Angina Pectoris"Angina" meaning to choke.• When the demand for myocardial oxygen exceeds the ability of the coronary arteries to supply the heart, myocardial ischemia occurs. o The clinical manifestation of this is: Angina pectoris o Can be caused by: An increase in demand for oxygen A decrease in oxygen transport in the blood o Almost 90% of cases involve some level of atherosclerosis o symptoms dont develop until the lumen of the coronary artery narrows 75%.
Why do we care about Angina andCoronary syndromes?
Causes of Angina PectorisLack of Supply to the myocardium: • Blood flow factors or low blood pressure (hemodynamic factors). • Vasospasms • Cardiac Factors • Hematologic Factors o low hgb/hctMost often (>90%) of cases, lack of blood supply to themyocardium is caused by atherosclerosis of a main coronaryartery
Causes of Angina PectorisMyocardium demands an increase in blood supply(increased need for O2) • High Systolic BP • Increased Ventricular Volume • Increased Heart Rate and Contractility
Patterns of Angina1. Stable Angina (Chronic Stable Angina)2. Variant or Prinzmentals angina3. Unstable Angina4. Silent Ischemia
Stable AnginaThis is caused by a fixed coronary obstruction that causesintermittent decreases in blood flow and a lack of vesselflexbility (the vessel cant dilate to allow more blood flow). • symptomatic chest pain or pressure that is associated with transient myocardial ischemia • usually precipitated by some sort of activity or stress that causes an increased need for oxygen in the myocardium • usually resolves with rest or by alleviating the stressor, use of nitrates to increase coronary blood flow also can reduce the pain • pain usually resolves within 3-5 minutes.
Variant or Prinzmentals AnginaThis is an angina pain that occurs mainly at rest, and resultsfrom vasospasm of the coronary arteries (strong contraction ofthe smooth muscle in the coronary artery). • Vasospasm can occur in individual who have no underlying coronary disease, but can also confound the problem of CAD in individuals. • Seen in patients with a history of migraine headaches and Raynauds disease. • Thought to occur due to increased myocardial demand and increased levels of certain substances. • Treated with nitrates and primarily calcium channel blockers • Often see anginal pain and ST segment elevation
Unstable AnginaThis form of angina, also called crescendo angina, is new onsetangina, angina that occurs at rest (but is not due tovasospasm), or angina that is worsening in pattern (increasedfrequency of events, increased intensity of events). • s/s include: fatigue, SOB, anxiety, indigestion (and can also include the chest pressure and pain associated with stable angina), ST segment depression. • A result of an unstable plaque (post rupture, where there is platelet aggregation and thrombus formation). • This is considered an emergency, and often is seen pre- myocardial infarction
Silent IschemiaThis is ischemia that occurs in the absence of anginal pain. • Diagnosed often with an EKG showing ischemic changes in the heart. • Thought to be the same pathophysiology as stable angina (r/t atherosclerotic disease). • Why dont they feel pain (different theories): o these episodes may be shorter and involve less tissue o the patient may have a defect in their pain threshold or pain tolerance patients with diabetes mellitus have a higher incidence of silent ischemia (have some cardiac autonomic nerve dysfunction)
Clinical manifestations of anginapectorisThink about what disease process may be causing these s/s? • Substernal chest discomfort, described as squeezing, constricting, or suffocating. o usually steady, increasing in intensity at the beginning and the end of the attack • Can radiate to the left shoulder, jaw, arm, between the shoulder blades, or other areas of the chest. • May complain of indigestion or a burning sensation in the epigastic region • Can be associated with a feeling of apprehension, impending doom
Potential Medical Complications1. Myocardial Infarction2. ArrhythmiasThese are both worse case scenarios, as both have a highmortality rate, especially when left untreated.
Myocardial InfarctionsThis occurs as a result of sustained ischemia. Heart musclecan tolerate 20 minutes of sustained hypoxia. Then cellulardeath begins to occur. After 4-6 hours, if the ischemia persists,there entire thickness of the myocardium can becomenecrosed. • This is a worst case scenario
Clinical manifestations of an MI• Pain: Severe, immobilizing chest pain that is not relieved by rest, position change, or nitrate administration o commonly in the early morning hours o pain is from the buildup of toxic metabolites in the heart cells• Sympathetic Nervous System activation: epinephrine and norepinephrine are released in large amounts from the damaged myocardial cells. Activates the sympathetic nervous system and causes peripheral vasoconstriction and diaphoresis. Patient will appear pale and feel cool, and clammy to the touch.• Nausea and Vomiting: there is reflex stimulation of the vomiting center in the medulla by the severe pain
Clinical Manifestations of an MI• Cardiovascular Manifestations: the release of the epi/norepi can initially increase the BP and HR. but the BP eventually drops due to decreased cardiac output. May decrease renal perfusion and ARF and decreased renal output. Left ventricular dysfunction may cause blood to back up in the lungs causing crackles.• Fever: Temperature increase up to a week post MI due to the systemic manifestation of inflammation from myocardial cell death.
Potential complications of an MI• Dysrhythmias: Occur in 80% of patients post acute MI. Life threatening dysrhythmias often occur with anterior wall infarctions. Ventricular fibrillation is a common cause of sudden cardiac death and often occurs within 4 hours of an acute MI• Heart Failure: the pumping power of the heart is diminished.• Cardiogenic shock: occurs when the heart is not perfusing the tissues because of severe Left ventricular failure. o very emergent if it occurs• Ventricular Aneurysms: the infarcted myocardial wall thins and develops an outpouching that doesnt function with normal contractile properties.
EKG/ECGThere are classic ECG changes that can occur with Angina andMI. • T-wave inversion • ST-segment elevation • Development of an abnormal Q-waveThese findings can vary based on the duration of the ischemicevent (acute vs. evolving), extent of ischemia (subendocardialvs. transmural), and the location.Findings may "disappear" when the angina isnt occuring, needto check ECG with the anginal pain.
Serum Enzyme Level TestsThe damaged heart muscle will often release proteins into thebloodstream that are indicative of cardiac damage. • These levels can be checked with a blood test • There are varying levels of specificity for cardiac vs. general muscle damage. o CK-MB o Troponin I, Troponin T o Myoglobin o Beta type Natiuretic peptide (BNP) • Albumin Cobalt Binding Test
Serum Enzyme Level TestsCK-MB: Troponin:• Creatinine Kinase MB is • This protein regulates the an intracellular enzyme Ca++ mediated Actin- found in the muscle cells Myosin contractile process• increases outside the • Troponin I/T begin to rise normal range within 4-8 within 3 hours after the hours post myocardial onset of MI and may injury remain elevated for 3-4• there are 3 bands of CK days post MI enzymes • More sensitive then CK-• CK-MB is very specific MB for cardiac muscle damage
Serum Enzyme Level TestsMyoglobin:• oxygen carrying protein, which is normally present in cardiac and skeletal muscle.• It is a small molecule, so it is released into the system quickly• Starts rising 1 hour post cardiac damage, peaks 4-8 hours post MI• myoglobin is rapidly excreted in the urine, so blood levels return to normal within 24 hours post MI• Not Cardiac Specific
Serum Enzyme Level TestsCobalt Albumin binding Beta-type Natriuretictest: peptide: • in an MI, albumin • this is used for diagnosis, molecules in the blood are assessment of severity altered, and unable to bind and prognosis of cobalt properly congestive heart failure. • Helpful to determine if the • peptide that is produced by patient didnt have a heart the ventricular myocardium attack if their ECG and • studies are showing that troponins are negative. it can predict the risk for • negative predictive value cardiac death in patients post MI
Serum Lipid PanelsElevated serum lipids are one of the most firmly establishedrisk factors for coronary artery disease.• Trigylcerides• Total Cholesterol• Cholesterol Fractionation: This usually includes HDL/LDL and total cholesterol.• C-reactive protein- inflammatory marker that is associated with recurrent cardiovascular events• N-High Sensitivity C-Reacitve Protein-tested with Cholesterol to help manage atherosclerosis
Exercise Stress Test• Treadmill exercise testing is an important diagnostic test done for the patient with chronic stable angina.• Patient is on a treadmill (or is injected with adenosine if they cant tolerate exercise) with a ECG/EKG hooked up and a BP cuff on. The patient then walks for however long they can tolerate it, and they are to stop and report chest pain or pressure if it occurs.• ST segment and T-wave abnormalities are used as an INDIRECT MEASURE of CORONARY PERFUSION• Can differentiate anginal chest pain from other chest pain.
Nuclear Cardiology ImagingA small amount of blood is removed and a radionucleotide dyeis mixed and the "tagged" blood is returned to the body. Theradiologic machine can then scan the body and assess: • Blood flow • Ventricular structures/Motion of the ventricles • Areas darkness where infarctions have occured ("cold spots") • Perfusion of the myocardium
Coronary Calcium ScanThis is a specialized CT scan that is able to assess the amountof calcium that has built up in the arteries of the heart: • A score is attached to the amount of calcifications seen • Can help determine amount of atherosclerosis in the coronary vessels • INDIRECT MEASURE OF CORONARY BLOOD FLOW
Coronary AngiographyA catheter is inserted into one of the larger arteries of the heartand is advanced to the coronary arteries, where dye is injected. • DIRECT EVALUATION OF CORONARY BLOOD FLOW • helps to evaluate collateral circulation • can assess the extent of the coronary vascular disease • only way to evaluate if the angina is variant type or due to obstruction • Need to assess platelets, PT, INR, PTT, and kidney function prior...why? • Also, can engage in therapeutic management during PCI
Acute AttacksShort acting nitrates are the first line therapy for anginalattacks, the drug works by: 1. dilating peripheral blood vessels (decreases SVR, increased blood return to the heart) 2. dilating coronary arteries and collateral vessels (increases coronary artery circulation, increases O2 to the heart)Sublingual Nitroglycerin:for an acute attack: give 0.4-0.6mg sublingual x1, may repeat2 more times every 5 minutes if no pain relief. o 1 pill sublingual, or 1 metered spray sublingual
Chronic Anginal ProphylaxisNitroglycerin Ointment:• Nitropaste is a 2% nitroglycerin topical ointment.• Dosed by inch• place on the skin, in an area free of hair and scars.• lasts 3-6 hours, especially good for nocturnal and unstable anginaTransdermal Nitrates: • Small, thin adhesive patch • Apply to a intact, hairless skin q24hours • Allows for a steady state of drug
Chronic Anginal ProphylaxisLong-Acting Nitrates: Sublingual Nitroglycerin: • Extended release • take a pill or a nitrospray tablets/capsules 5-10 minutes before • Taken every 8 to 12 hours engaging in a activity that • work to reduce the could precipitate anginal incidence of anginal attack attacks • Better to use before the • Imdur and Isordil (both pain develops isosorbide base) • increases exercise tolerance and stress tolerance
Chronic Anginal ProphylaxisBeta-Adrenergic Blockers: Calcium Channel Blockers:• These are the preferred • Drug of choice for drugs to help manage prinzmentals angina chronic stable angina • Inhibits the transport of• decrease myocardial calcium into the contractility myocardial and smooth• decrease HR, SVR, and muscle vasculature BP (dec. renin secretion) inhibiting muscle• can decrease morbidity contraction and mortality in patients • cause systemic who are s/p MI vasodilation, decreased• Counsel patients not to myocardial contractility, stop beta-blockers abruptly and coronary vasodilation
Chronic AnginalProphylaxis/ManagementAspirin (ASA): Clopidogrel (Plavix):• Inhibits cyclooxygenase, • Inhibits platelet which decreases the aggregation (ADP Blocker) productions of • Alternative for patients thromboxane A2, a potent who cant tolerate ASA platelet activator • indicated in combination• 81mg po qd with aspirin in patients whove had a heart attack or ACS • 75mg po qd
Fibrinolytic TherapyThis is a rapid and available method to break up a blockage ina coronary artery. • Aimed at dissolving the thrombus in the coronary artery and reperfusing the heart. • IV infusion of a thrombolytic agent • Will break down any clot...not just in the heart, need to watch for bleeding. • Nursing Management: o Assess V/S, pulse Ox, ECG o heart and lung assessments • Should see an improvement in the ST segment changes • Watch for reperfusion arrhythmias • Likely start heparin drip in the immediate post fibrinolytic period to prevent reocclusion.
Percutaneous Transluminal CoronaryAngioplasty (PTCA)• Catheter is inserted through a large peripheral vessel and advanced to the coronary vessels where a dye is injected (see previous slides)• Allows for a direct assessment of coronary blood flow• The atherosclerotic plaques can be shaved off and circulation to the coronary myocardium improved.• Need to assess: o PT/INR, PTT, Platelets, Kidney function o V/S and continuous monitoring of pulse ox and ECG before, during and post procedure.
Intracoronary Stents• PTCA with intravascular stent over a balloon• The catheter that is advanced to the coronary arteries had a balloon that can push aside the plaque and a stent is placed holding open the vessel.
Invasive Management of Angina/ACSLaser Angioplasty: Atherectomy: • A laser tipped angio • Plaque is shaved off using catheter is introduced via a a rotational blade large peripheral vessel • removes atheromas • the laser vaporizes the • Can embolize the plaque and creates atheroma channels between the left ventricle and microcirculation • used in patients who are not a CABG Candidate and who have failed maximal medical treatment for their angina
Coronary Artery Bypass GraftThis is the construction of new passages for block around ablocked coronary vessel • Traditional CABG involves a stenotomy and the use of cardiopulmonary bypass • A vessel is harvested from the saphenous vein area or internal mammary artery and are grafted from the aorta or left subclavian to an area beyond the occlusion (bypassing it) • Significant morbidity and recovery period (6-8 weeks off work)MIDCABG: (minimally invasive) thorascopic approach to theheart and beta-blockers or adenosine are used to slow theheart and allow for suturing of the bypass
Prehospital Emergency Care of ChestPainFor person with Unknown For Person with KnownCHD: CHD: • Recognize symptoms- • Recognize symptoms- Chest pain, SOB, nausea, Chest pain, SOB, Nausea, weakness weakness • Stop activity and sit or lie • Stop Activity, sit or lie down down • If pain persists for 5 • place 1 nitro-tab under minutes or more, activite your tongue or dispense the EMS one spray SL, repeat at 5 minute intervals x3 doses • If symptoms persist, activate EMS
Congestive Heart FailureImpaired cardiac function renderingthe heart unable to maintain proper output (PUMP FAILURE)
Cardiac Failure:High Output Failure: (not common) caused by an excessiveneed for cardiac output. The function of the heart may benormal to even excessive, but the body needs are higher. • severe anemia, thyroxicosis, conditions that cause arteriovenous shunting, and Pagets disease • Treatment involves treating the underlying diseaseLow Output Failure: (common) caused by failure of the heartas a pump • ischemic heart disease, cardiomyopathy, long standing hypertension • Treatment is focused on symptom management and slowing the natural disease state
General clinical features of heart failureThe failure of the compensatory mechanisms of the heartresults in heart failure: • heart rate fails to compensate for inadequate cardiac output • dilation of the heart fails to compensate for inadequate cardiac output • hypertrophy of the heart fails to compensate for inadequate cardiac output • kidneys, sensing decreased circulation, increase the production of renin, causing increased angiotensin II/increased SVR and Aldosterone/increasing blood volume
Systolic DysfunctionInvolves a decrease in cardiac contractility and ejection fraction • Caused by: o conditions that impair the contractile performance of the heart (ischemic heart disease and cardiomyopathy) o produce a volume overload (valvular insufficiency and anemia) o generate a pressure overload (hypertension and valvular stenosis) on the heartSymptoms result from reduction in ejection fraction and cardiacoutput
Diastolic DysfunctionThis accounts for 40% of all cases of CHFCharacterized by: • smaller ventricular chamber • ventricular hypertrophy • poor ventricular compliance (ability to stretch) • Symptoms: o because impaired filling, congestive symptoms predominate o symptoms increase in situations where the heart rate increasesCHF is often a combination of systolic and diastolicdysfunction
Compensatory Mechanisms in HeartFailureVentricular Dilation: Ventricular Hypertrophy: • Chambers stretch and • there is an increase in the dilate to allow more blood muscle mass and cardiac in the ventricle wall thickness in response • The ventricle can dilate to to overwork and strain the point of overstretching • occurs slowly and over where the actin and time myosin fibers are unable to • allows for initial increases contract properly and allow in CO, but demands more for a proper ejection of Oxygen, has poor blood contractility, is poorly • Frank Starling Law...page vascularized, and is prone 605 Porth to dysrhythmias
Compensatory Mechanisms in HeartFailureSympathetic Nervous Neurohormonal Response:System Activation: • Renin-Angiotensin- • decreased CO causes a aldosterone mechanism release of catecholamines with low CO to kidney (epinephrine and • Low CO to the brain norepinephine) causes increase ADH • initially increases HR, secretion, which increases myocardial contractility, preload and peripheral • Vascular endothelium vasoconstriction releases endothelin which • Overtime, causes an causes vasoconstriction overload on the failing (inc. SVR) heart (inc. O2 needs, inc. • Inflammatory cytokines are preload) released
Left Sided Heart FailureThe left side of the heart moves blood from a low pressurecircuit (the lungs) to a high pressure circuit (the peripheralcirculation). • S/S: o Decrease in cardiac output o Increase in Left Atrial and left ventricle end diastolic pressures o Congestion in the pulmonary circulation o Pulmonary edema • Most common cause is Acute Myocardial Infarction and Cardiomyopathy
Right Sided Heart FailureThis is the failure of the right of side of the heart. • S/S: o Jugular Venous Distention o Hepatomegaly o Splenomegaly o Vascular congestion of the GI tract get N/V/Reflux/hematemesis o Peripheral Edema • Caused by (most commonly) Left sided heart failure, 2nd primary pulmonary HTN , 3rd Right ventricle AMI o Lung disease can cause hypertrophy of the right ventricle called Cor Pulmonale
Clinical Manifestations of Heart Failure1. Fluid Retention and edema2. Respiratory manifestations3. Fatigue and limited exercise tolerance4. Cachexia and malnutrition5. Cyanosis
Clinical Manifestations of Heart Failure:Fluid Retention and EdemaEdema: Nocturia: • Common sign and usually • During the day, the appears in the dependent decreased CO causes areas decreased urine o peripheral edema production o liver • At night, with the patient o abdominal cavity lying back, the fluid from o lungs the interstitial space • Can be pitting (can indent moves back into the the skin with a finger tip) circulation where the • Acute development of kidneys are able to edema or wt. gain of >3lbs process it and make urine in 2 days is a sign of • Can be 6-7 times per night decompensation
Clinical Manifestations of Heart Failure:Respiratory ManifestationsPulmonary Edema: Paroxysmal Nocturnal• Sign of ADHF, caused by Dyspnea: increased pulmonary venous • Occurs in the middle of the pressure caused by the night when the patient is decreased efficiency of the LV recumbant• the lungs are less compliant • Fluid from the dependent and there is increased body areas are reabsorbed resistence in the small • often wake up in a panic with airways a feeling of suffocation• see dyspnea, anxiety, cool, Cough: pale, diaphoretic skin, cough • often persistent, dry, hacking with frothy sputum, orthopnea cough• Hear crackles, wheezes, and • sputum +/- rhonchi
Clinical Manifestations of Heart Failure:Fatigue and Limited Exercise ToleranceFatigue: Anxiety and Restlessness: • caused by decreased CO • Secondary to poor gas • fatigue occurs in activities exchange in the lungs and that were not previously impairment in cerebral tiring circulation • Anemia is often associated • Family may report anxiety, with CHF and compounds restlessness, confusion the fatigue and decreased attentionTachycardia: span • Early clinical sign • SNS response to decreased CO • Beta-blockers can mask this
Clinical Manifestations of Heart Failure:Weight Loss and MalnutritionWeight Loss: Malnutrition:• Cardiac Cachexia is a • closely linked to the condition hallmarked by cardiac cachexia tissue wasting o caused by fatigue and depression o also hepatomegaly and congestion of GI vasculature contributes to feeling of fullness o inflammatory mediators suppress hunger
Clinical Manifestations of Heart Failure:CyanosisThis is the bluish discoloration of the skin and mucousmembranes caused by excess desaturated hemoglobin in theblood. Often a late sign of heart failure.Central Cyanosis: caused by conditions that impairoxygenation of the arterial blood like pulmonary edema • Lips and mucous membranesPeripheral Cyanosis: caused by conditions that cause low-output failure that cause delivery of poorly oxygenated blood tothe peripheral tissues. • finger tips and toes
Complications of Heart Failure1. Pleural Effusion2. Arrhythmias3. Left Ventricular Thrombus4. Hepatomegaly
Pharmacologic TherapyACE Inhibitor: Inotropics:• Angiotensin Converting • Digitalis Glycosides Enzyme Inhibitors o good at reducing• Prevents the conversion of symptoms but doesnt angiotensin I to improve survival angiotensin II and also o Increase the force of inhibits the subsequent cardiac contraction release of aldosterone while decreasing the• Decreases both SV and rate of contraction PVR (preload and • Beta-Adrenergic Agonists afterload) o Dopamine/dobutamine• Decreases mortality due to • Calcium Sensitizers: in heart failure clinical trials here
Pharmacologic TherapyDiuretics: Vasodilators:• Utilized in CHF to mobilize • Class of drugs clearly edematous fluid and shown to improve survival decrease pulmonary in CHF venous pressure • Work to increase venous• Reduces vascular capacity, improve EF by volume/preload improving contractility,• Different types of diuretic slowing ventricular available, and they work in dysfunction, decreasing the different areas of the heart size, and avoiding kidney the neurohormonal o Potassium sparing vs. changes of CHF potassium wasting
Beta-Adrenergic Blocking AgentsMarked improvement in patient survival is seen in patients onbeta-blockers • Specifically Carvedilol (Coreg) and metorprolol (Toprol XL) • Blocks the negative effects of the SNS on the failing heart • Use in combination with other drugs and increase the dose slowly (because there can be a decrease in myocardial contractility)
Supportive Care of Heart FailureOxygen: Sodium Restricted Diet:• 2-6 lpm, increase amount • DASH diet of available Oxygen to the o <2.4gm sodium a day heart and the tissues o normal american diet is 7-10gms of sodium/dayRest:• decrease cardiac demand Fluid Restrictions: • In acute casesDaily Weights: • want to be careful in• Check for fluid retention emergency situations• Call provider if there is a weight gain of >3lbs in 2 days or 3-5lbs gain in 1 week
A particular slide catching your eye?
Clipping is a handy way to collect important slides you want to go back to later.