Cardiovascular Effects, Dr. C Sedacca, 4/5/14

Cardiovascular Effects of Systemic

Diseases

Cassidy Sedacca, MS, DVM, DACVIM (Cardiology)

[email protected]

Lecture Outline

Short description of disease Cardiac pathophysiology Diagnostics

◦ Cardiopulmonary physical examination◦ ECG◦ Radiography◦ Echocardiography

Therapy Prognosis Key Point

Systemic Diseases

Endocrine◦ Hyperthyroidism◦ Hypothyroidism◦ Cushing’s disease◦ Addison’s disease◦ Pheochromocytoma◦ Acromegaly◦ Diabetes mellitus

Metabolic◦ Hyperkalemia◦ Hypokalemia◦ Hypercalcemia◦ Hypocalcemia◦ Anemia◦ Uremia

Infectious/Inflammatory◦ Viral

◦ Bacterial

◦ Protozoal

◦ Mycotic

Miscellaneous◦ GDV

◦ Traumatic myocarditis

Neoplasia◦ Hemoangiosarcoma

◦ Lymphoma

◦ Ectopic thyroid carcinoma

Hyperthyroidism

Most common systemic disturbance to affect cardiac function in cats

Disease of middle-aged to geriatric cats (unusual before age 6)

Generally caused by thyroid adenoma in cats

Rare in dogs◦ Thyroid tumors usually nonfunctional adenocarcinomas

Hyperthyroidism

Cardiac Pathophysiology◦ Positive inotropic effects

Increased sarcolemma Na,K-ATPase activity

Increased synthesis and enhanced contractile properties of myosin

Increased # of L-type calcium channels

◦ Positive chronotropic effects

Increased rate of SA node firing

Decreased threshold of atrial activation

Shortened refractory period of conduction tissue

Hyperthyroidism

Cardiac Pathophysiology◦ Increased responsiveness to catecholamines

Number of β-receptors increase

Changes in intracellular G-protein populations

◦ “High cardiac output state” CHF

Increased metabolic rate increased tissue oxygen demands requires greater CO

Increased intravascular volume (preload)

Peripheral vasodilation = decreased SVR (afterload)

Increased contractility and HR

Hyperthyroidism

Cardiac Pathophysiology◦ Systemic hypertension

73% of cats in one study

Occurs in spite of peripheral vasodilation

Consequence of increased SV and HR

◦ Myocardial hypertrophy

Increased myosin protein synthesis

Increased responsiveness to catecholamines

Chronic volume overload

Systemic hypertension

CO = SV x HRBP = CO x SVR

Hyperthyroidism

Cardiopulmonary Examination◦ Tachycardia, premature beats, gallop sound, systolic murmur, forceful precordial impulse, hyperdynamic femoral pulses, jugular venous distension, episodic dyspnea even without CHF

ECG◦ Sinus tachycardia (42%), tall R waves (22%), R-BBB (7%), left anterior fascicular block (4%), APCs (5%), atrial tachycardia or a-fib (2%), VPCs (1%)

◦ Ventricular tachycardia and AV block (rare)

Hyperthyroidism

Radiography◦ Mild to severe cardiomegaly (50%)

◦ CHF = pulmonary edema or pleural effusion (< 5%)

Echocardiography◦ Symmetrical LV concentric hypertrophy, hyperkinetic wall motion, increased aortic outflow velocity, normal LA size to mild dilation

◦ “Burnt-out” ventricle: wall thinning, fibrosis, LV dilation, poor contractility, severe LA dilation

Hyperthyroidism

LV concentric hypertrophy “Burnt-out” ventricle

Hyperthyroidism

Management of hyperthyroidism◦ Radioactive iodine

◦ Surgical: thyroidectomy

◦ Medical: methimazole, carbimazole

Management of arrhythmias◦ Start medical treatment

◦ Beta-blockers (atenolol) for most

Careful of negative inotropic effects if CHF

◦ If CHF, diltiazem or digoxin for atrial ectopy

Hyperthyroidism

Management of hypertension◦ Control of hyperthyroid state

◦ Beta-blockers (atenolol) or vasodilators (amlodipine)

Management of CHF◦ Diuretics (furosemide) and ACE-inhibitors (enalapril, benazepril)

◦ Ancillary drugs (diltiazem, atenolol, pimobendan, digoxin, etc.)

Hyperthyroidism

Prognosis◦ Favorable – ECG, echocardiography, and blood pressure changes are reversible in most cases

◦ Poor – “burnt-out” ventricle and CHF

Key Point

The net effects of hyperthyroidism on CV system are enhanced contractility, tachycardia, cardiomegaly,

LV hypertrophy, high cardiac output, systemic hypertension, and occasionally high-output heart failure.

Hypothyroidism

Common endocrinopathy in dogs Most common causes: idiopathic atrophy

and immune-mediated thyroiditis Clinical signs usually develop middle age Rare as a naturally occurring condition in

cats Cardiac effects rarely have severe

consequences◦ Can aggravate CHF and complicate the management of cardiac patients

Hypothyroidism

Cardiac Pathophysiology◦ Opposite of hyperthyroidism

◦ Negative inotropic effects

Decreased Na, K-ATPase activity

Decreased synthesis and contractile properties of myosin

Decreased # of β-receptors

◦ Negative chronotropic effects

Decreased rate of SA node firing

Increased threshold of atrial activation

Prolonged refractory period of conduction tissue

Hypothyroidism

Cardiac Pathophysiology◦ Alters cholesterol and lipid metabolism Can result in atherosclerosis (rare)

Hypercoagulability leading to myocardial infarction or systemic/pulmonary thrombosis

◦ Decreases metabolic rate thus lessening the “required” cardiac output Correcting hypothyroidism increased workload on heart

◦ Hypothyroidism decreases digoxin clearance, predisposing to digoxin toxicity

Hypothyroidism

Cardiopulmonary Examination◦ Bradycardia, arrhythmias, weak precordial impulse, weak femoral pulses

ECG◦ Sinus bradycardia◦ Low voltage QRS complexes◦ Atrial and ventricular arrhythmias ◦ AV block◦ Prolonged QRS duration◦ Inverted T waves

Hypothyroidism

Echocardiography◦ Mild to marked decreases in indices of contractility

◦ Can cause a secondary form of DCM

Always check thyroid status when depressed contractility is noted in a breed not predisposed to heritable/primary DCM

Hypothyroidism

Treatment◦ Levothyroxine

◦ Cautious with treatment in patients with CHF

Supplementation increases metabolic rate and thus work required by heart

Start with ¼ standard dose and increase it by ¼ dose weekly

Prognosis◦ Favorable – most cardiac changes are reversible

Key Point

Hypothyroidism rarely causes congestive heart failure but can exacerbate cardiac function if underlying cardiac disease

is present.

Key Point

Evaluate thyroid status in any dog in congestive heart failurewith an inappropriately slow heart rate.

Addison’s Disease

Potentially life-threatening endocrinopathy

Uncommon in dogs; rare in cats

More common in females

Usually young to middle age

Immune-mediated destruction within adrenal gland◦ Zona glomerulosa = aldosterone

◦ Zona fasciculata = cortisol

Addison’s Disease

Cardiac Pathophysiology◦ Cortisol needed to maintain vascular integrity and responsiveness to catecholamines

Cortisol deficiency predisposes to hypotension

◦ Cortisol has a mild positive inotropic effect

Addison’s Disease

Cardiac Pathophysiology◦ Aldosterone acts on distal renal tubule and collecting duct to enhance Na+ retention and K+ excretion

Deficiency = hyponatremia and hyperkalemia

Hyponatremia intravascular fluid shifts causing

hypovolemia and hypotension

Hyperkalemia alters cardiac conduction and

repolarization leading to bradycardia and various dysrhythmias

Addison’s Disease

Hyperkalemia◦ Early: increases in Ikr affects repolarization phase (phase 3) of action potential Peaked T waves, QT interval shortening

◦ Persistent: reduces RMP inactivates INa

decreases rate of phase 0 of action potential reduction in myocardial conduction Prolongation of P wave, PR interval, and QRS complex

Loss of P wave and progressive widening of QRS

Sinoventricular rhythm (“atrial standstill”)

◦ Eventually: Ventricular fibrillation and asystole

Na+inK+out

RMP _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _

Addison’s Disease

Cardiopulmonary Examination◦ Weakness, collapse, dehydration, hypothermia, slow CRT, bradycardia, weak femoral pulses

ECG◦ Previously discussed

Radiography◦ Signs of hypovolemia

◦ Small caudal vena cava

◦ Microcardia

◦ Decreased pulmonary vascular markings

Addison’s Disease

Addison’s Disease

Addisonian Crisis Therapy◦ Volume replacement (0.9% saline)

◦ Glucocorticoid replacement (methylprednisolone, dexamethasone)

◦ Mineralocorticoid replacement (DOCP, Florinef)

◦ Hyperkalemia Calcium gluconate – counteracts effects on conduction

tissue; no effect on serum K+ levels

Saline infusion – causes rapid dilution of serum K+

NaHCO3 (if pH ≤ 7.0) – moves K+ inside cell by correcting acidosis

50% dextrose – stimulates endogenous insulin secretion which moves K+ inside cell

Regular insulin – moves K+ inside cell

Addison’s Disease

Maintenance Therapy◦ DOCP + Prednisone

◦ Florinef + Prednisone

Prognosis◦ Excellent with therapy

Key Point

Net CV effects are hypovolemia, systemic hypotension, altered cardiac conduction, and depressed myocardial function.

Cushing’s Disease

Common endocrinopathy in older dogs; rare in cats

Excessive cortisol levels◦ Pituitary (80-85%) – excess ACTH release

No sex predilection

◦ Adrenal – functional adrenocortical tumors

Females affected more frequently

◦ Rarely produces significant cardiac disease

◦ Systemic effects can exacerbate underlying cardiac disease

Cushing’s Disease

Cardiac Pathophysiology◦ Systemic hypertension Present in 57-82% of cushingoid dogs

Cortisol increases SVR by increasing smooth muscle sensitivity to catecholamines and increasing production of angiotensinogen

Can cause secondary LV concentric hypertrophy

Increased afterload can exacerbate mitral regurgitation

Cortisol enhances renal reabsorption of Na+ and secondary fluid retention increases intravascular volume

Cushing’s Disease

Cardiac Pathophysiology◦ Concentric hypertrophy of left ventricle

Primary – exact cause unknown

Secondary to systemic hypertension

Can lead to diastolic myocardial dysfunction but rarely causes CHF if concomitant heart disease not present

Cushing’s Disease

Cardiac Pathophysiology◦ Thromboembolism

Both pulmonary and systemic

High incidence of PTE in cushingoid patients

Cause of distal aortic thrombus in dogs

Cushing’s disease clearly causes hypercoaguability◦ Higher levels of clotting factors II, V, VIII, IX, XI,

protein C, protein S decreases aPTT

◦ Impaired fibrinolytic capacity increases clot lysis

time

Cushing’s Disease

Cardiac Pathophysiology◦ Panting/tachypnea/mild dyspnea

Altered ventilation mechanics

Weakness in muscles of respiration

Increased thoracic fat deposition decreases

chest wall compliance

Increased diaphragmatic abdominal pressure from excessive adipose tissue and hepatomegaly

+/- concurrent lower airway disease or pulmonary parenchymal disease

Cushing’s Disease

Cardiopulmonary Examination◦ Abdominal distension, hepatomegaly, muscle

weakness, obesity

ECG – no characteristic changes Radiography

◦ Calcification of tracheal and bronchial rings

◦ Osteoporosis of thoracic vertebrae

◦ Rarely metastatic pulmonary lesions from adrenal tumors

◦ Changes associated with PTE

Echocardiography◦ Primary or secondary LV concentric hypertrophy

Cushing’s Disease

Therapy◦ Pituitary dependent

Mitotane Trilostane

◦ Adrenal dependent Surgical removal of affected adrenal gland(s) Medical therapy

Prognosis◦ Excellent for resectable, benign adrenal tumors ◦ Poor for non-resectable or metastatic adrenal tumors◦ Most dogs with PD respond well to therapy◦ Systemic hypertension usually resolves with control

of hypercortisolism

Key Point

Hypercortisolism exacerbates concomitant heart disease by activating the RAAS, increasing intravascular volume,

increasing SVR (afterload), and potentially causing systemic hypertension and left ventricular concentric hypertrophy.

Acromegaly

Hypersomatotropism = abnormally high levels of growth hormone

Rare endocrinopathy in cats◦ Much more common in males

◦ Functional pituitary adenoma

Associated with generalized organomegaly◦ Increased protein synthesis and reduction in protein catabolism

◦ Modulation in glucose utilization and storage (often associated with diabetes)

Acromegaly

Acromegaly

Cardiac Pathophysiology◦ Myocardial hypertrophy, interstitial fibrosis,

myocytolysis, intramural arteriosclerosis

◦ Systemic hypertension

Cardiopulmonary Examination◦ Systolic murmur, gallop sound, signs of CHF

ECG – no characteristic changes Radiography

◦ Cardiomegaly

◦ Pulmonary edema and/or pleural effusion (CHF)

Echocardiography◦ LV concentric hypertrophy

Acromegaly

Acromegaly

Treatment◦ Surgery – hypophysectomy◦ Medical – somatostatin analogue (hypothalamic hormone that inhibits GH release from pituitary)

◦ Radiation – seems to be the best treatment option thus far

Prognosis◦ Survival ranges from 4 to 60 months◦ Most die or euthanized from CHF, renal failure, or expanding pituitary tumor

Pheochromocytoma

Catecholamine-secreting tumors derived from chromaffin cells of adrenal medulla

Excessive epinephrine and norepinephrine

Uncommon in dogs, extremely rare in cats

Usually older dogs

Locally invasive

Pheochromocytoma

Cardiac Pathophysiology◦ Alpha-1, beta-1, and beta-2 adrenergic agonistic effects of epinephrine and norepinephrine

Beta-1 (cardiac): positive inotropic, chronotropic, and dromotropic effects

Beta-2 (vessel): venous and arteriole vasodilation

Alpha-1 (vessel): venous and arteriole vasoconstriction◦ Dominant effect varies with receptor density

Pheochromocytoma


Alpha predominates in vascular smooth muscle so systemic hypertension is common (~50% of dogs)

◦ Arrhythmias from excessive catecholamines

Promote all 3 “mechanisms” of arrhythmias

Myocardial injury

Coronary vasoconstriction ischemia

◦ Local invasion into caudal vena cava

Thrombosis

Pheochromocytoma

Cardiopulmonary Examination◦ Clinical signs often episodic

◦ Collapse, syncope, weakness

◦ Pale MM, tachycardia, arrhythmias, pulse deficits

ECG◦ Nonspecific ST segment changes – myocardial

ischemia/hypoxia

◦ Sinus tachycardia very common

◦ Arrhythmias – APCs, VPCs, SVT, VT, etc.

Radiography and Echocardiography◦ Nonspecific

Pheochromocytoma

Therapy◦ Systemic hypertension

Alpha-blocking agents

Phenoxybenzamine (oral), Phentolamine (IV) –non-selective

Prazosin (oral) – alpha-1 only

◦ Tachyarrhythmias

Beta-blocking agents

Propranolol (oral, IV) – non-selective

Atenolol (oral), esmolol (IV) – beta-1 only

◦ Surgical removal definitive treatment

Key Point

Use of a beta-blocker without an alpha-blocker can cause severe hypertension.

Diabetes Mellitus

Insulin deficiency or resistance

CV system of dogs and cats is relative immune to the effects of hyperglycemia compared to humans

Humans ◦ Systemic hypertension

◦ Arrhythmias

◦ Coronary atherosclerosis

◦ Myocardial infarction

◦ “Diabetic cardiomyopathy”

Diabetes Mellitus


46% of dogs in one study

Severity associated with duration of disease in dogs

Less common in cats

Cause: not known◦ Changes in vascular compliance

◦ Changes in lipid profile

◦ Microangiopathy affecting the basement membrane

Diabetes Mellitus

Cardiac Pathophysiology◦ “Diabetic cardiomyopathy” Humans – myocardial hypertrophy, fibrosis, coronary microvascular endothelial proliferation, glycoprotein accumulation

Mild in humans without macrovascular coronary disease and systemic hypertension

Mild subclinical systolic myocardial dysfunction in dogs with experimental diabetes

Diastolic dysfunction mild and inconsistent in dogs

CHF not reported in dogs or cats

Increased risk for coronary artery disease notdemonstrated in dogs or cats

Key Point

Decreased cardiac performance in dogs and cats with diabetes is mild and unlikely to cause clinical problems unless accompanied by other forms of heart disease.

Hyperkalemia

95% of body K+ is intracellular ◦ 2-5% extracellular◦ Serum K+ values are not always reliable indicator of total body stores

Clinical causes◦ Decreased renal elimination (renal failure)◦ Ruptured urinary tract, urethral obstruction◦ Reperfusion injury (ie, aortic thromboembolism)

◦ Addison’s disease◦ Metabolic acidosis◦ Drugs (spironolactone, ACE-inhibitors)◦ Excessive supplementation

Hyperkalemia

Diagnosis, Therapy, and Prognosis◦ ECG changes discussed earlier

Depend on magnitude and rate of development

Poor correlation between serum K+ level and ECG changes

◦ Identification and treatment of underlying cause essential

Ancillary treatments during crisis

Hyperkalemia

Hypokalemia

Severe K+ loss leads to muscle weakness or paralysis

Clinical causes◦ Decreased intake (anorexia, K+ deficient fluids)

◦ Excessive GI loss (chronic vomiting, diarrhea)

◦ Overuse of enemas

◦ Excessive urinary loss (renal disease, drugs)

◦ Hyperaldosteronism (primary: tumor vs. secondary: liver failure, nephrotic syndrome)

◦ Metabolic alkalosis

Hypokalemia

Cardiac Pathophysiology◦ Hyperpolarization of nerve and myocyte cell

membrane, thus increasing RMP

◦ Delayed/abnormal repolarization

◦ Increased action potential duration

◦ Increased automaticity

ECG◦ Prolonged QT interval

◦ ST segment depression

◦ U wave (repolarization of

papillary m. and Purkinje

fibers)

◦ Ventricular arrhythmias

Hypokalemia

Tilley LP: Essentials of canine and feline electrocardiography, 3rd ed., 1992

Hypokalemia

Cardiopulmonary Examination◦ Muscle weakness

◦ Depression

◦ Ventroflexion of neck in cats

◦ Arrhythmias

Therapy◦ Treat underlying disease process

◦ Parental replacement

Do not exceed 0.5 mEq/kg/hr

◦ Oral supplementation if needed

Hypokalemia

Key Points◦ Increased likelihood of digoxin toxicity

Digoxin competes with K+ for same binding site on the Na+/K+-ATPase

◦ Increased risk of ventricular arrhythmias

◦ Decreased effectiveness of Class I antiarrhythmic agents (lidocaine, mexiletine, procainamide)

Hypercalcemia

Clinical causes◦ Normal in young, growing puppies◦ Paraneoplastic (lymphoma, anal sac carcinoma)◦ Addison’s disease◦ Renal failure◦ Skeletal lesions (osteomyelitis, multiple myeloma)

◦ Nutritional (hypervitaminosis D)◦ Primary hyperparathyroidism ◦ Severe hypothermia◦ Lab error

Hypercalcemia

Cardiac Pathophysiology◦ Little, if any, direct adverse effect on cardiac function

◦ Very high levels can cause arrhythmias

◦ Long-standing may predispose to calcification of myocardium, blood vessels, and other soft tissues (“metastatic calcification”)

Cardiopulmonary Examination◦ None specific

Hypercalcemia

ECG◦ ECG changes do not correlate closely with serum calcium concentration

◦ Short QT interval

◦ Sinus bradycardia

◦ Ventricular irritability and fibrillation at very high levels

Radiography/Echocardiography◦ None specific

Hypercalcemia

Therapy◦ IV fluids (0.9% saline) – promote renal excretion

◦ Calcitonin – parafollicular cells of thyroid (opposite of parathyroid hormone)

◦ Furosemide – promote renal excretion

◦ Corticosteroids – decrease intestinal absorption, limit bone resorption, increase renal excretion

◦ Bisphosphonates – limit osteoclastic resorption

Hypocalcemia

Clinical causes◦ Eclampsia

◦ Renal failure

◦ Acute pancreatitis

◦ Hypoparathyroidism

◦ Bilateral thyroid gland removal

◦ Post-op parathyroid tumor removal

◦ Ethylene glycol toxicity

◦ Hyperphosphatemia

◦ Relative (due to hypoalbuminemia)

Hypocalcemia

Cardiac Pathophysiology◦ Excitatory effect on nerve and muscle cells

Neuromuscular irritability, tetany, and seizures

◦ Decreased contractility

Only clinically important if concurrent heart disease

◦ Acute reductions can result in severe hypotension leading to cardiovascular shock

Cardiopulmonary Examination◦ None specific

Hypocalcemia

Synchronous diaphragmatic flutter◦ Synchronous contraction of the diaphragm with the heart beat

◦ Rhythmic abdominal contractions with heart beat

◦ Excitation of pericardial segment of phrenic nerve(s) by electrical activity of heart

◦ Most commonly seen in patients that are hypocalcemic from persistent vomiting

◦ Cause unknown – alkalosis or hypocalcemialeading to hyperirritability of phrenic nerve

Tiley LP, 1992.

Hypocalcemia

ECG◦ Classic: QT prolongation

Therapy◦ Calcium gluconate IV

while monitoring ECG

Slowly (15-30 min)

Temporarily stop if

bradycardia or ST segment elevation

Reinstate at slower rate

◦ Oral vitamin D

Increases intestinal Ca+2 absorption

Key Point

Calcium is cardiotoxic if replaced too quickly; even a normal serum concentration may be toxic if replaced too rapidly

Anemia

Sign of disease; not a disease entity

Symptoms of “reduced cardiac reserve”◦ Severity of anemia

◦ Rate of development

◦ Presence and extent of underlying cardiac disease

Anemia

Cardiac Pathophysiology◦ O2 delivery to tissues, blood viscosity SVR RAAS, ADH, SNS Na+ and H2O retention HR, SV, SVR CO and BP

◦ Depends on developmental rate of anemia

Acute – hypovolemic shock

Chronic – volume overload to all four cardiac chambers (eccentric hypertrophy), tachycardia,

SVR, increased myocardial oxygen demands

◦ Rarely causes CHF but certainly can exacerbate subclinical/pre-existing heart disease

Anemia

Cardiopulmonary Examination◦ Lethargy, exercise intolerance, weakness, collapse, syncope, stupor, exertional dyspnea

◦ Strong precordial impulse, hyperdynamicfemoral pulses (bounding), pale/icteric MM, prolonged CRT

◦ Soft (grade I-II/VI) systolic heart murmur due to blood viscosity and SV

Radiography◦ Cardiomegaly◦ Rarely, pulmonary venous distension, pulmonary edema, pleural effusion (CHF)

Anemia

ECG◦ Sinus tachycardia◦ Evidence of LV or LA enlargement (prolonged P wave or QRS duration, increased R wave amplitude)

◦ Ventricular arrhythmias from tissue (myocardial) hypoxia

Echocardiography◦ LV, LA, RV, and RA chamber dilation (volume overload)

◦ Hyperdynamic systolic myocardial function

Anemia

Therapy◦ Treatment depends on underlying cause

◦ Cautious with IV fluids when cardiomegaly present in the face of significant anemia

◦ If blood transfusion needed, packed RBCs are preferred b/c of smaller volume

◦ Furosemide if CHF present

Often can be discontinued once anemia corrected

Uremia

Clinical manifestation of azotemia

Can effect cardiac function

Reduce elimination of many cardiac drugs

Uremia

Cardiac Pathophysiology◦ Systemic hypertension common in CRF of both dogs (50-93%) and cats (65%)

◦ RF can cause elevations or reductions of K+ and Ca+2

Associated ECG changes

◦ Volume overload from chronic anemia

◦ Secondary pericarditis

Serositis of parietal pericardium

Small volume pericardial effusion

Uremia

Cardiac Pathophysiology◦ Pulmonary or systemic thromboembolism

Protein-losing nephropathy (antithrombin)

◦ Uremic pneumonitis

Rare cause of non-cardiogenic pulmonary edema

Uremia

Cardiopulmonary Examination◦ Uremic pneumonitis can cause dyspnea

◦ Metabolic acidosis can cause compensatory hyperventilation (tachypnea)

◦ Both can be confused with signs of CHF

ECG◦ Nonspecific

Electrolyte abnormalities

Pericardial effusion (decreased R wave amplitude)

◦ Conduction abnormalities (high grade 2nd or 3rd

degree AV block in cats???)

Uremia

Radiography◦ None specific

Echocardiography◦ LV concentric hypertrophy secondary to systemic hypertension

◦ Volume overload from chronic anemia

◦ Small volume pericardial effusion

Therapy◦ IV fluids, protein/P restriction, phosphate binders, calcitriol, erythropoietin

Uremia

Uremia

Challenge of managing azotemia with concurrent heart disease◦ “Cardiorenal Syndrome” in people

◦ Azotemia both pre-renal and renal

◦ Two subsets of patients

Subclinical heart disease

Congestive heart failure

◦ Uremic and currently in CHF?

No – reduce diuretic doses, improve cardiac output, or administer parental fluids

Yes – “rock and a hard place” unless Ultrafiltration

Uremia

Therapeutic considerations in azotemicpatients with heart disease◦ Use IV fluids cautiously

Slowly correct azotemia by reducing fluid rates

Consider low-Na+ fluids (half-strength saline)

Continually monitor for CHF (body weight, RR, thoracic auscultation, radiographs)

◦ No reason for simultaneous diuretic and parental (IV/SQ) fluid administration

Uremia

Therapeutic considerations in azotemicpatients with heart disease◦ Reduce doses of renally-excreted drugs Digoxin, sotalol, atenolol

◦ Careful with ACE-inhibitors Angiotensin II causes preferential vasocontrictionof efferent arteriole of glomerulus

Enalapril vs Benazepril

Safe to use other vasodilators (pimobendan, amlodipine, hyralazine, prazosin)

Spironolactone (aldosterone antagonist) as an alternative

Myocarditis

Inflammation involving cardiomyocytes, interstitium, or coronary vessels

Myocardial injury1. Direct invasion by an infectious agent

◦ Fungal, Toxoplasma, Neospora, Trypanosoma, Bartonella, viral (parvovirus, distemper virus, others)

2. Myocardial toxin produced by the agent◦ Trypanosoma, bacterial (endotoxin)

3. Secondary immune-mediated reaction◦ Vaccine, Lyme, rickettsial, bacterial (sepsis), neoplasia,

idiopathic/auto-immune

Myocarditis

Wide range of clinical disease◦ Subclinical myocarditis

◦ Array of arrhythmias and conduction abnormalities

◦ Secondary DCM-phenotype leading to CHF

Cardiac troponin-I◦ Released with cardiomyocyte damage, swelling, or necrosis

◦ Highly specific (compared to CPK) but notsensitive

Myocarditis

ECG◦ Supraventricular or ventricular ectopy◦ Bundle branch block◦ High-grade 2nd or 3rd degree AV block

Echocardiography◦ No changes at all◦ Acute – hypoechoic or mottled myocardium with concentric hypertrophy, small volume pericardial effusion

◦ Chronic – dilated chambers with decreased contractility and thin walls (2o DCM)

Myocarditis

ChronicAcute

Myocarditis

Therapy◦ Treat the primary agent IF KNOWN

◦ Treatment usually supportive and focused on the most prominent systemic manifestation

◦ Often permanent/irreversible damage even if treated appropriately

Prognosis◦ Highly variable

Key Point

If an underlying infectious agent cannot be determined, anti-inflammatory doses of corticosteroids are

often administered.

Gastric Dilation-Volvulus

Life-threatening emergency in dogs

Most common in large, deep-chested dogs

Exact etiology yet to be determined◦ Exercise following a large meal

Arrhythmias in up to 40% of cases◦ Most are ventricular

◦ Usually occur within 36 hours of admission

◦ Presence of arrhythmias does not worsen prognosis


Cardiac Pathophysiology◦ Exact mechanism for arrhythmias not known

◦ Theories

Acid-base imbalances

Electrolytes imbalances

Autonomic nervous system imbalances

Myocardial hypoxia

Myocardial depressant factor


Cardiopulmonary Examination◦ Pale MM, weak pulses, tachycardia, arrhythmias, signs of shock

ECG◦ All types of ventricular arrhythmias

Accelerated idioventricular rhythm most common

◦ Occasionally atrial arrhythmias

◦ ST segment changes myocardial

ischemia/hypoxia


Accelerated idioventricular rhythm◦ Wide, bizarre rhythm

◦ Rate similar to sinus rate (< 160 bpm)

◦ As sinus rate slows, ventricular rate may “capture” the heart rhythm

◦ Fusion beats common


Radiography◦ Microcardia and small caudal vena cava

◦ Decreased venous return

Therapy◦ Gastric decompression

◦ Shock therapy

◦ Treatment of arrhythmias

See above

Lidocaine for malignant ventricular ectopy

Traumatic Myocarditis

Arrhythmias that occur following blunt trauma

Trauma does not have to occur directly to chest

Exact mechanism for arrhythmias notknown◦ Direct damage to myocardium from trauma not necessary

◦ Autonomic nervous system imbalances?◦ Reperfusion of ischemic tissue?


ECG◦ All types of ventricular arrhythmias Accelerated idioventricular rhythm common

◦ Supraventricular arrhythmias

Therapy◦ Main goal is supportive care (pulmonary contusions, shock, hemorrhage, pain, etc.)

◦ Treatment of arrhythmias if hemodynamically significant Causing tachycardia, hypotension, malignant characteristics, etc.


PPVP Diniz, DS Schwartz, RC Collicchio-Zuanaze. Arq. Bras. Med. Vet. Zootec, 59: 2007


Treatment of ventricular arrhythmias◦ Lidocaine – class Ib (Na+ blocker)

◦ Procainamide – class Ia (Na+ blocker)

◦ Esmolol – class II (beta-blocker)

◦ Magnesium chloride

Treatment of supraventricular arrhythmias◦ Diltiazem – class IV (Ca+2 blocker)

◦ Esmolol

◦ Procainamide


Prognosis◦ Arrhythmias generally resolve after 2-5 days and do not require maintenance oral therapy

◦ Arrhythmias generally not lethal

◦ Progression of underlying disorders, not arrhythmias, usually lead to patient’s demise

Systemic Neoplasia

Systemic neoplasia with a cardiac manifestation◦ Hemangiosarcoma

◦ Lymphoma

◦ Ectopic thyroid carcinoma

Clinical signs◦ Pericardial effusion/cardiac tamponade

◦ CHF from myocardial dysfunction or ventricular inflow or outflow obstruction

◦ Arrhythmias

Hemangiosarcoma

Originates from endothelial cells

Systemic sites of origin◦ Spleen, liver, lungs, skin, etc.

Can be seen in any portion of heart◦ Right atrium and right auricle most common

Metastasis is common

Most common in large breed dogs

Rare in cats

Hemangiosarcoma

Lymphoma

Most common tumor that metastasizes to heart in cats

Infiltrative myocardial disease◦ Ventricular hypertrophy

◦ Severe changes to myocardial architecture and echogenicity

◦ Can produce a well-defined mass

◦ Pericardial effusion

Thank You!

Cardiovascular Effects, Dr. C Sedacca, 4/5/14

Health & Medicine

Transcript of Cardiovascular Effects, Dr. C Sedacca, 4/5/14