Patho Test 2 Cardio Review

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Pooling
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Terms in this set (73)
Pooling
-caused by drugs that dilate veins

-Veins hold 64% of the blood (more)
-Veins have a lower pressure system so the blood gets back by one-values, contractions, and "suck" RA
Cardiac Output (CO)=
stroke volume (SV) x heart rate (HR)
-Average adult CO= 5 L/min
Stroke Volume
The volume of blood pumped from a ventricle of the heart with each contraction

-Effected by:
--Myocardial Contractility
--Cardiac after load and preload
--Muscular Synchrony
Preload
Amount of blood returning to the heart (right side)
-Increase PL=Increased SV
-Measured by central venous pressure
After load
Resistance the heart has to work against to pump out
-Arterial pressure in the LV must overcome to eject blood
-Increase AL= Decrease SV
Frank-Starling Law of the Heart
-the relatively longer the cardiac muscle fibers, the greater the force of contraction

-A= Use an IV, or drink fluids to get to B
-B= Beautiful (perfect)
-C= To much fluid now so in heart failure and have pulmonary edema
-D= Death
Contractility
ability to shorten forcibly when stimulated
-Increase by myocardial O2 supply
Arterial Pressure (AP)=
PR (peripheral resistance) x CO
Arterial pressure is regulated by:
Autonomic nervous system (ANS)
Renin-angiotensin system
Kidneys (Natriuretic peptides)
Rapid control by the ANS: the Baroreceptor reflex
Constriction of nearly all arterioles
Constriction of veins
Acceleration of heart rate
Baroreceptors locatedcarotid bodies and aortic arch -Let you know your pressure is to lowrenin-angiotensin-aldosterone system-constriction of arterioles and veins (angiotensin II=powerful vasoconstrictor) -retention of sodium and water by the kidney (aldosterone) (so will increase BP)Natriuretic peptides (happy hormones)-secreted by atrial myocardium of the heart in response to high blood pressure (ventricles are to full) -Effects are opposite of aldosterone and so they cause loss of Na and H2Oautonomic nervous systemA subdivision of the peripheral nervous system. Controls involuntary activity of visceral muscles and internal organs and glands. -Sympathetic= Adrenergic -Parasympathetic= CholinergicSelectivity-Most desirable quality a drug can have -Able to alter a disease process while leaving other physiologic processes largely unaffectedAgonistBind directly to receptors and activate themAntagonistsBind to receptors and block themB1 and B2 receptorsB1--found in heart; increase rate and force of contraction and conductivity when NE/Epi binds B2--found in bronchial smooth muscle; causes bronchodilation when bind with NE/EpiAlpha 1 receptorsWhen NE binds or an A1 agonist causes vasoconstriction and increase BP -Ocular: MydriasisDrug SelectiveIf a drug interacts w/ 1 type of receptor, if the receptor regulates a few processes then drug relatively selective.Physiologic selectivityDoes the receptor do more than one thing?Cholingeric receptors (Parasympathetic)All receptors that mediate responses to AChAdernergic Receptors (Sympathetic)All receptors the mediate responses to Epi and NE -A1, A2, B1, B2, and DopamineSomatic-Voluntary muscle movements -Transmitter= ACh -Receptor= Nicotinic-M (muscle) (cholinergic)Autonomic functions-Regulation of Heart -Regulation of Glands -Regulation of Smooth Muscle (bronchi and Blood vessels)parasympathetic function-Slow heart -Most cholinergic drugs affect: GI, Bladder, eyeSympathetic functions-Cardiovascular system -Body temperature -Stress: Fight or flight --Increase HR and BP --Shunt blood from skin and viscera to muscles --Dilation of bronchi --Dilation of pupils --Mobilization of stored energy: glucose, fatty, acidsAlpha-2Inhibits release of norepinephrineBeta 1 receptors-Heart: Inc in HR (chronotropic), Increase heart work (inotropic), and increase conductivity (dromotropic) -Kindey: Stimulate release of renin leading to vasoconstriction (increase Na and H2O)Inotropicstrength of contraction (increase heart work)Chronotropicincrease heart rateDromotropicincrease conductivity of heartBeta 2 receptors-Arterioles in the heart, LUNGS, skeletal muscle= VasodilationDopamine receptorsOnly known function of PNS dopamine receptor= -Dilation of renal arteries --> enhances renal perfusionDecrease PSNS impulses (Decrease O2, High CO2 and low pH)-Leads to increase Sympathetic impulses so you want to rub carotid arteries, cough, and bar down which stimulates to vagus nerve to lower the HR and increase Parasympathetic impulsesheart failure (HF)-Is a syndrome NOT a disease -Associated with long-standing or uncontrolled hypertension (most), coronary artery disease (CAD), and myocardial infarction (MI) (muscle necrosis to myocytes)Risk factors of HFPrimary: -CAD -Advancing Age Contributing: -Hypertension (increase 3 fold) -Diabetes -Tobacco use -Obesity -High serum cholesterolsystolic failureDecrease in the left ventricular ejection fraction (EF)*** -Caused by: --Impaired contractile function (MI) --Increased after load (hypertension) (= decrease SV) --Cardiomyopathy --Mechanical abnormalities (value disease) -Do a Echocardiogram to check EFejection fractionmeasurement of the volume percentage of left ventricular contents ejected with each contraction -Normal= 55%-70%Diastolic failure-More often in elderly, women, and obese patients -Impaired ability of the ventricles to relax and fill during diastole, resulting in decreased SV and CO -Diagnosis based on the presence of pulmonary congestion, pulmonary hypertension, left ventricular hypertrophy from chronic hypertension, hypertrophic cardiomyopathy, and aortic stenosis (narrowing)mixed systolic and diastolic failureSeen in disease states such as dilated cardiomyopathy (DCM) Poor EFs (<35%) High pulmonary pressures Biventricular failure= Both ventricles may be dilated and have poor filling and emptying capacityCompensatory mechanisms (CM) of heart failureActivated to maintain adequate CO -THESE ARE NOT GOOD= lead to worsening HFCM: First and least effective= Sympathetic NS activation-Increased HR -Increased Myocardial contractility -Peripheral vasoconstriction -Overtime these mech. are detrimental as they INCREASE the workload of the failing myocardium and the need for O2CM: 2nd= Neurohormonal responses (Kidneys release renin)-Renin --> angiotensiongen --> AI --> AII by ACE (from lungs) = Release of aldosterone from adrenal glands (Increase Na and H2O) and increases peripheral vasoconstriction (increase BP) -Give ACE inhibitors and beta blockersNeurohormonal responses PART 2-Low CO causes a decrease in cerebral perfusion pressure so ADH is secreted and causes H2O reabsorption in renal tubules causing increased BP -Endothelin is then stimulated by ADH, Epi, and NE, and AngioII causing --Arterial vasoconstriction --Increase in cardiac contractility --HypertrophyNeurohormonal responses PART 3-Pro-inflammatory cytokines (tumor necrosis factor): Rebased by cardiac myocytes in response to cardiac injury -Depress cardiac function by causing cardiac hypertrophy, contractile dysfunction, and death of myocytes -Overtime, a systemic inflammatory response is mounted and results in --Cardiac wasting --Muscle myopathy --FatigueConsequences of compensatory mechanisms: Dilation (systolic HF)-Enlargement of the chambers of the heart that occurs when pressure in the left ventricle is elevated -Initially an adaptive mechanisms -Eventually this mechanism becomes inadequate and CO decreases -Thin heart muscles -Systolic HF= reduced EFDiastolic or HFpEF (Heart failure with Preserved Ejection Fraction)-Impaired relation -HF preserve EF= will be the normal EF 55-70% but since smaller space because of hypertrophied heart chambers there is less volume so low SVSystolic or HFrEF (heart failure with REDUCED ejection fraction)-Enlarged LV chamber with ineffective "squeeze" -Reduced left ventricle ejection factionConsequences of compensatory mechanisms: HypertrophyIncrease in muscle mass and cardiac wall thickness in response to chronic dilation, because can't relax, resulting in... -poor contractility -higher O2 needs -poor coronary artery circulation -risk for ventricular dysryhthmiasCounter Regulatory processes: Natriuretic peptidesNatriuretic peptides are endothelia and aldosterone antagonists. -Released in response to increase in atrial volume and reticular pressure -Promote venous and arterial vasodilation, reducing preload and afterload -Chronic HF leads to a depletion of these factors -Enhance diuresis -Block effects of the RAASHow does vasodilation decrease preload and after load?Preload decreases= Afterload decreases -Vasodilation causes pooling in veins --> Volume going back to heart decreases --> Preload decreases -If after load is reduced by a medication it is easier for the heart to pump blood out. -THIS IS GOODCounter Regulatory Process: Nitric Oxide-Released from the vascular endothelium in response to compensatory mechanisms -Nitric Oxides relaxes arterial smooth muscle resulting in vasodilation and decrease after load. -THIS IS GOODTypes of HF: Left Sided (most common)-from left ventricular dysfunction -Backup of blood into the left atrium and pulmonary veins -Blood flows backwards into lungs Causes: pulmonary congestion and edema (increases pulmonary pressure)Left Ventricular DysfunctionsMI, hypertension, CAD, cardiomyopathyManifestation of Pulmonary EdemaPink, Frothy, SputumTypes of HF: Right Sided HF NOT with Left Sided HFCaused by lung problems or disease.Types of HF: Right Sided HF WITH Left Sided HFBackup of blood into the right atrium and venous systemic circulation. It causes: -JVD: Jugular vein distention -Hepatomegaly, Splenomegaly -Vascular congestion of GI tract -Peripheral edemaManifestations of Acute Decompensated Heart Failure (ADHF): Pulmonary EdemaEarly: -Increase in respiratory rate -Decrease in PaO2 Later: -Tachypnea (about 24- too fast) -Respiratory acidosisMost common cause of pulmonary edema?acute left ventricular failure secondary to CADPhysical Findings of Acute Decompensated Heart Failure-Orthopnea -Dyspnea, tachypnea -Use of accessory muscles -Cyanosis -Cool and clammy skinPhysical Findings of Pulmonary Edema-Cough with pink, blood-tinged sputum -Breath sounds: crackles, wheezes, rhonchi -Tachycardia (HR increases) -Hypotension (SEVERE: low cardiac output) or hypertension)Hemodynamic associated with ADHFDry-Warm: -Normal PAWP, no congestion, Normal perfusion (CO) Wet-Warm: -CO normal, PAWP not normal (fluid in heart) Dry-Cold: -Normal PAWP, low perfusion (low CO) Wet-Cold: -WORST! -CO low, PAWP abnormal, can result in shockManifestations of Chronic HF-Fatigue due to low perfusion to tissues -dyspnea, orthopnea (discomfort laying down), parozysmal nocturnal dyspnea (laying down at night, blood pools in heart all at once) -persistent, dry cough, unrelieved with position change or over-the-counter cough suppressants -Tachycardia -Dependent/Pitting edema -Nocturia -Cool skin, absent hair growth, pigment change -Restlessness, confusion, decreased memory -Chest pain (angina) -Weight ChangeComplications of HFPleural effusion Atrial fibrillation High risk fatal dysrhythmias (EF < 35%) Renal insufficiency or failure Hepatomegaly Pulmonary edemaDiagnostic StudiesGoal is to determine and treat underlying cause -History and physical examination -Chest x-ray -EKG (electrocardiogram) -Lab studies (increased # of cardiac markers = worse HF) -Hemodynamic assessment -Echocardiogram (pumping action) -Stress Testing -Cardiac catheterization (coronary arteries) -Ejection Fraction by echocardiogramManagement of ADHF1. Decrease intravascular volume- reduces venous return= decreased preload -give loop diuretics (Lasix) -Ultrafiltration or aquapheresis 2. Decrease venous return (preload) -Reduces the amount of volume returned to the LV during diastole ---IV nitroglycerin (will dilate Veins and arteries) 3. Decrease Preload -Improves CO and decreases pulmonary congestion (all these drugs dilate) --Nipride --Morphine sulfate --Nesiritide (Natrecor) 4. Improve gas exchange and oxygenation 5. Improve cardiac function -For pt. who do not respond to conventional therapies -Inotropic= Overtime will make heart remodeling worse but will save you if dying nowCollaborative Management of Chronic HF-Treating the underlying cause and contributing factors -Maximize cardiac output -Improve ventricular function -Improve quality of life -Preserve traget organ function -Oxygen administration -Physical and emotional restAngiotensin receptor-neprilysin inhibitorSacubitril/valsartan (Entresto)Therapeutic goal for Chronic HF-Correction of Na and water retention and volume overload -Reduction of cardiac workloadDrug therapies for chronic HF1.Diaretics --Thiazide, Loop, Spironolactone (K sparing/aldosterone antagonist) 2. ACE inhibitors (-prils) 3. AngioII receptor blockers (-sartan) 4. Aldosterone antagonist (-one) 5. Nitrates 6. B-Adrenergic blockers (-lol) 7. Positive inotropic agents --Digitalis + Diuretics (can cause hypokalemia)Nursing Diagnosis for Chronic HF-Activity intolerance -Fluid volume excess -Impaired gas exchange -Anxiety -Deficient knowledgeBeta Blockersdecrease heart rate and dilate arteries by blocking beta receptors -Can mimic hypoglycemia