Diseases and Conditions Index: Angina; American

Heart Association.Angina Pectoris Treatment;Patient Health International.Angina Fact and Figures;American Heart Association. Transmyocardial

Revascularization (TMR); American Heart Association. Heart Disease and Stroke Statistics-2004 Update. Dallas,Tex. American Heart Association;2003.



VENTRICULAR INVOLVEMENT:

Right Heart Failure:

Ineffective right ventricular contractile function

Secondary to acute conditions such as:

1. Pulmonary embolism

2. MI

3. Secondary to Left-sided heart failure or

backward failure

Heart Failure



Heart Failure




Right Heart Failure:Common Manifestations:

Weakness

Peripheral edema

JVD

Organomegaly

Elevated CVP

Compromised peripheral perfusion

GI: anorexia, nausea, feeling of fullness

Heart Failure




Left Failure:

Disturbed contractile function of the left side of

the ventricle resulting in:

Pulmonary congestion & edema

Decreased CO


1. Left ventricular MI

2. Aortic or MV stenosis

3. Hypertension

Heart Failure




Left Heart Failure:Common Manifestations:

Tachypnea, tachycardia

Cough

Basilar crackles

Pulmonary edema, Hemoptysis

Decreased peripheral perfusion (weak,

diminished pulses; cool, pale extremities;

peripheral cyanosis

Eventual right side of the heart involvement

Heart Failure


26/31

8/7/20



Heart Failure



PRESSURE COMPROMISE: Forward Heart Failure

Inadequate delivery of blood into the arterialsystem

Occurs when there is increased systemic vascular

resistance (afterload) causing decreased CO


1. Aortic stenosis

2. Hypertension

Heart Failure



PRESSURE COMPROMISE: Backward Heart Failure

Causes inadequate emptying of the ventricle


1. LV systolic dysfunction d/t MI

2. Cardiomyopathy

Manifests as:

1. Increased LVEDP

2. Secodary increased atrial pressure &

pulmonary pressure

Heart Failure



CHRONICITY:

Acute

Sudden onset, no compensatory mechanism

Experienced as acute pulmonary edema, low

cardiac output, or cardiogenic shock

Heart Failure



CHRONICITY:

Chronic With compensatory mechanism involvement CO

1. Frank-Starling mechanism

2. Sympathetic reflexes

3. RAA system

4. Myocardial hypertrophy

Hypervolemic with Na and H2O retention; chamber

changes

Deterioration secondary to: dyrhythmias, acute

ischemia, cessation of medication

Heart Failure



Heart Failure

Systolic VS Diastolic Failure


27/31

8/7/20



COMPENSATORY MECHANISMS:

1. Adrenergic System

2. Renin-Angiotensin-Aldosterone System

3. Sinus Tachycardia

4. Ventricular Hypertrophy

Heart Failure



Possible Complications:

1. Shortness of Breath

Dyspnea

Orthopnea

Paroxysman Nocturnal

Dyspnea

Cardiac Asthma

2. Pulmonary Edema

Heart Failure



SHOCK

is a complex clinical syndrome characterized by

impaired cellular metabolism due to decreased

tissue perfusion.

inadequacy in tissue perfusion results in cellular

hypoxia, accumulation of cellular metabolic

wastes, cellular destruction , and, ultimately,

organ and system failure.



Cardiogenic Shock

it results from the impaired ability of the heart topump blood severe in perfusion

is a complex clinical syndrome characterized by:

Hypotension

Tachycardia

impaired mentation

urinary output level below 20ml/hour, and

peripheral vascular collapse



Cardiogenic Shock

it results from the impaired ability of the heart topump blood severe in perfusion

symptoms are caused by inadequate delivery of

blood to major body organs, particularly the

heart, brain, and kidneys.


28/31

8/7/20



CLASSIFICATIONS other than CARDIOGENIC:

1. HYPOVOLEMIC Shock

exists when the volume of blood is inadequate to

fill the intravascular space.

2. DISTRIBUTIVE Shock

happens when there is massive peripheralvasodilation because the blood volume, althoughwithin normal limits, is insufficient to fill theenlarged vascular capacity.



Differentiating Cardiogenic Shock



Distributive shock

SEPTIC

- any type of microorganism can produce septic shock,cellular derangement precede and contribute tocardiovascular abnormalities.

ANAPHYLACTIC

as the result of a severe allergic, antigen-antibodyreaction.

NEUROGENIC

there is a reduction in vasomotor tone, which occurs inthe vasomotor centers in the brainstem and causes

decreased vasoconstriction, resulting in generalizedsystemic vasodilation



Cardiogenic Shock

Possible Causes:

1. MYOPATHIC factors

SYSTOLIC dysfunction

Ex: Acute MI, congestive cardiomyopathy

DIASTOLIC dysfunction

Ex: cardiac tamponade

2. MECHANICAL factors regurgitant lesions

ruptured interventricularseptum

3. DYSRHYTHMIAS Bradydysrhythmias



Cardiogenic Shock

Etiologic Classifications:

1. Coronary occurs when a significant amount of the

LV myocardium has been destroyed

More common

Eg. Anterior wall MI

2. Non-Coronary usually r/t severe metabolic

problems and tension pneumothorax

Eg. Severe hypoxemia, acidosis, hypoglycemia,

hypocalcemia




29/31

8/7/20

Primary ventricular

ischemia

Structural problems Arrhythmias

Systolic dysfunction: ineffective forward movement of blood

Decreased stoke

volume

Diastolic dysfunction:

ineffective filling

Decreased cardiac

output

Increased pulmonary

pressures

Pulmonary edema

Decreased oxygenation

Decreased cellular oxygen supply

Decreased tissue perfusion

Impaired cellular metabolism



Cardiogenic Shock

Clinical Manifestations:

1. Anginalpain

2. Dysrhythmia

3. Hemodynamic

instability

Initial Stage

CompensatoryStage

ProgressiveStage

RefractoryStage



Stages of Cardiogenic Shock

INITIAL: no apparent signs or symptoms

subtle nonspecific changes occur at the

cellular level




COMPENSATORY: there is declining systemic arterial blood pressure,

right ventricular failure, and acidosis

SNS is stimulated and so second stage of chock

begins

Nervous, Endocrine, Chemical Homeostatic

compensatory mechanism are triggered


30/31

8/7/20

3




PROGRESSIVE: compensatory mechanism are not enough to reverse

the shock state. They will eventually fail destructive cellular and systemic changes ensue

there will be impaired cellular function related tonutritional blood flow

results to anaerobic metabolism and eventuallyacidosis

increase capillary hydrostatic pressure forces fluid tothe extravascular spaces.




PROGRESSIVE: Heart eventually fails from deprivation of adequate

perfusion Cerebral blood flow is decreased as a result of the

reduced cardiac output secondary to altered capillarydynamics

Decreased pulmonary vascular blood flow causesischemic and necrotic cellular changes.

The already compromised lungs become wet, stiff, andnoncompliant




REFRACTORY:

when death is imminent the patient in shock no longer

responds to any form of therapy

severe vasoconstriction continues

cardiac output falls even further

build up of acidosis further impairs respiratory and

cerebral function and tissue perfusion.



ORGAN/

SYSTEM

COMPENSATORY

Mechanisms

S/Sx of Decompensation

Brain/Neuroph

ysiologic

>decreased impulse transmission

of Baroreceptors

>vasomotor center removes

inhibition of the vasoconstriction

>SNS stimulation

>anterior pituitary and

hypothalamus is stimulated

>restlessness

>deterioration in sensorium

>cerebral ischemia/infarct

Heart and

vascular system

>increased heart rate

>enhanced contractility

>coronary vessels dilate

>peripheral vessels constrict

>decreased tissue perfusion

>myocardial ischemia/infarct

>congestive heart failure

>arrythmias

>failure of microcirculation

>DIC



ORGAN/

SYSTEM

COMPENSATORY

Mechanisms

S/Sx of Decompensation

Pulmo >chemoreceptor senses

poor ventilatory status

>increase in respiratory rate>stimulation of vasomotor

center

>hypoxia

>acidosis

>decreased pulmonary compliance>pulmonary interstitial edema

GIT >severe vasoconstriction

>RBCs are squeezed into

the circulation by liver and

spleen

>intestinal ischemia

>depressed protective action of RES

>anoxic liver

>release of toxic substances

>impaired portal blood flow

Renal >excitation of renal pressor

substance

>activation of R-A-A-S

>decreased renal perfusion

>oliguria/anuria

>renal shutdown



Renal >triggers posterior pituitary for

release of ADH

>stimulates erythropoeitin

production which stimulates the bone

marrow to produce RBC

>loose ability to regulate electrolyte

and acid-base balance

Endo

Hormone

>adrenal medulla releases

epinephrine and norepinephrine

>pitiutary gland releases ACTH to

stimulate adrenal cortex to produce

cortocisteroids:

-hydrocortisone

-aldosterone

>prolonged sever vasoconstriction

>enhances fluid retention and fluid

shift aggravating interstitial edema

Skin/

musculo

skeletal

>needs less oxygen and blood supply >peripheral circulatory prolapse

>cool,pale, clammy, mottled skin

>cyanosis

>muscle and tissue wasting


31/31

8/7/20



Given the following diseases conditions, identify the pathophysiologic mechanisms involved in

terms of its effects on the pump variables (Preload, Afterload, Contractility), possible causes &

Clinical Manifestations.

Condition Variable

OR Possible

Causes

Signs & Symptoms

MI Contractility CAD, chronic

HPN

S: Chest pain unrelieved by rest

O: diaphoresisLabs: cardiac enzymes

Aortic/Mitral

Regurgitation

Pulmonary HPN

Cardiomyopathy

VSD

Pulmonic Valve

stenosis

Systemic HPN

Cardiogenic Shock

Arrhythmia HODS - November 2006 197

altin oxygenation_heart as a pump

Documents