Emily Tetil, MSN, CRNP

Flow of Blood
The 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.

Definitions
Cardiac 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/beat CO = HR x SV Ejection fraction (EF): amount of blood ejected from the ventricle, 55-75% EF = SV / end diastolic volume

Definitions
Preload: 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 Failure

Systolic Failure - classic Impaired ability of the ventricle to eject blood = decreased EF, CO Almost always occurs with diastolic dysfunction Causes: Decreased muscle mass (after MI) Ventricular hypertrophy Volume overload Pressure overload (pulmonary or systemic hypertension, aortic or pulmonic valve stenosis)

Left Heart Failure

Diastolic Dysfunction Impaired diastolic relaxation and filling or increased stiffness of the ventricular wall or both = preserved EF >45% Can occur independently Causes: Ventricular hypertrophy causing increased ventricular stiffness HTN most common cause Ischemia after MI Pericardial disease, pericarditis, pericardial tamponade

Right Heart Failure

Causes: 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 Manifestations
Frank-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.

Signs
JVD - right
Hepatomegaly - right Edema right

Tachycardia
Rales/crackles Cardiomegaly Pulmonary vascular congestion Elevated BNP

Symptoms
Dyspnea on exertion
Paroxysmal nocturnal dyspnea Orthopnea

Fatigue
Lower ext. edema It is difficult to distinguish systolic from diastolic

failure based on physical findings alone.

Treatment
Control 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 patients risk for developing heart failure. Identify and correct underlying cause if able.

Diuretics
Reduce 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

Vasodilators
Help 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 Blockers
Improve LV systolic function, decrease HR and

ventricular stress thereby reducing myocardial oxygen demand. Carvedilol (coreg) Metoprolol (lopressor)

Coronary Artery Disease

CAD
CAD: Myocardial Ischemia and Infarction
CAD: virtually any vascular disorder that narrows or

occludes the coronary arteries Ischemia: disruption in myocardial blood supply Infarction: ischemia severe enough to cause cell necrosis
#1 cause: atherosclerosis

Risk Factors
Non-modifiable: advanced age, male gender or women

after menopause, family history Modifiable: dyslipidemia, HTN, cigarette smoking, DM, obesity, sedentary lifestyle, diet

Myocardial Ischemia = Angina

Stable 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 Ischemia = Angina

Myocardial Infarction
aka acute coronary syndrome
MI: 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 wasnt reversed it caused necrosis and cell death (infarction).

Myocardial Infarction
aka acute coronary syndrome
NSTEMI: 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

Symptoms
Chest pain, epigastric pain, shoulder pain, jaw pain,

back pain Nausea Dizziness, palpitations Shortness of breath Weakness, tiredness Leg swelling Weight gain

STEMI

Treatment of UA and NSTEMI

Primary 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 STEMI
ASA (antiplatelet), heparin (anticoagulant), beta

blockers, nitrates Fibrinolytic therapy causing lysis of the occlusion and restoring blood flow Percutaneous Coronary Intervention (PCI) with stenting or angioplasty Medications: ASA, plavix, BB, ACE-I, statins

Questions??