Congestive heart failure/shock physiology Flashcards
Diastolic heart failure leads to? Systolic heart failure leads to?
Heart failure occurs when?
Heart failure occurs when the heart is unable to supply adequate blood flow to peripheral tissues or requires elevated filling pressures to do so. Thus, heart failure can result from an impaired ability of the heart muscle to contract (systolic failure) or impaired filling of the heart (diastolic failure).
Explain systolic failure’s effects on frank starling curves and PV loops?
Effects of systolic failure on left ventricular Frank-Starling curves. Systolic failure decreases stroke volume and leads to an increase in ventricular preload
At the same left ventricular end diastolic volume, stroke volume or cardiac output is reduced
How does pulmonary congestion occur in heart failure?
The reduced stroke volume results in an increased preload and increased pulmonary capillary wedge pressure. The figure on the right presents pressures recorded in the right atrium, right ventricle, pulmonary artery and finally pulmonary artery wedge pressure when passing a catheter (with a balloon attachment) along this path. Pressure following balloon inflation (downstream) is similar to left atrial pressure because the occluded vessel and its distal branches that eventually form the pulmonary veins act as a long catheter that measures the blood pressures within the pulmonary veins and left atrium. Reduced stroke volume leads to an increased end systolic volume and increased pressure. This pressure “backs” up pressure in the left atrium and eventually into the lungs causing pulmonary edema.
The Frank-Starling mechanism is a compensatory mechanism explain its effects with CHF? (increasing preload)
The increase in preload activates the Frank-Starling mechanism. The FrankStarling mechanism helps maintain stroke volume despite the loss of inotropy. Accordingly, the Frank-Starling mechanism is an important compensatory mechanism. Specifically, without the increased preload, the decline in stroke volume would be much greater for a given loss of inotropy. Unfortunately, as systolic failure progresses, the ability of the heart to compensate by the Frank-Starling mechanism becomes limited (discussed below). The loss of inotropy and its effect on stroke volume, enddiastolic volume, and endsystolic volume are illustrated using ventricular pressurevolume loops right (figure redrawn by author). As shown, systolic failure decreases the slope of the end-systolic pressure volume relationship (reduced inotropy). Furthermore, at any given ventricular volume, less pressure can be generated during systole and therefore less volume ejected. This leads to an increase in end-systolic volume. Significantly, end diastolic volume increases (compensatory increase in preload). Ventricular preload increases because as the heart loses its ability to eject blood, more blood remains in the ventricle at the end of ejection. This results in the ventricle filling to a larger end-diastolic volume as venous return enters the ventricle. The increase in end-diastolic volume, however, is not as great as the increase in end-systolic volume. Therefore, the net effect is a decrease in stroke volume (decreased width of the pressure-volume loop).
This results in a substantial reduction in ejection fraction occurs. Ejection fraction is normally greater than 55%, but it can fall below 20% in severe systolic failure.
Contractility is known as? What is an index of inotropy?
Contractility is also known as inotropy Inotropy is independent of preload and afterload.
The Change in pressure over the change in time is an index of inotropy.
Diastolic heart failure is caused by?
Diastolic heart failure (reduced ventricular filling) Diastolic heart failure is caused by impaired ventricular filling due to a decreased ventricular compliance (e.g., as occurs with ventricular hypertrophy) or impaired relaxation (decreased lusitropy).
Reduced ventricular compliance shifts?
As shown above, reduced ventricular compliance shifts the ventricular enddiastolic pressure-volume relationship up and to the left and importantly less ventricular filling (decreased end-diastolic volume) and a greater end-diastolic pressure occurs. Stroke volume, therefore decreases. Ejection fraction may or may not change. For this reason, reduced ejection fraction is useful only as an indicator of systolic failure
Increased ventricular end-diastolic pressure often results in?
Increased ventricular end-diastolic pressure often results in serious consequences because left atrial and pulmonary capillary pressures rise. This can lead to pulmonary edema when the pulmonary capillary wedge pressure exceeds 20 mm Hg. Specifically, the increase in end-diastolic pressure is reflected back into the right atrium and pulmonary venous and capillary systems and lead to peripheral edema and abdominal ascites.
diastolic dysfunction increases the slope of the______? why? What does this do?
Combination heart failure?
Systolic and diastolic dysfunction. Chronic heart failure can be a combination of both systolic and diastolic dysfunction In both systolic and diastolic dysfunction, the slope of the end-systolic pressure- volume relationship is decreased (reduced inotropy) and the slope of the passive filling curve is increased (reduced compliance). As a result, this causies a dramatic reduction in stroke volume. The dramatic reduction in stroke volume occurs because end-systolic volume is increased and end-diastolic volume is decreased (loss of the Frank-Starling compensatory mechanism).
Systolic and disatolic HF lead to? which itself leads to? how do we compensate for this?
Both systolic and diastolic heart failure, because of the reduced stroke volume, cause a reduction in cardiac output. A reduced cardiac output results in a decreased arterial pressure and increased central venous pressure. The reduced aortic pressure and increase in right atrial pressure activate compensatory neurohumoral mechanisms that attempt to restore cardiac output and arterial pressure.
Reduced arterial pressure results in the activation of the sympathetic nervous system, the renin-angiotensin-aldosterone system, and vasopressin. The sympathetic nervous system, angiotensin and vasopressin cause an increase in systemic vascular resistance, while angiotensin, aldosterone and vasopressin increase blood volume, and central venous pressure.
Summary of neurohumoral changes associated with heart failure.
Explain how increasing Central venous pressure helps HF and is part of the starling mechanism?
The increased central venous pressure helps to enhance cardiac output by the Frank-Starling mechanism, however it may also lead to pulmonary and systemic edema. Similarly, although the increased systemic vascular resistance helps to maintain arterial pressure, it may eventually impair cardiac output because of increased afterload. After load is the Pressure Keeping Aortic Valve Shut. Low afterload requires less pressure to open valve. High after load requires more pressure to open valve. Redrawn by author Increased right atrial pressure stimulates the synthesis and release of atrial natriuretic peptide to counter-regulate the renin-angiotensin- aldosterone system. Although, these compensatory mechanisms initially help, they can eventually aggravate heart failure by increasing ventricular afterload (which depresses stroke volume) and increasing preload to the point at which pulmonary or systemic congestion and edema occur.
The compensatory mechanisms for HF result in? When cardiac performance is limited what happens?
The compensatory mechanisms described above for the decreased cardiac function result in an increase venous return and increased cardiac (pump) function via the Frank-Starling mechanisms. In addition, the heart undergoes hypertrophy to improve pump function.
However, when cardiac performance is limited the short-term compensations (i.e. Frank-Starling mechanism) and the long-term adaptive response (i.e. hypertrophy) are overcome.
That is because as the ventricular chamber becomes more and more distended, which takes advantage of the Frank-Starling mechanism, this leads to an increase in ventricular wall tension. Specifically, as the ventricular muscle in dilated it must generate greater contractile force (tension) to generate a normal systolic blood pressure. This is explained by the LaPlace Law.
Tension developed by the myocyte is equal to?Contractile Force (tension) is determined by the?
With systolic failure and compensatory increases in blood volume, the chamber undergoes?
Tension developed by the myocyte is equal to ventricular systolic pressure, ventricular radius and ventricular wall thickness.
Contractile Force (tension) is determined by the pressure generated by the ventricle, the radius of the ventricle and the wall thickness of the ventricle.
With systolic failure and compensatory increases in blood volume, the chamber undergoes volume overloading and an increased radius and small increase in wall thickness. This leads to greater wall tension.
With diastolic heart failure, the compensatory mechanisms lead to? Pro’s and Con’s of this?
With diastolic heart failure, the compensatory mechanisms lead to a pressure overload and increased ventricular pressure, slightly smaller ventricular radius and thicker ventricular wall.
What is systemic hypotension? due to?
Systemic hypotension is defined clinically as a systolic arterial pressure less than 90 mm Hg, or a diastolic pressure less than 60 mm Hg.
Hypotension is due to a decrease in cardiac output or a decrease in systemic vascular resistance.
Autonomic dysfunction problems with systemic vascular resistance?
Autonomic dysfunction can also decrease systemic vascular resistance, for example, in individuals with diabetes who experience autonomic neuropathy. The figure below illustrates the drop in arterial pressure and heart rate in response to autonomic ganglionic blockade in a conscious rat. Ganglionic blockade eliminates sympathetic tone to the vasculature reducing peripheral resistance and arterial blood pressure.
Effect of a short pause in heart rate on arterial pressure?
This figure shows the effect of a short pause in heart rate on arterial pressure. Even a short compensatory pause (arrows) following an early ventricular depolarization resulted in a fall in arterial pressure.
Bradycardia induced hypotension?
Reduced heart rate mediated by excessive vagal activation of the SA node or AV node may result in hypotension.
This figure shows the response to vagal efferent activation on arterial pressure. Vagal efferent activation stopped SA node firing and arterial pressure plummeted!
Excessive vagal tone may?
Note the p wave without a corresponding qRS complex and the resulting drop in arterial pressure
Explain tachycardia induced hypotension?
The figure below, presents mean arterial pressure (MAP) and the electrocardiogram (ECG) in a mouse where a single electrical pulse (#, or arrow inset) was sent within the vulnerable zone of the cardiac cycle and induced ventricular tachycardia. Ventricular tachycardia was identified on the electrocardiogram as rapid, wide QRS complexes with concomitant reduction in arterial pressure.
monomorphic v-tach leads to?
This figure show ischemia induced monomorphic ventricular tachycardia. The ischemia induced tachycardia reduced cardiac filling time, reducing stroke volume, cardiac output and arterial blood pressure.
Polymorphic tachycardia leads to?
The ischemia induced tachycardia reduced cardiac filling time, reducing stroke volume, cardiac output and arterial blood pressure.
What is vasovagal syncope?
The vasovagal reflex can lower heart rate and arterial pressure sufficiently to cause hypotension and syncope. The vasovagal syncope involves an increase in parasympathetic activity and a decrease in sympathetic activity. An increase in parasympathetic activity and a decrease in sympathetic activity lowers heart rate and cardiac output and thus arterial pressure. The decreased sympathetic activity, also mediates vasodilation, with a consequent decrease in TPR and a large drop in arterial blood pressure.
Activating vagal efferent fibers can cause A-V block with a reduction in arterial pressure (arrow).
Short Term Compensatory Responses to Hypotension in the Autonomic Nervous System?
Organization of sympathetic and vagal innervation of the heart and circulation. The tenth cranial nerve (vagus; parasympathetic) arises from the brainstem. Preganglionic fibers (solid red line, A) travel to the heart, where they synapse with cell bodies of short postganglionic fibers that innervate the heart. Preganglionic sympathetic nerves (solid black lines) arise from thoracic (T1–T12) and lumbar segments of the spinal cord. Some of these fibers (B) enter the paravertebral ganglia (sympathetic chain) on both sides of the spinal cord, and travel within the ganglia to synapse above (B) or below their entry level, or at their level of entry (C). Postganglionic fibers (dotted black lines) from the upper thoracic ganglia primarily innervate the heart, whereas those from lower thoracic ganglia travel to blood vessels and to the heart. Preganglionic fibers from lower thoracic and upper lumbar segments generally synapse in prevertebral ganglia (D), from which postganglionic fibers travel to blood vessels.
Compensatory mechanisms during hypotension?
Initial short-term mechanisms attempting to restore arterial pressure involve the arterial baroreceptor reflex. Unloading arterial baroreceptors results in a reduction in cardiac vagal activity and an increased cardiac and peripheral sympathetic activity. This increases heart rate, contractility, conduction and constricts systemic vascular beds to increase venous return, cardiac output and arterial pressure. The increases arterial pressure helps to maintain normal cerebral and coronary perfusion.
The baroreceptor compensatory mechanism for hypotension that results from blood loss (hemorrhagic hypotension) is summarized below.
Activation of baroreceptor mechanisms following acute blood loss (hemorrhage). Blood loss reduces cardiac preload, which decreases stroke volume, cardiac output and arterial pressure. The reduced arterial pressure and reduced stretch on the vessels, reduces firing of arterial baroreceptors which reduces cardiac vagal activity and activates the sympathetic nervous system. Reduced vagal activity and increased sympathetic activity stimulates cardiac function, and constricts resistance and capacitance vessels. These actions increase systemic vascular resistance, central venous pressure, and cardiac output, thereby partially restoring arterial pressure.
Supine to standing effects?
The effects of gravity while standing cause venous pooling which decreases venous return, stroke volume and arterial pressure. A sudden decrease in arterial pressure, as occurs when a person suddenly stands up from a supine position, decreases baroreceptor firing, activating sympathetic nerves and inhibiting parasympathetic (vagal) nerves. Figure drawn by author This change in autonomic balance increases cardiac output (CO) and systemic vascular resistance (SVR), which helps to restore normal arterial pressure. CNS, central nervous system.
Sympathetic activity on the heart?
Sympathetic Activity releases norepinephrine onto alpha-adrenergic receptors. Activation of alpha-adrenergic receptors constricts arterioles, trapping blood on the arterial system and increasing arterial blood pressure.
Sympathetic Activity constricts veins, increasing venous return, stroke volume and cardiac output and, by doing so, increasing arterial blood pressure.
Sympathetic Activity increases heart rate, contractility, conduction and relaxation thus increasing cardiac output and arterial blood pressure
Explain the muscle and respiratory pumps?
The respiratory and muscle pumps help to maintain venous return and stroke volume.
More slowly activated, long term compensatory mechanisms include the reninangiotensin-aldosterone system and vasopressin. These hormone systems, serve to increase blood volume and reinforce the vasoconstriction caused by increased sympathetic activity.
