chapter 16

Chapter 16: Altered Perfusion — Active-Reading Notes

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Big Picture

• This chapter is mainly about perfusion, which means moving blood through vessels into tissues so cells receive oxygen and nutrients.

• The main disease process is altered perfusion:

  • Tissues are not getting enough oxygenated blood.

  • Blood flow may be blocked, reduced, mismatched with ventilation, or unable to meet tissue demand.

• Perfusion matters because every cell depends on:

  • Oxygen delivery

  • Nutrient delivery

  • Waste removal

  • Normal cardiac output

  • Blood pressure regulation

  • Patent circulation

• Pay attention to:

  • How the heart pumps blood

  • How ventilation and perfusion must match

  • What blocks or reduces blood flow

  • How altered perfusion causes ischemia, infarction, shock, heart failure, stroke, and DIC

  • Cues that show poor oxygen delivery: cyanosis, fatigue, dyspnea, edema, mental status changes, poor urine output

Key Vocabulary

• Perfusion: Movement of blood/fluid through vessels into tissue vascular beds to deliver oxygen and nutrients.

• Altered perfusion: Inability to adequately oxygenate tissues at the capillary level.

• Ventilation: Movement of air into and out of the lungs.

• Diffusion: Movement of oxygen across the alveolar-capillary membrane.

• Ventilation-perfusion ratio: Relationship between air movement into the lungs and blood flow through pulmonary capillaries.

• Cardiac output: Amount of blood pumped by the heart per minute.

• Stroke volume: Amount of blood pumped from one ventricle with each beat.

• Heart rate: Number of heartbeats per minute.

• Preload: Ventricular filling/stretch before contraction.

• Afterload: Pressure/resistance the ventricle must overcome to eject blood.

• Contractility: Ability of the heart muscle to increase force of contraction.

• Blood pressure: Pressure of blood within systemic arteries.

• Pulse pressure: Difference between systolic and diastolic blood pressure.

• Mean arterial pressure: Measure of systemic tissue perfusion.

• Atherosclerosis: Lipid deposits in the intima of large/medium arteries.

• Thrombosis: Formation of a blood clot.

• Thrombus: Blood clot attached in a vessel.

• Embolus: Traveling plug of material that can obstruct a vessel.

• Infarct: Area of necrosis caused by sudden insufficient blood supply.

• Infarction: Process of vessel obstruction causing tissue necrosis.

• Ischemia: Reduced blood flow/oxygen supply to tissue.

• Shock: Circulatory failure with impaired perfusion of vital organs.

• Hypertension: Elevated blood pressure.

• Myocardial infarction: Total coronary artery occlusion causing myocardial ischemia and tissue death.

• Heart failure: Inadequate heart pumping to maintain circulation.

• Stroke/CVA: Acute neurologic injury caused by impaired cerebral circulation.

• DIC: Uncontrolled clotting followed by depletion of clotting factors and massive hemorrhage.

Main Chapter/Module Patho Chain

Perfusion problem → poor oxygen delivery → tissue hypoxia → cellular dysfunction → anaerobic metabolism → acidosis → cell injury/death → organ dysfunction

More specific chain:

• Ventilation problem, circulation problem, cardiac output problem, or excessive tissue demand
  ↓

• Tissues receive inadequate oxygenated blood
  ↓

• Cells cannot maintain normal aerobic metabolism
  ↓

• ATP production decreases
  ↓

• Ion pumps fail
  ↓

• Sodium enters cells, potassium leaves cells
  ↓

• Cells swell, rupture, and die
  ↓

• Organ function decreases
  ↓

• Severe cases: shock, infarction, stroke, heart failure, DIC, death

Organized Notes by Section

Introduction

• The four-chambered heart pumps blood through:

  • Pulmonary circuit

  • Systemic circuit

• The cardiac conducting system distributes impulses through heart muscle.

• These impulses allow cardiac muscle cells to contract.

• The heart continuously goes through contraction-relaxation cycles called the cardiac cycle.

• Cardiac output is the amount of blood the heart pumps.

• Cardiac output is determined by:

  • Heart rate

  • Stroke volume

• The heart works with the lungs:

  • Lungs oxygenate blood.

  • Lungs remove carbon dioxide.

  • Heart distributes oxygenated blood to tissues.

• The heart is central to tissue perfusion.

Module 1: Perfusion

Perfusion

• Perfusion is the process of forcing blood or other fluid to flow:

  • Through a vessel

  • Into the vascular bed of tissue

  • To provide oxygen and nutrients

Requirements for Effective Perfusion

• Adequate ventilation and diffusion

  • Person must breathe in oxygen.

  • Oxygen must move across capillaries.

  • Required for oxygen distribution to tissues.

• Intact pulmonary circulation

  • Required for oxygen uptake from inspired air.

• Adequate blood volume and components

  • Blood volume must be sufficient to:

    • Carry oxygen on hemoglobin

    • Maintain blood pressure

• Adequate cardiac output

  • Needs:

    • Optimal stroke volume

    • Optimal heart rate

    • Efficient heart rhythm

• Intact cardiac control center in the medulla

  • Regulates:

    • Heart rate

    • Force of cardiac contractions

    • Response to blood pressure changes

• Intact receptors

  • Sense changes in:

    • Cardiac function

    • Blood pressure

  • Send feedback to the cardiac control center.

• Intact parasympathetic and sympathetic nervous systems

  • Autonomic nervous system mediates cardiovascular changes based on body demands.

• Intact cardiac conduction

  • Electrical impulse conduction stimulates cardiac contractility.

• Intact coronary circulation

  • Maintains blood flow to cardiac structures.

  • Allows the heart to pump oxygenated blood to the rest of the body.

• Intact systemic circulation

  • Distributes oxygenated blood to tissues and organs.

• Adequate oxygen uptake in tissues

  • Cells and tissues must be able to receive and use oxygen and nutrients.

From Ventilation to Perfusion

• Adequate ventilation and diffusion are required for:

  • Oxygen intake

  • Oxygen transport

  • Carbon dioxide removal

• Perfusion with oxygenated blood cannot happen without:

  • Oxygen inhalation

  • Oxygen diffusion

• Oxygen moves across the alveolar-capillary junction.

• Pulmonary circulation then takes up and distributes oxygen.

• Effective gas exchange depends on a reasonably equal match between:

  • Ventilation = oxygen intake

  • Perfusion = blood flow movement of oxygen from lungs to blood

Ventilation-Perfusion Ratio

• The relationship between ventilation and perfusion is called the ventilation-perfusion ratio.

• Normal ratio is typically 0.8:0.9.

  • Ventilation is slightly less than perfusion.

• Largest volume of ventilation and perfusion occurs in the lower lobes of the lungs.

Why Lower Lobes Have More Ventilation/Perfusion

• Ventilation is optimal because:

  • Alveolar surface tension is lowest.

  • Lungs are most easily inflated.

• Perfusion is optimal because:

  • Blood pressure through lower lobes allows maximal blood flow.

Gravity and Ventilation-Perfusion

• Ventilation-perfusion is affected by gravity.

• Lung tissue that is most dependent/closest to the ground is most ventilated and perfused.

Circulation

• Effective perfusion requires blood vessels to:

  • Deliver oxygen and nutrients to tissues

  • Remove wastes

• Circulation is discussed through three connected pathways:

  • Pulmonary circulation

  • Cardiac/coronary circulation

  • Systemic circulation

Effective Circulation Depends On

• Patent blood vessels

• Microcirculation adjustment to tissue demands

• Arteries transport blood away from the heart.

• Veins transport blood toward the heart.

• Arterioles, capillaries, and venules form the microcirculation.

• Microcirculation is the primary site for nutrient exchange.

• More capillaries = more surface area for exchange.

• Organs with high oxygen needs, like the heart, have extensive capillary networks.

• When organ demand increases:

  • Vasodilation occurs.

  • More blood flow is directed to that organ.

• Increased cell metabolism/energy use increases perfusion needs.

Pulmonary Circulation

• Pulmonary circulation allows exchange of:

  • Oxygen

  • Carbon dioxide

• Pulmonary circulation includes:

  • Right side of the heart

  • Pulmonary arteries

  • Pulmonary capillaries

  • Pulmonary veins

• Important:

  • Pulmonary arteries carry deoxygenated blood to the lungs.

  • Pulmonary veins carry oxygenated blood to the left side of the heart.

• Pulmonary circulation functions at lower pressure than systemic circulation.

• Blood moves slowly past the lungs to allow maximum gas exchange.

Systemic Circulation

• Systemic circulation includes:

  • All arteries, capillaries, and veins except pulmonary circulation.

• Systemic circulation functions at higher pressure than pulmonary circulation.

• Blood must work against resistance to reach peripheral tissues.

• Systemic circulation is powered by the left side of the heart.

• The left ventricle is the strongest pumping chamber.

Coronary Circulation

• Coronary circulation is part of systemic circulation.

• It is discussed separately because the heart is the pump that supplies oxygenated blood to the body.

• Heart is a vital organ.

• Cardiac muscle cells need constant oxygen and nutrients.

• Cardiac cells have little storage capacity.

• Coronary circulation supplies oxygen and nutrients to the heart.

• Two major vessels branch directly off the aorta:

  • Right coronary artery

  • Left coronary artery

• These perfuse the right and left myocardium.

• The heart also has collateral circulation:

  • Accessory arterial and venous branches

  • Develops more when blood flow demand increases or obstruction occurs

Movement of Blood Through the Circulation

• Heart structures promote movement of blood:

  • Through arteries

  • To capillaries

• The heart has three layers:

  • Pericardium

  • Myocardium

  • Endocardium

Layers of the Heart

Pericardium

• Outer covering of the heart.

• Holds heart in place in the chest cavity.

• Contains receptors that help regulate:

  • Blood pressure

  • Heart rate

• Forms a first line of defense against infection and inflammation.

• Has two layers:

  • Inner visceral layer = epicardium

  • Outer parietal layer

• Pericardial fluid:

  • Found between pericardial layers

  • Cushions heart

  • Lubricates heart

  • Reduces friction during heartbeat

Myocardium

• Thick muscular middle layer.

• Thickness varies by location.

• Left ventricle has the thickest myocardium because it pumps against systemic resistance.

• Myocardium can undergo hypertrophy when workload increases.

Endocardium

• Inner lining of the heart.

• Continuous endothelial layer.

• Connects arteries and veins to the heart.

• Helps form a closed circulatory system.

Heart Chambers and Valves

• Heart has four chambers:

  • Right atrium

  • Left atrium

  • Right ventricle

  • Left ventricle

• Right and left sides are separated by the interventricular septum.

• Blood passes through valves:

  • Between atria and ventricles

  • Between ventricles and pulmonary artery/aorta

• Valves are one-way structures.

• Valves promote forward blood flow.

Blood Flow Through the Heart

Step-by-step pathway:

1. Venous blood returns to heart.

2. Blood from head and arms enters through the superior vena cava.

3. Blood from trunk and legs enters through the inferior vena cava.

4. Blood enters the right atrium.

5. Blood moves through the tricuspid valve.

6. Blood enters the right ventricle.

7. Blood moves through the pulmonary valve.

8. Blood enters the main pulmonary artery.

9. Deoxygenated blood goes to lungs.

10. Ventilation-perfusion exchange oxygenates blood.

11. Blood returns through pulmonary veins.

12. Blood enters the left atrium.

13. Blood moves through the bicuspid/mitral valve.

14. Blood enters the left ventricle.

15. Blood moves through the aortic valve.

16. Blood enters the aorta.

17. Blood goes to systemic circulation.

18. Blood returns by venous return to the right side.

Chordae Tendineae

• Fibrous strands attached to cusps of atrioventricular valves.

Cardiac Cycle

• Cardiac cycle = one contraction phase + one relaxation phase.

• Systole

  • Contraction phase.

  • Moves blood out of ventricles.

• Diastole

  • Relaxation phase.

  • Allows ventricles to fill with blood.

S1 Heart Sound

• Occurs when AV valves close.

• AV valves:

  • Bicuspid/mitral valve

  • Tricuspid valve

• Closure makes first heart sound:

  • “Lub”

  • Also called S1

S2 Heart Sound

• During systole:

  • Ventricular pressure becomes greater than pressure in aorta and pulmonary artery.

  • Semilunar valves open.

  • Blood ejects from ventricles.

• Semilunar valves:

  • Aortic valve

  • Pulmonary valve

• After blood ejection:

  • Ventricles relax.

  • Aorta and pulmonary artery pressure becomes higher than ventricular pressure.

  • Semilunar valves close to prevent backflow.

• Closure makes second heart sound:

  • “Dub”

  • Also called S2

Additional Heart Sounds

• S3

  • May occur with rapid ventricular filling.

  • Associated with weak, distended, or impaired ventricle.

• S4

  • May be heard during atrial contraction.

Conduction of Impulses

• Cardiac contractions rely on:

  • Ion movement

  • Electrical impulses

  • Cell-to-cell conduction

• Key ions:

  • Sodium

  • Calcium

  • Potassium

• Electrical activity occurs through action potentials.

Action Potential Phases

1. Rapid depolarization

2. Early repolarization

3. Plateau

4. Rapid repolarization

5. Resting phase

Depolarization

• Change in polarity.

• Fast sodium channels open.

• Sodium moves rapidly into the cell.

• Cell voltage changes suddenly.

Plateau Phase

• Calcium and sodium enter slowly through slow calcium-sodium channels.

• Calcium influx helps prolonged contraction of cardiac muscle fibers.

Repolarization

• Regrouping phase.

• Cell membrane becomes polarized again.

• Sodium and calcium channels close.

• Potassium exits the cell.

• Cell returns to resting polarity.

ECG/EKG Waves

• Electrical activity can be measured by an electrocardiogram.

ECG Components

• P wave

  • Depolarization of the atria through the SA node.

• P-Q interval

  • Depolarization of the AV node and bundle fibers.

• QRS complex

  • Depolarization of the ventricles.

• T wave

  • Repolarization of the ventricles.

• U wave

  • Repolarization of Purkinje fibers.

Cardiac Conduction Pathway

• Specialized myocardial cells create orderly impulse conduction.

SA Node

• Sinoatrial node.

• Pacemaker of the heart.

• Generates rhythmic impulse in atria.

• Stimulated by slow response through calcium-sodium channels.

AV Node

• Atrioventricular node.

• Connects conduction between atria and ventricles.

• Slows impulse to allow atria to empty fully into ventricles.

Bundle of His and Purkinje Fibers

• AV node impulse travels to:

  • AV bundle/bundle of His

  • Right and left bundle branches

  • Purkinje fibers

• Purkinje fibers stimulate ventricles to contract.

• Blood is ejected from ventricles.

Cardiac Output

• Cardiac output measures heart pumping efficiency.

• Formula:

CO = SV × HR

• CO: cardiac output

• SV: stroke volume

• HR: heart rate

• Stroke volume = amount of blood pumped from one ventricle per beat.

• Heart rate = beats per minute.

• Cardiac output varies with:

  • Age

  • Body size

  • Metabolic needs

• Adult average cardiac output:

  • 3.5 to 8.0 L/min

• During exercise:

  • Cardiac output can increase fourfold.

Box 16.1: Major Factors Impacting Cardiac Output

Preload

• Work imposed on the heart just before contraction.

• Also called ventricular end-diastolic volume.

• Represents pressure in ventricles before systole.

• Depends on:

  • Adequate venous return

  • Adequate cardiac muscle stretching

• Needed to eject optimal blood volume.

Cardiac Contractility

• Ability of heart to increase contraction force.

• Does not require changing diastolic/resting pressure.

• Affected by calcium ions.

Afterload

• Pressure in the ventricle toward the end of cardiac contraction.

• Resistance the ventricle must overcome to eject blood.

• Affected by resistance from:

  • Aorta

  • Main pulmonary artery

• Increases when valves are impaired.

Heart Rate

• Part of cardiac output equation.

• Must adjust to body demands.

• Slower heart rate allows greater diastolic filling.

• Excessively rapid heart rate moves blood quickly but reduces filling time.

Blood Volume

• Quantity and quality of blood affect heart workload.

• Excessive blood increases pressure.

• Deficient blood lowers pressure.

• Increased blood viscosity increases pressure.

• Thinner blood lowers vascular resistance and blood pressure.

• Heart adjusts to maintain optimal stroke volume.

Blood Pressure

• Blood pressure = pressure/tension of blood inside systemic arteries.

• Needed to perfuse vital organs.

• Maintained by:

  1. Contraction of left ventricle

  2. Peripheral vascular resistance

  3. Elasticity of arterial walls

  4. Blood viscosity and blood volume

• Blood pressure is a product of:

  • Cardiac output

  • Arterial resistance

Systolic Blood Pressure

• First number.

• Pressure during left ventricular contraction and blood ejection into aorta.

• Affected by:

  • Stroke volume

  • Heart rate

  • Resistance in the aorta

• Can increase with:

  • Exercise

  • Smoking

  • Cardiovascular disease

  • Stress

Diastolic Blood Pressure

• Second number.

• Pressure remaining in aorta during resting phase.

• Elevated diastolic pressure may show arteries are not resting appropriately.

• Low diastolic pressure may result from:

  • Lack of adequate resistance in aorta

  • Backflow through the aortic valve

Pulse Pressure

• Difference between systolic and diastolic pressure.

• Narrowing/convergence may reflect loss of systolic pressure.

• Example:

  • Severe blood loss decreases systolic pressure while diastolic may remain unchanged.

Mean Arterial Pressure

• Measure of systemic tissue perfusion.

• Formula:

  • One-third pulse pressure + diastolic pressure

Neural Control of Blood Pressure and Cardiovascular Adaptation

• Cardiovascular regulation is controlled by neurons in:

  • Medulla

  • Pons

• These neurons act on the autonomic nervous system.

Sympathetic Nervous System

• Increases:

  • Heart rate

  • Cardiac contractility

  • Blood vessel tension/resistance

• Can cause artery and arteriole vasoconstriction.

• Increases peripheral vascular resistance.

Parasympathetic Nervous System

• Acts on the heart to decrease heart rate.

Blood Pressure Regulation Responds To

1. Baroreceptors and chemoreceptors in arteries

2. Renin-angiotensin-aldosterone system

3. Kidneys

Baroreceptors

• Located throughout blood vessels and heart.

• Sense pressure changes.

• If arterial stretch decreases/low BP:

  • Baroreceptors alert cardiac control center in brainstem.

  • Brainstem stimulates sympathetic nervous system.

  • Beta-1 receptors in heart increase cardiac output.

  • Alpha-1 receptors in blood vessels cause vasoconstriction.

• When BP becomes optimal:

  • Sympathetic stimulation decreases.

Chemoreceptors

• Located in:

  • Aorta

  • Carotid arteries

• Detect changes in:

  • Oxygen

  • Carbon dioxide

  • Blood pH

• Provide feedback to:

  • Alter ventilation

  • Promote vasoconstriction as needed

  • Maximize oxygenation of vital organs

Renin-Angiotensin-Aldosterone System

• Renin is produced by kidneys.

• Renin converts angiotensinogen into angiotensin I.

• Angiotensin I is converted to angiotensin II by an enzyme in the lungs.

• Angiotensin II:

  • Potent vasoconstrictor

  • Increases blood pressure

  • Stimulates adrenal cortex to release aldosterone

• Aldosterone:

  • Increases salt and water retention by kidneys

  • Expands blood volume

Other Blood Pressure Regulators

• Antidiuretic hormone/vasopressin

  • In high doses, causes vasoconstriction.

  • Promotes fluid retention.

  • Increases blood volume.

• Epinephrine

  • Increases heart rate.

  • Increases cardiac contractility.

  • Promotes vessel tension.

Module 2: Altered Perfusion

Altered Perfusion

• Altered perfusion = inability to adequately oxygenate tissues at the capillary level.

• May result from:

  • Low oxygen level

  • Poor oxygen utilization

Factors That Alter Perfusion

• Ventilation-perfusion mismatching

• Impaired circulation

• Inadequate cardiac output

• Excessive perfusion demands

Ventilation-Perfusion Mismatching

• Most common cause of hypoxemia.

• Can occur due to:

Inadequate Ventilation in Well-Perfused Lung Areas

• Blood flow exists, but air movement is poor.

• Occurs with:

  • Asthma

  • Pneumonia

  • Pulmonary edema

Inadequate Perfusion in Well-Ventilated Lung Areas

• Air movement exists, but blood flow is poor.

• Occurs with vascular obstruction, such as:

  • Pulmonary embolus

Impaired Circulation

• Circulation problems lead to inadequate or excessive blood flow.

• Can result from:

  • Vessel injury

  • Obstructive processes

  • Inadequate blood movement

  • Inadequate blood volume

Vessel Injury and Hemorrhage

• Vessel injury causes loss of vessel integrity.

• Hemorrhage = blood loss through vessel wall.

• Most common cause:

  • Trauma-related vascular injury

• Other causes:

  • Aneurysms

  • Coagulation disorders

  • Vessel degradation by neoplasms

Obstruction in Vessels

• Obstruction blocks normal blood flow.

• Occluded arteries prevent oxygenated blood from reaching peripheral tissues.

• Occluded veins restrict venous return and cause congestion.

• Obstruction commonly occurs through thrombus formation.

Thrombosis

• Formation of a blood clot.

• Normal clotting is essential for wound healing.

• Undesired thrombi can form in arteries or veins and block blood flow.

Virchow Triad

Three major factors responsible for thrombus formation:

1. Vessel wall damage

2. Excessive clotting

3. Altered blood flow

   • Turbulence

   • Sluggish blood movement

• Injury to vessel endothelium followed by atherosclerosis is the most common cause of arterial thrombus formation.

• Endothelial injury also contributes to venous thrombosis.

Atherosclerosis

• Irregular lipid deposits in the intima of large/medium arteries.

• Begins with injury to the intima.

• Possible injury sources:

  • Hypertension

  • Smoking

  • Environmental exposures

Atherosclerosis Patho Chain

• Intima injury
  ↓

• LDL filters into artery lining
  ↓

• LDL becomes trapped
  ↓

• LDL becomes oxidized
  ↓

• Macrophages engulf oxidized LDL
  ↓

• Foam cells form
  ↓

• Foam cells + lipids create fatty streaks
  ↓

• Fatty streaks become fibrous plaques
  ↓

• Platelet caps expand over injury sites
  ↓

• Plaques may occlude artery

Turbulent or Stagnant Blood Flow

• Turbulent or stagnant flow contributes to thrombus formation.

Common Sites

• Bifurcations

  • Areas where vessels branch.

  • Blood slows or backs up while moving through narrowed pathways.

• Aneurysms

  • Local bulges caused by weakness in vessel wall.

  • Vessel wall damage promotes aneurysm development.

  • Loss of wall pressure slows blood transit.

• Venous stasis

  • Reduced venous return.

  • Blood pools, especially in legs.

  • Promoted by:

    • Heart failure

    • Varicose veins

    • Prolonged bed rest

    • Immobilization

Hypercoagulability

• Excess clotting allows unregulated thrombi formation.

• Can be congenital or acquired.

Acquired Causes

• Autoimmune mechanisms activating platelets and altering coagulation factors

• Cancer or myeloproliferative disorders

• Thrombocythemia

• Sickle cell disease

• Polycythemia vera

• Oral contraceptive use

• Vascular changes in late pregnancy

Outcomes of Thrombus Formation

1. Thrombus grows and completely occludes vessel.

2. Thrombus is degraded by enzymes and decreases in size.

3. Part or all of thrombus breaks off and travels.

Thromboembolus/Embolus

• Once a thrombus breaks off and travels, it becomes a thromboembolus or embolus.

• Embolus = any plug of material traveling in circulation that can obstruct vessel lumen.

• Emboli may include:

  • Thrombi

  • Air

  • Neoplasms

  • Microorganisms

  • Amniotic fluid

Infarct and Infarction

• Infarct: Area of necrosis due to sudden insufficient blood supply.

• Infarction: Process of vessel obstruction causing infarct formation.

• Loss of blood supply causes:

  • Necrosis

  • Loss of function in affected tissue

Severity Depends On

• Size of emboli

• Location of emboli

• Amount of collateral circulation

Emboli Effects

• Small emboli:

  • Smaller necrotic areas

  • Less significant damage

• Large emboli:

  • Can lodge in large vessels

  • Can block tributaries

  • Can cause sudden death

Venous Thromboemboli

• Often originate in deep leg veins.

• Can break off and travel to pulmonary arteries.

• Lodge where vessels narrow and bifurcate.

Arterial Thromboemboli

• Often originate from atherosclerotic plaques in the heart.

• Can travel to:

  • Brain

  • Intestines

  • Lower extremities

  • Kidneys

Inadequate Cardiac Output

• Cardiac output is inadequate when the heart cannot eject enough blood to pulmonary and systemic circulation.

Major Causes

• Changes in blood volume, composition, or viscosity

• Impaired ventricular pumping

• Structural heart defects

• Conduction defects

• Excessive or reduced peripheral vascular resistance

Blood Volume, Composition, and Viscosity Changes

• Blood volume and viscosity altered by:

  • Hypercoagulation

  • Dehydration

  • Hemorrhage

• DIC illustrates coagulation disorders and hemorrhage effects on perfusion.

• Anemia alters oxygen transport.

• In anemia:

  • Not enough RBCs carry oxygen.

  • Heart tries to move fewer RBCs faster.

  • Heart becomes overtaxed.

Impaired Ventricular Pumping

• Heart is a muscle.

• Loss of muscle activity prevents effective forward blood movement.

• Causes:

  • Arterial flow impairment

  • Venous congestion

  • Impaired venous return

• Heart failure illustrates impaired ventricular pumping and venous insufficiency.

Structural Heart Defects

• Structural defects impair smooth, directional blood flow through heart chambers.

Examples

• Atrial septal defect

• Ventricular septal defect

• Transposition/reversal of great vessels

• Coarctation/narrowing of great vessels

• Patent ductus arteriosus

• Valve stenosis

• Valve regurgitation

• Valve prolapse

Septal Defects and Shunting

Atrial Septal Defect

• Opening between left and right atria.

Ventricular Septal Defect

• Opening between left and right ventricles.

Two Major Problems

1. Oxygenated and deoxygenated blood mix.

2. Blood flow volume changes, affecting cardiac output.

Shunting

• Blood moves across chambers instead of following normal pathway.

• Blood moves from higher pressure to lower pressure.

Left-to-Right Shunt

• Blood moves from left side of heart to right side.

• Oxygenated blood recirculates into right side.

• Right heart and pulmonary circulation pressure increase.

• Large defects can cause:

  • Excessive right ventricular pressure

  • Pulmonary edema

  • Reduced systemic output from left ventricle

Right-to-Left Shunt

• Blood moves from right side to left side.

• Deoxygenated blood enters systemic circulation.

• Small defects may be asymptomatic.

• Large defects can cause:

  • Overtaxed left ventricle

  • Severe hypoxemia

Valvular Defects

• Can be congenital or acquired.

• Most often affect:

  • Bicuspid/mitral valve

  • Aortic valve

Acquired Causes

• Infection

• Inflammation

• Trauma

• Degeneration

Stenosis

• Valve narrowing.

• Valve cannot open adequately.

• Causes:

  • Increased resistance

  • Turbulent flow

  • Increased ventricular workload

Regurgitation

• Valve incompetence.

• Valve cannot close properly.

• Allows backflow/reflux of blood.

• Heart chamber works harder against constant backflow.

Conduction Defects

• Alter optimal heart rate and rhythm.

• Cardiac dysrhythmias show inefficient rhythm.

• Can originate from problems with:

  • SA node

  • AV node

  • Cells joining SA and AV nodes

  • Atrial conduction systems

  • Ventricular conduction systems

Why Conduction Defects Matter

• Without efficient rhythm, tissues are not adequately perfused.

• Ventricular conduction problems are most serious because ventricles pump blood to:

  • Aorta

  • Pulmonary artery

Ventricular Fibrillation

• Ventricle vibrates instead of pumping effectively.

Atrial Fibrillation

• Similar ineffective rhythm occurring in atria.

Defibrillator

• Uses electrical current to shock heart.

• Goal: reestablish efficient rhythm.

Heart Block

• Obstruction of cardiac conduction, often at AV node.

• Atria and ventricles lose coordination.

• Blood movement becomes inefficient.

Excessive Perfusion Demands

• Tissue metabolism can become excessive.

• Even if ventilation/diffusion works, tissue demand is too high.

• Can result from:

  • Extreme prolonged exertion

  • Metabolic alterations such as hyperthyroidism

General Manifestations of Altered Perfusion

From Impaired Cardiac Output

• Cyanosis

• Edema

• Shortness of breath

• Impaired growth

• Tachycardia

• Tachypnea

• Fatigue

From Blood Volume or Peripheral Resistance Changes

• Hypotension

• Hypertension

From Obstructive Processes

• Loss of organ function from ischemia

• Pain

• Edema

Deep Vein Thrombosis Cues

• Calf tenderness

• Tenderness with dorsiflexion of foot = Homans sign

• Total venous occlusion:

  • Edema

  • Coolness

  • Pallor

  • Cyanosis of lower extremity

Hemorrhage Skin Cues

• Ecchymoses: Bruises from superficial bleeding into skin.

• Petechiae: Pinpoint hemorrhages.

• Purpura: Diffuse hemorrhages of skin or mucous membranes.

• Hematoma: Larger accumulation of blood in tissue.

Valve or Septal Defect Cue

• Heart murmur

Diagnosing and Treating Altered Perfusion

• Diagnostic tools identify altered perfusion.

• Treatments aim to:

  • Improve cardiac output

  • Maintain circulation integrity

Module 3: Clinical Models

Hypertension

Definition

• Hypertension is a progressive cardiovascular syndrome.

• Detected by elevated blood pressure.

• American Heart Association threshold:

  • Systolic above 130 mm Hg

  • Or diastolic above 80 mm Hg

• Associated with:

  • Obesity

  • Diabetes

  • Chronic kidney disease

• Often asymptomatic.

• Many people are unaware without routine screening.

Hypertension Pathophysiology

Types

• Primary hypertension/essential hypertension

  • 90% to 95% of hypertension cases.

  • Cause often unknown.

  • Multifactorial.

  • Involves genetic and environmental triggers.

• Secondary hypertension

  • High BP caused by another condition.

  • Examples:

    • Coarctation of aorta

    • Kidney disease

• Isolated systolic hypertension

  • Systolic elevated without diastolic elevation.

• Isolated diastolic hypertension

  • Diastolic elevated without systolic elevation.

• Mixed systolic/diastolic hypertension

  • Both systolic and diastolic pressures elevated.

Risk Factors for Primary Hypertension

• Family history

• Aging

• Chronic stress

• Decreased nephron number

• Diabetes mellitus

• Excess dietary sodium intake

• Obesity

• Sedentary lifestyle

• Nutrition factors

• Excessive alcohol intake

• Smoking

Hypertension Mechanism

• Hypertension reflects:

  • Increased cardiac output

  • Or increased peripheral resistance

Increased Cardiac Output Caused By

• Increased stroke volume

• Increased heart rate

Increased Peripheral Resistance Caused By

• Restricted peripheral blood flow

• Increased blood viscosity

• Vasoconstriction

Impaired Regulatory Mechanisms

• Sympathetic nervous system overstimulation:

  • Systemic vasoconstriction

• RAAS overstimulation:

  • Vasoconstriction

  • Salt and water retention

  • Increased blood volume

• Impaired sodium excretion by kidneys:

  • Salt and water retention

  • Increased blood volume

Chronic Hypertension Vessel Damage

• Prolonged high pressure injures intima.

• Inflammatory response increases capillary permeability.

• Vessel wall damage worsens.

• Vessel walls adapt through:

  • Hypertrophy

  • Hyperplasia

• Vessel lumen permanently narrows.

Body Systems Affected by Hypertension

CNS

• Severe hypertension overwhelms cerebral blood flow control.

• Normally cerebral arterioles vasoconstrict when BP rises.

• In hypertensive crisis:

  • Arteriolar control is overwhelmed.

  • Fluid leaks into brain tissue.

  • Arterioles are damaged.

  • Intracranial pressure increases.

  • Oxygen transport decreases.

  • Brain function decreases.

Cardiovascular System

• Hypertension contributes to atherosclerosis.

• Can cause arterial obstruction.

• Small vessels in target organs are vulnerable:

  • Kidneys

  • Eyes

  • Brain

  • Heart

• Left ventricle works against pressure resistance.

• Left ventricular hypertrophy develops.

• Ineffective left ventricular pumping causes:

  • Impaired venous return

  • Impaired systemic perfusion

  • Pulmonary edema

  • Myocardial ischemia

  • Peripheral hypoxemia

Renal System

• Prolonged kidney arteriole pressure causes:

  • Chronic injury

  • Inflammation

  • Nephrosclerosis

• Nephrosclerosis = overgrowth/hardening of kidney connective tissue.

• Reduced kidney blood flow stimulates:

  • Renin

  • Aldosterone

• Blood volume expands.

• Blood pressure increases further.

Hypertension Clinical Manifestations

• Primary hypertension is often asymptomatic.

• Symptoms often reflect years of undetected hypertension.

CNS Cues

• Headache

• New blurred vision

• Nausea

• Vomiting

• Weakness

• Fatigue

• Confusion

• Mental status changes

• Cerebral vessel rupture can cause stroke.

Cardiovascular Cues

• Pulmonary edema signs

• Heart failure manifestations

Renal Cues

• Poor urinary output

• Hematuria

• Proteinuria

• Problems eliminating urinary waste

Hypertension Diagnostic Criteria

• Diagnosis requires:

  • Patient history

  • Physical exam

  • Lab/diagnostic tests

• History should include:

  • Family history

  • Risk factors

• Physical exam includes:

  • Proper blood pressure measurement

  • Assessment for target organ damage

  • Assessment for cardiovascular disease

• Hypertension diagnosis is not based on one elevated reading.

• Usually requires three properly performed BP measurements over 3 to 6 months.

AHA BP Categories

Labs/Diagnostics

• Electrolytes

• Urinalysis

• BUN

• Creatinine

• Lipid profile

• Blood glucose

• Chest radiograph in crisis if assessing:

  • CHF

  • Pulmonary edema

  • Coarctation of aorta

• CT brain if assessing:

  • Intracranial bleeding

  • Edema

  • Infarction

  • Secondary hypertension causes

• ECG for:

  • Cardiac ischemia

  • Infarction

Hypertension Treatment

• Goal: reduce cardiovascular risk.

• Lifestyle measures:

  • Weight reduction

  • Decreased alcohol intake

  • Decreased salt intake

  • Decreased saturated fat intake

  • Increased aerobic activity

  • Increased fruits/vegetables/potassium

  • Vitamin D intake

  • Smoking cessation

• Medication categories mentioned:

  • Diuretics: decrease fluid volume

  • Calcium channel blockers: decrease cardiac contractility/cardiac output

  • ACE inhibitors: decrease peripheral vascular resistance

  • ARBs: decrease peripheral vascular resistance

• Goal BP: below 130/80 mm Hg.

• Many people need two or more medications.

• Pharmacotherapy does not cure hypertension.

• It reduces symptoms and long-term complication risk.

Shock

Definition

• Shock = circulatory failure with impaired perfusion of vital organs.

• Often associated with hypotension.

• Hypotension is a late sign and indicates ineffective compensation.

Shock Pathophysiology

• Effective circulation requires:

  • Cardiac output

  • Adequate blood volume

  • Peripheral vascular resistance

Types of Shock

Cardiogenic Shock

• Caused by inadequate/ineffective cardiac pumping.

• Most common cause:

  • Myocardial infarction

• Basic problem:

  • Impaired pumping

  • Reduced cardiac output

  • Low BP

  • Restricted oxygenated blood movement

• Leads to:

  • Systemic hypotension

  • Pulmonary edema

• Mortality is approximately 70% without rapid revascularization.

Hypovolemic Shock

• Caused by inadequate blood/plasma volume.

• Typically occurs when volume decreases by 15% to 20%.

• Causes:

  • Severe hemorrhage

  • Burns

  • Diarrhea

  • Polyuria, such as diabetes insipidus

• Problem:

  • Fluid loss in vascular space

  • Deficient venous return

  • Reduced circulation

  • Reduced RBC volume decreases oxygen transport

• Without correction:

  • Inadequate perfusion

  • Multiple organ failure

Septic Shock

• Caused by overwhelming systemic infection.

• About half caused by Gram-positive microorganisms.

• Closely followed by Gram-negative microorganisms.

• Sometimes exact pathogen unknown.

• Gram-negative microorganisms contain endotoxin.

• Endotoxin can trigger massive inflammatory response.

• Chemical mediators cause widespread tissue injury.

• Endothelial cells:

  • Vasodilate

  • Become permeable

  • Allow fluid to escape intravascular space

  • Become damaged

• Leads to vascular collapse.

• Mortality approximately 30% to 50%.

Neurogenic Shock

• Caused by:

  • Brain injury

  • Spinal cord injury

  • Depressant drugs

  • General anesthesia

  • Hypoglycemia

  • Hypoxia

• Mechanism:

  • Altered neural transmission

  • Loss of sympathetic control of vessel tension

  • Unregulated vasodilation

  • Decreased peripheral vascular resistance

  • Decreased BP

  • Reduced vital organ perfusion

• Rarest cause of shock.

• Readily treatable.

• Generally responds well to therapy.

Anaphylactic Shock

• Caused by massive type I/IgE-mediated hypersensitivity response.

• Similar to septic shock:

  • Massive vasodilation

  • Increased vascular permeability

• Effects:

  • Reduced peripheral vascular resistance

  • Fluid shifts out of vascular space

  • BP decreases

  • Circulation impaired

Shock Cellular Patho Chain

• Any type of shock
  ↓

• Cells deprived of oxygen and nutrients
  ↓

• Impaired cellular metabolism
  ↓

• Acidosis
  ↓

• Compensation begins
  ↓

• If prolonged, compensation fails
  ↓

• Hypoxia worsens
  ↓

• Anaerobic metabolism
  ↓

• Metabolic acidosis
  ↓

• Ion pump failure
  ↓

• Sodium accumulates inside cells
  ↓

• Potassium leaves cells
  ↓

• Cell swelling, rupture, death
  ↓

• Multiple organ failure

Compensatory Mechanisms

• Sympathetic nervous system stimulation:

  • Increases HR

  • Increases contractility

  • Alters vessel tone

  • Vasodilates vessels to heart and brain

  • Vasoconstricts less vital areas

• RAAS stimulation:

  • Renin and angiotensin promote vasoconstriction.

  • Promotes sodium and water reabsorption.

  • Increases intravascular volume.

Goals of Compensation

1. Shunt blood to heart and brain.

2. Increase cardiac output through:

   • Increased intravascular volume

   • Increased HR

   • Increased contractility

Shock Clinical Manifestations

Early Cues Depend on Cause

• Cardiogenic shock/MI:

  • Chest pain

  • Shortness of breath

  • Labored breathing

  • Diaphoresis

  • Nausea

  • Vomiting

• Hypovolemic shock:

  • Related to amount of blood/plasma loss

• Septic shock:

  • Fever

  • Flushed, warm skin

• Anaphylactic shock:

  • Generalized skin flushing

  • Possible airway obstruction

Circulatory Collapse Cues

• Marked tachycardia

• Tachypnea

• Cool clammy extremities

• Poor peripheral pulses

• Decreased arterial BP

• Cyanosis

• Pallor

• Restlessness

• Apprehension

• Decreased mental function

• Poor urinary output

• General organ dysfunction

Shock Diagnostic Criteria

• No single test confirms shock.

• Diagnosis based on:

  • Patient history

  • Physical exam

  • Labs/diagnostics

• History may reveal:

  • MI

  • Massive hemorrhage

  • Systemic infection

  • Spinal cord injury

  • Anaphylaxis

• Physical assessment:

  • Skin color

  • Skin temperature

  • Pulses

  • Capillary refill

  • Heart rate

  • Blood pressure

  • Urine output

  • Mental status

• Cardiogenic shock labs/tests:

  • Cardiac enzymes

  • CBC

  • Electrolytes

  • ABGs

  • Coagulation tests

  • ECG

  • Echocardiogram

Shock Treatment

• Shock is a medical emergency.

• Priority: airway, breathing, circulation.

• Treatment depends on:

  • Shock cause

  • Fluid volume

  • Contractile ability of heart

• Hypovolemic patients:

  • Supine with legs elevated unless contraindicated

  • Blankets to keep warm

• Treatment focuses on correcting underlying cause.

Cardiogenic Shock Treatment

• Revascularize heart at obstruction point.

• Improve cardiac output.

• Maintain BP.

• Reduce heart workload.

• Provide oxygen.

• Regulate fluid volume.

• Inotropes increase myocardial contractility.

  • Epinephrine/norepinephrine: vasoconstricting effects

  • Dobutamine: vasodilating effects

Hypovolemic Shock Treatment

• IV fluid/blood replacement.

• Identify and correct bleeding/fluid loss.

• Oxygen depending on hypoxemia.

Septic Shock Treatment

• Treat infection source.

• Support circulation.

• Broad-spectrum antimicrobials.

• Vasopressors for vasoconstriction.

Anaphylactic Shock Treatment

• Corticosteroids may decrease systemic inflammatory response.

Neurogenic Shock Treatment

• Identify and correct cause if possible.

• Support vasoconstriction with inotropic medications.

All Shock Patients

• Frequent monitoring of:

  • Vital organ function

  • Hemodynamic status

Research Note: Pacemakers and Cell Phones

• Radio frequency energy from cell phones can potentially interfere with pacemakers.

• Called electromagnetic interference.

• Cell phones do not appear to pose significant risk.

• FDA advises:

  • Hold phone to ear opposite pacemaker side.

  • Do not carry phone in shirt/coat pocket directly over pacemaker.

• Testing continues.

Myocardial Infarction

Coronary Heart Disease

• CHD = any problem of impaired coronary circulation.

• Atherosclerosis is primary cause.

• Consequences range from:

  • Compensation through collateral circulation

  • Sudden death from myocardial anoxia

• Loss of coronary circulation may cause:

  • Impaired conduction

  • Impaired myocardial pumping

  • Heart failure

Myocardial Infarction Pathophysiology

• MI/heart attack = total occlusion of one or more coronary arteries causing ischemia and myocardial tissue death.

• Most common cause:

  • Atherosclerosis

• Atherosclerotic plaque can:

  • Directly obstruct artery

  • Break off and trigger platelet aggregation/thrombus formation

MI Risk Factors

• Family history

  • Male first-degree relative with MI/sudden coronary death before 55

  • Female first-degree relative before 65

• Hypertension and smoking

  • Injure endothelial lining

  • Promote atherosclerosis

  • Systolic BP above 160 mm Hg linked to threefold increased CHD risk

  • Diastolic elevations also significant

• Blood cholesterol

  • Especially high LDL

  • Promotes lipid vessel accumulation

• Diabetes mellitus

  • Type 2 diabetes associated with elevated blood lipids

• C-reactive protein

  • Inflammatory marker

  • High-sensitivity CRP used as risk indicator

  • Inflammation linked to atherosclerosis

• Hyperhomocysteinemia

  • Homocysteine from dietary amino acid in animal protein

  • Plays role in coagulation

  • High levels toxic to endothelial cells

  • May promote excessive coagulation and thrombus formation

  • About half of acute MI or stroke patients have hyperhomocysteinemia

MI Severity Depends On

• Size of occlusion

• Location of occlusion

• Duration of occlusion

• Presence of collateral circulation

Left Coronary Artery

• Supplies left side of heart.

• Branches:

  • Anterior descending left coronary artery

    • Mainly left ventricle

  • Circumflex left coronary artery

    • Mainly left atrium and parts of left ventricle

• Obstruction affects left ventricle and systemic pumping.

• Ventricular fibrillation is a major cause of sudden death from MI.

Right Coronary Artery

• Perfuses right side of heart.

• Also perfuses SA and AV nodes.

• Obstruction affects impulse conduction.

• Can cause rhythm irregularities.

• Right heart failure impairs venous return management.

Myocardial Oxygen Deprivation

• Myocardium can withstand oxygen deprivation for about 20 minutes.

• After that, cell death is irreversible.

• Necrotic myocardial cells are replaced by nonfunctional scar tissue.

MI Clinical Manifestations

• Chest pain

• Crushing pressure

• Pain radiating to:

  • Left arm

  • Shoulder

  • Jaw

• Dizziness

• Sweating

• Indigestion/heartburn pain

• Nausea

• Vomiting

• Fatigue

• Weakness

• Anxiety

• Cool moist skin

• Pallor

• Shortness of breath

• Patient may deny pain is MI-related.

• Women may have subtle/atypical cues:

  • Fatigue

  • Syncope

  • Weakness

Angina Pectoris

• Chest pain/pressure associated with myocardial ischemia.

• Caused by reduced coronary blood flow from atherosclerosis, often with vasospasm.

• Exacerbated by increased cardiac workload.

• Often reduced by rest.

• With MI:

  • Rest or nitroglycerin does not relieve angina.

MI Diagnostic Criteria

• Diagnosis based on:

  • Symptoms

  • ECG findings

  • Cardiac biomarkers

ECG Findings

• ST segment elevation may show ventricular repolarization problems.

• Larger infarcts may show prolonged Q wave.

Imaging/Procedures

• Angiography:

  • Determines obstruction location and extent.

• Echocardiography:

  • Shows wall motion abnormalities and ventricular function.

• Chest radiograph:

  • Detects complications such as CHF or pulmonary edema.

Cardiac Biomarkers

Troponin-T and Troponin-I

• Specific to cardiac muscle.

• Primary biomarkers for cardiac injury.

• Detected 6 to 8 hours after MI.

• Peak at 12 to 24 hours.

• Remain elevated 7 to 10 days.

CK-MB

• Cardiac-specific creatine kinase isoenzyme.

• Rises 4 to 9 hours after myocardial injury.

• Peaks at 24 hours.

• Returns to baseline in 48 to 72 hours.

Myoglobin

• Found in skeletal and cardiac muscle.

• Released 1 hour after injury.

• Peaks at 4 to 12 hours.

• Returns to normal soon after peak.

• Used with troponin or CK-MB to rule out MI if inconsistent with injury.

MI Treatment

• Initial goal:

  • Stabilize airway, breathing, circulation

• Rapid treatment within 90 minutes preferred to restore coronary perfusion.

• Before ED arrival:

  • IV access

  • Supplemental oxygen

  • Oral aspirin

• Aspirin and anticoagulants may improve coronary perfusion.

• Nitroglycerin and morphine for active chest pain.

• Emergency treatment may be medical or surgical.

Percutaneous Coronary Intervention

• Treatment of choice for many MI patients.

• Group of techniques to relieve coronary narrowing.

Percutaneous Transluminal Coronary Angioplasty

• Thin wire inserted into coronary artery via cardiac catheterization.

• Balloon inflated at obstruction site.

• Stenotic vessel pushed open.

• Stent often placed to keep vessel patent.

Other Treatments

• Coronary artery bypass surgery if other interventions fail.

• Thrombolytics + platelet inhibitor if PCI unavailable within 90 minutes.

• Continued:

  • Oxygen

  • Nitroglycerin

  • Analgesics

  • Aspirin

Long-Term Treatment

• Support:

  • Cardiac conduction

  • Cardiac output

  • Blood pressure

• Often includes:

  • Aspirin

  • Beta-blockers

  • ACE inhibitors

  • ARBs

• Lifestyle/risk modification:

  • No smoking

  • Reduced alcohol intake

  • Nutritious diet

  • Weight loss

  • Prescribed rest/exercise

Heart Failure

Definition

• Heart failure = inadequate heart pumping that fails to maintain blood circulation.

• Altered perfusion occurs due to:

  • Impaired cardiac function

  • Excess workload demands the heart cannot meet

• Heart failure occurs secondary to other conditions.

Conditions Causing Impaired Cardiac Function

• MI

• Structural heart defects

• Infection/inflammation of heart tissue layers

Conditions Increasing Heart Workload

• Hypertension

• Fluid volume overload

• Anemia

Heart Failure Pathophysiology

• Forward movement of blood is restricted.

• Causes congestion and edema in:

  • Pulmonary tissues

  • Peripheral tissues

• Cardiac reserve is used up even at rest.

• Simple tasks become taxing.

Left Heart Failure

• Left ventricle cannot meet cardiovascular demands.

• Forward blood movement is inhibited.

• Fluid accumulates in lung tissue.

Systolic Failure

• Loss of contractile ability.

• Heart cannot pump enough blood into circulation.

Diastolic Failure

• Stiff ventricle.

• Loss of relaxation ability.

• Heart cannot optimally fill between contractions.

Left Heart Failure Chain

• Left ventricle ineffective
  ↓

• Cannot eject enough blood into aorta
  ↓

• Blood backs up into pulmonary vein
  ↓

• Blood backs up into lung tissue
  ↓

• Pulmonary edema

Congestive Heart Failure

• Another term used to describe left heart failure.

Causes of Left Heart Failure

• Impaired left ventricular pumping:

  • MI

• Increased left ventricular workload:

  • Aortic valve disorders

  • Bicuspid/mitral valve disorders

  • Stenosis

  • Regurgitation

Right Heart Failure

• Begins on right side of heart.

• Impairs movement of deoxygenated blood to pulmonary circulation.

• Blood backs up into systemic circulation.

• Causes peripheral edema.

Dependent Edema

• Swelling occurs in dependent areas.

• Lower extremities most commonly affected.

Systemic Congestion Can Affect

• Liver

• Spleen

• GI tract

• Peritoneum

• Hepatic veins

• Portal circulation

Causes of Right Heart Failure

• Any process restricting blood flow into lungs.

• Cor pulmonale:

  • Alteration in right ventricular structure/function due to primary respiratory disorder.

• Lung problems implicated:

  • Lung injury

  • Infection

  • Inflammation

  • Pulmonary edema

• Common link:

  • Pulmonary hypertension

• Left heart failure can cause right heart failure due to pulmonary edema.

• Only primary lung conditions are termed cor pulmonale.

• Tricuspid and pulmonary valve defects can strain right ventricle.

Compensatory Mechanisms in Heart Failure

Improving Venous Return

• Vein tension increases.

• Blood movement forward improves.

• Preload increases.

• Cardiac output temporarily improves.

Sympathetic Nervous System Stimulation

• Increases:

  • Heart rate

  • Cardiac contractility

  • Vascular tone

• Goal: perfuse vital organs.

RAAS Stimulation

• Kidneys increase renin secretion.

• Angiotensin II increases.

• Vasoconstriction occurs.

Enlarging Heart Muscle

• Myocardial hypertrophy occurs due to workload demands.

• Initially improves contractility.

Why Compensation Becomes Harmful

• Prolonged venous congestion overwhelms compensation.

• Sympathetic stimulation can:

  • Trigger dysrhythmias

  • Reduce oxygen delivery to skin, muscle, kidneys

• Poor renal perfusion:

  • Increases sodium and water retention

  • Worsens venous return strain

• Aldosterone:

  • Increases sodium and water retention

• Myocardial hypertrophy:

  • Initially helps contractility

  • Eventually impairs diastole

  • Promotes myocardial oxygen deprivation

  • Makes myocardium noncompliant

  • Reduces chamber size

Heart Failure Clinical Manifestations

Left Heart Failure Cues

• May be absent early.

• Related to decreased cardiac output and pulmonary congestion.

• Pulmonary congestion:

  • Shortness of breath

  • Coughing

  • Lung crackles

• Poor tissue/organ perfusion:

  • Cyanosis

  • Exercise intolerance

  • Poor urinary output

  • Fluid and sodium retention

  • Anorexia

  • Fatigue

Right Heart Failure Cues

• May be absent or subtle early.

• Early:

  • Fatigue

  • Exertional dyspnea

  • Syncope with exertion

• Reflects inability to increase cardiac output and decreased systemic arterial pressure with exertion.

• Chest pain with exertion can occur from:

  • Right ventricular ischemia

  • Pulmonary artery stretching

• Advanced:

  • Anorexia

  • Weight loss

  • Gastric pain

  • Right upper quadrant pain

  • Jaundice

  • Extremity swelling

Heart Failure Diagnostic Criteria

• Based on:

  • Patient history

  • Physical exam

  • Clinical manifestations

• Chest radiography:

  • Detects pulmonary congestion

• Two-dimensional echocardiography:

  • Pumping ability

  • Chamber size/thickness

  • Valve abnormalities

  • Heart pressures

• ECG:

  • Conduction impairments

• Cardiac catheterization:

  • Structural defects

  • Pressure levels in heart chambers

• Severity based on activity restriction.

Heart Failure Treatment

• Focused on correcting cause when possible.

• Examples:

  • Replace defective valves

  • Treat respiratory infection

  • Treat anemia

• Many causes cannot be reversed.

• Lifestyle modifications:

  • Smoking cessation

  • Limit/stop alcohol

  • Salt restriction

  • Fluid restriction

  • Weight management

• Treatment goals:

  • Supplemental oxygen

  • Improve cardiac output

  • Correct volume overload

  • Reduce peripheral vascular resistance

  • Improve quality of life

• Heart failure is often chronic and progressive.

• Five-year survival rate approximately 50%.

Stroke

Definition

• Stroke = acute neurologic injury from impaired cerebral circulation.

• Can result from:

  • Shock

  • Cerebral hemorrhage

  • Ischemia

  • Infarction

• Also called cerebrovascular accident/CVA.

Major Risk Factors

• Hypertension

• Smoking

• Diabetes

Stroke Pathophysiology

Types

• Thrombotic stroke

• Embolic stroke

• Hemorrhagic stroke

Thrombotic Stroke

• Caused by occlusion of cerebral arteries.

• Often due to atherosclerosis.

• Common atherosclerosis site:

  • Common carotid artery bifurcation

Transient Ischemic Attack

• Transient neurologic dysfunction.

• Focal transient neurologic symptoms.

• Risk of permanent neurologic injury and stroke.

• Often caused by intermittent vascular obstruction.

Increased Stroke Risk After TIA

• Age greater than 60

• High blood pressure:

  • Systolic ≥140

  • Diastolic ≥90

• Stroke symptoms:

  • Unilateral weakness

  • Speech disturbance

• Symptoms lasting 1 hour or more

Completed Stroke

• Causes permanent neurologic deficits.

Embolic Stroke

• Emboli dislodge from distant sites.

• Travel to brain.

• Occlude small arteries.

Hemorrhagic Stroke

• Caused by cerebral bleeding.

• Causes:

  • Trauma

  • Cerebral vessel defects

  • Persistent hypertension

  • Neoplasia

• Bleeding fills and compresses:

  • Adjacent brain tissue

  • Brain ventricles

Cellular Stroke Patho Chain

• Blood flow disrupted to brain area
  ↓

• Ischemia and inflammation begin
  ↓

• Neurons lose perfusion within seconds-minutes
  ↓

• Neurons depolarize
  ↓

• ATP depleted
  ↓

• Membrane ion transport fails
  ↓

• Calcium influx triggers neurotransmitter release
  ↓

• Excitatory receptors on other neurons activate
  ↓

• More neurons depolarize
  ↓

• More calcium influx
  ↓

• More neural excitation and expanding ischemia
  ↓

• Destructive enzymes, free radicals, chemical mediators worsen injury
  ↓

• Infarct core forms within hours

Stroke Clinical Manifestations

• Abrupt onset of focal brain injury symptoms.

• Cerebral edema varies based on cellular injury.

• Loss of function depends on brain area affected.

• Hemorrhage near medulla can affect respiratory/cardiac centers and cause sudden death.

• Cerebellar stroke impairs coordination.

Common Stroke Cues

• Hemiparesis: weakness on one side

• Vision loss

• Visual field deficits

• Diplopia: double vision

• Dizziness

• Ataxia: lack of coordinated movement

• Aphasia: language impairment

• Sudden decreased level of consciousness

• Severe headache

• Sensory deficits

• Vomiting

Side-to-Side Rule

• Cerebral stroke on one side causes weakness/paralysis on opposite side.

• Example:

  • Left-sided weakness suggests right cerebrum obstruction/hemorrhage.

Stroke Diagnostic Criteria

• Based on:

  • Patient history

  • Physical exam

  • Labs/diagnostics

• If patient is aphasic:

  • Use observer reports for time of onset and symptom progression.

• Neurologic evaluation:

  • Mental status

  • Level of consciousness

  • Cranial nerves

  • Motor function

  • Sensory function

  • Cerebellar function

  • Gait

  • Deep tendon reflexes

• Stroke scales may quantify severity/progress.

Labs

• CBC

• Blood chemistry panel

• Coagulation studies

• Cardiac enzymes

Imaging

• CT scan

• MRI

• Used to identify:

  • Type of stroke

  • Location of infarction

• Imaging determines treatment path.

  • Thrombotic stroke may receive thrombolytics.

  • Hemorrhagic stroke does not receive thrombolytics.

Stroke Treatment

• Based on cause.

• Initial efforts:

  • Reduce cerebral edema

  • Reduce increased intracranial pressure

• Thrombotic/embolic stroke:

  • IV thrombolytic or anticoagulant therapy early

  • Long-term oral antithrombotic therapy to reduce recurrence

• Hemorrhagic stroke:

  • Prevent further bleeding

  • Aspirate accumulated blood if indicated

• Rehabilitation:

  • Adapt to reduced function

  • Maximize independence

Disseminated Intravascular Coagulation

Definition

• DIC = uncontrolled activation of clotting factors.

• Causes widespread thrombi formation.

• Followed by depletion of coagulation factors and platelets.

• Leads to massive hemorrhage.

Triggers

• Endothelial or tissue injury from:

  • Trauma

  • Surgery

  • Burns

  • Malignant neoplasms

  • Infections

  • Shock

  • Obstetric complications during labor/delivery

DIC Pathophysiology

• Injury triggers imbalance between clotting and fibrinolysis.

• Fibrinolysis = clot dissolution.

• Clotting factors, thrombin, and platelets accumulate throughout cardiovascular system.

• Especially dangerous in microcirculation.

• Microclots cause widespread tissue ischemia.

• Clotting mechanisms may become depleted.

• Clot-dissolving mechanisms may increase.

• Massive systemic hemorrhage can occur.

• DIC requires immediate recognition and treatment.

DIC Patho Chain

• Tissue/endothelial injury
  ↓

• Excess clotting activation
  ↓

• Widespread thrombi form
  ↓

• Microcirculation blocked
  ↓

• Tissue ischemia
  ↓

• Clotting factors/platelets depleted
  ↓

• Fibrinolysis increases
  ↓

• Massive bleeding/hemorrhage
  ↓

• Shock/organ failure risk

DIC Clinical Manifestations

• Effects vary depending on excessive clotting vs hemorrhage.

Acute Hemorrhagic DIC

• Caused by widespread clot dissolution from excess plasmin.

• Common causes:

  • Infection

  • Acute tissue injury

  • Obstetric complications

• Cues:

  • Bruising

  • Petechiae

  • Epistaxis

  • Blood in sputum

  • Blood in stool

  • Blood in emesis

  • Blood in urine

• Severe bleeding can cause hypovolemic shock.

Chronic/Subacute Clotting DIC

• Characterized by excess clotting/thrombin.

• More common with:

  • Malignancy

  • Chronic renal disease

  • Venous thrombosis

  • Certain connective tissue disorders

• Manifestations depend on thrombus location.

Organ-Specific Clotting Cues

• Brain:

  • Headache

  • Weakness

  • Seizures

  • Coma

• Kidneys:

  • Poor urine output

  • Renal failure progression

• Heart/lungs:

  • Cough

  • Shortness of breath

  • Respiratory distress

  • Chest pain

• Larger vessel occlusion:

  • Infarction in affected organ

DIC Diagnostic Criteria

• Must identify underlying cause:

  • Infection

  • Malignancy

  • Major trauma

  • Labor/delivery complication

  • Recent surgery

• Screening labs:

  • PT

  • PTT

  • Platelet count

  • Fibrinogen level

• D-dimer:

  • Measures fibrin degradation products

  • Significant for both thrombus formation and breakdown

  • Detects simultaneous thrombin and plasmin formation

  • Strongly suggests DIC

Coagulation Tests

PT

• Evaluates extrinsic clotting system.

• Includes factors:

  • I/fibrinogen

  • II/prothrombin

  • V

  • VII

  • X

• Expected range usually 11 to 14 seconds.

• Prolonged PT suggests deficiency in one or more factors.

PTT

• Evaluates intrinsic clotting system.

• Broader screening test.

• Factors:

  • I

  • II

  • V

  • VIII

  • IX

  • X

  • XII

  • XII listed in text

• Expected range approximately 22 to 34 seconds.

• Prolonged PTT is significant.

Fibrinogen

• Screens for factor I.

• Reduced fibrinogen commonly caused by DIC.

DIC Treatment

• Focused on correcting underlying cause.

• Depends on whether hemorrhage or thrombosis dominates.

• Goal: replace missing blood components.

• Massive clotting:

  • Anticoagulation therapy

• Massive hemorrhage:

  • Administration of clotting factors

  • Platelet replacement

• Treatment is a careful balance to restore appropriate coagulation.

Quick Review

Must-Know Facts

• Perfusion depends on:

  • Ventilation

  • Diffusion

  • Pulmonary circulation

  • Blood volume/components

  • Cardiac output

  • Cardiac conduction

  • Coronary circulation

  • Systemic circulation

  • Tissue oxygen uptake

• Cardiac output = stroke volume × heart rate.

• Blood pressure depends on cardiac output and peripheral vascular resistance.

• Altered perfusion means tissues are not adequately oxygenated at the capillary level.

• V/Q mismatch is the most common cause of hypoxemia.

• Atherosclerosis begins with endothelial/intimal injury.

• Virchow triad:

  • Vessel wall damage

  • Excessive clotting

  • Altered blood flow

• Infarct = necrotic tissue from sudden insufficient blood supply.

• Shock is circulatory failure and hypotension is late.

• MI is coronary artery occlusion causing myocardial tissue death.

• Heart failure causes congestion because forward flow is impaired.

• Stroke causes focal neurologic deficits based on brain area affected.

• DIC causes both clotting and bleeding.

Must-Know Cues

Altered Perfusion General Cues

• Cyanosis

• Edema

• Shortness of breath

• Tachycardia

• Tachypnea

• Fatigue

• Pain with ischemia

• Organ dysfunction

Hypertension Cues

• Often asymptomatic

• Headache

• Blurred vision

• Nausea/vomiting

• Confusion

• Mental status changes

• Poor urine output

• Hematuria/proteinuria

Shock Cues

• Tachycardia

• Tachypnea

• Cool clammy skin

• Weak pulses

• Low BP late

• Cyanosis/pallor

• Restlessness

• Decreased mental function

• Poor urine output

MI Cues

• Chest pain/pressure

• Pain radiating to left arm, shoulder, jaw

• Sweating

• Nausea/vomiting

• Shortness of breath

• Fatigue/weakness

• Cool moist skin

• Women may have subtle fatigue, syncope, weakness

Left Heart Failure Cues

• Pulmonary congestion

• Shortness of breath

• Cough

• Crackles

• Cyanosis

• Fatigue

• Poor urine output

Right Heart Failure Cues

• Peripheral edema

• Lower extremity swelling

• GI/liver congestion

• Right upper quadrant pain

• Jaundice

• Exertional dyspnea/syncope

Stroke Cues

• Sudden hemiparesis

• Aphasia

• Ataxia

• Diplopia

• Vision loss

• Dizziness

• Severe headache

• Vomiting

• Decreased level of consciousness

DIC Cues

• Bruising

• Petechiae

• Epistaxis

• Blood in sputum/stool/emesis/urine

• Poor urine output

• Respiratory distress

• Chest pain

• Seizures/coma in brain involvement

Must-Know Causes/Risk Factors

Hypertension

• Family history

• Aging

• Stress

• Diabetes

• High sodium

• Obesity

• Sedentary lifestyle

• Alcohol

• Smoking

• Kidney disease for secondary hypertension

MI

• Atherosclerosis

• Family history

• Hypertension

• Smoking

• High LDL

• Diabetes

• Inflammation/CRP

• Hyperhomocysteinemia

Shock

• MI → cardiogenic

• Hemorrhage/burns/diarrhea/polyuria → hypovolemic

• Infection → septic

• Brain/spinal injury/anesthesia/hypoglycemia/hypoxia → neurogenic

• IgE hypersensitivity → anaphylactic

Stroke

• Hypertension

• Smoking

• Diabetes

• Atherosclerosis

• Emboli

• Trauma/vessel defects/persistent hypertension for hemorrhagic stroke

DIC

• Trauma

• Surgery

• Burns

• Cancer

• Infection

• Shock

• Obstetric complications

Must-Know Pathophysiology Points

• Poor perfusion causes cellular hypoxia.

• Cellular hypoxia causes anaerobic metabolism and acidosis.

• Severe hypoxia causes ion pump failure, cell swelling, rupture, and death.

• Atherosclerosis narrows arteries and promotes thrombus formation.

• Thrombi can become emboli and cause infarction.

• Hypertension damages vessel intima and narrows vessel lumen over time.

• Shock starts with compensation but can spiral into organ failure.

• MI damage depends on artery blocked, duration of occlusion, and collateral circulation.

• Left heart failure backs blood into lungs.

• Right heart failure backs blood into systemic circulation.

• Stroke symptoms depend on location of brain ischemia/bleeding.

• DIC is dangerous because clotting factors get used up, causing both thrombi and hemorrhage.

Common Things Students May Confuse

• Perfusion vs ventilation

  • Ventilation = air movement.

  • Perfusion = blood flow to tissues.

• Pulmonary arteries vs pulmonary veins

  • Pulmonary arteries carry deoxygenated blood.

  • Pulmonary veins carry oxygenated blood.

• Systole vs diastole

  • Systole = contraction/ejection.

  • Diastole = relaxation/filling.

• S1 vs S2

  • S1 = AV valves close.

  • S2 = semilunar valves close.

• Preload vs afterload

  • Preload = filling/stretch before contraction.

  • Afterload = resistance to ejection.

• Thrombus vs embolus

  • Thrombus = clot attached in vessel.

  • Embolus = traveling plug.

• Ischemia vs infarction

  • Ischemia = reduced blood flow.

  • Infarction = tissue death from blood supply loss.

• Left vs right heart failure

  • Left = lungs.

  • Right = body/peripheral edema.

• TIA vs completed stroke

  • TIA = transient neurologic dysfunction.

  • Completed stroke = permanent neurologic deficit.

• DIC

  • Not just bleeding.

  • It is both uncontrolled clotting and later bleeding from depleted clotting factors.