heart failure

Heart Failure&

CAD

Emily Tetil, MSN, CRNP

Flow of BloodThe superior and inferior vena cava empty into the

right atrium through the tricuspid valve into the right ventricle. From there it passes through the pulmonic valve into the pulmonary artery where it is circulated through the lungs and the CO2 is exchanged for O2. The pulmonary vein then returns the oxygenated blood back to the heart into the left atrium. The blood then passes through the mitral valve into the left ventricle. From there is goes through the aortic valve, into the aorta, and distributed throughout the body.

DefinitionsCardiac output (CO): volume of blood ejected

per minute, 4-8 L/min Stroke volume (SV): volume of blood ejected

with each heart beat, 50-100 mL/beatCO = HR x SVEjection fraction (EF): amount of blood

ejected from the ventricle, 55-75%EF = SV / end diastolic volume

DefinitionsPreload: amount of stretch on the ventricle at

the end of diastole, before contraction, approximated by the end diastolic volume

Afterload: the resistance that the ventricle must overcome to eject the blood, approximated by blood pressure

Contractility (inotropy): strength of contraction

What is heart failure?Heart failure is defined as the inability of the

heart to pump blood at a sufficient rate to meet the metabolic demands of the body. Heart failure can be defined as diastolic or systolic dysfunction. The leading causes of heart failure include coronary artery disease and hypertension with the primary clinical symptoms of dyspnea, fatigue, and fluid retention.

Left Heart FailureSystolic Failure - classic

Impaired ability of the ventricle to eject blood = decreased EF, CO

Almost always occurs with diastolic dysfunctionCauses:

Decreased muscle mass (after MI)Ventricular hypertrophyVolume overloadPressure overload (pulmonary or systemic

hypertension, aortic or pulmonic valve stenosis)

Left Heart FailureDiastolic Dysfunction

Impaired diastolic relaxation and filling or increased stiffness of the ventricular wall or both = preserved EF >45%

Can occur independentlyCauses:

Ventricular hypertrophy causing increased ventricular stiffness

HTN – most common causeIschemia after MIPericardial disease, pericarditis, pericardial

tamponade

Right Heart FailureCauses:

Occurs when the right ventricle faces a sudden increase in afterload and is unable to compensate for the increased workload. The response is increase in systemic venous circulation.

Other causes: pulmonary embolism, pulmonic valve stenosis, COPD, pulmonary hypertension

Most common cause: presence of left sided heart failure

Clinical ManifestationsFrank-Starling mechanism (increase in preload

results in an increase in stroke volume). The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return.

Activation of the RAAS. Renin is released which is responsible for the conversion of angiotensinogen to angiotensin 1. ACE then converts angiotensin I to angiotensin II which is a potent vasoconstrictor. Angiotensin II also stimulates the adrenal glands to release aldosterone which promotes retention of sodium and water.

SignsJVD - rightHepatomegaly - rightEdema – rightTachycardia Rales/cracklesCardiomegalyPulmonary vascular congestionElevated BNP

SymptomsDyspnea on exertionParoxysmal nocturnal dyspneaOrthopneaFatigueLower ext. edema

It is difficult to distinguish systolic from diastolic failure based on physical findings alone.

TreatmentControl of blood pressure and risk factors for

cardiovascular disease such as smoking cessation, treatment of lipid disorders, diabetes management are important ways to reduce a patient’s risk for developing heart failure.

Identify and correct underlying cause if able.

DiureticsReduce intravascular volume therefore

reducing venous return to the heart results in decreased preload.

Should only be used in the setting of pulmonary congestions or peripheral interstitial fluid accumulation

Loop: furosemide (lasix) bumetanide (bumex)Thiazide: hydrochlorothiazide, zaroxolyn

VasodilatorsHelp reverse the adverse effects of

compensatory mechanisms including vasoconstriction (increases afterload) and volume retention (increases preload) (remember the RAAS)

Venous (nitrates): decreases venous pressure therefore decrease preload

Arterial (hydralazine): reduces systemic vascular resistance and therefore LV afterload

Venous and arterial (ACE inhibitors, ARBs): augment the RAAS

Beta BlockersImprove LV systolic function, decrease HR

and ventricular stress thereby reducing myocardial oxygen demand.

Carvedilol (coreg)Metoprolol (lopressor)

Coronary Artery Disease

CADCAD: Myocardial Ischemia and InfarctionCAD: virtually any vascular disorder that

narrows or occludes the coronary arteriesIschemia: disruption in myocardial blood

supplyInfarction: ischemia severe enough to cause

cell necrosis

#1 cause: atherosclerosis

Risk FactorsNon-modifiable: advanced age, male gender

or women after menopause, family historyModifiable: dyslipidemia, HTN, cigarette

smoking, DM, obesity, sedentary lifestyle, diet

Myocardial Ischemia = AnginaStable angina: last 3-5 minutes, heaviness or pressure,

may radiate. Caused by gradual narrowing and hardening of the arterial walls so that the affected vessels cannot dilate in response to increased myocardial demand associated with physical exertion or emotional stress. Relieved by rest and nitrates.

Prinzmetal Angina: caused by vasospasm of the coronary artery with or without associated atherosclerosis

Unstable Angina: result of reversible myocardial ischemia and is a warning sign of an impending infarction

Myocardial Ischemia = Angina

Myocardial Infarction aka acute coronary syndromeMI: prolonged ischemia causing irreversible

damage to the heart muscle. Majority of cases the results is due to rupture of an atherosclerotic plaque with subsequent platelet activation and aggregation with activation of the clotting cascade.

MI is the result of untreated unstable angina where the vessel was occluded for a length of time that cause ischemia and when it wasn’t reversed it caused necrosis and cell death (infarction).

Myocardial Infarction aka acute coronary syndromeNSTEMI: the thrombus has broken up before

complete distal tissue necrosis has occurred therefore the infarct will only involve part of the myocardium.

STEMI: the thrombus has lodged permanently in the vessel and the infarction extends through the myocardium (from endocardium to epicardium) – emergent treatment needed

SymptomsChest pain, epigastric pain, shoulder pain,

jaw pain, back painNausea Dizziness, palpitationsShortness of breathWeakness, tirednessLeg swellingWeight gain

Treatment of UA and NSTEMIPrimary focus: anti-ischemic therapy to restore

balance of myocardial oxygen supply and demand and antithrombotic therapy to stabilize the coronary thrombus

Anti-ischemic therapy: Beta blockers, Nitrates, CCB

BB: decrease oxygen demand through reducing heart rate

Nitrates: venodilation decreases preload therefore less ventricular stress therefore decreased oxygen demand

Treatment of STEMIASA (antiplatelet), heparin (anticoagulant),

beta blockers, nitratesFibrinolytic therapy causing lysis of the

occlusion and restoring blood flowPercutaneous Coronary Intervention (PCI)

with stenting or angioplastyMedications: ASA, plavix, BB, ACE-I, statins

Questions??