NU608 Cardiac Output PDF

1 If you haven’t done so already…please make sure you review the two videos on cardiac output that are located in the module Cardiac output is the amount of blood that the heart ejects in a minute. Cardiac output varies with activity, age and gender but in general ranges from 4.2 to 8 Liters. The...

1 If you haven’t done so already…please make sure you review the two videos on cardiac output that are located in the module Cardiac output is the amount of blood that the heart ejects in a minute. Cardiac output varies with activity, age and gender but in general ranges from 4.2 to 8 Liters. The heart’s ability to increase its output according to body’s needs depends on stroke volume (the amount of blood ejected with each beat). Preload or, filling of the ventricles (ie end-diastolic volume (EDV) Afterload  or, resistance to ejection of blood from the heart Contractility  determined by the interaction of the actin & myosin filaments of cardiac muscles Stroke volume = EDV – ESV EDV (end diastolic volume) is the amount of blood in the ventricle at the end of diastole and the average is ~120 ml ESV (end systolic volume) is the amount of blood that is left at the end of contraction (the heart never fully empties) of that 120ml initially in the ventricle there is ~50ml remaining. So stroke volume would be 120 – 50 = 70ml Cardiac output = SV x HR Heart rate  which determines the frequency with which blood is ejected from the heart So if someone had a SV of 70ml and a HR of 74 bpm – CO would be 70 x 74 2 = 5.18L 2  Preload  represents the volume work of the heart It is called preload because it is the work imposed on the heart before the contraction begins. It represents the amount of blood that the heart must pump with each beat & is largely determined by: the venous return to the heart and, the accompanying stretch of the muscle fibers Preload is the amount of stretch applied to the ventricles as it fills with blood. It’s the distending force (stretch) on muscle fibers prior to contraction it is the volume of blood stretching the heart muscle it is determined mainly by venous vascular volume so, it can be affected by venous vascular volume vascular tone  constriction can increase preload, dilation decreases preload obstruction to blood returning to heart can decrease preload  tamponade, tension pneumothorax, high peep respiratory diseases treatment decreasing venous return to heart The maximum force of contraction occurs when an increase in preload stretches muscle fibers of the heart to approximately 2 ½ times their resting length Frank-starling (mechanism) law of the heart states that there is a direct relationship between the volume of blood in the heart and the stretch or length of cardiac fibers at the end of diastole and the force of contraction during the next systole in a normal functioning heart. The failing or dilated heart may not be able to respond to increased filling because its fibers are already lengthened maximally. 3 Afterload  is the pressure or tension work of the heart. It is the pressure that the heart must generate to move blood into the aorta. Relates to the vascular resistance or the tone of the vascular bed against which the ventricle is pumping. It is called afterload because it is the work presented to the heart after the contraction has commenced. It represents the force that the contracting heart must generate to eject blood from the filled heart. afterload is the amount of resistance to that ejection main component of afterload is systemic vascular resistance the effectiveness of SV proportional to afterload  the greater the SVR, the greater the intra-ventricular pressure must be generated to get that blood out so in a compromised heart cardiac output may decrease Ventricular oxygen consumption directly proportional to afterload the greater the SVR the harder the heart has to work 4 Contractility is the other component of cardiac output  intrinsic ability of the heart muscle to contract, the ability of the cardiac muscle to develop tension (or the degree of myocardial fiber shortening) It refers to the ability of the heart to change its force of contraction without changing its resting (diastolic) length. The contractile state of the myocardial muscle is determined by biochemical & biophysical properties that govern the actin and myosin interactions of the cardiac muscle. Contractility is influenced by inotropes. An inotropic influence is one that modifies the contractile state of the myocardium. Positive inotropes  increase contractility (increase the velocity of myocardial contraction)  sympathetic stimulation (dopamine, epi, norepi, isuprel, calcium salt infusion, digoxin, excess thyroid hormone) Negative inotropes  decreases contractility (decrease in the velocity)  beta blockers, hypoxia, alcohol, glucose, inflammatory mediators, ischemia 5 Blood pressure is determined by the cardiac output (SV x HR) and the resistance that the blood encountered as it moves through the peripheral vessels (systemic vascular resistance). BP = CO / SVR BP can be changed by alterations in CO (which means it can be changed by factors affecting stroke volume) An increase in CO without a decrease in peripheral (also referred to as systemic) resistance will cause both arterial volume and mean BP to increase The higher arterial pressure increases blood flow thru the arterioles Decrease in CO causes an immediate drop in MAP and arteriolar flow PVR (peripheral vascular resistance): Determined primarily by a change in diameter of the arterioles Arteriole constriction raises MAP by preventing free flow of blood into capillaries Dilatation the opposite effect. Reflex control of vasoconstriction & vasodilatation is mediated by effects of sympathetic nervous system Mean arterial blood pressure represents the average blood pressure in the systemic circulation. The MAP is determined by the CO/PVR. It is a good indicator of tissue perfusion, and is monitored along with systolic & diastolic 6 ry system 7 Many hormones cause contraction & relaxation of arteriolar smooth muscle Epinephrine  released from adrenal medulla. Causes vasoconstriction (in most vascular beds) – except in the liver and skeletal muscles Norepi  (from sympathetic NS) – more vasoconstrictive effects ADH, RAAS, and natriuetic peptides  influence BP by influencing the changes in the total volume of fluid in the circulation Adrenomedullin Peptide present in numerous tissues Has powerful vasodilator activity Synthesized and secreted from vascular endothelium and smooth muscle cells Released in various cardio-renal diseases such as hypertension, chronic renal failure and CHF Role in fluid and electrolyte balance Insulin Direct vascular actions that contribute to vascular protection and injury Increases release of nitric oxide thereby decreasing the inflammatory reaction Decreases binding of macrophage/macrophages on vessel wall Insulin resistance (type II diabetes) have threefold increase of coronary artery disease & cause of atherosclerosis 8 8 There are two ways renin is stimulated: 1. The primary stimulus for secretion is renal hypoperfusion… when renal perfusion is decreased  renin release is stimulated. So, anytime renal blood flow is decreased renin will be released. The second way... There are specialized cells in the distal tubule (macula densa) These cells sense the amount of Na+ and Cl- arriving at the site When the concentration of Cl- at macula densa falls renin is released 2. Renin then enters the general circulation acting on angiotensinogen (which is a protein produced in the liver) to convert it to Angiotensin I. 3. Angiotensin I passes through the lung and is converted (by ACE…angiotensin converting enzyme) to Angiotensin II. 4. Angiotensin II is physiologically active and is a potent vasoconstrictor.... Increasing PVR (peripheral vascular resistance) leading to increased BP 5. Angiotensin II also stimulates the adrenal cortex to release aldosterone (a salt-retaining hormone) Aldosterone acts mainly on distal tubule…in the presence of aldosterone Na (and H2O) is reabsorbed and K is secreted 9 Hypertension: Sustained elevation of arterial blood pressure Diagnosis when average of two or more BP measurements made on two or more consecutive visits documents diastolic 90 or greater or a systolic of 140 or greater. Systolic hypertension (even when not accompanied by an increase in diastolic pressure) is the most significant factor in causing target organ damage. 10 Caused by increases in: cardiac output  any condition that increases HR or SV total peripheral resistance  increased by any factor that increases blood viscosity or reduces vessel diameter Types of hypertension primary secondary isolated 11 Can you believe …it’s 30y/o for the onset of hypertension …but… it’s usually not detected until later in life 12 Increased PVR 13 Primary Hypertension  specific cause not yet identified though thought to be combination of genetics and environment. Also, known as essential or idiopathic hypertension affects 90-95% of individuals with hypertension. The above is a path map showing the contribution of increased PVR and increased blood volume leading to sustained hypertension. Next slide shows factors associated with the interplay of genetics and environment. 14 15 Secondary Hypertension caused by systemic disease process that raises (increases) PVR or cardiac output if cause identified and removed before permanent structural damage occurs  BP can return to normal 16 17 Complicated hypertension basically means that there is the presence of end organ damge. Chronic hypertension damages the walls of systemic blood vessels. Walls undergo hypertrophy and hyperplasia associated with fibrosis of the tunica intima & media  known as vascular remodeling This reduces blood flow & eventually organ dysfunction Target organs for hypertension  kidney, brain, heart, extremities and eyes CVS  LVH, L heart failure (CHF), CAD, MI, sudden death Renal  parenchymal damage, renal arteriosclerosis, renal failure Eyes  see changes in the vascular bed noted by viewing the arterioles of the retina  hemorrhage CNS  TIAs, stroke, cerebral thrombosis, aneurysm, hemorrhage Malignant hypertension Rapidly progressive hypertension in which diastolic pressure is usually above 140 mm Hg High hydrostatic pressure in the capillaries cause vascular fluid to move into the interstitial space Causes encephalopathy, profound cerebral edema  loss of consciousness Encephalopathy  d/t high pressures render arterioles of regulating blood flow Hypertensive emergency 18 Isolated Systolic hypertension (ISH) caused by increased cardiac output can be secondary to: Dysfunction of aortic valve (insufficiency) Thyroid storm Beriberi (thiamine deficiency) PVR can be increased Rigidity of proximal large arteries  chief cause in elderly. The rigidity most often caused by arteriosclerosis (which we will look at in next weeks module) 19 Although usually thought of as an adult problem – children can develop hypertension. While most pediatric hypertension is secondary (such as renal disease or coarctation of aorta), unfortunately, primary hypertension is becoming increasingly diagnosed in young adults d/t obesity & decreased activity. Systemic hypertension in pediatric patients is defined as systolic and diastolic blood pressure levels greater than the 95% for age and gender on at least three different occasions 20 As you will learn when you get into health assessment and your clinical management courses – assessment focuses on two things: 1. Before we start treating someone with primary hypertension we want to make sure we are not missing a cause of secondary hypertension 2. And, then we need to assess to see if there is any end-organ damage that may already be present. If there is and depending on what it is – it may change our treatment plan for the patient. 21  Fundoscopic exam – looking for arteriosclerotic and hypertensive changes such as the presence of AV nicking, arteriolar narrowing, exudates, papilledema. AV nicking occurs as chronic hypertension narrows the arteries and creates indentation in the veins where the arteries cross over them – this can be identified on eye exam. If AV nicking is present in elderly patients with hypertension – it has been shown to correlate with the presence of LVH in those individuals. Neck - look for distended veins, bruits, or thyroid enlargement CVS – assessing for evidence of hypertrophy or failure, murmurs, gallops Abd – asses for the presence of masses or bruits (especially over renal arteries) Peripheral pulses Neuro exam Assess for evidence of gout, thyroid or Cushings – all can impact hypertension 22 Above are diagnostic testing that may be needed in the hypertensive patient. Next week we look at the development atherosclerosis and CAD (which unfortunately tend to go hand-in-hand with many who have evidence of primary hypertension. 23