cardiovascular pathophysiology - accredited cme … ncvh/5-29-fri/nurse-cath/6 ncvh rci… ·...

Cardiovascular

Pathophysiology

Thank You To:

AHA/ACC

SICP

Philip B. Adamson, MD

cardiovillage.com

Disclosures

Speaker’s Bureau:

• None

Honorarium:

• None

Consultant:

• None

Stockholder:

• None

Grant/Research Support:

• None

Medical/Scientific Boards:

• None

Outline• Coronary Artery Disease

– Angina

– Acute Coronary Syndrome (UA/NSTEMI, STEMI)

• Heart Failure

– Left and right side

• Valve Disease

– AS, AI, MS, MS

• Cardiomyopathies

– Dilated CMO

– Hypertrophic CMO

• Non-obstructive

• Obstructive

– Restrictive CMO

Coronary Artery Disease

the loss of elasticity of the

blood vessels

is a narrowing of the vessels

due to fatty deposits

Arteriosclerosis Atherosclerosis

Risk Factors For CAD

• Family history

• Advancing age

• Gender is still a factor

• Total cholesterol >200, LDL>100 HDL< 35

• Hypertension

• Smoking

• Overweight/obesity

• Sedentary life-style

• Stress

• Diabetes Mellitus

Evolution of Plaque

LDL

Monocyte

endothelium

Cell Adhesion

factors

1

1. LDL enters

2. & Oxidizes

3. Monocytes adhere & 4.

cross intima differentiate

yeilding macrophages

Macrophage

5. Macrophages engulf

LDL yielding Foam

cells

6. muscle cells multiply &

7. Migrate towards intima

8. Muscle cells die

& harden plaque -

Calcium develops

Todd’s Cardiovascular Review Book, 1st Edition, Vol. 3: Hemodynamic Calculations

8

• TWO PROCESSES :

• First the fats:

• Lipid accumulation & oxidation

• Then the vessel deforms:

• Endothelial dysfunction

• Spastic vessels

Manifestations of Coronary Artery Disease

• Predictable

• Unbalanced

Supply &

Demand

• Reduced O₂

• Reduced

Blood Flow

• Responsive to

Medication

• Often related

to occlusive

thrombus &

plaque rupture

• Stasis of flow

• Loss of supply

with increase

in demand

• Irreversible

Myocardial

Damage

Stable Angina Myocardial InfarctUnstable Angina

• Pain which is

unpredicted, new or

occurs at rest

• Unbalanced Supply &

Demand

• Less/Unresponsive to

Medication

• Often related to transient

non-occlusive thrombus

Other Angina TypesPrinzmetals / Variant

• Typically occurs at rest

• Caused by focal spasm of angiographically normal coronary arteries. In the majority of patients there is also atherosclerotic coronary artery obstruction. In cases where there is atherosclerotic obstruction the vasospasm occurs near the stenotic lesion.

Post infarct• Secondary to ischemic tissue around the infarcted area.

Microvascular / Syndrome X• Angina without angiographic evidence of stenosis or disease

• Thought to be microvasculature circulation deficiency

Angina Management

• Lifestyle

• Nitrates

• Statins

• Beta Blockers

• CCB’s

• Aspirin

• PCI (if indicated)

Patient Presentation of the Acute

Myocardial Infarction

• Syncope or near syncope without other cause

• Impairment of cognitive function without other cause

• Chest pain described as a pressure sensation, fullness, or squeezing in the midportion of the thorax

• Radiation of chest pain into the jaw or teeth, shoulder, arm, and/or back

• Associated dyspnea or shortness of breath

• Associated epigastric discomfort with or without nausea and vomiting

• Associated diaphoresis or sweating

13

Thrombus Formation and ACS

UA NQMI STE-MI

Plaque Disruption/Fissure/Erosion

Thrombus Formation

Non-ST-Segment Elevation Acute

Coronary Syndrome (NSTEMI-ACS)ST-Segment

Elevation

Acute

Coronary

Syndrome

(STEMI-ACS)

Old

Terminology:

New

Terminology:

Cardiac Markers• Creatine Kinase- MB

– 4-6 hours after symptom onset

– Normal in 48-72 hours

• Myoglobin


– Normal in 24-36 hours

• Troponins (C, I, T)


– Remain elevated as long as 7-10 days

– I & T specific to cardiac muscle

http://upload.wikimedia.org/wikipedia/commons/8/80/AMI_bloodtests_engl.png

http://upload.wikimedia.org/wikipedia/commons/8/80/AMI_bloodtests_engl.png

15

Treatment of Acute Coronary

Syndrome

Initial Treatment of ACS

Long-Term Medical Management

UA/NSTEMI†STEMI*

Thrombolytics PCI or CABG PCI or CABG

Antiplatelet, anti-ischemic, or

anticoagulant therapy

Antiplatelet, anti-ischemic, or

anticoagulant therapy

*Boden WE, et al. N Engl J Med. 2001;344:1939-1942. and Braunwald E, et al. J Am Coll Cardiol. 2000;36:970-1062.

16

ACS Medicine Cabinet

• Aspirin

• Heparin

• Low Molecular Weight Heparin

• GP IIb/IIIa Inhibitors

• Direct Thrombin Inhibitors

• Warfarin

• Statins (HMG Co-A Reductase Inhibitors)

• Early Medical vs Early Invasive therapy

Anticoagulation

17

ACS Medicine Cabinet

• Bed Rest

• Nitroglycerin

• Supplemental O2

• Narcotics (Morphine)

• Beta Blockade

• Ace Inhibitor

• Diuretics

• Anti-arrthymics (PRN)

• Inotropic Agents (PRN)

• IABP (PRN)

• A compassionate listener

Anti-Ischemic Therapy

Complications of MI

• Dysrhythmias

– Heart blocks

– Bundle branch block

– Ventricular

• Heart Failure

• LV Aneurysm

• VSD

• Mitral Regurgitation

Basic Concepts of Heart Failure• Pathophysiological state in which cardiac

function fails to pump blood at a volume

commensurate with venous return to meet

metabolic demands.

• Inadequate forward flow with volume back up

to capillary beds “behind” the failing ventricle

• Can be Left or Right Ventricular in Nature

• RV failure is most commonly due to chronic

LV failure.

Hemodynamic Basis for

Left Sided Heart Failure Symptoms


Hemodynamics

Increase: LVEDP, LA, PCWP, PAP

Chronic Increase RHP, CVP

Decrease: CO, CI

Etiology of Left Ventricular Failure

Volume Over load: Regurgitate AO valveHigh output status

Pressure Overload: Systemic hypertensionOutflow obstruction (AS)

Loss of Muscle: Post MIChronic ischemiaConnective tissue diseases

Infection

Restricted Filling: Pericardial diseases Restrictive cardiomyopathy

Heart Failure


Left Sided Heart Failure Symptoms


Hemodynamics

Increase: LVEDP, LA, PCWP, PAP

Chronic Increase RHP, CVP

Decrease: CO, CI

Left Ventricular Dysfunction

Symptoms

Dyspnea on Exertion

Paroxysmal Nocturnal Dyspnea

Tachycardia

Cough

Hemoptysis

Physical Signs

Rales/Crackles

Pulmonary Edema

Pulsus Alternans

S3 Gallop

Pleural Effusion

Cheyne-Stokes Respiration

Clinical Note: Treatment for heart failure is directed at the etiology of failure.


Right Sided Heart Failure Symptoms


Hemodynamics

Increase: RVEDP, RA, CVP, JVP

Possible decrease: PAP, PCWP, CO, CI

Right Ventricular Dysfunction

Symptoms

Associated with dec. CO

Abdominal Pain

Anorexia

Nausea

Bloating

Swelling

Physical Signs

Peripheral Edema

Jugular Venous Distention

Abdominal-Jugular Reflux

Hepatomegaly

Weight gain

Clinical Note: Treatment for heart failure is directed at the etiology of failure.

Assessing Heart Failure

• ECG Monitor

• O2 Sat Monitor

• Chest X-ray

• Pulmonary Artery Catheter

– SVR / PVR

– CO/CI

– PCWP

– CVP

Functional Classifications

(New York Heart Association)

• Class I: No symptoms with activity.

• Class II: Slight limitations to physical activity, comfortable at rest, physical activity results in fatigue, palpitations, SOB, or angina

• Class III: Marked limitations to physical activity, comfortable at rest, slight physical activity results in fatigue, palpitations, SOB, or angina

• Class IV: Unable to carry out any physical activity without discomfort

29

Pharmacologic/Medical Management• Oxygen

• Digoxin

• Diuretics

• ACE Inhibitors

• Beta-Blockers

• Aldosterone Antagonists

• Angiotensin Receptor Blockers (ARBs)

• Dopamine/Dobutamine

• Intra Aortic Balloon Pump

• Underlying Cause

Heart Failure Summary

• Heart failure is a chronic, progressive disease that is generally not curable, but treatable

• Most recent guidelines promote lifestyle modifications and medical

• It is estimated 15% of all heart failure patients may be candidates for cardiac resynchronization therapy

• Close follow-up of the heart failure patient is essential, with necessary adjustments in medical management

Aortic Stenosis• Normal aortic valve area

is 2.5 to 3.6 cm2

• Critical severe aortic stenosis

less than 0.7 cm2 (can vary)

You can Learn a lot From a Garden Hose

Richard E. Klabunde, PhD -Cardiovascular Physiology Concepts

Chronic Aortic Stenosis• Compensation

– Pressure overload

– Starlings law

– Initially inc LVEDV,

inc cont

Aortic Stenosis

• LVOT obstruction

• LVH initially

• Pulsus parvus/tarvus-narrow pulse pressure

• Decreased systemic perfusion

• Inc. LVEDP, LA, PCWP, PA

• Pulmonary congestion

• LV-AO Systolic gradient

• Systolic murmur

• SAD-syncope, angina, dyspnea

Cardiac Self Assessment, Wes Todd, RCIS

Normal Aortic StenosisAO dec systolic

Narrow pulse pressure

LV Inc sys

Inc Dias, LVEDP

Michael Ragosta, MD, www.cardioVillage.com

AS Hemodynamic Manifestations

– AO

• Pulsus Parvous et Tarvus– May be brisk in elderly with non

compliant vessels

– PCWP

• Inc

– PA

• Inc

– SV & CO/CI

• Dec

– LV & AO systolic gradient

– Varies on the severity


Aortic Insufficiency

• Leakage of blood

backwards across the

closed aortic valve

during ventricular

diastole

Diagnosis in the Cardiac Cath

Lab• Wide pulse pressure

• LVEDP may normal in

chronic AI, markedly

elevated in acute AI

• No aortic gradient

unless AS is also

present

Mitral Stenosis• LV inflow obstruction

• Dec. LV filling and preload

• Decreased CO and systemic perfusion

• Inc. LA, PCWP, PA, PVR

• A Fib


• Diastolic murmur

• Left Atrial enlargement


Baim DS, Grossman’s Cardiac Catheterization, Angiography, and Intervention, 7th ed.

Recording a MS Case• Hemodynamics

– PCWP/LA, LV, HR, CO

Mitral StenosisLV/PCW

LV Down stroke

Bisects V-wave of PCW

Mean pressure gradient

across the mitral valve

in diastole

LA or PCW pressure vs.

LV pressure

The PCW tracing must

be phase shifted

Cardiac output must be

measured

Mitral valve orifice

calculated using the

Gorlin equation

Mitral Valve Stenosis

A normal mitral valve has an area of 4 – 6 cm2

• Hemodynamically significant changes occur when the valve area is reduced to 2 cm2 or less.

– Other Hemodynamic changes that may occur with significant mitral stenosis:

• Increased a-wave in left atria

• Pulmonary hypertension

• Right heart pressures increase in reaction to pulmonary hypertension, possibly leading to right heart failure.

Mitral Valve Stenosis• Mitral valve stenosis evaluated

hemodynamically by comparing LA or PCWP to LVEDP

– In the normal heart, the mean LA or Wedge pressure should equal the LV EDP.

– If the mean pressure is greater than the LV EDP, this indicates that there is a restriction between the chambers, forcing the atrial pressures to be higher than necessary.

• This is the classic sign of Mitral Stenosis

Note: If LV EDP is higher than the Mean of the LA, your transducers may not be

properly leveled or balanced.

Mitral Stenosis Evaluation

The greater the gradient, the more significant the disease

Mitral Regurgitation

Leakage of blood across a closed mitral valve during ventricular systole


• LV ejecting into LA, PV’S

• Decreased CO and systemic perfusion

• Inc. LA, PCWP, PA

• Systolic murmur

• A Fib


• LA/PCPW inc V wave

• Left Atrial enlargement


Classification of Mitral Regurgitation

• Classification of Mitral Regurgitation is often performed following Left Ventriculography.

• Classification is based upon the amount of contrast flowing back into the left atrium during ventricular systole.

– Class I+ - Trace amounts of contrast flow into the LA, but it clears during atrial contraction

– Class II+ - Moderate insufficiency; contrast is visible within the entire LA, and does not clear

– Class III+ - Moderately severe MR; contrast opacifies the LA, and becomes more dense with each contraction of the left ventricle

– Class IV+ - Severe regurgitation; wide open MR, contrast completely opacifies the LA during the first contraction of the LV


• LA/PCWP inc.

– V wave inc

• PA inc

• CO/CI dec

• S & S pulm edema

Richard E. Klabunde, PhD -Cardiovascular Physiology Concepts

Mitral Valve Regurgitation

• Mitral valve regurgitation is assessed by evaluating the V-wave of the left atrial or pulmonary arterial wedge pressure.

– The V-wave reflects atrial filling following ventricular contraction

– Due to the regurgitant valve, volume will rapidly enter the atrium from the left ventricle in a retrograde fashion, adding to the volume normally received from the right ventricle contraction.

Mitral Valve Regurgitation

Large

V-

wave

LV and Wedge recorded

simultaneously. Notice the very

large V-waves

V Waves

Michael Ragosta, MD, www.cardiovillage.com

Cardiomyopathy

A disease of heart

muscle often in

the absence of a

known etiology

Is a significant

cause of morbidity

and mortality

Cardiomyopathy

• World health organization has classified

the cardiomyopathies into three

categories-

– Dilated cardiomyopathy

– Hypertrophic cardiomyopathy

– Restrictive cardiomyopathy

• Distinctions not always absolute often

overlapping features

Normal Dilated Cardiomyopathy

Dilated Cardiomyopathy• Most common form of cardiomyopathy

• Formerly called congestive

• Gross dilation LV and all 4 chambers, decrease contractility

• Often symptoms of congestive heart failure

Dilated Cardiomyopathy-Etiology

May be linked to:• Idiopathic

• Alcohol

• Cobalt

• Pregnancy

• Infections-HIV-Post Myocarditis

• Toxins (Adriamycin)

Dilated

Cardiomyopathy

• Gross dilation

• Thin ventricular walls

• Decrease systolic function

• Thrombus formation

• Mitral & Tricuspid regurgitation

• Increase in diastolic and systolic volumes

Dilated Cardiomyopathy-LV Gram

Dilated Cardiomyopathy

LV pressure waveform

Findings in the Cardiac Cath Lab

Hemodynamics

Elevated LVEDP, PCWP, PA

Elevated SVR and PVR

May assess responsiveness to vasodilators for PVR

V-wave on PCWP

Possible increase in right heart pressures

Decreased EF% and CO

Angiographic Evaluation

LV-gram dilated, poorly contractile LV

Global LV hypokineticmovement

Assess coronaries to rule out CAD as a cause of poor contractility

Mitral regurgitation common

Dilated Cardiomyopathy-TreatmentManage Heart Failure

• Digitalis • Diuretics• Ace inhibitors • Beta blockers• Nitrates

Manage Coagulation

• Aspirin• Coumadin

Resynchronization Therapy

If secondary to alcohol-STOP DRINKING

Hypertrophic

Cardiomyopathy

Hypertrophic Cardiomyopathy

• Marked hypertrophy of the heart, especially the interventricular septum without obvious cause (hypertension, aortic stenosis)

• May be diffuse, asymmetrical (IVS) or apical

• With and without obstruction (aprox. 95% without and 5% with obstruction)

• Hypertrophic obstructive cardiomyopathy(HOCM)

• Preserved or enhanced contractile function

Background HOCM

• Prevalence approximately 1:500

• HOCM- #1 killer of young athletes

• More prevalent in men

• Genetically transmitted autosomal dominant with variable expression- Congenital

• May involve all ventricular walls, apex, interventricularseptum

• Acquired hypertrophic cardiomyopathy

– Usually associated with hypertension

HOCMDynamic LVOT obstruction

Gradient increased with reduced

afterload & preload, and increased

contractility

Gradient reduced with increased

preload & afterload, and reduced

contractility

Gradient only occurs in HOCM

with ASH

Hypertrophic Obstructive Cardiomyopathy


HOCM

• Hypertrophied septum results in narrowing of LV outflow tract

• Forms obstruction below the aortic valve

• The mitral leaflet that forms lateral wall of LV outflow tract actively involved

• Elevated LVEDP

• Frequent mitral regurgitation

• May have diastolic dysfunction due to stiff non compliant LV

• Pulsus Bisferiens

Cardiac Cath Lab Findings

• Right heart pressures may be normal

• Pressure gradient may not exist at rest

• Provocative maneuvers– Valsalva maneuver (reduces preload)

– Amyl nitrate (reduces afterload)

– Isoproterenol (increases contractility)

• Careful analysis of location of gradient

• Post ectopic beat– Normally would result in increased pulse pressure

– Result in increase in obstruction and reduced stroke volume, “Brockenbrough’s phenomenon”

Pullback in HOCMUse end hole catheter, not a pigtail


Treatment Options

Sigwart U. Non-Surgical myocardial reduction for hypertrophic obstructive cardiomyopathy. Lancet 1995;346:211-14.

• AICD for sudden

death

• Surgical•Myotomy/myomectomy with

mitral valve replacement

•Alcohol ablation

• Transplant

Restrictive

Cardiomyopathy

Restrictive Cardiomyopathy

• Least common form of cardiomyopathy

– In western countries, more common in third world

• Impaired diastolic filling

– Rigid ventricular walls

• Systolic function usually preserved

• May result from a variety of local or systemic

diseases or radiation treatments

• Important to differentiate from constrictive

pericarditis

The Restrictive Cardiomyopathies

• Scleroderma• Systemic sclerosis produces fibrotic thickening

• Loeffler’s Endocarditis• Eosinophils lining the endocardium & in the myocardium

• Amyloidosis• Most common in US

• Protein deposits

• Hemochromatosis• Iron deposits

• Sarcoidosis• Granulomatous infiltration

Pathophysiology

• Abnormal diastolic function caused by

infiltration of the endocardium/myocardium

• Excessively rigid stiff ventricular walls

• Decrease in ventricular filling

• Contractility unimpaired

• Normal systolic emptying of ventricles

• Hemodynamically resembles constrictive

pericarditis

Hemodynamics Restrictive Cardiomyopathy

– Preserved Systolic function

– Early rapid ventricular fill associated with decreased ventricular compliance

– Dip and plateau(square root) configuration in LV and RV diastolic pressure wave forms

– RA & LA/PCWP prominent x and y descents-M or W pattern

– LV diastolic ~5mmhg greater than RV diastolic

– With exercise pressure separates further-LV pressure increases more than RV

– Pulmonary hypertension usually exists


Clinical Note: RV & LV diastolic pressures will

separate with exercise


Restrictive Cardiomyopathy S&S

• Gradually worsening shortness of breath

• Chest Pain/Palpatations

• Progressive exercise intolerance

• SOB/Paroxysmal nocturnal dyspnea

• Fatigue

• Abdominal discomfort or liver tenderness

• JVD, Hepatamegaly, Ascites

• Atrial Fibrillation

• Thromboembolic events

• Hemodyamic findings as discussed

• Kussmals Sign

• Distant heart sounds

– S3 or S4 heart sounds possible

• Narrowed pulse pressure

Symptoms Signs

Restrictive Cardiomyopathy &

Constrictive Pericarditis

Restrictive Cardiomyopathy & Constrictive Pericarditis

• Filling occurs in early diastole

• Rapid Y-descent of the atrial pressure tracings

• Rapid early filling waveform in the ventricular pressure

• Square root sign in atrial and ventricular diastolic filling

• Kussmaul’s Sign

Kussmaul’s Sign

Restrictive Cardiomyopathy Management

• Usually poor prognosis

• Optimally treat any systemic disease

process of underlying cause

• Diuretics for systemic and pulmonary

congestion

• Antiarrhythmics

Thank You

Cardiovascular

Pathophysiology

Thank You To:

AHA/ACC

SICP


cardiovillage.com

cardiovascular pathophysiology - accredited cme … ncvh/5-29-fri/nurse-cath/6 ncvh rci… ·...

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